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feat: reorganized articles

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Nick 2024-09-16 17:29:06 -05:00
parent 4a51ade97e
commit 6afc244c09
94 changed files with 20159 additions and 34671 deletions
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2
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@ -42,6 +22,11 @@
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https://x.com/DrGaryMcGowan/status/1835376100836348042

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Recently, a controversial paper reviewing both the health and environmental benefits of animal foods was published to the journal, Animal [[1](https://pubmed.ncbi.nlm.nih.gov/35158307/)]. This was brought to my attention by one of my patrons, who specifically requested that I respond to the first section of the article, titled "why the nutritional case against animal source foods may be overstated". My response was originally supposed to be a reaction video for my patrons. But, the more of the paper that I read, the more I realized that this would require a much more systematic appraisal.
Although I have only reviewed one section of the paper, I am told that the rest of the paper is also filled with questionable claims, falsehoods, half-truths, and dubious reasoning. As such, I will leave it to people with more domain knowledge to comment on the latter sections of the paper. As for the section that I was tasked with critiquing, I'm completely comfortable with systematically evaluating the claims contained within it. So, let's get into it.
> "Even though advocacy for moderate to heavy restriction [of animal foods] is echoed by various public heath institutions worldwide, suggesting apparent consensus, the scientific debate is not settled as the evidence has been challenged by various scientists, both for red meat (Truswell, 2009; Hite et al., 20100; Alexander et al., 2015; Klurfeld, 2015; Kruger & Zhou, 2018; Händel et al., 2020; Hill et al., 2020; Johnston et al., 2019; Leroy and Cofnas, 2020; Sholl et al., 2021)"
**Weasel words:**
Citing a couple of authors to represent the "public heath institutions" that advocate for animal food restriction, whilst also citing ten authors who challenge this notion, is a painfully misleading move. The evidence for reducing most animal foods is actually extensive, with only a small handful of exceptions. Not only that, but it's also questionable whether or not any public health institutions actually advocate for the moderate or heavy restriction of these exceptions. It's unclear, because the terms "moderate" and "heavy" are not clearly defined.
**Motte and Bailey:**
The paragraph began by referencing the presumed attitudes of "public health institutions" toward animal foods more broadly. A truly extraordinary claim that is not supposed by any of the their reference material. They then follow it up by citing authors who have pushed back specifically on these institutions' attitudes toward red meat and saturated fat. Most public health institutions that are concerned with nutrition do indeed advocate for the restriction of these foods.
> "...and saturated fat, which is not exclusive to animal source foods (Astrup et al., 2020; Krauss & Kris Etherton, 2020)."
**Red herring:**
While there are some plant foods that are high in saturated fat, we need not consume them. Those sources of saturated fat can be avoided on an animal food restricted diet. This is less true of the animal foods that these authors are specifically attempting to defend. Not only that, but no public health institutions are advocating for the consumption of plant foods like coconut or palm oil. So, I'm not even sure what this point is meant to address.
> "Among other concerns, one of the objections is that pleas for restriction are based on conflicting findings and observational relationships that are not necessarily causal, suffering from confounding and bias (Grosso et al., 2017; Händel et al., 2020; Hill et al., 2020; Leroy & Barnard, 2020; Nordhagen et al., 2020)."
**Potential contradiction:**
Confounding is a causal concept. All posited confounders need to be validated as genuine confounders using evidence that meets these authors' bar for causal inference. Otherwise we don't have a reason to consider them confounders at all. The truth is that virtually all accepted confounders in this domain are validated via epidemiological data itself. I can formalize the argument like this:
**P1)** If evidence that is stronger than the best animal food epidemiology is required to demonstrate causality and confounding is a causal concept, then evidence that is stronger than the best animal food epidemiology is required to validate potential confounders.
**(E∧C→P)**
**P2)** Evidence that is stronger than the best animal food epidemiology is required to demonstrate causality.
**(E)**
**P3)** Confounding is a causal concept.
**(C)**
**C)** Therefore, evidence that is stronger than the best animal food epidemiology is required to validate potential confounders.
**(∴P)**
In the above syllogism, the authors could very easily be affirming E and ¬E. If the authors are rejecting epidemiological evidence while simultaneously positing confounders that will be validated with epidemiological evidence, their position would entail a contradiction.
> "Unwarranted use of causal language is nonetheless widespread in the interpretation of nutritional epidemiological data, thereby posing a systemic problem and undermining the field’s credibility (Cofield et al., 2010; Ioannidis, 2018)."
**Red herring:**
Firstly, there is no reference for the claim that causal language is widespread in the interpretation of nutritional epidemiological data. Secondly, even if it were true, nutritional epidemiology has excellent validation for both its results as well as the underpinning methodology, considering its limitations and shortcomings.
If the goalpost for causal inference is human experiments, then the use of causal language is likely to be warranted more often than it is unwarranted. This is due to the high degree of concordance between the results of nutritional epidemiology and randomized controlled trials [[2](https://pubmed.ncbi.nlm.nih.gov/34526355/)][[3](https://pubmed.ncbi.nlm.nih.gov/23700648/)][[4](https://pubmed.ncbi.nlm.nih.gov/34308960/)]. Regardless, it's not clear how the widespread use of causal language poses either a systemic problem or undermines the field's credibility. Again, it just isn't clear what the point of these claims is supposed to be.
> "Moreover, the associations between red meat and metabolic disease have not only been evaluated as weak..."
**Red herring:**
It is not true that these associations are weak. When meta-analytically summated the associations are often close to linear. Not only for total mortality but also for many major chronic diseases [[5](https://pubmed.ncbi.nlm.nih.gov/28446499/)][[6](https://pubmed.ncbi.nlm.nih.gov/29039970/)][[7](https://pubmed.ncbi.nlm.nih.gov/28397016/)]. The associations generally only appear weak when there are certain sources of bias present, such as inadequate exposure contrasts, follow-up times, participant numbers, or even overadjustment for mediators.
> "...translating into small absolute risks based on low to very low certainty evidence (Johnston et al., 2019)..."
**Red herring:**
Absolute risk and certainty are concepts that don't strongly interact. You can have low absolute risks and a high degree of certainty, such as with successful human trials with event-based stopping conditions. You can also have high absolute risks and low certainty, such as with underpowered human studies with high event rates.
It's also not clear why the authors would choose to favour absolute risk over relative risk, considering that the maximum possible absolute risk differences are going to be dictated by event rates in the comparator population. This concept can be easily illustrated referring to populations that have longer follow-up times, such as with the literature on LDL and cardiovascular disease risk [[8](https://pubmed.ncbi.nlm.nih.gov/30571575/)].
The distance between the two green lines represents the absolute risk difference between low and high LDL over 10 years. Whereas the distance between the two red lines represents the absolute risk difference between low and high LDL over 30 years. Here we can see that if insufficient follow-up is observed, absolute risk differences will inevitably be smaller. This is because event rates naturally increase with time.
The meta-analysis by Vernooij et al. (2019) that the authors cited to support the claim of "small" absolute risk differences with red meat had a median follow-up time of 10.5 years for cardiovascular disease [[9](https://pubmed.ncbi.nlm.nih.gov/31569217/)]. Despite this limitation, Vernooij et al. did not appear to have made any substantive attempt to explore the heterogeneity between their included studies with subgroup analyses or meta-regression analyses. Had they done so, they could have subgrouped by follow-up time and inevitably found that the absolute risks were higher in cohorts with longer follow-ups.
But we can take it a step further. We can reveal the inconsistency in their reasoning by formalizing their argument against nutritional epidemiology, and showing that their criticisms apply to, say, human experiments as well.
**Definitions:**
V := human studies are vulnerable to bias and small effect sizes
D := human studies can demonstrate causality or support causal inference
G := are garbage
e := human experiments
**P1)** If human studies are vulnerable to bias and small effect sizes, then human studies cannot demonstrate causality or support causal inference.
**(∀x(Vx→¬Dx))**
**P2)** Human studies are vulnerable to bias and small effect sizes.
**(∀x(Vx))**
**P3)** If human experiments are human studies that cannot demonstrate causality or support causal inference, then human experiments are human studies that are garbage.
**(¬De→Ge)**
**C)** Therefore, human experiments are human studies that are garbage.
**(∴Ge)**
Using the authors' own logic, we can show that they would have to dismiss human experimental evidence on the same basis. This is because human experimental evidence is vulnerable to the same types of limitations that the authors are positing as presumably invalidating for nutritional epidemiology.
> "Associations are particularly noticeable in North America, where meat is often consumed through a fast-food window and where high-meat consumers tend to also eat less healthy diets and follow less healthy lifestyles in general. In a Canadian study, eating more meat was only associated with more all-cause cancer incidence for the subpopulation eating the lowest amounts of fruits and vegetables (Maximova et al., 2020)."
**Potential contradiction:**
Again, the authors appear to be dismissing nutritional epidemiological evidence on the basis of confounding, without justifying their asymmetrical attitudes toward the supporting evidence for the confounders they're positing. What is true of the evidence between fruits and vegetables and cancer and the evidence between meat and cancer, such that we can infer causality for one and not the other?
**Equivocation:**
This is the second time the authors have shifted the goalpost regarding what types of animals foods that are in question. First they were discussing animal foods simpliciter, only to shift the goalpost to red meat. Now they were talking about red meat, and have shifted goalposts to meat as a broad category. Whether this is intentional or just the result of sloppy writing, it is not a good look for the authors.
> "Several large-scale population-based studies, performed in individuals with ‘healthy lifestyles’, such as the Oxford-EPIC Study (Key et al., 2003) and the 45-and-Up Study (Mihrshahi et al., 2017), also find that the negative effects of red meat consumption on all-cause mortality become benign."
**Red Herring:**
From the wider literature, the typical threshold for harm with meat is at approximately 100g/day on average [[5](https://pubmed.ncbi.nlm.nih.gov/28446499/)].
The Oxford-EPIC cohort lacks power in those ranges [[10](https://pubmed.ncbi.nlm.nih.gov/23497300/)]. Data on the exposure contrasts in the 45-and-Up Study are even more unpersuasive [[11](https://pubmed.ncbi.nlm.nih.gov/28040519/)]. We have far more robust data than this, with better internal validity, follow-up times, and measurements.
In this Japanese cohort with a follow-up of 14 years, diet and lifestyle covariates were largely balanced across the quantiles of red meat intake [[12](https://pubmed.ncbi.nlm.nih.gov/33320898/)]. In fact, many covariates we'd suspect to be detrimental actually favoured meat consumption. Despite this, total meat was still associated with a statistically significant 21% increase in all-cause mortality among men between the ages of 65 and 79 years old, and a borderline-significant 41% increase in all-cause mortality risk among women between the ages of 45 and 54 years old.
These results could indicate that meat consumption is more likely to lead to premature death due to an unmeasured cause earlier in life than with men. Perhaps the seemingly premature increase in mortality could plausibly be attributed to an unmeasured female-specific endpoint, such as breast cancer [[13](https://pubmed.ncbi.nlm.nih.gov/31389007/)].
Again, just to hammer the point home, we can actually defeat the authors' position with a simple modus tollens.
**P1)** If meat consumption is likely to decrease mortality risk, then those consuming the most meat do not die more than those consuming the least meat.
**(P→¬L)**
**P2)** Those consuming the most meat do die more than those consuming the least meat.
**(L)**
**C)** Therefore, meat consumption is not likely to decrease mortality risk.
**(∴¬P)**
Given the weight and strength of the evidence in favour of meat restriction for longevity, it would be quite hilarious to see the authors attempt to reject P2. The evidence they referenced from the Oxford-EPIC cohrot and the 45-and-Up Study could be used in an attempt to reject P2. However, that evidence is very easily superseded by higher internal validity evidence with greater power, not to mention in populations that don't suffer from the same supposed confounding.
> "If red meat were indeed causally driving the associations, one would anticipate finding stronger effects in systematic reviews looking specifically at red meat intake (able to evaluate a large intake gradient) compared to dietary pattern studies (smaller intake gradient) (Johnston et al., 2018)."
**Potential contradiction:**
The association between all-cause mortality and red meat consumption is stronger than the inverse association between all-cause mortality and fruit and vegetable consumption in the most well-done systematic reviews [[5](https://pubmed.ncbi.nlm.nih.gov/28446499/)]. Again, what is true of the association between fruits and vegetables and all-cause mortality and red meat and all-cause mortality, such that we can infer causality for one and not the other?
> "On the contrary, the absolute risk reductions from both reviews specific to intake versus dietary pattern (Johnston et al., 2019) were very similar in their magnitude of effect, indicating the possibility that, even after adjustment, a multitude of other diet or lifestyle components may be confounding the associations irrespective of whether they are negative or positive (Zeraatkar & Johnston, 2019)."
**Red herring:**
This literally just doesn't make any sense. Similar effect sizes are not indicators of multicollinearity or interaction between exposures. I have no idea how the authors come to this conclusion. If I punch people in the face on Mondays and kick people in the balls on Wednesdays, the risk of injury is equal between both Mondays and Wednesdays, but Mondays and Wednesdays aren't the same thing. Just as dietary patterns and individual foods aren't the same thing.
Just because the contribution of meat and diet/lifestyle factors have similar magnitudes of effect doesn't mean a mutual adjustment would do anything to either effect. Both exposures could be interacting with the outcome without interacting with each other. This is easily one of the most bizarre claims in the entire paper. They're also comparing effect sizes between analyses investigating different populations. It's just unfounded speculation.
> "While such troubling incongruity can be partially ascribed to differences in methodological set-up between studies, it has been hypothesised that the associations found in the West could at least partially be seen as cultural constructs generated by responses to norms of eating right (Hite, 2018)."
**Red herring:**
Again, these associations are seen in populations that are not consuming Westernized diets [[12](https://pubmed.ncbi.nlm.nih.gov/33320898/)]. I'm not entirely sure why the authors seem to believe that these associations are limited to Western populations eating Western diets with Western attitudes toward health.
> "An important question to consider, therefore, is "whether intake of animal and plant proteins is a marker of overall dietary patterns or of social class" (Naghshi et al., 2020). Upper-middle classes, who are particularly sensitive to the ideologies of eating virtuous, tend to eat less red meat and saturated fat because of what they symbolise, and because of what they are being told by authorities and moralising societal discourse (Leroy & Hite, 2020). However, those same people are also more educated, wealthier, and healthier in general (Leroy & Cofnas, 2020)."
**Equivocation:**
Yet again, the authors have shifted their goalpost. They went from animal foods to red meat, from red meat to meat, and now from meat to animal protein. Again, it's unclear if this is intentional or just really atrocious writing on the part of the authors. But, I will attempt to keep my rebuttals relevant to the authors' most recently stated goalpost.
**Bullshit:**
These associations are seen even when socioeconomic status are largely balanced across the quantiles of animal protein intake [[14](https://pubmed.ncbi.nlm.nih.gov/33624505/)]. In fact, in this analysis of the Women's Health Initiative Observational Study by Sun et al. (2021), those who consumed the most plant protein were typically in the lower socioeconomic strata. This is in direct opposition to their speculation about socioeconomic status confounding. Additionally, replacing animal protein with plant protein associates with a reduced risk of all-cause mortality even in populations that are situated in a higher socioeconomic stratum [[15](https://pubmed.ncbi.nlm.nih.gov/27479196/)].
> "Even if multivariable models are used to account for such confounding effects as smoking, alcohol consumption, or obesity, it may not be possible to disentangle the effects of all dietary and lifestyle factors involved, especially given the low certainty of evidence."
**Potential contradiction:**
Yet again, we find ourselves needing to ask the authors what is true of the evidence between smoking/alcohol/obesity and health outcomes and animal foods/red meat/meat/animal protein and health outcomes such that we can infer causality for one and not the other? Thus far, the authors have not divulged any clear answers to this question in their paper.
> "Therefore, WHO (2015) mentions that eating unprocessed red meat "has not yet been established as a cause of cancer” (emphasis added)..."
**Appeal to authority:**
Causal inference is an epistemic question, informed and largely adjudicated by statistics. It's rather interesting that the authors tend to offer next to no critical appraisal of methodology or interpretation when the results concord with their (obvious) biases. So far any evidence against animal food consumption as been scrutinized extensively, albeit fallaciously, but the same attempt at rigour is not extended to the counterevidence.
> "...while IARC (2015) stated that "chance, bias, and confounding could not be ruled out” with respect to the association between red meat intake and colorectal cancer. According to some (e.g., Hite, 2018), nutritional epidemiology of chronic disease is thus at risk of capturing cultural artefacts and health beliefs within observational relationships, rather than reliably quantifying actual health effects. Such observations are then used to reinforce dietary advice, potentially creating a positive feedback loop (Leroy & Hite, 2020)."
**Red herring:**
This is true of any association, as per the Duhem-Quine thesis [[16](https://en.wikipedia.org/wiki/Duhem%E2%80%93Quine_thesis)]. Causal inference is a separate consideration, and the fact that auxiliary hypotheses can be proposed is tangential. The authors imply that the ability to appeal to these auxiliary hypotheses presents a barrier to reliably quantifying actual health effects. What type of evidence do they propose needs to be used, then? Because no scientific evidence is free from this limitation.
> "This problem is further underlined by the lack of support from intervention trials (O’Connor et al., 2017; Turner & Lloyd, 2017; Leroy & Cofnas, 2020), which are designed to account for known and unknown confounders, and the fact that the mechanistic rationale for red meats remains speculative at best (Delgado et al., 2020; Leroy & Barnard, 2020)."
**Equivocation:**
The authors' references don't support the claim. Until this point they were discussing the impact of meat products on disease outcomes, not disease risk markers or biochemical mechanisms. However, one of the only studies that did attempt to replace animal foods in the diet also showed one of the largest effect sizes in reducing the risk of acute myocardial infarction [[17](https://pubmed.ncbi.nlm.nih.gov/7911176/)]. On top of that, the most well-controlled human mechanistic studies also support the inference that meat increases CVD risk factors [[18](https://pubmed.ncbi.nlm.nih.gov/31161217/)].
> "Taken together, various public health organisations make a case for the reduction of animal source foods based on their interpretation of the prevailing scientific evidence. Others, however, argue that conclusive proof for (some of) these recommendations is missing, particularly given the contribution of animal source foods to closing essential micronutrient gaps (Leroy & Barnard, 2020)."
**Potential contradiction:**
The authors need to define "conclusive proof", and demonstrate how it has been shown for all variables that they are positing as confounding. However, it's beginning to sound as though they're getting close to planting their goalpost at human experimental evidence. However, this would be a mistake, as they've already posited a number of confounders for which we have no human experimental evidence for causal interaction with the outcomes that have been discussed.
> "Arguing for strong reductions contradicts common-sense approaches, especially from an anthropological perspective (Gupta, 2016; Leroy et al., 2020a). Meat, marrow, and seafood are evolutionary components of the human diet, even if they may have displayed some nutritional and biochemical differences compared to what is produced today in intensified operations, e.g., with respect to fat composition (Kuipers et al., 2010; Manzano-Baena & Salguero-Herrera 2018) and the presence of phytochemicals (van Vliet et al., 2021a, and 2021b). The health impact of these differences may be significant but remains difficult to quantify, though polyunsaturated fatty acids/saturated fatty acids and omega 3/6 ratios of wild ruminants living in current times are similar to pasture-raised (grass-fed) beef, but dissimilar to grain-fed beef (Cordain et al., 2002b). Be that as it may, the abundant consumption of animal source foods over 2.5 million years has resulted in an adapted human anatomy, metabolism, and cognitive capacity that is divergent from other apes (Milton, 2003; Mann, 2018). Also, many hunter-gatherer populations consume far larger amounts of meat and other animal source foods (sometimes > 300 kg/p/y), than what is now consumed in the West (around 100 kg/p/y). This is likely still much below what was once valid for early humans preying on megafauna (Ben-Dor & Barkai, 2020). On a caloric basis, the animal:plant ratio of Western diets (about 1:2 in the US; Rehkamp, 2016) is the inverse of most pre-agricultural diets (mean of 2:1; Cordain et al., 2000). Such high amounts of animal source foods are not necessarily indicative of a health advantage, but it can be assumed that animal source foods are at least compatible with good health."
**Equivocation:**
Apparently we've gone from talking about animal foods to talking about red meat, from talking about red meat to talking about meat, from talking about meat to talking about animal protein, and now from talking about animal protein to to talking about meat, marrow, and seafood. This is truly astonishing. Especially considering that now they're including seafood, which no major public health institution recommends that we eschew.
**Appeal to nature:**
Just because meat is an integral part of our evolutionary history does not actually mean that it is necessarily beneficial for the long-term health of modern humans. In fact, there are valid reasons to suspect that foods to which we are most strongly adapted may actually be more detrimental for long-term health, via antagonistic pleiotropy. I discuss this in a previous blog article [[19](https://www.the-nutrivore.com/post/should-we-eat-like-hunter-gatherers)].
Appeal to nature fallacies basically affirm that because something is natural (or in this case, "evolutionary"), it then follows that it is good. However, taking this position leads to hilarious consequences. Let me demonstrate by formalizing the authors' position once more.
**P1)** If the behaviour is evolutionary, then the behaviour is good.
**(∀x(Ex→Ox))**
**P2)** Meat consumption is a behaviour that is evolutionary.
**(Ea)**
**C)** Therefore, meat consumption is a behaviour that is good.
**(∴Oa)**
It should be obvious straight away why this is problematic. There are plenty of things that are natural or "evolutionary" that we also consider to be undesirable, and we can illustrate that with a reductio ad absurdum.
**P1)** If the behaviour is evolutionary, then the behaviour is good.
**(∀x(Ex→Ox))**
**P2)** Murder is a behaviour that is evolutionary.
**(Em)**
**C)** Therefore, murder is a behaviour that is good.
**(∴Om)**
If animal foods are good by virtue of them being natural or "evolutionary", the authors will have to explain to me why something like murder is not good. As they share the same property of being evolutionary.
> "So-called "diseases of modernity" were rare in ancestral communities, in contrast to what is now seen in regions where Western diets rich in energy-dense foods and (sedentary) lifestyles prevail. In the US, 71% of packaged foods are ultraprocessed (Baldridge et al., 2019)..."
**Red herring:**
There are a number of epistemic barriers that challenge inferences about the long-term health value of more primitive living conditions for modern humans, such as survivorship bias [[20](https://pubmed.ncbi.nlm.nih.gov/25489027/)]. Primitive cultures tend to have very high rates of infant and child mortality, which modern medicine can rescue. When those children are _not_ saved, the population will appear more robust by weeding out less resilient people. When those children _are_ saved, you increase the number of less resilient people within the population.
> "Even if this has been described as a "paradox” (Cordain et al., 2002a), it mainly indicates that today’s assumptions about healthy diets, as being de facto low in red meat and saturated fat, are flawed and represent a romanticised Western viewpoint."
**Strawman:**
No public health institutions are suggesting that healthy diets are _defined_ by the absence of red meat and saturated fat. Rather, diets lower in red meat and saturated fat tend to be healthier than diets that are higher in red meat and saturated fat. But, this doesn't mean that other factors don't also matter. These dietary patterns have many other characteristics that contribute to healthfulness that have nothing to do with red meat or saturated fat.
> "To sum up, although animal source foods are primary components of the Western diet, they are also evolutionary foods to which the human body is anatomically and metabolically adapted, up to the level of the microbiome (Sholl et al., 2021), and has always obtained key nutrients from."
**Appeal to nature:**
The status of red meat as an evolutionary food is tangential to the question of whether or not red meat increases long-term disease risk in modern populations. Investigations into the health status of primitive cultures is insufficient to inform this question.
> "Although further research may be needed, their role in chronic diseases could as well be a mere artefact based on association with the actual damage from other dietary and lifestyle factors. It is uncertain yet possible that high intake of red meat could become problematic in a contemporary Western context."
**Red herring:**
Again, this is true of any association. Causal inference is a separate consideration, and the fact that auxiliary hypotheses can be proposed is, again, tangential.
**Potential contradiction:**
For the last time, posited confounders require validation that meets the authors' bar for causal inference. Thus far, no such bar has been provided and no validation was offered for any of the confounders that were posited. That which is stated without evidence can be dismissed without evidence. Anyone can baselessly speculate.
> "Moreover, contemporary cultures that have maintained traditional diets and lifestyles typically have low burdens of chronic disease (e.g., Kaplan et al., 2017)."
**Red herring:**
The authors reference a cross-sectional analysis of the Tsimane population conducted by Kaplan et al. (2017) [[21](https://pubmed.ncbi.nlm.nih.gov/28320601/)]. It's questionable whether or not their results qualify as low burdens of chronic disease for that population in the first place.
This is made even more questionable after accounting for ~15-year age overestimations that were likely to have biased their results [[22](https://immunityageing.biomedcentral.com/articles/10.1186/s12979-019-0165-8)][[23](https://pubmed.ncbi.nlm.nih.gov/27511193/)][[24](https://pubmed.ncbi.nlm.nih.gov/34038540/)]. After this adjustment, the cardiovascular disease burden within the Tsimane is likely largely comparable with the results of the MESA cohort.
Here on the chart above we see Tsimane age estimates using DNA methylation on the Y axis, against Tsimane age estimates using the methods of Kaplan et al. on the X axis. Kaplan et al. (2017) estimated the ages of the Tsimane participants using written records, relative age lists, dated events, photo comparisons of people with known ages, and cross-validation of information from independent interviews of kin.
Apparently such methodology would appear to introduce a fair amount of bias, as the more objective measures of age tend not to agree with them. Furthermore, all of these more robust measures of age seem to point to overestimations on the party of Kaplan et al. that are all roughly in the same ballpark of 10-20 years.
**Equivocation:**
The category of "chronic disease" is a superset, including many individual diseases. The only disease endpoint investigated in the authors' reference was cardiovascular disease progression (measured by coronary artery calcification). So, I'm not sure why they feel justified in referring to chronic disease as a broad category with this single reference.
To wrap this up, I'd just like to say that I've never before seen a peer-reviewed publication that was so densely packed with logical fallacies and inconsistencies. Mind you this is only the first section, related to disease risk. I was only responsible for appraising this section, but from what I've been told about the remainder of the paper it could potentially be even more absurd. Which is scary to me.
Altogether the authors were guilty of eleven red herrings, six potential contradictions, five equivocations, and eight other assorted fallacies. From what I've read, no truly persuasive arguments were offered in favour of their view, and their attempts to criticize the prevailing paradigm were uniformly hollow and superficial.
Ultimately, the authors actually describe the absurdity of their approach better than I could in the introduction of their paper. Truly astonishing.
> _"Due to constraints in format, we restrict ourselves to generating a perspective that favours concepts over details and methodological data."_
Thanks for reading! If you enjoy my writing and want more content like this, consider pledging to my [Patreon](https://www.patreon.com/thenutrivore)!
**References:**
[1] Leroy, Frédéric, et al. ‘Animal Board Invited Review: Animal Source Foods in Healthy, Sustainable, and Ethical Diets - An Argument against Drastic Limitation of Livestock in the Food System’. _Animal: An International Journal of Animal Bioscience_, vol. 16, no. 3, Mar. 2022, p. 100457. _PubMed_, [https://doi.org/10.1016/j.animal.2022.100457](https://doi.org/10.1016/j.animal.2022.100457.)
[2] Schwingshackl, Lukas, et al. ‘Evaluating Agreement between Bodies of Evidence from Randomised Controlled Trials and Cohort Studies in Nutrition Research: Meta-Epidemiological Study’. _BMJ (Clinical Research Ed.)_, vol. 374, Sept. 2021, p. n1864. _PubMed_, [https://doi.org/10.1136/bmj.n1864](https://doi.org/10.1136/bmj.n1864)
[3] Moorthy, Denish, et al. _Concordance Between the Findings of Epidemiological Studies and Randomized Trials in Nutrition: An Empirical Evaluation and Citation Analysis: Nutritional Research Series, Vol. 6_. Agency for Healthcare Research and Quality (US), 2013. _PubMed_, [http://www.ncbi.nlm.nih.gov/books/NBK138246/](http://www.ncbi.nlm.nih.gov/books/NBK138246/)
[4] Beyerbach, Jessica, et al. ‘Evaluating Concordance of Bodies of Evidence from Randomized Controlled Trials, Dietary Intake, and Biomarkers of Intake in Cohort Studies: A Meta-Epidemiological Study’. _Advances in Nutrition (Bethesda, Md.)_, vol. 13, no. 1, Feb. 2022, pp. 48–65. _PubMed_, [https://doi.org/10.1093/advances/nmab095](https://doi.org/10.1093/advances/nmab095)
[5] Schwingshackl, Lukas, et al. ‘Food Groups and Risk of All-Cause Mortality: A Systematic Review and Meta-Analysis of Prospective Studies’. _The American Journal of Clinical Nutrition_, vol. 105, no. 6, June 2017, pp. 1462–73. _PubMed_, [https://doi.org/10.3945/ajcn.117.153148](https://doi.org/10.3945/ajcn.117.153148)
[6] Bechthold, Angela, et al. ‘Food Groups and Risk of Coronary Heart Disease, Stroke and Heart Failure: A Systematic Review and Dose-Response Meta-Analysis of Prospective Studies’. _Critical Reviews in Food Science and Nutrition_, vol. 59, no. 7, 2019, pp. 1071–90. _PubMed_, [https://doi.org/10.1080/10408398.2017.1392288](https://doi.org/10.1080/10408398.2017.1392288.)
[7] Schwingshackl, Lukas, et al. ‘Food Groups and Risk of Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of Prospective Studies’. _European Journal of Epidemiology_, vol. 32, no. 5, May 2017, pp. 363–75. _PubMed_, [https://doi.org/10.1007/s10654-017-0246-y](https://doi.org/10.1007/s10654-017-0246-y)
[8] Abdullah, Shuaib M., et al. ‘Long-Term Association of Low-Density Lipoprotein Cholesterol With Cardiovascular Mortality in Individuals at Low 10-Year Risk of Atherosclerotic Cardiovascular Disease’. _Circulation_, vol. 138, no. 21, Nov. 2018, pp. 2315–25. _PubMed_, [https://doi.org/10.1161/CIRCULATIONAHA.118.034273](https://doi.org/10.1161/CIRCULATIONAHA.118.034273)
[9] Vernooij, Robin W. M., et al. ‘Patterns of Red and Processed Meat Consumption and Risk for Cardiometabolic and Cancer Outcomes: A Systematic Review and Meta-Analysis of Cohort Studies’. _Annals of Internal Medicine_, vol. 171, no. 10, Nov. 2019, pp. 732–41. _PubMed_, [https://doi.org/10.7326/M19-1583](https://doi.org/10.7326/M19-1583)
[10] Rohrmann, Sabine, et al. ‘Meat Consumption and Mortality--Results from the European Prospective Investigation into Cancer and Nutrition’. _BMC Medicine_, vol. 11, Mar. 2013, p. 63. _PubMed_, [https://doi.org/10.1186/1741-7015-11-63](https://doi.org/10.1186/1741-7015-11-63)
[11] Mihrshahi, Seema, et al. ‘Vegetarian Diet and All-Cause Mortality: Evidence from a Large Population-Based Australian Cohort - the 45 and Up Study’. _Preventive Medicine_, vol. 97, Apr. 2017, pp. 1–7. _PubMed_, [https://doi.org/10.1016/j.ypmed.2016.12.044](https://doi.org/10.1016/j.ypmed.2016.12.044)
[12] Saito, Eiko, et al. ‘Association between Meat Intake and Mortality Due to All-Cause and Major Causes of Death in a Japanese Population’. _PloS One_, vol. 15, no. 12, 2020, p. e0244007. _PubMed_, [https://doi.org/10.1371/journal.pone.0244007](https://doi.org/10.1371/journal.pone.0244007)
[13] Lo, Jamie J., et al. ‘Association between Meat Consumption and Risk of Breast Cancer: Findings from the Sister Study’. _International Journal of Cancer_, vol. 146, no. 8, Apr. 2020, pp. 2156–65. _PubMed_, [https://doi.org/10.1002/ijc.32547](https://doi.org/10.1002/ijc.32547)
[14] Sun, Yangbo, et al. ‘Association of Major Dietary Protein Sources With All-Cause and Cause-Specific Mortality: Prospective Cohort Study’. _Journal of the American Heart Association_, vol. 10, no. 5, Feb. 2021, p. e015553. _PubMed_, [https://doi.org/10.1161/JAHA.119.015553](https://doi.org/10.1161/JAHA.119.015553)
[15] Song, Mingyang, et al. ‘Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality’. _JAMA Internal Medicine_, vol. 176, no. 10, Oct. 2016, pp. 1453–63. _PubMed_, [https://doi.org/10.1001/jamainternmed.2016.4182](https://doi.org/10.1001/jamainternmed.2016.4182)
[16] ‘Duhem–Quine Thesis’. _Wikipedia_, 13 Jan. 2022. _Wikipedia_, [https://en.wikipedia.org/w/index.php?title=Duhem%E2%80%93Quine_thesis&oldid=1065410241](https://en.wikipedia.org/w/index.php?title=Duhem%E2%80%93Quine_thesis&oldid=1065410241)
[17] de Lorgeril, M., et al. ‘Mediterranean Alpha-Linolenic Acid-Rich Diet in Secondary Prevention of Coronary Heart Disease’. _Lancet (London, England)_, vol. 343, no. 8911, June 1994, pp. 1454–59. _PubMed_, [https://doi.org/10.1016/s0140-6736(94)92580-1](https://doi.org/10.1016/s0140-6736(94)92580-1)
[18] Bergeron, Nathalie, et al. ‘Effects of Red Meat, White Meat, and Nonmeat Protein Sources on Atherogenic Lipoprotein Measures in the Context of Low Compared with High Saturated Fat Intake: A Randomized Controlled Trial’. _The American Journal of Clinical Nutrition_, vol. 110, no. 1, July 2019, pp. 24–33. _PubMed_, [https://doi.org/10.1093/ajcn/nqz035](https://doi.org/10.1093/ajcn/nqz035)
[19] Hiebert, Nick. ‘Should Modern Humans Eat Like Hunter-Gatherers?’ _The Nutrivore_, 14 May 2021, [https://www.the-nutrivore.com/post/should-we-eat-like-hunter-gatherers.](https://www.the-nutrivore.com/post/should-we-eat-like-hunter-gatherers.)
[20] Perrin, James M., et al. ‘The Rise in Chronic Conditions among Infants, Children, and Youth Can Be Met with Continued Health System Innovations’. _Health Affairs (Project Hope)_, vol. 33, no. 12, Dec. 2014, pp. 2099–105. _PubMed_, [https://doi.org/10.1377/hlthaff.2014.0832](https://doi.org/10.1377/hlthaff.2014.0832)
[21] Kaplan, Hillard, et al. ‘Coronary Atherosclerosis in Indigenous South American Tsimane: A Cross-Sectional Cohort Study’. _Lancet (London, England)_, vol. 389, no. 10080, Apr. 2017, pp. 1730–39. _PubMed_, [https://doi.org/10.1016/S0140-6736(17)30752-3](https://doi.org/10.1016/S0140-6736(17)30752-3)
[22] Li, Mingde, et al. ‘Age Related Human T Cell Subset Evolution and Senescence’. _Immunity & Ageing_, vol. 16, no. 1, Sept. 2019, p. 24. _BioMed Central_, [https://doi.org/10.1186/s12979-019-0165-8](https://doi.org/10.1186/s12979-019-0165-8)
[23] Horvath, Steve, et al. ‘An Epigenetic Clock Analysis of Race/Ethnicity, Sex, and Coronary Heart Disease’. _Genome Biology_, vol. 17, no. 1, Aug. 2016, p. 171. _PubMed_, [https://doi.org/10.1186/s13059-016-1030-0](https://doi.org/10.1186/s13059-016-1030-0)
[24] Irimia, Andrei, et al. ‘The Indigenous South American Tsimane Exhibit Relatively Modest Decrease in Brain Volume With Age Despite High Systemic Inflammation’. _The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences_, vol. 76, no. 12, Nov. 2021, pp. 2147–55. _PubMed_, [https://doi.org/10.1093/gerona/glab138](https://doi.org/10.1093/gerona/glab138)

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It's basically a sound induction at this point that anti-seed oil clowns won't debate me. My comprehensive, 15,000+ word, 200+ reference [article](https://www.the-nutrivore.com/post/a-comprehensive-rebuttal-to-seed-oil-sophistry) on seed oils is almost three years old, and since it was published, nobody from the opposition has offered even a shred of substantive criticism toward it. A few have tried, but ultimately their efforts were akin to taking halfhearted swats at low-hanging fruit and ultimately failing, rather than actually meaningfully engaging with my core findings and the arguments underpinning my interpretations. They really are just a pathetically weak lot of human beings.
At the risk of sounding self-aggrandizing, I think I have a pretty good idea why these people won't debate me—I have the tools to dismantle them. I'm well-versed on the relevant empirics, I'm intimately familiar with several formal systems of reasoning, I use semantic analysis to make sure my interlocutor's term meanings and usages are understood and remain consistent, I have decent knowledge of philosophy and, more specifically, scientific epistemology, and I deploy an algorithmic debate strategy. I am essentially kryptonite to anti-seed oil quacks. That's probably why they never show up to debate.
My most recent exposure to anti-seed oil cuckery was so profoundly egregious that it warranted writing about it here on my main blog. This extra special example of subhuman behavior comes from Cate Shanahan herself, or as I like to call her, Cate Shenanigans. If you want more info on Cate Shenanigans' history of debate-dodging, I have compiled an inventory [here](https://www.the-nutrivore.com/dodgers). For now, let me start from the beginning.
Nearly a year ago, I was [invited](https://x.com/zbitter/status/1668413822388916224) by Zach Bitter, via X, to debate the proposition "seed oils are not a significant, independent concern for public health" on his podcast with a willing interlocutor. Cate Shenanigans was [tagged](https://x.com/NTxLoneRider/status/1673811898645598211) in this post but did not reply. In fact, every single high-profile seed oil skeptic who responded to the thread declined my invite, while others, like Cate Shenanigans, were pinged and never replied. The nutrition debate arena was a ghost town that day. Not an ounce of courage was to be found among the anti-seed oil clowns.
However, nearly a year after that, Cate Shenanigans put out a general [invite](https://x.com/drcateshanahan/status/1773836787196346592) to debate. Even going so far as to [suggest](https://x.com/drcateshanahan/status/1774490576362062311) that I was scared to face her, to which I replied. Shortly after, she actually decided to engage and [replied](https://x.com/drcateshanahan/status/1774681584907559220) to me, encouraging me to DM her (presumably to work out the details of the debate). After some minor miscommunications, she instructed me in another [reply](https://x.com/drcateshanahan/status/1774830896006185446) to contact her via email. I did. I never received a reply. Some time passed, and Zach Bitter once again started [prodding](https://x.com/zbitter/status/1778171569967190413) at Cate Shenanigans about the status of her debate invitation to me (presumably with the intention of once again offering to host it). A day later, after a brief back and forth, Cate Shenanigans [replied](https://x.com/drcateshanahan/status/1778430104617603232) with what seemed like an alteration in the conditions to debate. At least this is how I interpreted it, as someone who has an interest in her arguments. I [pressed](https://x.com/TheNutrivore/status/1778456234078662984) her for clarification, and even quoted her in a [post](https://x.com/TheNutrivore/status/1778490825124552875) later that day about it, and received no reply. But not before she made her own [post](https://x.com/drcateshanahan/status/1778483241755787308) in a different thread, which I didn't initially see, wherein she withdrew from the debate that day. What a bizarre series of behaviours.
Fast forward to June 2nd, 2024, and I was DMed by another third party looking to coordinate yet another debate between Cate Shenanigans and myself. I won't reveal this person's identity and throw this individual under the bus, because they were nothing but cordial and respectful to me. After a short exchange, I was CC'd into an email chain with Cate Shenanigans, and this is where the fun begins. But rather than narrate the exchange, I'll just post it here:
**Host:**
> Hi cate
>
> Nick, CCed, would be down to do the seed oil debate for my show… Are you game? If so my team, CCed, can help to arrange…
**Nick:**
> If the debate proposition is clear and I disagree with it, then absolutely. I generally won't debate anything vague or normative, though. I'll happily debate a proposition like "seed oil consumption increases the risk of heart disease", for example.
**Shenanigans:**
> HI Host
>
> Someone else wanted to set up a debate on their podcast between myself and Nick. But what was proposed looked more like just an unstructured argument, and that is not something I’m interested in. I don’t know if the disconnect was with that host or with Nick….? So I’d like to make sure we’re all on the same page about what a debate is.
>
> A debate starts with an assertion and the two participants who are debating take opposing sides.
>
> So if Nick wants to debate, then the assertion could be “RBD vegetable oils are part of a healthy diet.”
>
> Sound good?
**Host:**
> What do you think Nick?
**Nick:**
> First of all, it's not just that someone else has previously wanted to set up a debate between Cate and myself. Cate herself put out what I (quite reasonably) interpreted as a general invitation to those challenging her positions, which can be found [here](https://x.com/drcateshanahan/status/1773836787196346592), on March 29th. I accepted the invite, to which Cate replied on March 31st with an invitation to me to DM her (presumably to set up a debate), which can be found [here](https://x.com/drcateshanahan/status/1774681584907559220). I responded via email on April 1st, after she invited me to do so [here](https://x.com/drcateshanahan/status/1774830896006185446), on the same day. There was no third party present at this time. This was Cate clearly inviting me, personally, to debate. Just to be clear about the facts.
>
> Furthermore, while we're being clear about the facts, Cate also presumably withdrew from the debate for what would be completely bizarre reasons that are ultimately orthogonal to the debate itself, which can be found [here](https://x.com/drcateshanahan/status/1778483241755787308). But, not before implying that she had altered the necessary conditions for a debate, which can be found [here](https://x.com/TheNutrivore/status/1778490825124552875). Whatever the case, declining to debate someone on an empirical position because they disagree with you on an unrelated normative position is **beyond** strange, and honestly it was so outlandish that I just flagged it as a blatant excuse not to debate. I hope, Host, you can also see that this is the most reasonable interpretation of her behaviour.
>
> Now that that's out of the way and clarified, I'd be happy to debate Cate on a number of propositions. So long as she's done making excuses. Specifically, I might want to debate against [this](https://x.com/drcateshanahan/status/1516786219841073153) proposition:
>
> "current levels of seed oil consumption are the main driver of the obesity and chronic disease epidemics that now represent an existential threat to human populations around the world.
>
> Out of all of her claims, this could easily be one of the most egregious, depending on how the semantics are unpacked. So, I'd need some of those semantics clarified. Cate, when you say seed oils are the main driver, do you mean that in a counterfactual scenario wherein all the seed oils in the food supply were replaced with low-PUFA alternatives like butter or tallow, those same diseases epidemics would be less likely to occur? If yes, I disagree with the proposition and will happily debate it. If not, what do you mean?
>
> As for the stuff about what the debate would be. I typically don't do "structured" debates in the traditional sense. They seem closer to theatrics than debates, with time limits and scheduled topic shifts, opening statements, closing statements, etc. I prefer a linear, continuous Socratic debate format where the truth value of a proposition can be scrutinized to completion with no get-out-of-jail free cards granted by the clock. If it takes many hours to reach a concession, so be it. Other formats typically just make sophistry and dodging easier to get away with, because one party can just filibuster until the clock runs out.
>
> Also, Cate, my debate style is far from unstructured. My debate algorithm can be found [here](https://drive.google.com/file/d/1QQaN6HRwzp3kY2DAcnHVBxeX6jBhrvkw/view). So everyone knows what to expect of me. No rational person would look at this and conclude that my approach to debate is unstructured. I just refuse to debate with my hands tied behind my back, or debate under conditions where the proposition can't be scrutinized to completion.
**Host:**
> Thanks Nick!
> Cate, you game to schedule?
**Shenanigans:**
> Dear Nick and Host,
>
> Nick, my tweet "sure I’ll take all comers,” was a casual proposition subject to agreeing on further details, which we have yet to do.
>
> Host, from Nick's email it looks like he wants to argue against a primary thesis of my book, without having read my book. That doesn’t seem like a debate to me. 
>
> In Dark Calories I lay out the groundwork to support my claims across multiple chapters, each with scores of scientific references to support the arguments I make in the book. I can’t skip that information and jump right into a debate on my conclusions. 
>
> Maybe an analogy will help, here. Let’s say, hypothetically, that after publishing his theory of relativity, Einstein announced in a public forum “Hey everyone I think E=MC squared. Read my paper for supporting arguments." And then, someone wanted to debate his paper without having read it. Einstein would have been in a position to have to spell out many details of his complex thesis, including technical information that would probably not be interesting to a lay audience. (Not when presented in debate format. A good documentarian or science writer would be able to make it interesting, however.) In order to “win” the debate, Einstein may even have had to defend the veracity of fundamental principles of physics. That would take the form of a lecture, or a series of lectures. That’s not a debate. It’s a college course.
>
> Therefore, I’ve proposed we debate this: “Vegetable oils are heart healthy.” After all, that is what the AHA claims. It’s also what docctors learn, and it is influencing public policy, what American farmers grow, and what every child and adult eats. It’s an important topic that merits debate. I would argue against and Nick would argue for.
>
> Nick, are you willing to do that?
**Host:**
> I love that proposition “Vegetable oils are heart healthy.”
>
> What do u think Nick?
**Nick:**
> Just ignoring the fact that, in a blatant display of unbridled narcissism, Cate has unabashedly compared herself to Einstein, and her work to Einstein's theory of relativity, I'd like to ask Cate a few questions:
>
> 1. If I read your book, Dark Calories, will you debate the proposition I suggested (provided you actually unpack your semantics in a way that leads me to disagree with it)? If yes, surely you'd be willing to provide me with a free PDF of Dark Calories for me to scrutinize, no?
>
> 2. If you wish to debate what I believe on the subject, surely you've done me the likewise courtesy of reading my [article](https://www.the-nutrivore.com/post/a-comprehensive-rebuttal-to-seed-oil-sophistry) on the subject, right? If yes, why did you not suggest a proposition directly from my work?
>
> I also have some further objections to Cate's reasoning. Unlike Einstein's theories and models, the predictions of which could only be confirmed many decades later (if not a century later in some cases), Cate's thesis has been tested (and ultimately falsified with respect to human outcome data), which is why the debate would likely lead heavily into empirics and not require a whole book's worth of lectures on fundamentals. So no, I don't need to read her book to show that the proposition is false. Her reasoning here is ridiculous.
>
> Respectfully, Host and Cate, "vegetable oils are heart healthy" is an awful proposition, for a number of reasons:
>
> 1. It's not my proposition.
> 2. I don't represent the AHA.
> 3. I don't even care what the AHA says about seed oils.
> 4. I don't even know what it means because it's so semantically vague.
> 5. I can think and reason for myself and can defend my own propositions, thank you.
>
> How about we narrow the scope of the proposition I suggested down to a single disease? Since Cate quantifies the detrimental effects of seed oils over the entire scope of chronic diseases that qualify as epidemics, it is entailed logically that we could choose any disease within that scope. So, how about we meet half way on the subject and debate this proposition:
>
> "current levels of seed oil consumption are the main driver of heart disease."
>
> To the degree that Cate affirms that heart disease is an epidemic, she should affirm that the proposition is true. I affirm that the proposition is false. So, we simply exchange the relevant empirics and have the debate. EZPZ.
**Shenanigans:**
> Dear Host and Nick,
>
> I am interested in a debate on the topic I proposed. But I feel this particular email chain is no longer constructive. 
>
> Resorting to character attacks during what should be a civil conversation is outside the realm of what I consider acceptable discourse.
>
> Respectfully,
> Cate
**Nick:**
> You've attacked my character on multiple occasions, Cate. I don't care about that. Let's just discuss the arguments, and hammer out a path toward a productive debate.
>
> It's also ridiculous to imply that I'm not contributing productively to the conversation. I literally suggested a proposition that seems to satisfy us both. If I've failed to do that, please explain how so I can improve upon further suggestions.
>
> Just give me a yay or nay, Cate. I don't want to waste my time if you're not interested in actually defending your views or answering any clarifying questions.
**Shenanigans:**
> Nick,
>
> As I said two emails ago, because most people, including you, are not familiar with the scientific underpinnings of my work I would first need to explain them, and that is not a debate.
>
> What I proposed is a debate. If you are not interested in that debate then I believe we have reached the conclusion of this discussion.
>
> Best wishes to you.
**Nick:**
> And I explained to you how that's a dodge. Again, I don't need a lecture on the theoretical underpinnings when the predictions of the hypothesis have been tested and there is tons of empirical data on it. We only need to have a discussion about the empirics that test the hypothesis' fruitfulness, not the theoretical underpinnings. Insisting that I read your book is just filibustering.
>
> But hey, I'm still super curious to hear the answer to this question that I already asked you. If I were to read your book, would you debate the prop? Yes or no. If yes, then would you be willing to supply me with a free PDF of your book as a good faith gesture that you're interested in having your work scrutinized? Yes or no.
>
> I'm likewise super curious to hear the answer to this further question that I also already asked you. If you instead want to debate my beliefs, have you paid me the likewise courtesy of reading my work? Yes or no. If yes, then why haven't you picked a prop that has been extracted from my work directly? Why in the world do you want me to defend the AHA's prop and not a prop of my own?
**Shenanigans:**
> Nick I am responding to your questions and only your questions and I hope that can be the end of it.
>
> "And I explained to you how that's a dodge. Again, I don't need a lecture on the theoretical underpinnings when the predictions of the hypothesis have been tested and there is tons of empirical data on it. We only need to have a discussion about the empirics that test the hypothesis' fruitfulness, not the theoretical underpinnings. Insisting that I read your book is just filibustering.
>
> But hey, I'm still super curious to hear the answer to this question that I already asked you. If I were to read your book, would you debate the prop? Yes or no."
>
> No. For reasons I explained. Just because you’ve read the book does not mean the audience has and I will still be in the position to essentially give a lecture on the topics in my books. Its simply not suitable for normal debate format. Furthermore, I’m not interested in debating someone who thinks familiarizing himself with the basic underpinnings of the topic being debated is optional.
>
> "If yes, then would you be willing to supply me with a free PDF of your book as a good faith gesture that you're interested in having your work scrutinized? Yes or no.
>
> N/A
>
> "I'm likewise super curious to hear the answer to this further question that I also already asked you. If you instead want to debate my beliefs, have you paid me the likewise courtesy of reading my work?
>
> I am familiar with your thoughts. You cite the same type of evidence that the AHA uses to support its heart healthy claim.
>
> "Yes or no. If yes, then why haven't you picked a prop that has been extracted from my work directly?
>
> Not all propositions are equally interesting. I want to debate something interesting.
>
> "Why in the world do you want me to defend the AHA's prop and not a prop of my own?
>
> See above. Additionally, keep in mind that I did not bring you into this conversation.
**Nick:**
> So basically you're just dodging. Got it.
>
> Before we killscreen the entire enterprise, I would like one more answer to a question, because it might provide for a way forward. With respect to the AHA prop that you bizarrely want me to defend, what does it mean to say that seed oils are heart healthy? For example, does that mean that seed oils decrease the risk of heart disease?
>
> Because if that prop cashes out into a prop that I'd be willing to defend, then I don't see a reason why we couldn't debate it. If it means what I think it means, it'll just lead into the exact same empirical debate that you're currently dodging, so it makes no difference to me.
**Host's Producer:**
> Hi Nick and Cate,
>
> Host's Producer here; I'm the producer at [redacted]. Host and I agreed that we would like to conclude this discussion and explore other debate topics. The tone of the email discourse is not what we had in mind for our debut episode of this new podcast.
>
> We appreciate your consideration.
**Nick:**
> I'd be happy to debate cordially with somebody who is not a sophist. Cate, unfortunately, is one of the most dishonest actors in this entire space and deserves zero respect from anybody (though I would give her more than what she deserves and actually be respectful to her in a verbal discussion for the betterment of your podcast). There are people I could recommend who disagree with me who I don't think are dishonest but rather just confused about the empirics. If you guys are still interested in having a productive seed oil debate, I'd be happy to provide a list.
>
> Also if you're worried about my tone during the debate, you need not be concerned. I don't think anybody can actually find more than a single example of me being rude to my interlocutor across what is probably dozens of verbal debates by now. Other than that one exception, which I actually think was justified anyway, I am always polite and cordial with my interlocutor in verbal discussions.
This is where the email exchange ended. So much of what Cate Shenanigans said was just brain-dead lunacy. Let's go through the list.
**A) Suggesting that I defend a proposition that isn't my own**
Why? Why in the world would I be asked to defend a proposition that I, myself, am not even sure I affirm? I'm not even sure what the proposition "seed oils are heart healthy" even means. Does it mean that seed oils will increase your VO2 max? Does it mean seed oils will cure hypertension? Who the hell knows. It was just beyond strange that it was even suggested and demonstrates to me that Cate Shenanigans is operating with a level-zero debate meta.
Furthermore, if she was truly interested in contesting my views, why did she not pay me the likewise courtesy of reading my article and selecting a proposition directly from my own writing? Seems not only to be ridiculously stupid, but also a ridiculously stupid double-standard. Yet another example of Shenanigans-level cuckery.
**B) Shifting the goalpost three times**
Months ago, she dodged me on the grounds that I haven't read her book and that reading her book was necessary to have a debate. I [offered](https://x.com/TheNutrivore/status/1778490825124552875) to read her book then to satisfy the criteria and got no reply. Now, she dodged me for the second time on these grounds, and when I directly offered to read her book and satisfy her criteria, she shifted the goalpost a third time. Apparently, it's not good enough that I read her book, but now the entire audience needs to read her book in order for us to debate. This is just the most cuckish form of sophistry imaginable, and she should be ashamed.
**C) Her goalposts are dumb anyway**
To anyone with even a modicum of understanding with respect to scientific epistemology, it should be quite clear that Cate Shenanigans is dodging. Essentially, the strength of a scientific hypothesis does not rest upon its complexity, its elegance, its creativity, or any other such quality. It rests upon how scientifically virtuous it is, and this is determined by testing the hypothesis' compatibility with the theoretical virtues of science. I wrote a lengthy article on the subject [here](https://www.the-nutrivore.com/post/the-hitchhiker-s-guide-to-quack-smashing).
To determine if a hypothesis is strong, we should ask three fundamental questions, compared to other hypotheses:
1. Does this hypothesis make more novel predictions?
2. Does this hypothesis explain a wider breadth of phenomena?
3. Does this hypothesis make fewer overall assumptions?
There are other questions some philosophers think we should ask, but generally speaking, philosophers of science do not disagree about these three core questions. So, let's take them one by one.
Firstly, the hypothesis doesn't really seem to make very many novel predictions at all. In fact, as I had previously discussed in another blog [article](https://www.the-nutrivore.com/post/a-comprehensive-rebuttal-to-seed-oil-sophistry), the overall weight of the literature heavily favours the negation of Cate Shenanigans' hypothesis. When confronted with this fact on a [podcast](https://gimletmedia.com/shows/science-vs/mehwdgww) (33:00), Cate Shenanigans had no compelling answers and merely insisted that it "didn't make any sense" and that every single study on the subject (150-300 studies by her count) was "flawed". Very persuasive, Dr. Shenanigans. Gold fucking star.
As for the second question, the scope of her hypothesis is actually quite impressive. As she stated in the linked podcast above, seed oils literally have a causal role to play in every disease. That is quite an impressive scope. Think of all the phenomena this accounts for. Looks great for the hypothesis, except when we try to answer the third question.
With respect to the final question we're asking, every disease Cate Shenanigans blames on seed oils in an attempt to inflate her scope, she piles on more and more assumptions. Assumptions that empirically verifiable pathophysiological mechanisms that explain a number of diseases, that have nothing to do with seed oils, are either wrong or so incomplete that they might as well be wrong. This produces an insane amount of assumptions. And that's not even counting the assumptions that are stacked in virtue of the hypothesis' failures to make novel predictions.
As I explained in a previous article, The Hitchhiker's Guide to Quack-Smashing, quacks will often inflate scope at the expense of parsimony and/or fruitfulness. They want to be able to capture the widest scope of phenomena with their hypothesis without actually having evidence or having to explain a damn thing.
No, Dr. Shenanigans, I don't need to read your book in order to debate your proposition that seed oils are responsible for all disease, or chronic disease, or even just heart disease. As I explained in the email exchange, the only thing that is required is an investigation into the empirical data that tests your hypothesis. We can test the fruitfulness, we can test the scope, and we can test the parsimony. You're just dodging because you are scared.
Thanks for reading! If you enjoy my writing and want more content like this, consider pledging to my [Patreon](https://www.patreon.com/thenutrivore)!

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Firstly, I'd like to thank all of the people who volunteered days of their time in order to make this article possible!
Some time ago, the YouTube channel, [What I've Learned](https://www.youtube.com/@WhatIveLearned), release the video called "[Vegan diets don't work. Here's why](https://www.youtube.com/watch?v=MpxgZGnEF7E)", wherein the channel's host, [Joseph Everett](https://twitter.com/JEverettLearned), tells a cautionary tale regarding the health-related pitfalls of so-called "vegan" diets. In this article, Joseph will be exposed as the shameless fabulist that he is. Most of the references are taken out of context or cherry-picked, while others actually directly contradict the claims that they were cited to support.
In order to save on characters, I'm forced to truncate my introduction. So, I'll just take this time to say that you, Joseph, are a complete sophist, and you should be utterly ashamed for misleading the millions of people who consume your content. The effort that it took to write this article is more than you deserve, but its contents are more than deserved by your viewers. Your viewers deserve the truth— not cringey narratives about maverick dentists and cave paintings. With that, let's begin.
**Claim #1 (**[**00:00**](https://youtu.be/MpxgZGnEF7E?t=1)**):**
> It’s well understood that each of these vitamins have many functions in the body, but what does this have to do with nice teeth or looking attractive? Well, research later confirmed that along with things like protein and calcium, these vitamins indeed work together to transport minerals to support proper formation of the bones. [[1](https://pubmed.ncbi.nlm.nih.gov/29138634/)][[2](https://pubmed.ncbi.nlm.nih.gov/33801011/)] And of course your facial structure which includes the dental arch depends on proper development of your facial bones.
This is incredibly unscientific evidence on this hypothesis. The potential for selection bias with this particular body of evidence is enormously high, and on multiple levels. Of course we do not want to assume bad faith on the part of the researcher himself, but no credible scientific establishment would consider this evidence to be anything above laughable on the hypothesis specified. The specified hypothesis is that vitamin K2 (presumably in conjunction with other fat soluble vitamins) is responsible for teeth being straight rather than crooked.
It's not clear at all how the evidence presented even interacts with the hypothesis. These traditional peoples were not screened for vitamin K2 status or intake. There were no prospective analysis. No intake measurements. No biomarker measurements. Just storytelling. In fact, four years ago Joseph published a video that present a far more plausible hypothesis for the appearance of strong jaws and straight teeth in traditional populations eating traditional diets. In the video he cites [a researcher named Clark Spencer Larson from Ohio State University](https://youtu.be/zbzT00Cyq-g?t=591), who claims that stronger jaws and straighter teeth seen in ancestral populations are a consequence of the repetitive chewing of tough, fibrous plant material.
There is also evidence that [straighter teeth tend to be more worn down in traditional populations](https://www.youtube.com/watch?v=ybRD4UPN3D4&t=505s), which supports the chewing hypothesis. [[3](https://www.aegisdentalnetwork.com/cced/2009/06/interdisciplinary-analysis-origins-of-dental-crowding-and-malocclusions-an-anthropological-perspective)] In fact, Joseph references the pictures from Weston A Price's Nutrition and Physical Degeneration as evidence for the chewing hypothesis. [He remarks that the straight teeth in the traditional populations appear more worn down](https://www.patreon.com/file?h=24534404&i=3265485).
Has Joseph changed his view? It's unclear why, as this is a far more plausible hypothesis, and can actually subsume the vitamin K2 hypothesis. If vitamin K2 intake is a correlate for traditional diets, and traditional diets are more likely to be high in fibrous, tough plant foods, and straighter teeth tend to be more worn then crooked teeth, then the chewing hypothesis would appear to be more parsimonious.
Also, if insufficiency of K2 and the other fat soluble vitamins are to blame for crowded teeth due to their role in bone formation, why is there no mention of any of these people have any other issues associated with those sorts of nutritional insufficiencies? Like rickets, blindness, poor skin, or even haemophilia? It doesn't make sense.
**Claim #2 (**[**01:01**](https://youtu.be/MpxgZGnEF7E?t=61)**):**
> If eating zero animal foods improves health so much, why would a 2016 study find that 84% of vegans eventually quit their diet? [[4](https://faunalytics.org/a-summary-of-faunalytics-study-of-current-and-former-vegetarians-and-vegans/#:~:text=84%25%20of%20vegetarians%2Fvegans%20abandon,former%20vegetarians%2Fvegans%20was%20health)]
First of all, the claim of 84% of vegans quitting is just blatantly incorrect according to his own citation, which found a 70% dropout rate for vegans. Second of all, this is a ridiculous question. People stop doing health promoting things for all sorts of reasons, and it probably would have been a good idea for him to read the goddamn reference instead of resorting to conspiracy theories. The study includes an inventory of explanations for participant recidivism, and [the craving of animal products only occurred in the minority of recidivists](https://faunalytics.org/wp-content/uploads/2016/02/Faunalytics-Study-of-Current-and-Former-Vegetarians-and-Vegans-%E2%80%93-Secondary-Findings-.pdf).
Furthermore the study includes a table of motivations for pursuing veganism. Only a measly 1-3% of participants had motivations that were purely ethical in nature. While most motivations were health related. So, it seems like people are generally going on plant-based diets for health related reasons, and abandoning the diets without generally suffering health related costs. This isn't the only reason the question is stupid. Plenty of health promoting behaviours have high recidivism rates, such as exercise.
The Faunalytics study [from the previous year](https://faunalytics.org/wp-content/uploads/2015/06/Faunalytics_Current-Former-Vegetarians_Full-Report.pdf) actually explicitly stated that health did not present a noticeable difficulty for study participants, with the exception of vitamin B12 monitoring. Very few people actually reported any health issues at all, and it's not clear how many of them were actually supplementing B12.
The study had 54 current vegans and 129 former vegans. Of those 129 former vegans, 123 gave reasons. Of those 123, 104 reported no health issues. Of the remaining 19, 7 had no health issues, but rather just "felt" like they weren't getting enough nutrients or were concerned for no particular reason. One seemed to quit because they doubted the benefits. Only 11 reported actual health issues.
Of those 11, 6 were vague like "sick", "lightheaded", "not healthy", and "health issues", and doctors and/or dietitians were rarely, or never, involved to actually confirm that the diet was the issue. In conclusion, if we're being outrageously generous to his position, 6% of those who tried a vegan diet reported any health issues at all. But as we discussed above, it's unclear if this is just a result of poor supplementation practices.
It's not clear why we should accept the implication that a diet is healthy if and only if it can be generally adhered to. There are many examples of diets with poor adherence rates that I don't think Joseph would sign off on being unhealthy, and there are plenty of examples of diets with high adherence rates that Joseph wouldn't consider healthy at all.
**Definitions:**
**D** := (x) diet is great
**G** := people generally adhere to (x) diet
**s** := Standard American Diet
**k** := Ketogenic Diets
**P1)** A diet is great if and only if people generally adhere to it.
**(∀x(Dx↔Gx))**
**P2)** People generally adhere to SAD and not keto.
**(Gs∧¬Gk)**
**C)** Therefore, SAD is great and keto isn't.
**(∴Ds∧¬Dk)**
**Claim #3 (**[**04:59**](https://youtu.be/MpxgZGnEF7E?t=299)**):**
> So it’s interesting to observe that the Dutch are competing with Montenegrins for the tallest people in the world title (animation source: USA data) and they happen to be 2nd and 3rd on the list for the most milk consumed per capita in the world. A study of 105 countries in the journal Economics & Human Biology noted that animal food, particularly dairy, most correlated with increases in height. [[5](https://pubmed.ncbi.nlm.nih.gov/26948573/)]
This is actually the first claim where he actually starts citing peer reviewed research and not just the 1930s equivalent of a blog article with no citations.
Firstly, this is an ecological fallacy. Essentially, Joseph is looking at two temporally concurrent variables and implying a causal relationship. Specially, the research that Joseph cites does not look at individuals, their animal food/dairy consumption in childhood, nor their attained height in adulthood. These heights aren't compared to height projections or heights of peers consuming different diets.
Instead, this research is just looking at the average height of each entire country and the average intake of said foods. Such studies are susceptible to something called the [ecological fallacy](https://en.wikipedia.org/wiki/Ecological_fallacy), meaning what applies on a country average level may not apply on an individual level.
In this graph on average as X increases, so does Y. But if you look at each cluster separately, as X increases Y decreases. A real life example of this is the relationship between smoking and longevity.
If you plot each country's smoking rate and lifespan you'll see that [the more people smoke the longer they live](https://www.thefunctionalart.com/2018/07/visualizing-amalgamation-paradoxes-and.html). This correlation, of course, breaks at an individual level.
I very much doubt that Joseph would approve of this ecological study. [[6](https://pubmed.ncbi.nlm.nih.gov/1140864/)]
The study makes no attempt to adjust for socioeconomic or genetic differences in the countries involved. Richer countries tend to have access to more expensive sources of calories, but also have fewer infections and cleaner water, among many other things conducive to better health. They also tend to eat meat. This doesn't tell us what's happening within each of those populations across the spectrum of meat consumption.
Also it's likely that the reason animal protein correlates strongly with height in Joseph's reference is that it's the main source of protein calories in most diets around the world. For example, in Europe where they essentially consume no plant protein (most plant foods consumed lack significant protein), highly correlated protein (defined by the authors as milk, eggs, pork, beef and potatoes), as well as animal protein and total meat associate more with height than total calories and total protein. If you look at Asia where people eat more plants protein, you'll see total protein and total calories correlate better. Also, inequality adjusted human development index unsurprisingly was more strongly correlated with height than any food.
**Claim #4 (**[**05:30**](https://youtu.be/MpxgZGnEF7E?t=330)**):**
> I recently interviewed Yovana Mendoza who had essentially made a career based around her vegan lifestyle when she had health issues she tried her best to solve them while staying on the diet, using all kinds of supplements and troubleshooting strategies but she eventually had to prioritize her health and quit the diet after 6 years … even though she had every motivation to keep being vegan. Reintroducing animal foods fixed her health issues. Yovana’s case is a peak at how complex it can be to replace animal foods in your diet.
Yovana Mendoza was a so-called "raw" vegan. As you can see from the picture he flashed, she was on a meme starvation diet of only raw food averaging an abysmal ~1000 calories a day.
Raw food diets are associated with many stupid beliefs revolving around self-purification, including extensive fasting periods (49% of study participants), not supplementing B12 (7% took any supplement at all), and enemas (16% of them). [[7](https://pubmed.ncbi.nlm.nih.gov/10436305/)]
Some believe once you are "purified" you lose your period which is a sign you're clean, for example. As you approach 100% raw food, pretty much half of them complain of amenorrhea, probably due to insufficient calories.
As you can see, raw diets associate with considerably low BMI scores.
Rawvana also [made a video](https://youtu.be/hMO4m0rZAB8?t=27) telling us how since she's gotten healthier on her raw vegan diet her "eyes have become greener", so I don't know how much stock we should put in her health advice, Joseph.
As illustrated by [Anna's analysis](https://youtu.be/iqDK_0iaVCE), this seems to be an extremely common pipeline. People go raw vegan, influenced by social media morons, they don't eat enough calories, because their diets aren't formulated correctly, and then they return to some omnivorous diet and claim that veganism failed them. No. Veganism didn't fail you. You played a stupid game and you won a stupid prize.
**Claim #6 (**[**06:18**](https://youtu.be/MpxgZGnEF7E?t=378)**):**
> Take Vitamin A - you might think the average vegan has way more vitamin A because it comes from vegetables like carrots or sweet potatoes - but that’s not vitamin A, that’s beta carotene that has to be converted into vitamin A …and the conversion rate is very poor - about 12:1. [[8](https://pubmed.ncbi.nlm.nih.gov/20237064/)] Though it’s more like 21:1 when you account for the hampering effect of fiber in the diet. [[9](https://pubmed.ncbi.nlm.nih.gov/12221270/)] Not only that, the more you eat, the worse the conversion rate becomes. Further, depending on your genes, your conversion rate could be even lower - [this is the case for me](https://www.youtube.com/watch?v=gWiC4ZCS55Y&t=421s) and for potentially as much as 37% of people of European descent (See also, 57% lower. [[101](https://pubmed.ncbi.nlm.nih.gov/35571879/)][[1](https://pubmed.ncbi.nlm.nih.gov/35571879/)[12](https://pubmed.ncbi.nlm.nih.gov/19103647/)] Actual vitamin A only comes from animal foods or synthetic supplements.
Firstly, let's cut to the chase. Is there a risk of vitamin A deficiency among those only relying on non-retinol sources of vitamin A? That's the question. We'll get to the mechanistic speculation, and why it's so dumb, but for now let's focus on actual outcomes. To my knowledge there are two studies assessing retinol status in vegans after excluding those who supplement. [[13](https://pubmed.ncbi.nlm.nih.gov/24394311/)][[14](https://pubmed.ncbi.nlm.nih.gov/26502280/)]
Both studies showed that vegans had statistically significantly lower retinol status than omnivores, but the differences were not clinically significant. We're free to speculate all we want, but at the end of the day there is no reason to believe that the differences in status actually amount to any differences in expected health outcomes between the two groups.
Now, let's get to the mechanistic fuckery. Joseph claims that there are genetic differences in carotenoid to retinol conversion capacity that could lead to deficiency in some who are relying on carotenoids over retinol. Right off the bat, Joseph's own reference contradicts his claim, as the entire variance in the population sample had fasting plasma retinol within the reference range.
> _...the lowest plasma concentration was 963.8 nM, indicating that all volunteers had adequate serum vitamin A concentrations._
Even the people with the worst impairments maintain adequate retinol status, despite only getting an average of a measly 133mcg/day of retinol. The only thing that changes is that the ratio of beta-carotene to retinol is increased based on the severity of the impairment in conversion rates. That's all.
But, we can take this a step further and actually see what happens when we try to correct vitamin A deficiency using dietary carotenoids in human subjects. [[15](https://pubmed.ncbi.nlm.nih.gov/15883432/)][[16](https://pubmed.ncbi.nlm.nih.gov/17413103/)][[17](https://pubmed.ncbi.nlm.nih.gov/9808223/)][[18](https://pubmed.ncbi.nlm.nih.gov/10584052/)][[19](https://pubmed.ncbi.nlm.nih.gov/15321812/)][[20](https://pubmed.ncbi.nlm.nih.gov/16210712/)] On the whole, eating foods rich in carotenoids reliably improves and/or normalizes vitamin A status. Even foods that have been genetically engineered to have higher levels of carotenoids reliably improve vitamin A status in humans. [[21](https://pubmed.ncbi.nlm.nih.gov/19369372/)] In fact, a newer study published in 2020 found no differences in retinol status between BCO1 genotypes in a population consuming low amounts of preformed retinol. [[22](https://pubmed.ncbi.nlm.nih.gov/32560166/)]
Let me explain what's happening here. These genetic variants likely aren't changing the total amount of retinol converted from carotenoids. Likely the only thing that's happening here is that the conversion curve is changing shape without a change to the area under that curve. Meaning that across these genetic variants, people are capable of converting the same amount of retinol from carotenoids, but the rate at which they make that conversion is slightly longer in those with the so-called impairments. In my opinion, this is the most parsimonious way to reconcile the data.
As a side note, the only cases of vitamin A toxicity (hypervitaminosis A) from whole foods that I could find in the literature involved the consumption of preformed retinol from liver. [[23](https://pubmed.ncbi.nlm.nih.gov/25850632/)][[24](https://pubmed.ncbi.nlm.nih.gov/21902932/)][[25](https://pubmed.ncbi.nlm.nih.gov/10424294/)][[26](https://pubmed.ncbi.nlm.nih.gov/31089689/)][[27](https://pubmed.ncbi.nlm.nih.gov/3655980/)] In one case, a child died from consuming chicken liver pate sandwiches. I could find no case reports of such vitamin A toxicity related to carotenoids.
**Claim #7 (**[**06:58**](https://youtu.be/MpxgZGnEF7E?t=418)**):**
> A 2021 study found vegan Finnish children had insufficient vitamin A and a 2020 German study found vegans to have a lower vitamin A level than omnivores. [[28](https://pubmed.ncbi.nlm.nih.gov/33471422/)][[29](https://pubmed.ncbi.nlm.nih.gov/33161940/)]
In both studies, vegan participants had lower vitamin A status, but again, this seemed to be clinically irrelevant. With the authors of the Finnish study concluding that none of the vegans could be classified as deficient, and the the authors of the German study reporting that Vitamin A status among vegans was still well within the reference range.
We should be starting to see a pattern here, and this should lead us to question the utility of having higher vitamin A status as a consequence of consuming preformed retinol. Even if we granted that you will boast a higher vitamin A status as an omnivore, it's not clear that possessing a higher status actually has any clinical benefit or advantage. I don't know why it would be desirable. Is Joseph prepared to resign himself to affirming that more is simply better? Shall we coin this the Everett Fallacy?
**Claim #8 (**[**07:26**](https://youtu.be/MpxgZGnEF7E?t=446)**):**
> Vitamin D is pretty much only found in animal foods with some exceptions like some mushrooms and some algae. Some people can get enough vitamin D from the sun, but if you live at latitudes above 37 degrees, your skin barely makes any vitamin D from the sun except for in summer. [[30](https://www.health.harvard.edu/staying-healthy/time-for-more-vitamin-d#:~:text=Except%20during%20the%20summer%20months,risk%20for%20vitamin%20D%20deficiency)]
This is one of those times where I won't say anything I will just let his citation speak for itself.
> "Lack of sun exposure would be less of a problem if diet provided adequate vitamin D. But there aren't many vitamin D–rich foods (see chart, below), and you need to eat a lot of them to get 800 to 1,000 IU per day...For these and other reasons, a surprising number of Americans — more than 50% of women and men ages 65 and older in North America — are vitamin D–deficient, according to a consensus workshop held in 2006."
His own citation notes that a massive portion of the population is deficient and the treatment for that is sun exposure or supplementation, not goose liver.
**Claim #9 (**[**07:40**](https://youtu.be/MpxgZGnEF7E?t=460)**)**
> A 2016 Finnish study found vegans’ levels of vitamin D to be 34% lower than omnivores. [[31](https://pubmed.ncbi.nlm.nih.gov/26840251/)]
They had lower intake and therefore lower levels. According to Joseph's previous reference, they should probably be supplementing more.
**Claim #10 (**[**07:52**](https://youtu.be/MpxgZGnEF7E?t=472)**):**
> Unless you’re eating fermented foods, you’ll only find vitamin K2 in animal foods. The richest sources of K2 are going to be animal livers (especially goose liver), egg-yolks, hard cheese and full-fat dairy. Unfortunately New York City made it illegal for schools to serve whole milk in 2006. [[32](https://www.politifact.com/factchecks/2021/jun/07/lorraine-lewandrowski/whole-milk-prohibited-being-offered-new-york-schoo/)] The fermented soybean dish natto does in fact have a ton of K2 and sauerkraut has some too. Vitamin K2 helps put calcium into the right places like your bones and keeps it out of your heart which is thought to be one reason higher vitamin K2 strongly correlated with reduced risk of heart disease. [[33](https://pubmed.ncbi.nlm.nih.gov/34785587/)][[34](https://pubmed.ncbi.nlm.nih.gov/28639365/)]
Here's a quick intro for vitamin K2. There are many different vitamin K isomers (or vitamers). We have vitamin K1 from plants and vitamin K2, primarily from fermented foods or animal products. There is only one vitamin K1, but vitamin K2 has many forms, including MK4 and MK7, which have been studied most. The form of K2 you can not obtain from fermented foods is MK4, but it doesn't appear to be bioavailable at nutritional doses.
First, we'll look at bioavailability of MK4. He mentions animal livers (especially goose liver), egg-yolks, hard cheese and full-fat dairy. I couldn’t find any study on bioavailability of MK4 from foods rather than supplements. But, we can look at studies with doses one could plausibly obtain from diet alone. In probably the best study on this subject, researchers assessed **420 μg of MK-4 compared to 420 μg of MK-7**. [[35](https://pubmed.ncbi.nlm.nih.gov/23140417/)] As you can see from this chart, the only reasonable way to obtain this is with goose liver. [[36](https://pubmed.ncbi.nlm.nih.gov/11356998/)]
The other things he recommended simply don’t have enough. To get this amount it would take **8.9 kilograms of hard cheese, 52.5 liters of whole milk, or 52.4 average eggs.** The amount of goose liver it would take to get this dose of MK-4 is roughly **115g of liver,** however this has **over 10,000μg of retinol, the upper limit is 3000μg** and hypervitaminosis A is no joke.
But regardless, let’s say someone managed to eat this amount of MK-4 regularly. Is it actually absorbed? It wouldn't appear so.
At no time point after the oral administration of 420μg of MK4 is it actually detectable in the blood.
In summary, Joseph suggests food items like hard cheese and whole milk for vitamin K2 when they have abysmal amounts that probably aren't even absorbed. Worth noting that the natto he dismissed contains MK7 which is actually bioavailable, as evidenced by the same reference. Natto also contains it in concentrations over **700 times that of hard cheese**, which is the richest source of MK7 out of the foods he listed.
**Claim #11 (**[**08:25**](https://youtu.be/MpxgZGnEF7E?t=505)**):**
> Speaking of all these nutrients for the skeleton, a 2021 polish study found vegan children to have weaker bones and were 3cm shorter than their meat eating counterparts. [[37](https://pubmed.ncbi.nlm.nih.gov/33740036/)]
What Joseph didn't mention was that 29% of the vegan children did not consume vitamin B12 supplements or fortified foods, and only 32.7% used vitamin D supplements. Those who did actually consume vitamins B12 and D had comparable B12 and D status to omnivores. It's entirely plausible, if not probable, that this high percentage of non-supplementing participants was enough to drag down the average for the entire group.
I mention this because it's clear that a large chunk of the cohort was not actually supplementing vitamin B12 and vitamin D. Both of which are nutrients that are strongly associated with normal growth. There was also little to no consideration for other dietary variables, and the analysis itself is cross-sectional with extremely small sample-sizes.
Perhaps also worth noting are the similar lean mass, lower fat mass, and preferable LDL-C and hs-CRP values of the vegans. But he didn't mention that.
**Claim #12 (**[**08:27**](https://youtu.be/MpxgZGnEF7E?t=507)**):**
> A British study and a Dutch study also found vegan children to be shorter. [[38](https://pubmed.ncbi.nlm.nih.gov/3414589/)]
Let's start with the British study. These results are trivially explainable by the lower caloric intakes for vegans in his reference.
Also, while the vegans tended to fall below the 50th percentile for weight, the vast majority experienced normal growth, and the lower weight (and in some cases height) may be attributable to the lower caloric intake. The authors actually take note of this, but Joseph didn't mention it.
The authors also suggest that the lower fat intake may be the reason they had a lower caloric intake, and go on to state that dense fat sources can be important for children for that reason (eat your avocados, kids). They concluded that children can grow up to be "normal" and that there's no evidence of impairment to cognitive development.
Just as a side note, it's also funny to mention that the vegan diets were more nutrient dense than the average omnivorous UK diet. Even more hilariously, they explicitly state that there are healthy and unhealthy versions of vegan diets and that clowns will run with the occasional case reports on unhealthy vegan kids fed **inappropriate** diets. These authors were calling out Joseph in 1988.
On to the Dutch study. Firstly, the so-called "vegan" diet was actually a type of meme "vegan" diet called the macrobiotic diet. This diet is highly restrictive and often very low in protein. This is not representative of what a well-balanced "vegan" diet would look like.
Thus far, the studies he cited either haven't supported his claim or provide clear reasons for why there may be differences in growth. With the reasons provided not being intractable characteristics of vegan diets themselves. He also left out the studies where we do see similar growth between vegan and omnivorous kids with adequate diets.
In the Farm Study was a 1989 study involving children ages four months to ten years residing in a community in Tennessee. [[39](https://pubmed.ncbi.nlm.nih.gov/2771551/)] 75% of mothers were vegan through pregnancy and 73% of children were vegan since birth. These mothers consumed well balanced diets with fortified foods (soy milk and nutritional yeast), which they fortified themselves!
> The Farm community was generally well informed regarding issues related to vegetarianism, including complementing different protein sources, for example, grains and legumes and nonanimal sources of vitamins and minerals. Until 1983, the population followed a vegan diet, with soybeans being their primary source of protein. Supplements of vitamins A, D, and B12 were added to the soy milk produced on The Farm. Nutritional yeast (containing vitamin B12) and other vitamin and mineral supplements were also used. In the fall of 1983, some members of the community introduced eggs and dairy products into their diets.
Across vegan children, growth was skirting the 50th percentile on average. This is exactly where these growth trajectories should be.
Same for weight.
We also have the VeChi Diet Study. [[40](https://pubmed.ncbi.nlm.nih.gov/31013738/)] Vegan and omnivorous children had similar caloric intakes. Omnivores had the highest protein, fat, and added sugar intake, while vegans had the highest total carb and fibre intake. In fact, the vegans were still able to consume a median of 2.25g of protein per kg bodyweight. While there were a few outliers in each group, growth was generally very similar overall.
There are explanations for the children who may have been stunted or wasted, and they're nothing that is necessarily inherent to vegan diets themselves. These reasons include: short parents, inadequate caloric intake, exclusively breastfeeding longer than recommended (probably due to hippie vegan parents doing dumb hippie things).
> Regarding these eight children classified as stunted, two had very low reported energy intakes (534 kcal/day and 598 kcal/day, respectively), and both were exclusively breastfed >6 months (7 and 9 months, respectively). An overly long period of exclusively breastfeeding can result in an insufficient intake of complementary foods and inadequate low TEI because, after a certain age, human milk alone cannot supply energy and all nutrients in adequate amounts to meet a child’s requirements [71]. Furthermore, one of the two children as well as three other children classified as stunted had parents with a BH (mother: 161 cm, father: 170 cm) below the German average (167 cm and 180–181 cm of 25–55-year-old women or men, respectively) that might have influenced the child’s BH. The other child with low energy intake was also categorized as SGA, which is considered a risk factor for stunting [72]. Another stunted child was categorized as SGA, and its birthweight was only slightly above 2500 g (2545 g). The seventh child was exclusively breastfed for twelve months (the eighth child was breastfed for eight months), and it had parents with BHs (mother: 160 cm, father: 178 cm) below the German average.
We also have data on intake of micronutrients and fatty acids in the 1-3 year olds in this cohort. [[41](https://pubmed.ncbi.nlm.nih.gov/34855006/)] All diet groups had low iodine intake, and the vegans had the lowest intakes of saturated fat, cholesterol, and DHA (although omnivores had low intakes too), but higher intakes of ALA and LA. They also mention that vegan and vegetarian children had the more favourable intakes of several micronutrients and fatty acids.
In addition to evaluating nutrient intake, they also measured status in 6-18 year olds. [[42](https://pubmed.ncbi.nlm.nih.gov/34069944/)] Ultimately, the results are very similar to the those of the VeChi Diet Study that was previously mentioned, with preferable blood lipids in the vegans.
A further study on mothers consuming various dietary patterns supports that a vegan diet can support "normal and physiological growth" through pregnancy and the first year of life. Also of note, 95.2% (20/21) of the vegan mothers took supplements through pregnancy. [[43](https://www.minervamedica.it/en/journals/minerva-pediatrics/article.php?cod=R15Y9999N00A21041604)]
So some of Joseph's own references suggest vegan diets can support growth and development, and that is consistent with other research where vegans are consuming a balanced and appropriately supplemented diet.
**Claim #13 (**[**09:34**](https://youtu.be/MpxgZGnEF7E?t=574)**):**
> Most vegans know they need to supplement B12 which is very important for proper brain function. Yet, one study looking at B12 status in vegetarians and vegans found that 7% of vegetarians and 52% of vegans were not getting enough B12. [[44](https://pubmed.ncbi.nlm.nih.gov/20648045/)] However, in another study with a more sensitive testing method - they found a whopping 77% of vegetarians and 92% of vegans had insufficient B12 whereas only 11% of omnivores did. [[45](https://pubmed.ncbi.nlm.nih.gov/12816782/)] Perhaps these B12 supplements don’t work exactly like animal foods do. Also it can take years to deplete the body’s B12 store, so people can be lacking B12 for a while without realizing it.
Right off the bat, 81% of vegans did not supplement in the first study. In the second, the authors did not assess how many of them were supplementing, but we know 59% supplemented "B vitamins".
Joseph then concludes (from two studies were the majority did not supplement B12) that B12 supplements "don’t work exactly like animal foods do". If Joseph wanted to know if B12 supplements work at all he could've simply read his previous reference, Elorinne, et al. (2016). [[31](https://pubmed.ncbi.nlm.nih.gov/26840251/)] Had he done so, he would have noticed that 91% of that cohort took B12 supplements, and as you'd expect they were not B12 deficient.
If Joseph wanted to know if B12 supplements work differently than animal foods, he could turn his attention to this interventional study that found that fortified cereal was more effective at raising B12 than pork. [[46](https://pubmed.ncbi.nlm.nih.gov/31519167/)]
Also, various doses of cheapo, vanilla-ass cyanocobalamin rescue vitamin B12 deficiency in clinically deficient vegans. [[47](https://pubmed.ncbi.nlm.nih.gov/29499976/)] This is confirmed by clinically meaningful reductions in both methylmalonic acid and total homocysteine. If Joseph knows of any better biological correlates for B12 absorption and utilization, as well as evidence that they're uniquely affected by animal foods, I'd love to hear from him about it.
**Claim #14 (**[**11:38**](https://youtu.be/MpxgZGnEF7E?t=698)**):**
> ...another possibility is the vegan diet has impaired digestion.
The term "digestion" here is so unclear and nebulous, that it is uncertain what exactly to look for in the literature in order to test the hypothesis. However, if we assume that the hypothesis is referring to any symptoms related to digestion, we should expect to see increased rates of digestion-related symptoms, as reported as adverse events, in any of the randomized controlled trials that have been done on so-called "vegan" diets. But we can find close to none, which calls into question whether or not this is even an effect, let alone a generalizable effect.
**Claim #15 (**[**12:25**](https://youtu.be/MpxgZGnEF7E?t=745)**):**
> ...many [vegans] do quit the diet because of health issues.
If "many" is meant to be some sort of generalization, then his claim is straightforwardly contradicted by a study discussed in one of his own references on vegan recidivism rates, the 2015 Faunalytics study.
> Interestingly, health did not present a noticeable difficulty for study participants, with the exception of vitamin B12 monitoring. 2) Consider increasing awareness about the importance of B12: a far greater percentage of former (76%) than current (42%) vegetarians/vegans never had their B12 levels checked while they were adhering to the diet.
His only evidence for this claim is a montage of ex-vegan YouTubers who already have a demonstrable history of lying to people's faces. What the fuck are we even doing here, Joseph? These people were telling their audiences that they had newfound health on a vegan diet, and now they are once again telling their audiences that they have newfound health, but on a non-vegan diet. Joseph expects us to believe them. I can only guess that's because he is an idiot and doesn't understand what evidence is.
**Claim #16 (**[**13:21**](https://youtu.be/MpxgZGnEF7E?t=801)**):**
> A 2012 study found in 63 patients with constipation, reducing fiber intake improved symptoms but eating a zero fiber diet completely eliminated all symptoms. [[48](https://pubmed.ncbi.nlm.nih.gov/22969234/)]
This is a category mistake. Constipation isn't indigestion. Digestion precedes stool formation and colonic transit. Also, there is no mention of vitamin B12 deficiency or its related symptoms among the subjects in the reference Joseph provided. It's not clear how this is interacting with the claim.
I'll briefly entertain the tangent, though. The trial that Joseph references is not easily generalizable, because the subjects had idiopathic constipation. It's also not clear at all what this has to do with "vegan" diets. Additionally the researchers did not actually assess fibre intake. Fibre intake was assumed based on the researchers instructions to the subjects, which naturally is a very poor measurement to fibre intake.
Meanwhile, we see very consistently that increased consumption of fibre associates with a decrease in bowel transit time and improving symptoms of constipation. [[49](https://pubmed.ncbi.nlm.nih.gov/26950143/)][[50](https://pubmed.ncbi.nlm.nih.gov/35816465/)]
**Claim #17 (**[**13:46**](https://youtu.be/MpxgZGnEF7E?t=826)**):**
> As for B12, you need to have strong enough stomach acid to properly absorb it and dietary fiber is known to weaken the stomach acid. [[51](https://pubmed.ncbi.nlm.nih.gov/2823869/)][[52](https://www.tandfonline.com/doi/abs/10.3109/00365528709095891)][[53](https://pubmed.ncbi.nlm.nih.gov/6095709/)]
For the former claim, there is no reference. But what Joseph is probably referring to here is the requirement for a lower stomach pH in digesting food normally in general. Without a sufficiently acidic stomach acid, it is true that vitamin B12 may not be adequately liberated from a given food matrix.
However, this doesn't apply to supplements (as supplements do not have a food matrix that requires a particularly low pH stomach acid to digest), and therefore doesn't apply to "vegan" diets. Also, we can easily see from previously cited research that vegans can achieve and maintain normal B12 status on high fibre diets.
In fact, you can even absorb B12 adequately and rescue frank B12 deficiency syndromes by shoving it directly up your ass. [[54](https://pubmed.ncbi.nlm.nih.gov/5924495/)] Sublingual B12 supplements are effective in rescuing B12 deficiency. [[55](https://pubmed.ncbi.nlm.nih.gov/14749150/)] Both of these methods bypass the stomach completely.
**Claim #18 (**[**13:56**](https://youtu.be/MpxgZGnEF7E?t=836)**):**
> So the context matters - what else are you getting with the nutrients? For example, there are plenty of plant sources of iron, but plant foods like whole grains, legumes and nuts contain phytic acid that impairs iron absorption. [[56](https://pubmed.ncbi.nlm.nih.gov/12936958/)] Spinach is thought to be a great source of iron but you can only absorb 2% of it because of the oxalate in it. [[57](https://pubmed.ncbi.nlm.nih.gov/1745900/)]
Once again, Joseph shows that he either doesn't read the studies he cites or ignores where they contradict him. From the first study:
> Iron deficiency anemia appears to be no more prevalent among vegetarian women than among nonvegetarian women...Thus, although several reports indicate that vegetarians in Western societies have lower iron stores and may have lower hemoglobin concentrations, they do not indicate a greater incidence of iron deficiency anemia...Lowering iron stores without increasing the risk of iron deficiency anemia may confer a health advantage when vegetarian diets are chosen from an abundant food supply.
Joseph further shows that he is really good at constructing strawmen. What official public health authority in any developed country actually recommends spinach as a significant source of iron? Regardless, it's also a non-sequitur that just because spinach has a particularly poor bioavailability of iron that there exist no vegan sources of iron with good bioavailability. There even exist other green vegetables with good bioavailability, such as broccoli and cabbage. [[58](https://pubmed.ncbi.nlm.nih.gov/31394334/)]
**Claim #19 (**[**14:00**](https://youtu.be/MpxgZGnEF7E?t=840)**)**
> Then, where the heme-iron in animal foods is very easily absorbed, the non heme iron in plants and supplements is quite poorly absorbed. Two different literature reviews suggest that vegans are at greater risk for iron deficiency than omnivores [[59](https://pubmed.ncbi.nlm.nih.gov/28319940/)][[60](https://pubmed.ncbi.nlm.nih.gov/30783404/)].
No citation was provided for this claim and he says it as if it follows logically from what he said beforehand. Which it doesn't. Phytic acid in isolation impairing iron absorption in some plant foods high in phytic acid having low bioavailability of iron also doesn't imply that iron is poorly absorbed from all plant sources.
Firstly, despite whole wheat flour being higher in phytic acid than white wheat flour, it has better bioavailability of iron. [[61](https://pubmed.ncbi.nlm.nih.gov/10655952/)] Granted this is in animal models, but this is evidence Joseph has been known to accept in the past.
Secondly, other compounds that are common in plant foods but are absent (or virtually absent) from animal foods may have pleiotropic effects that mitigate or even overcome the effect of phytates on iron absorption, with vitamin C probably being the most prominent example. In regards of counteracting phytic acid, 50mg (less than an orange worth) does more than 50g of meat. [[62](https://pubmed.ncbi.nlm.nih.gov/2911999/)]
It also doesn't follow that one needs to consume animal products to meet iron needs, which Joseph heavily implies. Increased intake through diet and/or supplementation are clearly possible.
First of all, both the literature reviews Joseph cites are looking at vegetarians, not vegans. I thought his video was on so-called "vegan" diets, not vegetarianism. Even the authors of his own references disagree with his interpretation. Here's a quote from Pawlak, et al. (2017):
> Findings regarding individuals who adhere to specific vegetarian diet type, such as vegans, were underrepresented and thus, conclusions regarding iron status among such individuals were not possible.
And from another of Joseph's references, Pawlak, et al. (2018):
> Considering the limitations, it is reasonable to conclude that the findings are most likely not representative of the entire vegetarian populations nor are they representative of any one specific vegetarian subgroup. 3 of the studies were published in the 1990s and one in 1982. It is reasonable to assume that iron fortification practices have changed since the time of food availability has improved due to globalization. Consequently, this makes the generalization of the findings difficult
So, what is the point in wrongly applying or generalizing these findings with already questionable external validity from vegetarians onto vegans? That being said, just because the studies Joseph cites don't appropriately support his claim does not imply that his claim is wrong. For that, we need to go deeper.
There are three studies that were published before the two reviews that Joseph cited that differentiate between vegans and vegetarians, while also comparing them to omnivores with measurements of plasma ferritin. There are four that were published afterward. It would be valuable to go through them one by one.
In Schüpbach, et al. (2017), omnivores had higher plasma ferritin, but there was a lower percentage of vegans than omnivores in the range of deficiency, while vegans had almost double the iron intake of omnivores. [[14](https://pubmed.ncbi.nlm.nih.gov/26502280/)]
The more curious finding with respect to iron was that for omnivores and vegetarians, the correlation between iron intake and plasma ferritin was fairly strong and statistically significant (r = 0.247, p = 0.030; r = 0.331, p = 0.030, respectively), but not so for vegans (r = 0.168, p = 0.281).
The more concerning finding outside of iron was that despite a similar zinc intake across groups almost half of vegans were below the normal range compared to just 10% of omnivores. However, almost 60% of omnivores had folate levels below the normal range as well.
Vegans in Elorinne, et al. (2016) had much lower plasma ferritin than non-vegetarians despite higher intake. [[31](https://pubmed.ncbi.nlm.nih.gov/26840251/)] It's unclear whether there was a single subject with low ferritin and this result was not discussed anywhere in the text. However, there were funny sections about selenium in fertilizers and how a low LA intake might help vegans convert LNA to DHA.
Less than half the vegan children in Desmond, et al. (2021) used B12 supplements, almost a third got neither B12 supplements nor B12 fortified foods. [[37](https://pubmed.ncbi.nlm.nih.gov/33740036/)] Under their second adjustment model, the vegan children had 25% lower ferritin levels. 30% of the vegan children had ferritin levels below the cut-off, compared to 13% of the omnivore children. 2% and 6% of vegan children had moderate and mild iron deficiency anemia, respectively, compared to none of the omnivore children. The authors were (rightfully) much more concerned about the differences in bone mineral content and B12 deficiency. They also get props for looking at cardiovascular risk factors in children.
Another study, by Slywitch, et al. (2021), gets props for a 10 year long recruitment period and for differentiating between menstruating and non-menstruating women. [[63](https://pubmed.ncbi.nlm.nih.gov/34578841/)] However, for unknown reasons, these authors only differentiated between vegans and vegetarians for the analysis on BMI but not for ferritin. To be fair, they were more interested in how inflammation may mask iron deficiency, but still. It would have been nice to have that data.
Weikert, et al. (2020) represents one of the better studies on the subject, because the groups were similar in their characteristics and all but one vegan were actually using supplements. [[29](https://pubmed.ncbi.nlm.nih.gov/33161940/)] Plasma iron and ferritin levels were on average lower in vegans than omnivores, but not statistically significantly so, with the vegans having a 50% higher iron intake. 11% of vegans showed signs of iron deficiency compared to 8% of omnivores. Vegans who substituted iron had higher average ferritin than omnivores who did not substitute iron.
Another study by Alexy, et al. (2021) found statistically significantly lower plasma ferritin than omnivores despite 50% higher iron intake, but prevalence below the cut-off was called "low" by the authors and thrown into the supplemental. [[42](https://pubmed.ncbi.nlm.nih.gov/34069944/)] Weirdly, the authors were concerned about the high prevalence of B2 deficiency in all groups, using a cut-off of 199 µg/l.
In Wilsen, et al. (1999), despite the 50% higher iron intake, the vegans had almost 50% lower serum ferritin than omnivores, with 20% falling below 12 ng/ml. [[64](https://pubmed.ncbi.nlm.nih.gov/10201799/)] The difference in hemoglobin between vegans and omnivores was also statistically significant. On the other hand, 20% of omnivores had ferritin levels elevated above 200 ng/ml, which is indicative of inflammation.
In conclusion, even though Josephs citations don't support his claim, there is some truth to the matter. The literature is in unanimous agreement that iron in vegan diets has much lower bioavailability, but this is not due to phytates alone. Dietary fiber and polyphenols are important as well. Of course this is not enough to infer an outcome such as iron deficiency, let alone iron deficiency anemia, since vegans also have a much higher iron intake than omnivores. Furthermore, in many of the studies lower iron status is observed without a particularly increased risk of deficiency.
Vegans, especially those who menstruate, might want to err on the side of caution by regularly getting their ferritin checked whenever they get their B12 checked, and then supplementing accordingly. Pretty much the same is true for vegetarians, or even omnivores for that matter. But what these studies show overall is that no matter their diet, people kind of suck at hitting reference ranges of biomarkers for all nutrients.
**Claim #20 (**[**14:30**](https://youtu.be/MpxgZGnEF7E?t=870)**):**
> Now before we continue, why should we assume a meat containing diet was the natural default for humans rather than a plant-based diet? Well, to get a wide variety of nutrients, vegans have to eat a huge variety of modern fruits and vegetables, but the fruits and vegetables early humans had access to were nothing like modern ones. Before cultivation, they had far less actually edible material and far more fiber and seeds. Paleoanthropologist Daniel Lieberman has said that the sweetest fruit available would have been no sweeter than a modern day carrot.
Previously having less edible material is trivially true of animal foods produced from modern animal agriculture.
**Claim #21 (**[**14:58**](https://youtu.be/MpxgZGnEF7E?t=898)**):**
> We have stable isotope studies finding we ate pretty much whatever meat we could get our hands on… our earliest art is cave paintings of hunts. Lastly, the brain is a disproportionately energy expensive organ, hogging 20% of our oxygen and calories. [[65](https://pubmed.ncbi.nlm.nih.gov/30872714/)][[66](https://pubmed.ncbi.nlm.nih.gov/12149485/)] Our guts (also energy expensive) shrank in size to allocate more resources to the brain. [[67](https://pubmed.ncbi.nlm.nih.gov/22174868/)] Thus, to fuel our big brains, the more energy efficient animal fat became favored over fibrous plants that took time and energy to chew and digest.
What point is Joseph trying to make here? We could try to formalize it, perhaps.
**Definitions:**
**B** := (x) food make brain big
**G** := (x) food gud
**O** := ooga booga
**m** := meat
**p** := plants
**P1)** If food gud, then food make brain big.
**(∀x(Gx→Bx))**
**P2)** Meat gud.
**(Gm)**
**P3)** Plants no make brain big.
**(¬Bp)**
**P4)** Ooga booga.
**(O)**
**C)** Therefore, meat make brain big, plants no gud, ooga booga.
**(∴Bm∧¬Gp∧O)**
**Claim #22 (**[**15:34**](https://youtu.be/MpxgZGnEF7E?t=934)**):**
> Most people are not aware that animal foods are packed with far more of a huge variety of nutrients, especially ones critical for brain function. This may have a role in why a 2021 study found people who don’t eat meat to have significantly higher risk of depression and anxiety. [[68](https://www.tandfonline.com/doi/full/10.1080/10408398.2020.1741505)]
Again, in his typical style, the review Joseph linked contained only one randomized controlled trial and guess what that one trial showed. I'll quote the authors directly.
> Restricting meat, fish, and poultry improved some domains of short-term mood state in modern omnivores. To our knowledge, this is the first trial to examine the impact of restricting meat, fish, and poultry on mood state in omnivores.
Also, the authors overlooked a couple more trials, and didn't even mention them. I personally don't really see a reason for their exclusion. [[69](https://pubmed.ncbi.nlm.nih.gov/24524383/)][[70](https://pubmed.ncbi.nlm.nih.gov/20389060/)] They also rated the one RCT that they did include as "low quality" without providing a decent justification. In both trials, a benefit of so-called "vegan" diets was observed.
Not only that, but in a 2022 systematic review including more studies, they note that higher quality studies and studies that can distinguish temporal relationships (such as RCTs and cohort studies) the effects of plant-based diets on mental health are either positive or non-significant. This review contained two RCTs, one on vegetarians (which can be interpretated as a meat-restriction intervention, so it is still relevant) which showed improved confusion and stress and one on vegans which showed improvements in depression indicators.
Lastly, one of the two "high quality" studies in the review that Joseph cited evaluated the temporal relationship and suggests that the so-called vegan diet came **after** the development of mental health issues. [[71](https://pubmed.ncbi.nlm.nih.gov/22676203/)] When vegan, vegetarian, and semi-vegetarian diets are separated, meta-analyses suggest that semi-vegetarian diets are associated with higher prevalence of depression, while there is no statistically significant relationship between "vegan" or vegetarian diets and depression. [[72](https://pubmed.ncbi.nlm.nih.gov/33822140/)]
Here is the prevalence of depression forest plot from that meta-analysis.
And mean depression scores.
Also, just for flavour, I'll point out that Joseph's reference was funded by the beef industry.
> This study was funded in part via an unrestricted research grant from the Beef Checkoff, through the National Cattlemen’s Beef Association. The sponsor of the study had no role in the study design, data collection, data analysis, data interpretation, or writing of the report.
**Claim #23 (**[**17:17**](https://youtu.be/MpxgZGnEF7E?t=1037)**):**
> The peoples Weston price studied had an intuitive understanding of the importance of nutrient dense foods - especially in pregnancy and childhood. Even without a nutrition label, they knew that certain animal foods encouraged proper robust growth.
There is an implicit claim here that animal foods have some kind of special importance for pregnancy and childhood. Ultimately, this is just an anecdote, barely distinguishable from an appeal to authority. So, let's throw one back from the American Dietetic Association:
> ...appropriately planned vegetarian, including vegan, diets are appropriate for all stages of the life cycle, including pregnancy, lactation, infancy, and childhood
To be clear, I think hinging the truth value of any claims about the health value of either co-called "vegan" diets or omnivorous diets on either of these opinions is incredibly cringe. It's just not clear to me why we can't just counter anecdotes with anecdotes.
**Claim #24 (**[**18:12**](https://youtu.be/MpxgZGnEF7E?t=1092)**):**
> As Michael Pollan has argued in his book In Defense of Food - we frequently fall victim to this concept of 'nutritionism' that we don’t necessarily need whole foods, we just need their components.
Joseph, what does it mean to fall victim to a concept that is arguably true? Also, what do you mean by need? Is there some sort of necessity relation between whole foods and human health that you'd like to tell me about?
**Claim #25 (**[**18:34**](https://youtu.be/MpxgZGnEF7E?t=1114)**):**
> According to a 2012 study, despite taking prenatal supplements, 58% of pregnant woman had iron levels below normal. [[73](https://pubmed.ncbi.nlm.nih.gov/22113871/)]
Joseph makes this claim to vaguely support the notion that we should not rely on supplements. However, the study cited to support this claim is a study of 19 pregnant women who were given labelled iron supplements in order to better characterise placental iron transport. It is not a large scale study of prevalence of iron deficiency in pregnant women who take prenatal supplements and therefore does not support the claim.
On the contrary, a meta-analysis involving 43274 women shows that preventative daily oral iron supplementation reduces iron deficiency and iron deficiency anemia at term by 57% and 70%, respectively. [[74](https://pubmed.ncbi.nlm.nih.gov/26198451/)]
**Claim #26 (**[**18:40**](https://youtu.be/MpxgZGnEF7E?t=1120)**):**
> 90% of Americans are not getting enough [choline]. [[75](https://pubmed.ncbi.nlm.nih.gov/30853718/)]
While it is clear that choline is an essential nutrient for proper liver, muscle, and brain function, and this study does estimate 90% of Americans to fall short of the adequate intake, the same study caveats that:
> Current intakes cannot be deemed inadequate based upon the [adequate intake] value alone. Although [adequate intakes] may be useful in guiding individual dietary plans, by definition, they are established when the evidence is insufficient to calculate an [estimated average requirement]. Therefore it is not possible to conclusively assess the risk of inadequacy in a population.
In short, the way Joseph presents this study is essentially fear-mongering.
**Claim #27 (**[**18:47**](https://youtu.be/MpxgZGnEF7E?t=1127)**):**
> Choline from egg-yolk is better absorbed than choline from the common supplement, choline bitartrate. 150 calories of egg yolk (a little over 2 eggs) are enough to meet ones adequate choline intake.
While choline absorption from eggs is particularly high, choline intake in the American population is driven by egg intake and vegetarians have the lowest intakes among the US population, this does not support the notion that choline requirements cannot be met with proper supplementation.
On the other hand, the same authors as from the paper before state that choline is a precursor to betaine, another 'methyl donor' largely present in plant foods such as wheat bran, beets and spinach. Higher intakes of betaine may spare some of the potential negative consequences of low choline intake among vegetarian populations. [[76](https://pubmed.ncbi.nlm.nih.gov/31385730/)]
The main concern with choline deficiency is non-alcoholic fatty liver disease (NAFLD). If choline deficiency was an issue among vegans we'd expect a positive correlation between higher adherence to so-called "vegan" diets and NAFLD, an inverse correlation between consumption of animal foods and NAFLD, no change or an increase in liver enzymes for NAFLD patients being told to eat a "vegan" diet, and lower odds of NAFLD in people who eat more than 2 eggs per day (calculated from the calories from egg yolk needed to achieve adequate choline intake as given by Joseph (keep this number in mind).
However, we see the opposite. Higher adherence to plant-based diets, especially healthful plant-based diets is associated with lower likelihood of fatty liver. [[77](https://pubmed.ncbi.nlm.nih.gov/30578029/)][[78](https://pubmed.ncbi.nlm.nih.gov/36235752/)] Higher consumption of animal foods correlated with a higher prevalence of NAFLD, while a higher consumption of grains and vegetables was correlated with a lower prevalence of NAFLD in Chinese Adults. [[79](https://pubmed.ncbi.nlm.nih.gov/26083112/)] Also, in a pilot study with 26 NAFLD patients who agreed to eat a vegan diet for six months 20 normalised their liver function tests, independently of their improvements in body weight. [[80](https://pubmed.ncbi.nlm.nih.gov/33548123/)] Meanwhile, in a case-control study of 951 patients who had been referred to hepatology clinics, those participants who consumed 2-3 eggs per week (not per day) had over 3-times higher odds of having NAFLD than those who consumed less than 2 eggs. [[81](https://pubmed.ncbi.nlm.nih.gov/28443155/)]
It doesn't actually seem like consuming choline from animal products, particularly eggs, is even an effective means of avoiding NAFLD. This may be because animal-derived sources of choline are also typically high in fat, which would likely increase the choline requirement.
Consuming more fats means activating the bodies lipid transport system, such as lipoproteins, to a greater degree. Phosphatidylcholine is one of the primary phospholipids that make up the membranes of lipoproteins. The more fat you eat, the more choline you require. This is basically why choline deficiency can cause fatty liver.
So, even from a mechanistic standpoint, it would be unclear whether or not high fat animal-based diets would have an advantage over low fat plant-based diets.
**Claim #28 (**[**19:02**](https://youtu.be/MpxgZGnEF7E?t=1142)**):**
> Dietary calcium reduces risk of heart attack, calcium supplements increase the risk of heart attack.
This claim, which Joseph bases off of a single study that he fails to cite in his substack document, is not supported by the larger literature. A multitude of meta-analyses of prospective cohort studies with combined sample sizes of hundreds of thousands of patients show an inverse correlation of total calcium intake and all-cause mortality in the short term (≤ 10 years), but no statistically significant correlation in the long term (> 10 years). This difference is likely explained by the positive correlation between both dietary and supplemental calcium with cardiovascular mortality, following a U-shaped dose response curve that becomes statistically significant for intakes exceeding ~1200 mg/day. [[82](https://pubmed.ncbi.nlm.nih.gov/25912278/)][[83](https://pubmed.ncbi.nlm.nih.gov/33382441/)][[84](https://pubmed.ncbi.nlm.nih.gov/25252963/)]
The only statistically significant finding of the only meta-analysis of RCTs of calcium supplementation was a 9% increased risk of coronary heart disease incidence, driven by dosages exceeding 1000 mg/day in men, but no statistically significant difference in all-cause mortality. [[85](https://www.tandfonline.com/doi/full/10.1080/07315724.2019.1649219)]
Therefore, calcium supplementation in a range similar to reasonable dietary intakes should be regarded as safe. It is also effective at improving bone mineral density in both preadolescent children and adults with osteoporosis. [[86](https://pubmed.ncbi.nlm.nih.gov/36808216/)][[87](https://pubmed.ncbi.nlm.nih.gov/36810543/)]
**Claim #29 (**[**19:12**](https://youtu.be/MpxgZGnEF7E?t=1152)**):**
> Vegans have weaker bones and a 43% higher risk for fractures than omnivores. [[88](https://pubmed.ncbi.nlm.nih.gov/33222682/)]
On average, vegans do in fact tend to have a lower bone mineral density and higher hip fracture risk compared to non-vegans. This alone is uninteresting, though. We know that, on average, omnivores have a higher BMI than vegans. In this study the difference in BMI between the groups was 2.4 points, in the general population it is more than double that.
BMI has been shown to causally increase bone mineral density, which in turn has been shown to causally decrease risk of fracture. This effect mediation has been found independently in observational studies, and the differences in bone mineral density seem to align with what we would expect based on the differences in BMI. [[89](https://pubmed.ncbi.nlm.nih.gov/33784428/)][[90](https://pubmed.ncbi.nlm.nih.gov/36260985/)][[91](https://pubmed.ncbi.nlm.nih.gov/24862213/)][[92](https://pubmed.ncbi.nlm.nih.gov/15817133/)]
So the question that is interesting here, from a causal perspective, is whether vegans have weaker bones and higher risk of fracture independently of BMI and other important confounders such as calcium and vitamin D. Vitamin D has not been taken into account at all in the EPIC-Oxford study. BMI and dietary calcium were adjusted for, but only via categorisation, which is known to bias results when examining continuous variables with non-linear responses. [[93](https://pubmed.ncbi.nlm.nih.gov/17938055/)]
In the Adventist Health Study 2, a better prospective cohort study (more recent, bigger sample size, higher proportion of vegans, longer follow-up, etc), the same question was investigated. When adjusting for all known confounders (and unlike EPIC-Oxford using a proper adjustment model), only female vegans who did not supplement calcium and vitamin D were at a higher risk of hip fractures. [[94](https://pubmed.ncbi.nlm.nih.gov/33964850/)]
On the other hand, in another prospective cohort study, a higher ratio of animal protein to plant protein was found to increase rates of bone loss and fracture risk in postmenopausal women. [[95](https://pubmed.ncbi.nlm.nih.gov/11124760/)]
**Claim #30 (**[**19:52**](https://youtu.be/MpxgZGnEF7E?t=1192)**):**
> Dr. Francis Pottenger had been trying to formulate a healthy diet for his laboratory cats ... This had Dr. Pottenger conduct a 10 year study to puzzle out the effects of cooked meat versus raw meat on hundreds of cats. He found that the cooked meat cats consistently had health problems but the problems were even worse for their kittens.
This might be interesting if we continued to have an incomplete understanding of feline nutrition. But this isn't 1932. In fact we have such a strong understanding of feline nutrition these days, that we can even formulate nutritionally complete animal-free diets for cats.
There are plenty of plausible explanations for what happened to the cats. One plausible explanation is that cooking the meat destroyed the taurine content, as we understand that even mild temperatures can significantly reduce the taurine content of meat. [[96](https://pubmed.ncbi.nlm.nih.gov/22060873/)] Taurine is an essential nutrient in cats, and most of the symptoms described can be explained by a taurine deficiency.
At present, our understanding of human nutrition is such that many can live for years on total parenteral nutrition (TPN), which is a type of intravenous total dietary replacement. There has been plenty of literature pointing out that TPN is associated with a wide range of negative health outcomes. But, it's difficult enough to disambiguate the effects of the TPN and the effects of whatever led to the patient requiring TPN to begin with, let alone the ostensible effects of unknown, spooky mystery meat nutrients.
**Claim #31 (**[**25:05**](https://youtu.be/MpxgZGnEF7E?t=1505)**):**
> A huge 2020 review explained that saturated fat rich foods like whole-fat dairy or unprocessed meat themselves are not associated with an increase risk of heart disease and a 2022 systematic review found the previous evidence that shows unprocessed meat is linked to chronic diseases like cancer or heart disease to be far too weak to make the recommendation to reduce meat consumption.
The evidence used to buttress the JACC paper is the same sort of evidence that the BOP paper authors considers too weak to be reliable. Why even point it out if the evidence is shit?
But, just for clarification, it is understood that whole fat dairy blunts the effect of saturated fats on blood lipids, due to its unique food matrix and the presence of something called the milk fat globule membrane. [[97](https://pubmed.ncbi.nlm.nih.gov/26016870/)] It is also understood that chocolate, while high in saturated fat, is high in a particular type of saturated fat called stearic acid. This particular saturated fat does not have a significant effect on blood lipids. [[98](https://pubmed.ncbi.nlm.nih.gov/32998517/)]
This is just Joseph using these exceptions to the rule to obfuscate the effect that meat itself has on blood lipids, which is significant and replicable. [[99](https://pubmed.ncbi.nlm.nih.gov/31161217/)] Overall, we understand that the relationship between meat and heart disease is likely mediated by blood lipids, particularly LDL. Meat has a tendency to raise LDL, which just straightforwardly explains its strong association with heart disease.
**Claim #32 (**[**25:44**](https://youtu.be/MpxgZGnEF7E?t=1544)**):**
> Yet, the anti-meat push has gotten so strong that as investigative journalist Nina Teicholz reveals, a recent Tufts University ranking system bogusly ranks Reese’s Peanut Butter Cups as healthier than Eggs, Cheese or Ground Beef.
These data don't represent any official guidelines. And I'm not sure how shitty input data and shitty methodology constitutes an "anti-meat push", honestly. But Joseph is not even representing the results of the Food Compass accurately. While it's true that on average animal products get a mediocre score, it's not true that they rank lower than snacks and desserts on average. [[100](https://pubmed.ncbi.nlm.nih.gov/37117986/)] What he presented in his video is an example of cherry picking.
In fact, some animal foods rank higher than some plant foods, and in the aggregate there is non-inferiority between some animal foods and some plant foods. For example, seafood ranks particularly high, and is non-inferior to both fruits and vegetables. Both meat and dairy are also non-inferior to grains. If Joseph wants to make some kind of claim about a vegan conspiracy to suppress the health value of animal foods, he'll have to explain why seafood gets such a remarkable score here.
**Claim #33 (**[**26:04**](https://youtu.be/MpxgZGnEF7E?t=1564)**):**
> It’s easy to assume that our understanding of individual nutrients is so advanced that we don’t need to rely on outdated meat-based diets - we can make replacements. But, while the amount of knowledge on nutrition that’s been accumulated is incredible, is it as complete as we assume?
While this has the appearance of being a sound inductive sort of argument, it ultimately seems to be an argument that is halfway between an appeal to ignorance and some nutrition-focused flavour of Pascal's wager. I'm not sure why we should find this persuasive. If we don't know if there are any nutrients in meat that currently render meat indispensable, I would just be agnostic about the existence of those nutrients.
**Claim #34 (**[**27:26**](https://youtu.be/MpxgZGnEF7E?t=1646)**):**
> It wasn’t even until 1998 that the nutrient Choline was recognized to be essential. Liver disease, atherosclerosis and neurological dysfunction taught us that Choline is pretty important. [[101](https://pubmed.ncbi.nlm.nih.gov/19906248/)]
>
> A paper from just last year in 2022, suggests we underestimate the optimal intake of choline. [[102](https://pubmed.ncbi.nlm.nih.gov/34962672/)] This Cornell study found that seven-year-old children had better attention span if their mothers consumed twice the recommended amount of choline during their pregnancy.
It is known that prenatal DHA supplementation positively influences attention of infants and preschool children in a similar manner as found for choline in the Cornell study. [[103](https://pubmed.ncbi.nlm.nih.gov/27362506/)][[104](https://pubmed.ncbi.nlm.nih.gov/27604770/)] Additionally, there is high-quality emerging evidence that prenatal choline supplementation improves DHA status in pregnant women but not in lactating women (also no statistically significant difference for DHA concentration in breast milk) making it likely that the beneficial effect of prenatal choline supplementation on sustained attention is mediated through DHA. [[105](https://pubmed.ncbi.nlm.nih.gov/35575618/)][[106](https://pubmed.ncbi.nlm.nih.gov/33516092/)]
Therefore, it may be prudent for both vegan and non-vegan women, especially those with certain PEMT genotypes, to supplement choline in addition to DHA during the second and third trimester of their pregnancies. [[107](https://pubmed.ncbi.nlm.nih.gov/36145177/)]
**Claim #35 (**[**28:33**](https://youtu.be/MpxgZGnEF7E?t=1713)**):**
> If a mother can’t breastfeed or get donor milk, of course modern infant formula is basically a miracle. But even as a representative of Abbott, a leading infant formula manufacturer admits: “to mimic and replicate breast milk is not possible.” Yes, a newborn will have far more sensitive nutrient requirements than an adult or even a child, but it’s an example the difficulty of trying to make a complete replacement of a natural food.
The two scenarios are not analogous. In the case of vegan replacements for animal based foods, we generally don't see people on properly planned "vegan" diets experiencing negative health outcomes as a consequence. So, even if the association between formula feeding and negative health outcomes was strong, it's not clear how one functions as a plausible analogy for the other.
**Claim #36 (**[**29:28**](https://youtu.be/MpxgZGnEF7E?t=1768)**):**
> ...there is evidence that [insert non-essential animal nutrient here] has beneficial effects. [[108](https://pubmed.ncbi.nlm.nih.gov/32072297/)]
In most studies wherein a benefit of these animal-derived compounds is found, supranutritional doses are given to subjects. Not only that, but the minimum doses required to achieve maximum benefits (when benefits are even present) is often well above and beyond what we could reasonably obtain from diet alone. This just leaves us asking why omnivore shouldn't be relying on supplements too.
**Claim #37 (**[**29:38**](https://youtu.be/MpxgZGnEF7E?t=1778)**):**
> Just to look at two This 2002 paper argues that taurine may be essential in certain circumstances, and creatine supplementation has benefits for brain function in adults like improving memory, intelligence and mood and it reduces the negative effects of sleep deprivation. [[109](https://pubmed.ncbi.nlm.nih.gov/12514918/)][[110](https://pubmed.ncbi.nlm.nih.gov/29704637/)][[111](https://pubmed.ncbi.nlm.nih.gov/16416332/)] Further, creatine is transferred from the mother to her baby during pregnancy providing several benefits to the baby. [[112](https://pubmed.ncbi.nlm.nih.gov/24766646/)]
The "certain circumstances" here were premature infants on total parenteral nutrition. The authors say this is due to them being unable to synthesize their own taurine at this stage and depending on breast milk. How is this related to vegan diets or even animal foods?
Regarding creatine, all studies he cited were on supplemental creatine with doses that would require over 1kg of beef a day to get. For most individuals, beyond their caloric needs.
**Claim #38 (**[**30:14**](https://youtu.be/MpxgZGnEF7E?t=1814)**):**
> You could take substantial amounts of soy or pea protein powders to make up for the fact that most plant proteins are poorly absorbed and have lower amounts of amino acids and so on and so on.
I'm sorry, Joseph. But tracer studies disagree. [[113](https://pubmed.ncbi.nlm.nih.gov/33693735/)] In fact, tofu appears to be on par with pork, and better than eggs, in terms of its contribution to total positive protein balance in the human body.
If you're going to try to make this point to shit on tofu, would you please be consistent and also shit on pork and eggs?
**Claim #39 (**[**30:28**](https://youtu.be/MpxgZGnEF7E?t=1828)**):**
> Again, meat is so nutrient dense that you can get a decent amount of well absorbed zinc, iron, selenium, choline, various B-vitamins, vitamin A, calcium and other nutrients just eating a crappy cheeseburger.
Here, in another certified bruh moment, Joseph relies on vague language to make a point that nobody should care about. You can only eat around three Burger King Whopper cheese burgers before exceeding 2200 Kcal, but you'd also be deficient in most nutrients.
While it's true that you would get the RDA of a number of nutrients, you would also exceed your sodium RDA by 268%, the AI for potassium would be undershot by 50%, and only 50% of the conservative 600 IU of vitamin D would be obtained. Additionally, you would only get about 40% of the RDA of vitamin A, in exchange for over 40g of saturated fat.
While I am aware that Joseph is not advocating for cheeseburger consumption, it's just an incredibly stupid point to make. Which leads me to the next claim.
**Claim #40 (**[**30:40**](https://youtu.be/MpxgZGnEF7E?t=1840)**):**
> Ideally people shouldn’t eat crappy cheeseburgers… but the average busy person doesn’t have time to craft the perfect meal - convenience is important. This is evidenced by the fact that a 2021 paper found that the more people avoided animal products in their diet - the more they ate convenient ultra-processed foods with vegans eating the most processed foods. [[114](https://pubmed.ncbi.nlm.nih.gov/32692345/)]
In yet another instance of Joseph failing to read his own references, possibly because he's rushing for that confirmation bias induced YouTube money, he mentions convenience ultra-processed foods (UPF) but links a paper where the reason vegans seemingly ate more UPF (not convenience foods) was that the authors classified meat alternatives and plant based milks like soy milk as UPF.
> Concomitantly with the increased numbers of vegetarians or vegans, the offer of industrial plant-based meat and dairy substitutes on the market has been growing during the past decade in Western countries (e.g., tofu, textured vegetable foods such as vegetarian sausages or patties, and plant-based drinks such as soy “milk”) (9, 10). Most of these substitutes are ultra-processed foods (UPFs). The development of this industrial plant-based meat and dairy substitutes market (11, 12, 13, 14) may have contributed to the growing consumption of UPFs in countries such as France (15) by specific populations. For example, persons avoiding most animal-based foods may have high intakes of UPFs, driven by higher consumptions of plant-based meat and dairy substitutes.
The difference was so tiny as to be entirely explained by that classification.
> The proportion of energy from UPFs was significantly higher for vegetarians (37.0% of the total energy intake) and vegans (39.5%) than for meat eaters (33.0%) (Figure 1A). Comparing vegans to meat eaters, for example, vegans consumed a greater proportion of UPFs (+6.41%) (Figure 1B).
In addition, Joseph failed to mention that vegans eat more unprocessed foods than omnivores.
> The proportion of energy from unprocessed foods was significantly higher for vegans (31.2% of the total energy intake) than for meat eaters (29.0%) (Figure 1A and B).
**Claim #41 (**[**31:13**](https://youtu.be/MpxgZGnEF7E?t=1873)**):**
> Eating tons of processed soy protein and vegetable oils like sunflower oil is quite new to the human stomach. Sunflower oil seems like a simple swap for animal fat … but they are totally different. Many animal fats can be a good source of vitamin K2, but vegetable oil in fact hampers the activity of vitamin K, increasing your need for it. [[115](https://pubmed.ncbi.nlm.nih.gov/12032162/)][[116](https://pubmed.ncbi.nlm.nih.gov/27251151/)][[117](https://pubmed.ncbi.nlm.nih.gov/28962307/)][[118](https://pubmed.ncbi.nlm.nih.gov/29353277/)] It also oxidizes very easily so it will increase your need for the antioxidant vitamin E. [[119](https://pubmed.ncbi.nlm.nih.gov/26291567/)] Vegetable oil has several other negative effects which I have talked about in another video.
We already discussed vitamin K2 earlier, and touched on how animal foods are generally a pathetic source, but even if they weren't, it's not clear that animal-derived vitamin K2 is even bioavailable. Additionally, vegetable oil consumption is not an entailment of veganism, so I'm not entirely sure why it's being discussed here. Nor is UPF consumption, unless you're dense enough to categorize B12 and D3 supplements as UPFs. At best this is a red herring, at worst this is a non sequitur.
**Claim #42 (**[**31:47**](https://youtu.be/MpxgZGnEF7E?t=1907)**):**
> Vegans and vegetarians tend to rely on soy for protein a lot. The hormone disrupting effects of increased soy consumption is somewhat controversial, but it may explain why a study on almost 8000 boys found boys born to vegetarian mothers had a higher risk for a specific deformity in the genitals called hypospadias. [[120](https://pubmed.ncbi.nlm.nih.gov/10619956/)]
Risk is not exactly what is being assessed in this study. This is a case-control study, which means we're looking at odds ratios. This is the ratio of the odds of the outcome of interest between two groups at varying levels of exposure. Case-control studies are also missing a temporal component, which is often considered critical for making sound causal inferences. With case-control studies, the direction of causality is extremely difficult to ascertain. Additionally, the study did not even measure or assess soy intake.
In this case, the odds ratio for hypospadias from low to high soy exposure was actually non-significant. However, in a similar case-control study from 2013, phytoestrogen consumption was inversely associated with hypospadias incidence. [[121](https://pubmed.ncbi.nlm.nih.gov/23752918/)] At best I think we can say that the literature on soy is pretty mixed, ranging from non-significant increases in the odds of hypospadias to statistically significant decreases in the odds of hypospadias.
**Claim #43 (**[**32:09**](https://youtu.be/MpxgZGnEF7E?t=1929)**):**
> Soy contains the isoflavonoid genistein, which studies show has “detrimental effects on the male reproductive system…” [[122](https://pubmed.ncbi.nlm.nih.gov/35760341/)]
Bruh, this is a meta-analysis of rodent studies with a blurb about how the results may or may not translate to humans.
**Claim #44 (**[**32:17**](https://youtu.be/MpxgZGnEF7E?t=1937)**):**
> Lastly, impossible burger has tried to make their product taste meatier with something called leghemoglobin from the roots of genetically modified soy plants. [[123](https://www.canada.ca/en/health-canada/services/food-nutrition/genetically-modified-foods-other-novel-foods/approved-products/soy-leghemoglobin/document.html)]
>
> GMOscience.org writes that:
>
> A 28-day study commissioned by Impossible Foods in 2017 on soy leghemoglobin found that soy leghemoglobin caused statistically significant changes in weight gain, changes in the blood that can indicate the onset of inflammation or kidney disease, and possible signs of anaemia in the rats.
In isolation, leghemoglobin actually had better bioavailability than iron(II)-sulfate, and when part of a food matrix, here as fortification for corn tortillas, had similar (ie non stat sig different) bioavailability compared to bovine heme iron. [[124](https://pubmed.ncbi.nlm.nih.gov/16478282/)]
As an added fun fact that may blow up the brains of Joseph's audience, leghemoglobin is actually evolutionarily just as old as hemoglobin. See the following figure from Biochemistry 6th edition by Berg, Tymoczko and Styer.
**Claim #45 (**[**32:43**](https://youtu.be/MpxgZGnEF7E?t=1963)**):**
> Further studies did eventually persuade the FDA to designate leghemoglobin as safe, but Impossible Foods admitted that a quarter their new ingredient was composed of 46 “unexpected” additional proteins, none of which were assessed for safety in the dossier. [[125](https://twitter.com/ImpossibleFoods/status/1000397509196505089?s=20)]
These "unexpected additional" proteins are just unknown proteins, which in this context simply means that their biological behaviour is not yet known. If you analyse any food, including beef, there will be many, many such "unknown" proteins. It's not spooky. This characteristic likely quantifies over all foods, and as such we have no good reason to consider this a cause for any concern.
**Claim #46 (**[**33:27**](https://youtu.be/MpxgZGnEF7E?t=2007)**):**
> This is another big issue with trying to replace animal foods. The replacement almost always comes with plenty of other stuff. Kidney beans are a good source of protein need to be soaked and cooked to reduce the lectin content. Some boys in the UK showed up in the hospital with profuse diarrhea and vomiting because they ate 4 kidney beans that were soaked, but not cooked. [[126](https://pubmed.ncbi.nlm.nih.gov/2249712/)]
Okay, Joseph. Either you're not reading your references at all or you're just memeing at this point. The results are relevant to raw beans, which everyone agrees shouldn't be eaten. This isn't revelatory. Soaking your legumes is some level-zero Weston A Price bullshit. They need to be cooked, dude. **COOKED**.
Even without soaking, and instead pressure cooking, the time required to deactivate the lectins was well below the time required to make them edible. [[127](https://www.researchgate.net/publication/229968837_Effect_of_Heat_Processing_on_Hemagglutinin_Activity_in_Red_Kidney_Beans)]
Additionally, in the years between 1976 and 1989, the UK only saw 50 suspected incidents related to un- or under-cooked legumes were registered. Meanwhile, [according to the USDA](https://www.fsis.usda.gov/inspection/inspection-programs/inspection-poultry-products/reducing-salmonella-poultry/salmonella), poor meat preparation can account for approximately 1.35 million salmonella-related infections, 26,500 salmonella-related hospitalizations, and 420 salmonella-related deaths every year just in the United States.
Joseph also tries to address those who react to lectins in cooked kidney beans too. News flash. There are no fucking lectins in cooked kidney beans. [[128](https://pubmed.ncbi.nlm.nih.gov/34829077/)]
**Claim #47 (**[**33:56**](https://youtu.be/MpxgZGnEF7E?t=2036)**):**
> Phytic acid found in beans, seeds, nuts and grains inhibits fat digestion and the absorption of calcium, magnesium, phosphorus and Zinc. How much? Well, this study found about 35% less Zinc is absorbed in a vegetarian diet. [[129](https://pubmed.ncbi.nlm.nih.gov/31095149/)][[130](https://pubmed.ncbi.nlm.nih.gov/16401188/)][[56](https://pubmed.ncbi.nlm.nih.gov/12936958/)] Fiber itself worsens the activity of pancreatic lipase which is important for the absorption of fat soluble vitamins like A, D and K2. [[131](https://pubmed.ncbi.nlm.nih.gov/2819858/)]
Joseph's reference for this claim is the same paper that he cited for his claim about phytate-mediated inhibition of iron absorption. However, straight from the author's conclusions, we can read:
> The iron and zinc from vegetarian diets are generally less bioavailable than from nonvegetarian diets because of reduced meat intake as well as the tendency to consume more phytic acid and other plant-based inhibitors of iron and zinc absorption. However, in Western countries with varied and abundant food supplies, it is not clear that this reduced bioavailability has any functional consequences.
What's worse, Joseph's reference for phytate-mediated inhibition of hepatic lipase activity is an in vitro study. It's not clear why we should care.
**Claim #48 (**[**34:19**](https://youtu.be/MpxgZGnEF7E?t=2059)**):**
> A high intake of goitrogenic foods like cabbage, kale and turnips can interfere with iodine functioning.
Show me the study that actually divulges that any of these sorts of foods have any goitrogenic effects, please. We've tried to look for this effect in foods that are highest in these so-called goitrogens, such as broccoli sprouts, and we so far haven't found any generalizable effect. [[132](https://pubmed.ncbi.nlm.nih.gov/30735751/)] In fact, the number of subjects with subclinical hypothyroidism actually went down in the broccoli sprout group, compared to baseline.
**Claim #49 (**[**34:25**](https://youtu.be/MpxgZGnEF7E?t=2065)**):**
> Food Scientist Dr. Frederic Leroy has written an extensive article on the various examples of why it’s a challenge to acquire enough of certain nutrients just from plants due to inhibiting compounds like these. [[133](https://aleph-2020.blogspot.com/2019/05/animal-source-foods-provide-nutrients.html)] This nutrient challenge is part of the reason why The German Nutrition Society in 2016 and the French-speaking Pediatric HGN Group in 2019 recommend against a vegan diet for adolescents, children or mothers. [[134](https://www.ernaehrungs-umschau.de/english-articles/15-06-2016-vegan-diet/)][[135](https://pubmed.ncbi.nlm.nih.gov/31615715/)]
Well, as long as we're appealing to authorities, we should point out that both the French and German governments recommend limiting meat intake to no more than 500g per week and 600g per week, respectively.
**Claim #50 (**[**34:49**](https://youtu.be/MpxgZGnEF7E?t=2089)**):**
> Several studies have found babies born to vegan mothers to have a lower birth weight than babies of omnivore mothers. [[136](https://pubmed.ncbi.nlm.nih.gov/30909771/)][[137](https://journals.lww.com/ijcm/Abstract/1999/24020/A_STUDY_OF_EFFECT_OF_MATERNAL_NUTRITION_ON.4.aspx)][[138](https://pubmed.ncbi.nlm.nih.gov/32776295/)][[139](https://pubmed.ncbi.nlm.nih.gov/8172120/)][[140](https://pubmed.ncbi.nlm.nih.gov/33232446/)][[141](https://www.nichd.nih.gov/newsroom/news/122120-vegetarian-diets)][[142](https://pubmed.ncbi.nlm.nih.gov/28745335/)][[143](https://sciendo.com/article/10.5604/01.3001.0014.9343)]
> Birth weight can be a predictor of infant health and growth. [[144](https://pubmed.ncbi.nlm.nih.gov/15703531/)][[145](https://pubmed.ncbi.nlm.nih.gov/32928144/)][[146](https://pubmed.ncbi.nlm.nih.gov/26288495/)][[147](https://pubmed.ncbi.nlm.nih.gov/28840655/)] In fact, one study that meticulously analyzed the records of 4,300 adults who were in the Danish Medical Birth Register found that the lower their weight at birth, the shorter they would be as adults. [[148](https://pubmed.ncbi.nlm.nih.gov/10206622/)]
> This study points out that the growth of vegetarian children was adequate, but less than average. [[39](https://pubmed.ncbi.nlm.nih.gov/2771551/)] I wonder how people would react to a doctor saying “your son won’t be as tall as he could be, but don’t worry his height will be adequate.”
Firstly, it's probably not actually birth weights we should be caring about necessarily. It's whether or not the infants are considered small for gestational age. Secondly, Joseph's references don't actually provide very persuasive evidence to support the notion that vegan diets increase the risk of small for gestational age. One particularly strong reason for this is poor B12 supplementation practices, which is a known risk factor among vegans that has not been adequately accounted for.
For instance, Ferrara et al. found that only 15% of the vegan cohort supplemented B12, while only 5% supplemented D3. Similarly, Yisahak et al. conducted a tangential study on vegetarians, but even then no assessment for B12 or D3 supplementation was made.
In addition, the study by R.K. Sharma et al. was done in 1999 before fortification and supplementation standards were established. Although they found that low birth weights were largely explained by the height and weight of the mother and that anemia was a risk factor for small for gestational age. These authors also did not account for B12 supplementation.
Kesary et al. lumped B12, iron, folate, and multivitamins together, and participants were said to be taking supplements if they took supplements more than once per week. However, the odds of small for gestational age between vegans and omnivores was not significant after an adjustment for BMI. Therefore, it is difficult to draw a definitive conclusion about the relationship between "vegan" diets and small for gestational age from this study.
Basically if vegans tend to have lower baseline BMI and tend to gain less weight during pregnancy, normally they will give birth to smaller babies. By definition, since you shifted the distribution curve, more of them will fall bellow the 10th percentile. Any unique effect of vegan diets here are probably with respect to more powerfully resisting weight gain and than typical omnivorous diets.
Finally, two cautionary narrative review articles by Miedziaszczyk et al. and Pawlak et al. highlighted that most of the vegan populations mentioned had either high MMA, low B12 intake or status, or poor supplementation practices. These observations further emphasize the importance of adequate B12 supplementation when considering the risks associated with vegan diets during pregnancy. Here's a quote from one of the authors:
> It should be thus concluded that vegan diets are appropriate for pregnant and lactating women only if these women habitually use reliable B12 sources, preferably oral supplements.
**Claim #51 (**[**38:18**](https://youtu.be/MpxgZGnEF7E?t=2118)**):**
> What is the difference between enough nutrients and the optimal amount of nutrients...cutting out nutrient dense animal foods doesn’t seem like a move in the right direction for health
This just seems like pure speculation. Maybe optimal is not achievable without a supplement on any natural diet. I mean, think about it. What's the argument for omnivorous diets necessarily providing optimal amounts of all nutrients? If there's no argument for that, then it's possible that even the diet that he's recommending is horribly insufficient in some way.
How has Joseph determined that the optimal range for nutrient intakes aren't above what could be obtained from omnivorous diets? Seems like his argument here is begging the question. If it's the case that optimal levels of nutrients are only practical to obtain from supplements, then we'd all benefit— not just vegans.
It's also true that this works in reverse. If Joseph is arguing that we should eat more meat to hit some nebulous "optimal" ranges for all nutrients, what's the argument that this is not true for plant foods? Perhaps eating more meat displaces plant foods and keeps us from achieving an optimal intake of some other plant-derived nutrients as well, notably vitamin C, folate, fibre, potassium, manganese, or polyphenols. Yes, Joseph, I live in the real world where getting ample fibre intake is actually beneficial for the vast majority of people.
So perhaps the optimal intake of many of plant-derived nutrients cannot be achieved if you are eating a significant amount of meat. Since Joseph insists on discussing non-essential, animal-derived nutrients for which the evidence for benefit is paltry at best. There is literally more evidence of benefit for polyphenols than there is for carnitine, anserine, taurine, and perhaps even creatine.
**Claim #52 (**[**36:44**](https://youtu.be/MpxgZGnEF7E?t=2204)**):**
> For 99% of human history we relied on animal foods for nutrients - the an animal food containing diet has a strong track record that spans arguably over 1.7 million years. [[149](https://pubmed.ncbi.nlm.nih.gov/32508752/)][[150](https://bigthink.com/the-past/brain-evolution/)] Various cultures viewed animal foods as important to growth and despite the challenging circumstances they lived in, they were protected from infectious diseases, they didn’t have the modern diseases of civilization, and they enjoyed proper growth in their body, faces and mouths.
There is no source provided for Joseph's claim that "various cultures" do not suffer from the modern diseases of civilization. Joseph characterizes these diseases as "heart disease, cancer, osteoporosis, diabetes, and so on", but there is plenty of evidence against the notion that these diseases are somehow modern.
Cancer in humans is a phenomenon that is over a million and a half years old, for example. [[151](https://carta.anthropogeny.org/libraries/bibliography/earliest-hominin-cancer-17-million-year-old-osteosarcoma-swartkrans-cave)] Heart disease is prevalent in nearly every population we study, whether traditional, ancient, or modern. [[152](https://pubmed.ncbi.nlm.nih.gov/23489753/)] Even the Tsimane have advanced atherosclerosis. [[153](https://pubmed.ncbi.nlm.nih.gov/28320601/)] Even diabetes dates back millennia. [[154](https://pubmed.ncbi.nlm.nih.gov/26788261/)]
**Claim #53 (**[**37:07**](https://youtu.be/MpxgZGnEF7E?t=2227)**):**
> With that in mind, a plant-based diet is an experiment without any meaningful track record. It’s been a couple decades at best that people have been doing vegan diets, yet already many people quit for health reasons. Research is a promising story of progress - maybe one day we’ll learn enough to make sufficient plant-based replacements for animal foods. But it’s probably not happening any time soon.
It seems like the word "experiment" is being used in a strange way here. From what I can gather, Joseph is either trying to convey that there is significant risk entailed by being on a "vegan" diet OR that there is no historical precedent for animal-free diets and that we should apply some precautionary principle OR veganism is being used to test a hypothesis.
Either of these three propositions requires an argument. If "experiment" is just being used as it is commonly used, as something done to test a hypothesis, then it is not clear that veganism is an experiment on that construal. If "experiment" just means that there is a possibility of some undesirable outcome actualizing, then it seems trivially true and misleading to refer to veganism as an experiment. If "experiment" means that there is some demonstrably entailment to a poor outcome, then he would actually need to provide decent evidence for that.
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Back in August of 2021, I invited [Tucker Goodrich](https://twitter.com/TuckerGoodrich) to a debate about the health value of seed oils. Tucker agreed to participate immediately, but after a brief back-and-forth (which resulted in Tucker [contradicting himself](https://twitter.com/The_Nutrivore/status/1428064287059324929?s=20&t=rmYpT72-5Tan31MnU_ptlw)), he eventually [withdrew](https://twitter.com/TuckerGoodrich/status/1428062578668830720?s=20&t=rmYpT72-5Tan31MnU_ptlw) without an explicit justification. Shortly thereafter he wrote a [blog article](https://yelling-stop.blogspot.com/2021/12/thoughts-on-nick-hieberts-comprehensive.html), wherein he paints a caricature of the events that transpired, which included everything from exaggerations to full-throated lies. Despite this, I reinvited him to debate multiple times since the incident, with either no response or outright refusals in reply.
My initial invitation was prompted by my discovery that Tucker was actually just straight up [fabricating evidence](https://twitter.com/The_Nutrivore/status/1489863311155810304?s=20&t=DhYUMrwmqG260Ft7uNHozg) in a debate with a friend of mine, [Alan Flanagan](https://www.alineanutrition.com/about/). Needless to say, Tucker appears to be a particularly dishonest actor and a coward. When he wants to engage with me he does so in the safety of his blog, and critiques my writings and public statements with strawman arguments and red herrings, as well as just attacking very low-hanging fruit. At this point I don't think it's unfair to speculate that he conducts himself in this manner because he knows his arguments would not withstand scrutiny in a debate against me.
Recently I was invited to set the record straight and shed some light on some of Tucker's more misleading claims on [Mark Bell's Power Project](https://www.youtube.com/watch?v=omzCi2CGoxo). Naturally Tucker felt compelled to write [a response](http://yelling-stop.blogspot.com/2022/02/thoughts-on-nick-hiebert-on-mark-bells.html) that was also particularly low-level and ultimately did not provide any stable defeaters for any of my positions. That didn't stop him from writing the article as though my arguments had been thoroughly dispatched, despite his counterarguments not even meaningfully interacting with what I had said to begin with.
At this point I figured that enough was enough. So, I contacted an acquaintance of mine (who through this whole ordeal would become a friend), [Matthew Nagra](https://drmatthewnagra.com). I knew Matt was experienced in empirical debate and didn't hold any whacky heterodox views about seed oils, so I asked him if he'd be interested in debating Tucker. Matt agreed and promptly extended an invitation to Tucker. After Tucker agreed to a debate against Matt on [Simon Hill](https://twitter.com/theproof)'s [podcast](https://theproof.com/podcast/), it was time to get to work. With some help from [Matthew Madore](https://twitter.com/MattMadore576) over at [My Nutrition Science](https://www.mynutritionscience.com/authors-page/), we developed about 200 pages worth of debate-prep, syllogisms, and dialogue trees over approximately six weeks.
As you will see throughout this article, our hard work paid off in the sweetest way possible. Matt was able to tease an absolutely enormous amount of dodges, strawman arguments, and straight up contradictions out of Tucker. It was more than any of us could have hoped for, and it truly reveals just how weak Tucker's arguments really are. The number of self-defeating bullets Tucker tried to bite in order to stay ahead in the debate was exquisite— a true treat. All in all, I'm very pleased with the results. Matt did a truly phenomenal job. Enjoy!
**MATTHEW NAGRA VS TUCKER GOODRICH**
Let's start. Tucker and Matt both agree to the following:
**Debate Rules:**
1) The debate will be open and conversation-style.
2) Both parties will avoid talking over one another.
3) Both parties must answer questions directly.
4) Both parties will make and address one claim at a time.
5) Both parties will refrain from using personal insults.
6) Both parties will provide adequate time for response.
**Matt's Debate Proposition:**
"It is more reasonable to believe that seed oils are beneficial, rather than harmful, for coronary heart disease risk."
**Tucker's Definition of Seed Oils:**
"Oils made from seeds, like canola oil, soybean oil, sunflower oil, etc. Not the fleshy part of the fruit, like olive oil, palm oil, avocado oil, or coconut oil. With the primary focus being high linoleic acid oils."
Now let's get into the actual debate.
**Rule violation (**[**30:20**](https://youtu.be/5nZSV-DyVRM?t=1820)**,** [**30:38**](https://youtu.be/5nZSV-DyVRM?t=1838)**):**
Tucker breaks rule three twice. Matt provides evidence from three independent analyses that shows a concordance rate of 65-67% between nutritional epidemiology and nutritional randomized controlled trials (RCTs). Matt then asks Tucker if nutritional epidemiological evidence is concordant with nutritional RCTs two thirds of the time, which is a yes or no question. Tucker responds by saying its irrelevant due to being a tangent. However, it's not clear exactly how Matt's question is an irrelevant tangent, since it directly interacts with Tucker's opening claim at the beginning of the debate.
**Strawman (**[**32:09**](https://youtu.be/5nZSV-DyVRM?t=1929)**):**
Tucker finally answers "no" in response to Matt's question. When Matt asks why not, Tucker responds by saying "it's just a meta-analysis", which doesn't provide us with any clarity on why he provided the answer that he did. Tucker further elaborates with a strawman of Matt's position, stating that the data provided by Matt doesn't provide us with any information about the likelihood of a high-LA intervention being beneficial. However, this wasn't Matt's point. Matt's point was that Tucker's characterization of nutritional epidemiology on the whole was a red herring and false.
**Rule violation (**[**37:24**](https://youtu.be/5nZSV-DyVRM?t=2239)**):**
Tucker breaks rule three for the third time. Matt shows Tucker the power calculation from MCE, and demonstrates that the trial was actually underpowered. Matt then asks Tucker if the trial had adequate power. Tucker again says that the question is irrelevant, stating that when a trial shows harm, it shouldn't be discounted based on a P-value. This is a truly bizarre answer, as Matt has yet to discount the trial.
**Rule violation (**[**38:50**](https://youtu.be/5nZSV-DyVRM?t=2330)**):**
Tucker breaks rule four. Instead of resolving Matt's point about MCE, Tucker wants to pivot to the LA Veterans Administration Hospital Trial (LAVAT).
**Rule violation (**[**43:20**](https://youtu.be/5nZSV-DyVRM?t=2600)**):**
Tucker breaks rule three for the fourth time. Matt presents a subgroup analysis from MCE that shows that older subjects who maintained the intervention diet for more one year tended to see a benefit when compared to the control diet. Matt asks Tucker if the older subjects in MCE who were consuming the intervention diet for longer saw a benefit compared to the control diet. Tucker rejects the question, saying that Matt is citing a "sub-population" analysis, and that it is superseded by the total outcome. This answer doesn't interact with Matt's question.
**Rule violation (**[**42:56**](https://youtu.be/5nZSV-DyVRM?t=2576)**,** [**43:30**](https://youtu.be/5nZSV-DyVRM?t=2610)**):**
Tucker breaks rule three for the fifth time. Matt rephrases his question, asking Tucker if harm would be more likely if subjects were to maintain the intervention diet for a longer period of time as opposed to a shorter period of time in MCE. Tucker again, dismisses a yes-or-no question as being irrelevant without any clarifying explanation.
**Rule violation (**[**44:06**](https://youtu.be/5nZSV-DyVRM?t=2646)**):**
Tucker breaks rule two. Matt wants to elaborate on why his question is important, but Tucker cuts him off. Matt allows it, but Tucker shouldn't have done it to begin with.
**Rule violation (**[**48:18**](https://youtu.be/5nZSV-DyVRM?t=2898)**):**
Tucker breaks rule one and three. Tucker attempts an explanation for why MCE showed benefit for older subjects over two years. When Matt asks for further clarification, Tucker refuses to provide it. Not only is this directly dodging a question, this behaviour also calls into question whether or not Tucker is actually there for an open, conversation-style debate.
**Rule violation (**[**49:07**](https://youtu.be/5nZSV-DyVRM?t=2947)**):**
Tucker breaks rule four again. Instead of resolving Matt's point about MCE, Tucker wants to pivot to the Oslo Diet-Heart Study (ODHS).
**Strawman (**[**50:34**](https://youtu.be/5nZSV-DyVRM?t=3034)**):**
Tucker offers a strawman of Matt's position, claiming that Matt's conclusions were based on ODHS. In fact, Matt's position was not based on ODHS, and Matt even said that the evidence underpinning his position is virtually the same if ODHS is omitted completely.
**Strawman (**[**51:52**](https://youtu.be/oYsRgsJoZc4?t=3112)**):**
Tucker offers a strawman of Matt's position, claiming that the composition of fats in margarines would need to be known in order to conclude that trans-fats (TFA) were confounding in MCE. This isn't Matt's position. Matt's position was that TFA confounding is likely based on two pieces of evidence. Firstly, the vast majority of margarines during that time period contained TFA. Secondly, there was disagreement between the observed cholesterol changes and the predicted cholesterol changes in MCE. From these data Matt infers that TFA confounding was likely, which is merely a truism that can be soundly inferred a priori. Matt doesn't conclude that TFA confounding did in fact occur. He merely takes the position that is likely.
**Rule violation (**[**55:27**](https://youtu.be/oYsRgsJoZc4?t=3327)**):**
Tucker breaks rule three. Matt asks Tucker if he thinks that a cooking oil with 1% TFA would be equivalent to a cooking oil with 15% TFA, which is a yes or no question. Tucker responds by saying that TFA confounding would have to be a systematic issue across all of the RCTs using Matt's assumptions. However, this doesn't interact with Matt's question.
**Rule violation (**[**1:02:00**](https://youtu.be/oYsRgsJoZc4?t=3720)**):**
Tucker breakers rule three again. Tucker cites a result from the LAVAT that is incongruent with Matt's figures, so Matt asks him what Tucker's figure is representing. After Matt finishes explaining the incongruency, he asks Tucker where he is getting the number from. Instead of answering, Tucker just asks him what his point is.
**Potential contradiction (**[**1:08:00**](https://youtu.be/oYsRgsJoZc4?t=4080)**):**
Tucker concedes that LAVAT showed a slight benefit for vegetable oils compared to animal fats. However, earlier he characterized MCE as showing "harm", but it wasn't qualified as slight. However, LAVAT showed a statistically significant 49% increase in CVD mortality risk in the control group, but MCE showed a non-significant 24% increase in CVD mortality risk in the intervention group. If a non-significant 24% increase in CVD mortality is noteworthy in Tucker's view, why is a statistically significant 49% increase in CVD mortality risk only slight in his view as well?
Without further elaboration, would have to either accept that the increase in CVD mortality in LAVAT is noteworthy, or accept that the CVD mortality increase in MCE is at least just as unnoteworthy as LAVAT, if he wishes to stay consistent. We can syllogize the logical entailments of accepting the CVD mortality risk in MCE as "not slight" like this:
**Definitions:**
C := the trial has a CVD mortality risk that is over 23%
M := the trial has a CVD mortality risk that is not slight
e := MCE
v := LAVAT
**P1)** If the trial has a CVD mortality risk that is over 23%, then the trial has a CVD mortality risk that is not slight.
**(∀x(Cx→Mx)**
**P3)** MCE and LAVAT are trials that have CVD mortality risks that are over 23%.
**(Ce∧Cv)**
**C)** Therefore, MCE and LAVAT are trials that have CVD mortality risks that are not slight.
**(∴Me∧Mv)**
**Rule violation (**[**1:08:22**](https://youtu.be/oYsRgsJoZc4?t=4102)**,** [**1:08:34**](https://youtu.be/oYsRgsJoZc4?t=4114)**):**
Tucker breaks rule three two more times. Matt presented data from LAVAT that divulged that the intervention diet resulted in statistically significant benefits to CVD mortality and all-cause mortality. Matt asked Tucker if he though the data shows that the intervention diet in LAVAT resulted in a benefit to CVD mortality and all-cause mortality, which is again a yes or no question. First, Tucker dismisses the question, saying that LAVAT also saw an increase in cancer. When Matt asks again, Tucker says that he doesn't agree that studies can be "sliced and diced", which doesn't interact with Matt's question.
**Rule violation (**[**1:10:44**](https://youtu.be/oYsRgsJoZc4?t=4244)**,** [**1:14:22**](https://youtu.be/oYsRgsJoZc4?t=4462)**):**
Tucker breaks rule four two more times. Instead of resolving Matt's point about LAVAT, Tucker tries to pivot to talking about the standard American diet (SAD), which is tangential to the claim being discussed at that moment. When asked again, Tucker responds by talking about rates of acute myocardial infarction (AMI) in Africans, which is also tangential to the claim being discussed at that moment.
**Rule violation (**[**1:18:03**](https://youtu.be/QGNNsiINehI?t=4683)**):**
Tucker breaks rule three yet again. Matt attempts an internal critique by asking if Tucker would believe that adding vegetable oils to the SAD would be a benefit, based on the results of LAVAT. Tucker replies by saying that Lee Hooper would conclude that there is little to no benefit. A truly bizarre reply that doesn't interact with Matt's question at all.
**Potential contradiction (**[**1:21:11**](https://youtu.be/QGNNsiINehI?t=4871)**):**
Matt responds to ecological data that Tucker presented earlier, stating that he disagrees with the notion that it can be used to determine independent effects of seed oils. Tucker denies that he is making such a claim, and clarifies that he is speculating off that data. However, earlier in the debate Tucker objected to Matt's speculation regarding TFA confounding in MCE. Why is it OK for Tucker to submit speculation as evidence but not OK for Matt to submit speculation as evidence?
Without further elaboration, it's unclear why Tucker would not be OK with a priori inferences about the potentially confounding effects of TFA in MCE being used in debate, when he also relies on such a priori inferences. Such as when he infers from ecological data that seed oils are likely to be detrimental. We can syllogize the logical entailments of accepting the use of a priori inferences in debate like this:
**Definitions:**
N := speculation counts as evidence
B := speculation can be used in debate
n := a priori inferences about the effects of seed oils from ecological data
m := a priori inferences about TFA in MCE
**P1)** If speculation counts as evidence, then speculation can be used in debate.
**(∀x(Nx→Bx))**
**P4)** A priori inferences about the effects of seed oils from ecological data and a priori inferences about TFA in MCE are speculations that count as evidence.
**(Nn∧Nm)**
**C)** Therefore, a priori inferences about the effects of seed oils from ecological data and a priori inferences about TFA in MCE are speculations can be used in debate.
**(∴Bn∧Bm)**
**Rule violation (**[**1:32:15**](https://youtu.be/QGNNsiINehI?t=5535)**):**
Tucker breaks rule four once more. At this point, both are discussing Lyon Diet-Heart Study (LDHS), and the differential effects of the various dietary modifications that were made in that study, such as the reduction in LA. Matt takes the position that it is unlikely the the 73% reduction in AMI risk seen in LDHS is attributable to LA-reduction due to many other dietary variables changing alongside the reduction in LA. Tucker takes the position that reduction in LA explains the majority of the effect. Instead of resolving Matt's point about LDHS, Tucker wants to pivot to discussing the mechanisms of atherosclerosis.
**Potential contradiction (**[**1:35:45**](https://youtu.be/QGNNsiINehI?t=5745)**):**
Tucker holds the view that alpha-linolenic acid reduces risk, but he also holds the view that risk is mediated solely by LA-specific metabolites. However, this is true of all non-LA fatty acids. If the metabolites that confer harm are LA-specific, then shouldn't all non-LA fatty acids be equally non-atherogenic? He tries to reconcile this by saying that ALA "blocks" the negative effects of LA. Does that mean that ALA is an antioxidant? Does the mean that ALA detoxifies LA-specific metabolites somehow? He offers no further explanation.
**Rule violation (**[**1:47:53**](https://youtu.be/QGNNsiINehI?t=6473)**):**
Tucker breaks both rule two and rule six. In response to an objection from Tucker, Matt wanted to ask a question so that he could have specific clarity on Tucker's position, but Tucker cut Matt off before Matt could ask.
**Potential contradiction (**[**1:39:20**](https://youtu.be/QGNNsiINehI?t=5960)**):**
Matt uses one of Tucker's references to present an internal critique. The reference appears to contradict Tucker's model of CVD by stating that hyperlipidemia is sufficient to explain the development of CVD in all its manifestations. Tucker objects to this, saying that the paper is referring to the "genetic hypothesis" of CVD, which involves CVD risk being conferred via genetically mediated concentrations of LDL. Tucker elaborates by stating that if the hypothesis were true, there wouldn't be observable differences in CVD rates between people with the same genetic background between different environments. This appears to be discounting the possibility that LDL can vary between individuals within a genetically homogenous group. Yet, here he affirms that environmental factors like dietary modification can affect LDL levels.
**Strawman (**[**1:49:00**](https://youtu.be/QGNNsiINehI?t=6540)**):**
Matt claims that oxidation of LDL is virtually inevitable after LDL are irreversibly retained within the subendothelial space. Tucker objects, saying it is not inevitable. Matt asks for clarification, requesting evidence that oxidation can be abolished in the subendothelial space. Tucker informs Matt that the fat composition of the diet can influence LDL oxidation rates. After Matt tells Tucker that this isn't what he's asking about, Tucker insists that this is indeed what Matt is asking about, without any further explanation.
**Potential contradiction (**[**1:53:46**](https://youtu.be/QGNNsiINehI?t=6826)**):**
Tucker correctly states that the LA-derived metabolite, malondialdehyde (MDA), is responsible for oxidative modification of LDL particles. However, he also states that ALA can produce this metabolite as well. If Tucker's position is that MDA-mediated oxidative modification of LDL particles initiates CVD, then why would it matter if an intervention involves both LA and ALA? At **58:32**, Tucker states that the inclusion of ALA confounded LAVAT.
If Tucker wants to remain consistent, he'll have to explain why the atherogenic properties of ALA that are entailed from his stated position don't seem to matter. He seems to singling out LA based on characteristics that he admits are shared by ALA. Without further elaboration, Tucker should have to accept ALA as atherogenic, and the reasoning can be syllogized like this:
**Definitions:**
M := MDA is atherogenic
F := increase heart disease risk
x := MDA-producing fatty acids
n := ALA
**P1)** If MDA is atherogenic, then all MDA-producing fatty acids increase heart disease risk.
**(M→∀x(Fx))**
**P2)** MDA is atherogenic.
**(M)**
**C)** Therefore, ALA is an MDA-producing fatty acid that increases heart disease risk.
**(∴Fn)**
**Direct contradiction (2:18:19):**
Tucker directly contradicts himself when he suggests that corn oil is not a seed oil. At **1:43:50**, he cited two primary interventions that demonstrate that seed oils produce harm, but the sole oil used in those trials was corn oil.
**P1)** If MCE and RCOT used corn oil and MCE and RCOT demonstrate the harms of seed oils, then corn oil is a seed oil.
**(H∧R→O)**
**P2)** MCE and RCOT used corn oil.
**(H)**
**P3)** MCE and RCOT demonstrate the harms of seed oils.
**(R)**
**C)** Therefore, corn oil is a seed oil.
**(∴O)**
**Potential contradiction (**[**2:09:08**](https://youtu.be/QGNNsiINehI?t=7748)**):**
Tucker again concedes that LAVAT showed a "fairly small" benefit of vegetable oils compared to animal fats. Earlier in the debate, Tucker stated that other trials such as MCE as showed "harm". However, LAVAT showed a statistically significant 49% increase in CVD mortality risk in the control group, but MCE showed a non-significant 24% increase in CVD mortality risk in the intervention group. If a non-significant 24% increase in CVD mortality is noteworthy in Tucker's view, why is a statistically significant 49% increase in CVD mortality risk only "fairly small" in Tucker's view as well?
**Rule violation (**[**2:10:08**](https://youtu.be/QGNNsiINehI?t=7808)**,** [**2:10:41**](https://youtu.be/QGNNsiINehI?t=7841)**):**
Tucker breaks rule three another three times. After Tucker implies that the benefits seen in LAVAT are inconsequential, Matt once again presents the findings of LAVAT. Matt asks Tucker if he believes that a 33% reduction to all-cause mortality and a 35% reduction to CVD mortality is "small", which is a yes or no question. Rather than answering, Tucker starts talking about Christopher Ramsden's meta-analysis. When Matt asks again, Tucker continues talking about the Ramsden meta-analysis.
**Rule violation (**[**2:10:52**](https://youtu.be/QGNNsiINehI?t=7852)**):**
Tucker breaks rule one again. Matt attempts to explain what his question for Tucker is, but Tucker mind-reads and tries to tell Matt what he means instead of listening.
**Direct contradiction (**[**2:10:59**](https://youtu.be/QGNNsiINehI?t=7859)**):**
Tucker objects to Matt's use of LAVAT to demonstrate a potential benefit of seed oils, saying that "you can't take one single RCT and prove an effect". However, this is the exact manner in which Tucker relies on LDHS to demonstrate the benefits of LA reduction in the context of high ALA. There is no other study that included such an intervention.
Without additional clarification, Tucker would need to reject his own reliance on LDHS to prove the effect of LA-reduction in the context of an ALA-rich diet. Such an entailment can be syllogized like this:
**P1)** If a single study cannot be used to prove an effect, then one cannot use LDHS to prove the effect of LA-reduction in the context of an ALA-rich diet.
**(P→¬U)**
**P2)** A single study cannot be used to prove an effect.
**(P)**
**C)** Therefore, one cannot use LDHS to prove the effect of LA-reduction in the context of an ALA-rich diet.
**(∴****¬****U)**
**Rule violation (**[**2:13:03**](https://youtu.be/QGNNsiINehI?t=7983)**):**
In an astonishing feat, Tucker breaks rules two, four, five, and six all at the same time. Rather than engaging with Matt's question about the clinical significance of the LAVAT results, Tucker dodges by attacking Matt's intellectual integrity. When Matt attempts to interject, Tucker cuts Matt off, attempting to pivot to discussing meta-analyses despite agreeing to systematically discuss the relevant trials one by one.
**Strawman (**[**2:14:21**](https://youtu.be/QGNNsiINehI?t=8061)**):**
Tucker finishes his rant by suggesting that the LAVAT results don't show that increasing seed oils can "reduce heart disease by 30%", which was not at all what Matt was suggesting. All Matt asked Tucker was whether or not Tucker believed that the effects observed in LAVAT were small.
**Strawman (**[**2:14:33**](https://youtu.be/QGNNsiINehI?t=8073)**):**
Tucker claims that Matt agreed that you cannot "prove" something based on one study, and in fact meta-analysis is required for proof. Matt never committed himself to such a concept for causal inference. This is a truly bizarre move on Tucker's part.
**Rule violation (**[**2:16:32**](https://youtu.be/QGNNsiINehI?t=8192)**):**
Tucker breaks rules two and six again. Now discussing the paper by Hooper et al. (2020), Tucker asks Matt where in the paper can the evidence for his claims be found. Matt attempts to respond, but Tucker cuts Matt off again by asking the exact same question he just asked, but with a slightly more crazed inflection.
**Rule violation (**[**2:19:30**](https://youtu.be/QGNNsiINehI?t=8370)**,** [**2:19:38**](https://youtu.be/QGNNsiINehI?t=8378)**,** [**2:19:45**](https://youtu.be/QGNNsiINehI?t=8385)**):**
Tucker breaks rule three three more times. Tucker criticizes the Hooper (2020) meta-analysis by stating that the analysis found "little to no effect" of reducing saturated fat on CVD mortality. Not only is this tangential, but Matt humours the objection long enough to make the point that events is a much more sensitive endpoint than mortality, and events is where the benefit can be seen. Matt follows up by asking Tucker if he thinks reducing total CVD events is beneficial if all else was held equal, which is a simple yes or no question. Rather than answering, Tucker starts painting a caricature of Matt's question instead. When it is clear that Matt is not getting a straight answer, the moderator interjects and allows the yes-or-no question to be asked again. Again, Tucker dodges.
**Direct contradiction (**[**2:21:19**](https://youtu.be/QGNNsiINehI?t=8479)**):**
Tucker takes the position that silent and non-fatal AMIs are not important outcomes and we need not care about them. Yet, at [**1:16:22**](https://youtu.be/QGNNsiINehI?t=4582), Tucker makes it clear that silent and non-fatal AMIs are important and that we should care about them.
This one is pretty straight forward. Either silent and non-fatal AMIs are important and we should care about them, or they are not important and we shouldn't care about them. If Tucker wishes to remain consistent while also preserving his own arguments, we'd need to accept that silent and non-fatal AMIs are important, and that we should care about them. This entailment can by syllogized like this:
**P1)** If silent and non-fatal AMIs are important, then we should care about silent and non-fatal AMIs.
**(N→W)**
**P2)** Silent and non-fatal AMIs are important
**(N)**
**C)** Therefore, we should care about silent and non-fatal AMIs.
**(∴W)**
**Rule violation (**[**2:25:20**](https://youtu.be/QGNNsiINehI?t=8720)**):**
Tucker breaks rule four for the seventh time. After agreeing to discuss the results of Hooper (2020), Tucker suddenly attempts to steer the debate toward some sort of meta-level discussion about seed oil consumption in the general population.
**Rule violation (**[**2:30:31**](https://youtu.be/QGNNsiINehI?t=9031)**):**
Tucker breaks both rules four and six. The moderator poses a question to both Matt and Tucker, and gets a satisfactory answer from both Matt and Tucker. However, rather than returning the floor to the moderator or continuing with the debate, Tucker takes the opportunity to address points that Matt hasn't even made yet in the debate, and doesn't give Matt any amount of time to respond.
**Rule violation (**[**2:37:06**](https://youtu.be/QGNNsiINehI?t=9426)**):**
Tucker breaks rules two and four again. The moderator recognizes that Tucker's incoherent flow-of-consciousness monologue has been going on for nearly ten minutes, and the moderator tries to interject. Tucker cuts the moderator off and proceeds to ramble about vitamin E for another minute.
**Rule violation (**[**2:38:42**](https://youtu.be/QGNNsiINehI?t=9522)**):**
Tucker can't help but break rule four again. Tucker interjects, before Matt can even finish a single sentence, in order to tell Matt that ecological studies are the worst form of epidemiology. At this point it is fair to say that Tucker is breaking rule one as well. It's clear that Tucker is no longer here for an "open, conversation-style" debate.
**Direct contradiction (**[**2:38:50**](https://youtu.be/QGNNsiINehI?t=9530)**):**
Tucker takes the position that ecological studies are of critical importance, superseding all other forms of epidemiology. Yet, only moments earlier, Tucker took the position that ecological studies are the worst form of epidemiological evidence.
Again, we have another relatively simple inconsistency to address. In order for Tucker to make his case against seed oils, he systematically rejected all nutritional epidemiology except for ecological studies. Yet, claiming that ecological studies are the worst form of epidemiology entails a contradiction, as it means that Tucker is simultaneously holding the view that it is both the best and the worst form of epidemiology at the same time. If Tucker wished to resolve the inconsistency, he'd probably have to acknowledge that ecological studies are not the worst form of epidemiology. This can be syllogized like this:
**P1)** If ecological studies are the best form of nutritional epidemiology, then ecological studies are not the worst form of nutritional epidemiology.
**(B→¬W)**
**P2)** Ecological studies are the best form of nutritional epidemiology
**(B)**
**C)** Therefore, ecological studies are not the worst form of nutritional epidemiology.
**(∴¬W)**
**Direct contradiction (**[**2:42:37**](https://youtu.be/QGNNsiINehI?t=9757)**):**
Tucker makes the claim that we can't know whether or not the margarine used in Sydney Diet-Heart Study (SDHS) contained TFA. Moments later, at [**2:44:23**](https://youtu.be/QGNNsiINehI?t=9863) he suggests that it is valid to argue that we absolutely can know the margarine in SDHS did not contain TFA.
If Tucker maintains that it cannot be known whether or not TFA was confounding in SDHS, then he cannot posit that it can be known one way or the other. Either position that Tucker took could work for his argument on this subject, but they're just not compatible with each other, and that can be illustrated like this:
**P1)** If it cannot be known whether TFA was confounding in SDHS, then it is not reasonable to posit that we absolutely know that TFA wasn't confounding in SDHS.
**(¬T→¬S)**
**P2)** It cannot be known whether TFA was confounding in SDHS.
**(¬T)**
**C)** Therefore, it is not reasonable to posit that we absolutely know that TFA wasn't confounding in SDHS.
**(∴¬S)**
**Rule violation (**[**2:57:59**](https://youtu.be/QGNNsiINehI?t=10679)**,** [**2:58:53**](https://youtu.be/QGNNsiINehI?t=10733)**):**
Tucker breaks rule three two more times. While discussing a paper that models substitutions of olive oil for various other fats, Matt asks Tucker if he has any problems with the paper. Rather than answering, Tucker starts discussing issues he has with another paper published by the same group investigating dairy fat. Matt attempts to interject, but Tucker continues to discuss previous research on potatoes that was also published by this group.
**Rule violation (**[**2:59:44**](https://youtu.be/QGNNsiINehI?t=10784)**):**
Tucker breaks rules two, three, and four again. Matt once again asks Tucker if he has any issues with the olive oil substitution analysis. Rather than answering, Tucker cuts Matt off before he can finish asking his question, and Tucker starts asking why Matt included the paper in his references.
**Rule violation (**[**3:00:44**](https://youtu.be/QGNNsiINehI?t=10844)**):**
Tucker once again breaks rule three. Matt asks his yes-or-no question yet again, to which Tucker responds by stating that the mechanisms favour his position. This is just another dodge.
**Rule violation (**[**3:00:53**](https://youtu.be/QGNNsiINehI?t=10853)**,** [**3:02:18**](https://youtu.be/QGNNsiINehI?t=10938)**):**
Tucker breaks rule three again, despite it now being enforced by the moderator. The moderator notices that Matt is not getting an answer to his question, and the moderator steps and reminds Tucker of the question being asked. Rather than answering the question, Tucker continues to discuss mechanisms. The moderator again notices that this doesn't answer Matt's question, and implores Tucker to answer. Again, Tucker dodges the question and starts talking about the paper itself, rather than addressing Matt's question about Tucker's interpretation of the paper.
**Rule violation (**[**3:06:00**](https://youtu.be/QGNNsiINehI?t=11160)**):**
Tucker breaks rules one and six again. Not even one minute after Tucker grants Matt the floor to make a point about mechanistic data, Tucker interrupts Matt on the basis that Matt's point isn't relevant. Though, only moments before, the moderator gave Matt the floor to complete his point. It is clear that Tucker has no respect for the moderator's wishes, nor the debate parameters.
**Rule violation (**[**3:06:52**](https://youtu.be/QGNNsiINehI?t=11212)**):**
Tucker breaks rules one and six again. For the second time, Tucker interrupts Matt when he's been given the floor by the moderator to complete his point.
**Rule violation (**[**3:13:34**](https://youtu.be/QGNNsiINehI?t=11614)**):**
Tucker breaks rules two again. Rather than letting Matt complete his point about the olive oil substitution analysis, Tucker interrupts him.
**Direct contradiction (**[**3:15:10**](https://youtu.be/QGNNsiINehI?t=11710)**):**
Tucker concedes that margarine and mayonnaise are not the same thing as isolated vegetable oils. However, at [**3:14:30**](https://youtu.be/QGNNsiINehI?t=11670), Tucker rejects that there are differences between margarine, mayonnaise, and isolated vegetable oils. Another layer of hilarity would be to point out that if Tucker maintains that mayonnaise is the same as an isolated seed oil, he'd be holding the position that corn oil is not a seed oil, but mayonnaise is.
**Definitions:**
S := seed oils are the topic of debate
T := non-seed oil topics are not the topic of debate
m := mayonnaise and margarine
**P1)** If seed oils are the topic of debate, then non-seed oil topics are not the topic of debate.
**(S→(∀x(Tx))**
**P2)** Seed oils are the topic of debate.
**(S)**
**C)** Therefore, mayonnaise and margarine are non-seed oil topics that are not the topic of debate.
**(∴Tm)**
This is where the debate portion of the episode ends, with Matt and Tucker both giving their closing statements. Altogether, Tucker violated the rules at least 50 times and committed at least 18 fallacies, and that's not counting the various hilarious empirical and epistemic claims that Tucker made. For anyone interested in reading more about Tucker's errors, Matt published a comprehensive rebuttal to his personal blog, which can be found on [Matt's blog](https://drmatthewnagra.com/seed-oil-debate-with-tucker-goodrich/). From what I could tell, Matt did not really break the rules at all, except for perhaps a few minor instances when he attempted to interject when Tucker was rambling. Other than that, he conducted himself according to the rules.
Whether you're skeptical, supportive, or unsure of Tucker's work, I hope that this debate, as well as the breakdown contained within this article, gives you a decent perspective on just how bad his arguments actually are. I'm truly failing to imagine any good reasons for why someone with a stable position, which is truly robust to scrutiny, should struggle this hard to stay consistent in a debate. Tucker's performance was truly terrible, and should be eye-opening to anyone who thought that he might have even a scrap of credibility within this domain.
Thanks for reading! If you enjoy my writing and want more content like this, consider pledging to my [Patreon](https://www.patreon.com/thenutrivore)!

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Many Paleo diet advocates claim that hunter-gatherer diets optimally promote the long-term health of human beings. There are typically two primary justifications for this claim— firstly, the fact that hunter-gatherer populations typically appear to be robustly healthy, and secondly, the fact that humans evolved eating these types of diets. While these are technically statements of fact, I find myself forced to take a page out of the Paleo-dieter's playbook, as I remind them that correlation doesn't equal causation. So, let's dig into why their reasoning is flawed.
Firstly, let me hit you with a thought experiment for a moment. Do you think that the elderly people within a given population would appear either more healthy or less healthy if that population _never_ had access to modern medical technology? Think about this for a moment. You may understandably intuit that their health would probably be worse, correct? But that probably isn't what would happen. They would probably appear healthier, and I'll explain why.
If a population never had access to modern medical technology, one of the things you couldn't reliably do is save sick or injured children. No matter what culture you observe, a sizable proportion of children will develop infectious illnesses. These illnesses, like bacterial or viral infections, are generally mundane by modern standards. However, without modern medicine many children who developed these types of illnesses would likely not survive them.
Those who are more prone to illness likely do not have the same chances of survival as those who are less prone to illness. As such, why wouldn't the elderly in this hypothetical population present with more robust health as a result? Without medical intervention, the environment is essentially selecting for the fittest possible individuals in our hypothetical population. This would likely generate the appearance of more robust health in the elderly. Consider this carefully for a moment. If you weed out all of the weaker people, of course the remaining population is going to appear stronger.
This presents a significant problem for Paleo diet advocates who choose to cite the robust health of hunter-gatherer populations as a justification for the Paleo diet, or as a justification for recommending the diet to others. Most Paleo-dieters do seem to be aware of the environmental adversity faced by hunter-gatherer populations. But they often don't seem to appreciate how this also produces significant challenges for their narrative.
For example, if you remind a Paleo-dieter that hunter-gatherers typically had an average life expectancy of around 30 years, they will often immediately retort by stating that those estimates are confounded by infant and child mortality. But therein lies the problem— they can't have it both ways. A Paleo diet advocate cannot use that argument without tacitly admitting that infant and child mortality is typically enormously high among hunter-gatherer populations. Which it most certainly is [[1]](https://www.sciencedirect.com/science/article/abs/pii/S1090513812001237).
Approximately 26.8% of infants and 48.8% of prepubescent children die in hunter-gatherer populations. With such a high proportion of children dying, how could it be the case that the apparent health of elderly hunter-gatherers is **not** coloured by this? Remember, hunter-gatherer populations likely appear healthier because the least resilient members of those populations are already dead. Paleo diet advocates cannot admit that hunter-gatherer populations had high rates of infant and child mortality without also admitting that the resulting population is a heavily biased sample.
This type of confounding is known as survivorship bias. Basically, survivorship bias is a type of selection bias that can occur when those who did not survive a selection event or process are overlooked in favour of those who did survive. For example, let's say we were trying to construct better body armour for soldiers to wear in combat. Perhaps we might conduct a study of the soldiers who returned from battle. We could collect bullet wound distribution pattern data to help ascertain where soldiers were most likely to get shot.
However, as we see in the graphic above, this sort of analysis would exclude all those who were shot and did **not** survive. It would also overlook the sorts of bullet wound distribution patterns that tended to lead to death, which would actually have given us a significantly clearer picture of how we might construct better body armour.
Likewise, when Paleo diet advocates claim that we should eat like hunter-gatherers because hunter-gatherers are robustly healthy, they're not appreciating how survivorship bias is confounding their appraisal of hunter-gatherer health. They are essentially overlooking the other fifty percent of the hunter-gatherer population that didn't survive.
For this reason, it is dubious to use the apparent good health of hunter-gatherers as the basis for the assumption that their diets are appropriate for modern humans. Until Paleo diet advocates can figure out a way to explain why survivorship bias would not be confounding in an evaluation of hunter-gatherer health, they cannot rely on the apparent good health of hunter-gatherer populations to determine the applicability of hunter-gatherer diets to modern humans. In reality, the degree to which hunter-gatherer diets are appropriate for modern humans remains unclear.
But this isn't the only erroneous argument that Paleo-dieters will use to justify their claims. Often times Paleo diet advocates will also suggest that since we evolved eating certain foods, it is absurd to believe that any of the foods that we evolved eating could pose a long-term health risk to the average person. This reasoning has been used to dismiss robust and well-studied diet-disease relationships, such as saturated fat and cardiovascular disease, red meat and cancer, or even sodium and hypertension [[2]](https://pubmed.ncbi.nlm.nih.gov/32428300/)[[3]](https://pubmed.ncbi.nlm.nih.gov/28487287/)[[4]](https://pubmed.ncbi.nlm.nih.gov/27216139/)[[5]](https://pubmed.ncbi.nlm.nih.gov/28655835/).
Right off the bat it is quite easy to identify that this is a blatant appeal to nature fallacy, and can be outright dismissed on that basis alone. However, it is important to describe precisely why this line of reasoning fails. What we really want to know is whether or not foods are necessarily beneficial (or neutral) for long-term health merely because we evolved eating them.
To explore this question, let's first briefly consider how Darwinian natural selection works. Essentially, it is the process by which random gene mutations are selected for by different environmental challenges. Some mutations are better at dealing with certain environmental challenges than other mutations. As a result, these more adaptive mutations increase an organism's chances of producing offspring. These organisms subsequently pass on these adaptive mutations to their offspring as well.
In this image we see that black mice are less likely to get eaten by the bird than tan mice. For this reason, the random mutations that produces black mice rather than tan mice ends up being naturally selected for by the environment. However, environmental challenges like getting eaten aren't quite the same as environmental challenges that affect the long-term health of an organism.
Getting eaten when you're young is an acute event. Developing a life-threatening chronic disease in old-age, as a result of a life-long environmental exposure (like a food or nutrient), is a long, protracted event. It is unlikely that selection pressure applies to these two events symmetrically, because adaptations occur as a function of successful reproduction. As a result, the probability that _deleterious_ traits will be successfully selected against likely diminishes with age.
So, the question ends up being: how long after reproductive age does natural selection still robustly apply to human beings? Surely selection pressure doesn't end at reproductive age, because human children need human adults to raise them and care for them. But does selective pressure exist to a meaningful degree for those in the age ranges that typically associate with life-threatening chronic disease? Some scholars have attempted to estimate the force of natural selection as a function of age [[6]](https://pubmed.ncbi.nlm.nih.gov/30124168/).
Applying the above graph to human beings, our best estimations suggest that the forces of natural selection rapidly wane down to nil shortly after sexual maturity, which would be approximately 16 to 17 years of age. Around the ages of 30 to 40 is when humans likely enter the "selection shadow", which is the zone wherein natural selection no longer robustly applies.
It seems highly unlikely that the fate of a population could ever hinge on the fitness of middle-aged people who are past their prime. For fun, let's estimate the age range wherein peak human performance is likely to occur. Perhaps we could look at the average age range of Olympic athletes [[7]](https://venngage.com/blog/olympics/).
The average age range of Olympic athletes is between ~22.5 and ~25.5, which is well before the age range seen within the selection shadow. Which honestly makes sense if you think about it. As you age it becomes less likely that natural selection will select against deleterious traits, like losing athletic performance. Once inside the selection shadow, there is likely insufficient selective pressure to extend peak physical performance into higher and higher age ranges.
The selection shadow may actually be observable in some existing traditional populations as well, such as the Tsimané people of Bolivia. While they are technically hunter/forager-horticulturalists and not strictly hunter-gatherers, they are one of the only traditional populations for which we have decent data regarding the progression of chronic disease.
Using a measurement of atherosclerotic cardiovascular disease (ASCVD) progression known as coronary artery calcification (CAC) scoring, researchers were able to quantify the prevalence of ASCVD by age group among the Tsimané [[8]](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)30752-3/fulltext).
It should also be noted that CAC scores are indicative of advanced ASCVD [[9]](https://pubmed.ncbi.nlm.nih.gov/24530667/). The exclusive use of CAC scoring in this study of the Tsimané leaves us with many interpretive challenges. For example, if CAC scores are representative of advanced ASCVD (so called "hard plaques"), what proportion of less advanced ASCVD (so-called "soft plaque") might have been overlooked? It is difficult to say for sure. But the bottom line is that the Tsimané experience increases in chronic disease at approximately the same time as modern populations— well inside the selection shadow.
Granted, the prevalence of chronic disease in the Tsimané is overall lower than that of Western cultures. But, this could be expected given the fact that their diets and lifestyles are likely preferable to that of Western cultures as well. Not to mention the possible confounding due to survivorship bias, to which they are also not immune [[10]](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502712/). The Tsimané have infant mortality rates that are many fold higher than in Western cultures. This means that the Tsimané are vulnerable to the same type of confounding via survivorship bias that we discussed earlier, thus adding more layers of interpretive challenges.
The methods used to determine the age-ranges of the Tsimané were also questionable, and relied mostly on anecdote and personal judgement rather than objective measurements.
_“Birth years were assigned based on a combination of methods including using known ages from written records, relative age lists, dated events, photo comparisons of people with known ages, and cross-validation of information from independent interviews of kin.”_
When compared to more objective measures of age, the methods described above would appear to overestimate ages as the age of the subjects increases [[11]](https://pubmed.ncbi.nlm.nih.gov/27511193/). Below the age of 40, estimates appear to be rather accurate. However, the age estimations used by Kaplan et al. (2017) would seem to overestimate ages by approximately 15 years above the age of 60. After adjusting for this, it is unlikely that CAC prevalence among the Tsimané differs significantly from Western populations. In fact, it might actually be higher.
It is also imperative to mention that foods to which we are adapted might actually be more likely to be harmful for us as we age. This is because of a concept in evolutionary biology called antagonistic pleiotropy, which is the most widely accepted explanation for the evolutionary origin of aging [[12]](https://pubmed.ncbi.nlm.nih.gov/31870250/)[[13]](https://pubmed.ncbi.nlm.nih.gov/30524730/). The theory of antagonistic pleiotropy essentially posits some genetic adaptations can trade long-term health for short-term reproductive success. However, it can be inferred that most genetic adaptations are antagonistically pleiotropic.
Essentially, human DNA tends to degrade over time when it doesn't rightfully need to, as evidenced by the existence of biologically immortal organisms. Human DNA repair is also regulated and gene-specific. Given these facts, the interaction between gene degradation and gene repair is likely to be adaptive. This assigns every gene in our DNA that tends to degrade more with time a single antagonistically pleiotropic trait. Since most DNA in the human genome degrades over time, we can infer that over 50% of genes are antagonistically pleiotropic.
Since adaptations to foods are no more or less genetic than any other adaptations, we can infer that most adaptations to food are also likely to be antagonistic pleiotropic as well. From here we just infer that antagonistic pleiotropy applies more to ancestral foods than it does to novel foods. Which would suggest that the foods to which we are most strongly adapted would tend to be most antagonistically pleiotropic. This increases the likelihood that ancestral foods trade long-term fitness for short-term reproductive success.
For example, perhaps adaptations to sodium and saturated fat consumption, like regulated changes in blood pressure or lipoprotein secretion from the liver, may help to carry people to reproductive age without incident. However, those adaptations might actually increase the risk of poorer health later in life if those dietary exposures persist too long. This is why we cannot assume that natural diets are actually appropriate for maintaining the long-term health of modern humans. These adaptations to diet are likely to be antagonistic pleiotropic.
Without scientific evidence to help inform our attitudes toward the relative health value of novel foods, the health value of those foods remains is a black box. Due to the principle of indifference, we have no particular reason to suspect that truly novel foods will be either beneficial or detrimental. However, if it can be demonstrated that both an ancestral food and a novel food have the same thriving potential during the reproductive years, we can actually infer that the novel food is to be favoured.
Novel foods do not belong to the domain of foods that have the potential to be antagonistic pleiotropic, since we did not evolve consuming them. Conversely, the ancestral food in our scenario is likely to be antagonistically pleiotropic. Thus, the novel food is to be favoured over the ancestral food in this case. This concept can be illustrated clearly with a couple of simple tables.
To summarize, we can infer that ancestral foods are likely to have both positive short-term health value, as well as negative long-term health value. However, in the absence of empirical data, our doxastic attitude toward the health value of novel foods should be one of agnosticism. When the thriving potential of novel foods and ancestral foods show non-inferiority, we infer that the novel foods is less likely to be detrimental for long-term health. Altogether, the argument can be summarized like this:
**Definitions:**
**A** := a human trait (x) is antagonistically pleiotropic
**E** := the human trait (x) is an evolutionary adaptation
**N** := the human trait (x) mediates more than one downstream effect, one of which is negative in the post-reproductive window of the carrier
**D** := human genes succumb to degradation
**M** := human genes must be assumed to be antagonistically pleiotropic
**R** := humans have more genetic adaptations to ancestral foods than novel foods
**C** := antagonistic pleiotropy applies more to ancestral foods than it does to novel foods
**V** := there is a novel food that has non-inferior short-term health value compared to a given ancestral foods
**U** := there is a novel food that is likely to be superior to such an ancestral food in the long-term
**O** := there are unnatural diets that are preferable to ancestral diets.
**x** := human genes
**y** := trait of a human gene
**i** := the interaction between degradation and repair
**P1)** A human trait is antagonistically pleiotropic if and only if the human trait is an evolutionary adaptation and the human trait mediates more than one downstream effect, one of which is negative in the post-reproductive window of the carrier.
**(∀x(Ax↔(Ex∧Nx)))**
**P2)** The interaction between gene degradation and gene repair is an evolutionary adaptation.
**(Ei)**
**P3)** The interaction between gene degradation and gene repair mediates more than one downstream effect, one of which is negative in the post-reproductive window of the carrier.
**(Ni)**
**P4)** If the interaction between gene degradation and gene repair is antagonistically pleiotropic and all human genes succumb to degradation, then all human genes must be assumed to be antagonistically pleiotropic.
**(Ai∧D→M)**
**P5)** All human genes succumb to degradation.
**(D)**
**P6)** If all human genes must be assumed to be antagonistically pleiotropic and humans have more genetic adaptations to ancestral foods than novel foods, then antagonistic pleiotropy applies more to ancestral foods than it does to novel foods.
**(M∧R→C)**
**P7)** Humans have more genetic adaptations to ancestral foods than novel foods.
**(R)**
**P8)** If antagonistic pleiotropy applies more to ancestral foods than it does to novel foods and there is a novel food that has non-inferior short-term health value compared to a given ancestral food, then there is a novel food that is likely to be superior to such an ancestral food in the long-term.
**(C∧V→U)**
**P9)** There is a novel food that has non-inferior short-term health value compared to a given ancestral food.
**(V)**
**P10)** If there is a novel food that is likely superior to such an ancestral food in the long-term, then there are some unnatural diets that are superior to some ancestral diets.
**(U→O)**
**C)** Therefore, there are some unnatural diets that are superior to some ancestral diets.
**(∴O)**
Essentially, once you equalize advantages across a given novel food and a given ancestral food, the inherent disadvantages of antagonistic pleiotropy would leave us favouring the novel food over the ancestral food for long-term health. From here we can infer a priori that a diet that maximizes benefits and minimizes risks for the most amount of people is likely to be a diet that is on some level unnatural or non-ancestral. It is also important to discuss what this position is **not** arguing. It is **not** being argued that every novel food is going to be superior to every ancestral food, and it is **not** being argued that all ancestral foods are bad.
As an aside, one might point out that while ancestral foods like meat seem to increase the risk of many diseases, while other ancestral foods like fruit seem to decrease the risk of many diseases. So what gives? My arguments apply equally to fruit, and adaptations of fruit are also likely to be antagonistically pleiotropic. However, it is likely the case that the antagonistically pleiotropic pathways that are influenced by foods like fruit are less impactful than those influenced by foods like meat.
Diet is about substitutions. Replacing meat with fruit lowers risk, but that doesn't mean that fruit is without long-term harms or risks as well. Bearing this in mind, I posit that if we truly want to maximize the thriving potential of food, we must engineer our own food. Assuming that no diet of natural foods will actually lower risk to zero, if we wanted to improve the health value of food even more, how would we accomplish this without artificially manipulating those foods? In fact, we have evidence that the health value of natural foods can be improved, with examples like Golden rice.
**P1)** If the health value of natural foods can be improved via artificial manipulation, then there are unnatural foods that are preferable to some natural foods.
**(V→M)**
**P2)** The health value of natural foods can be improved via artificial manipulation.
**(V)**
**C)** Therefore, there are some unnatural foods that are preferable to some natural foods.
**(∴M)**
Lastly, it has also been suggested by some Paleo diet advocates that certain hunter-gatherer migrant studies provide us with a justification for why hunter-gatherer diets are appropriate for modern humans. This is due to the fact that these studies demonstrate that when certain hunter-gatherer populations transition from their traditional diets to more Westernized diets, they experience increases in chronic disease risk [[14]](https://pubmed.ncbi.nlm.nih.gov/6937778/)[[15]](https://pubmed.ncbi.nlm.nih.gov/7462380/). However, this is ultimately irrelevant to my point.
The fact that Western diets increase disease risk relative to certain hunter-gatherer diets does not actually lend any credibility to the notion that modern humans can achieve robust health that is equal to that of hunter-gatherers merely by emulating their diets. Perhaps the Western diet is so bad that it would negatively impact the health of any human population who ate it over the long-term. But, it could also be the case that hunter-gatherer diets are still inappropriate for modern humans in many ways— ways that may not be obvious for the reasons I've discussed throughout this article. These are not incompatible concepts.
The most I would have to grant is that a hunter-gatherer diet is likely an improvement over a Western diet. But that is a far cry from ascertaining that a hunter-gatherer diet is optimal for the long-term health of modern humans. This is just a gross overextrapolation from altogether irrelevant data.
The last inference is the icing on the cake, and a bit more convoluted, but it is necessary to argue it to an ancestral diet advocate. This is next argument cuts to the core of their epistemology regarding ancestral diets and health. All we need to do is prime the ancestral diet advocate for the inference by asking them if they identify as "**F**" (as defined below). If they do, then we proceed. If they don't, then their motivations for advocating for ancestral diets diets isn't clear at all.
**Definitions:**
**A** **:**= F(x) would be acting against their values to not be in favour of consuming N(y).
**F(x)** := someone who favours consuming ancestral foods to the exclusion of novel foods because they value reducing disease risk.
**N(y)** := a novel food that reduces disease risk when replacing an ancestral food.
**P1)** If there exists someone who favours consuming ancestral foods to the exclusion of novel foods because they value reducing disease risk, and there exists a novel food that reduces disease risk when replacing an ancestral food, then that person would be acting against their values to not be in favour of consuming that novel food.
**∃xF(x)∧∃yN(y)→∀x∀y(Axy)**
**P2)** There exists someone who favours consuming ancestral foods to the exclusion of novel foods because they value reducing disease risk.
**(∃xF(x))**
**P3)** There exists a novel food that reduces disease risk when replacing an ancestral food.
**(∃yN(y))**
**C)** Therefore, that person would be acting against their values to not be in favour of consuming that novel food.
**(∴∀x∀y(Axy))**
Essentially, if our interlocutor identifies as "**F**", then all we need to do is demonstrate to them that "**N**" exists, and we're essentially home free. If they accept that "**N**" exists and they also identify as "**F**", then they should be in favour of substituting such a novel food for such an ancestral food. If they don't, then they have a contradiction. This is where the ancestral diet advocate could face quite a dilemma.
However, there is a way around this for them, but it's absurd. They can simply reject the evidence for "**N**" existing. Which would be a hilarious move for them to make, but they can make it if they want. However, implicit in this move is the rejection of all evidence that supports "**N**" existing, regardless of the quality.
For example, if they maintain that animal fat consumption is more supportive of health than vegetable fat consumption, they'd need to reject the multiple meta-analyses and meta-regression analyses of randomized controlled trials on the subject, as well as the consistency of effect in seen in high internal validity epidemiology. The implications of taking such a position are hilarious, because they could very easily have to also reject many other diet/lifestyle-disease relationships that they likely take for granted on much weaker evidence. Such as exercise and alcohol consumption affecting cardiovascular disease risk.
It is likely that the vaunted "optimal human diet", which is to say a diet that maximizes long-term health for the greatest number of people, has actually yet to be discovered. Ultimately, to answer the question of what foods are healthy, we need science. We need robust outcome data on modern human beings, not speculation and appeal to nature fallacies. We need this science to teach us how to eat.
**UPDATE:**
Chris Masterjohn has apparently written a [lengthy response](https://chrismasterjohnphd.substack.com/p/ancestral-health-vs-antagonistic) to my position on antagonistic pleiotropy and how it relates to the long-term health value of ancestral foods. Many have asked me to rebut the article, but it's not clear to me why I should. He's not interacting with the argument at all. Let me give you an example to help illustrate my feelings in this matter. If I give someone an argument, and their response is to turn around and scream at a wall, should I feel any sort of drive to "rebut" the screaming? I don't think so.
Constructing a lengthy reply to Masterjohn's article would only serve to give readers the impression that he actually said anything of substance against my position, which he hasn't. When someone tells me that they disagree with an argument that I have presented, I take this to mean one of two things. Either they have an argument of their own that forms a conclusion that is the negation of at least one of my premises, or they give at least one of my premises such low credence that they just deny that it's true. Masterjohn didn't do either in his article.
Masterjohn just spends the article giving low credence to concepts that aren't even entailed from the argument itself, so why should I care? It's doubly hilarious to expect me to rebut his article when he actually signed off on the entailments of my position at least twice in our [debate](https://chrismasterjohnphd.substack.com/p/the-ancestral-health-debate) when he was actually interacting with the argument itself and not going off on tangents. Once at [58:26](https://youtu.be/n1I5xgvERbo?t=3506) and again at [1:39:16](https://youtu.be/n1I5xgvERbo?t=5956). Not sure what more there is to comment on here.
Thank you for reading! If you like what you've read and want help support my content, consider pledging to my [Patreon](https://www.patreon.com/thenutrivore). Every little bit helps! I hope you found the content interesting!
**References:**
[1] Anthony A. Volka and Jeremy A. Atkinson. Infant and child death in the human environment of evolutionary adaptation. Evolution and Human Behavior. Volume 34, Issue 3, May 2013, Pages 182-192. [https://www.sciencedirect.com/science/article/abs/pii/S1090513812001237](https://www.sciencedirect.com/science/article/abs/pii/S1090513812001237)
[2] Lee Hooper, et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2020 May. [https://pubmed.ncbi.nlm.nih.gov/32428300/](https://pubmed.ncbi.nlm.nih.gov/32428300/)
[3] Arash Etemadi, et al. Mortality from different causes associated with meat, heme iron, nitrates, and nitrites in the NIH-AARP Diet and Health Study: population based cohort study. BMJ. 2017 May 9. [https://pubmed.ncbi.nlm.nih.gov/28487287/](https://pubmed.ncbi.nlm.nih.gov/28487287/)
[4] Andrew Mente, et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet. 2016 Jul 30. [https://pubmed.ncbi.nlm.nih.gov/27216139/](https://pubmed.ncbi.nlm.nih.gov/27216139/)
[5] Rik H G Olde Engberink, et al. Use of a Single Baseline Versus Multiyear 24-Hour Urine Collection for Estimation of Long-Term Sodium Intake and Associated Cardiovascular and Renal Risk. Circulation. 2017 Sep 5. [https://pubmed.ncbi.nlm.nih.gov/28655835/](https://pubmed.ncbi.nlm.nih.gov/28655835/)
[6] Thomas Flatt and Linda Partridge. Horizons in the evolution of aging. BMC Biol. 2018 Aug 20.
[https://pubmed.ncbi.nlm.nih.gov/30124168/](https://pubmed.ncbi.nlm.nih.gov/30124168/)
[7] Ryan McCready. For Olympic Athletes, Is 30 the New 20? July 2016. [https://venngage.com/blog/olympics/](https://venngage.com/blog/olympics/)
[8] Hillard Kaplan, et al. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. Lancet. 2017 Apr 29. [https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)30752-3/fulltext](https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)30752-3/fulltext)
[9] Mahesh V Madhavan, et al. Coronary artery calcification: pathogenesis and prognostic implications. J Am Coll Cardiol. 2014 May. [https://pubmed.ncbi.nlm.nih.gov/24530667/](https://pubmed.ncbi.nlm.nih.gov/24530667/)
[10] Michael Gurven. Infant and fetal mortality among a high fertility and mortality population in the Bolivian Amazon. Soc Sci Med. 2012 Dec. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502712/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502712/)
[11] Horvath et al. An epigenetic clock analysis of race/ethnicity, sex, and coronary heart disease. Genome Biol. 2016 Aug. [https://pubmed.ncbi.nlm.nih.gov/27511193/](https://pubmed.ncbi.nlm.nih.gov/27511193/)
[12] J Mitteldorf. What Is Antagonistic Pleiotropy? Biochemistry (Mosc). 2019 Dec. [https://pubmed.ncbi.nlm.nih.gov/31870250/](https://pubmed.ncbi.nlm.nih.gov/31870250/)
[13] He and Zhang. Toward a molecular understanding of pleiotropy. Genetics. 2006 Aug. [https://pubmed.ncbi.nlm.nih.gov/16702416/](https://pubmed.ncbi.nlm.nih.gov/16702416/)
[14] J M Stanhope and I A Prior. The Tokelau island migrant study: prevalence and incidence of diabetes mellitus. N Z Med J. 1980 Dec. [https://pubmed.ncbi.nlm.nih.gov/6937778/](https://pubmed.ncbi.nlm.nih.gov/6937778/)
[15] J M Stanhope and I A Prior. The Tokelau Island Migrant Study: serum lipid concentration in two environments. J Chronic Dis. 1981. [https://pubmed.ncbi.nlm.nih.gov/7462380/](https://pubmed.ncbi.nlm.nih.gov/7462380/)

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Because every online diet camp purports that their pet diet cures every disease known to mankind, naturally each one will give you some fantastical mechanistic story about how said diet cures type 2 diabetes mellitus (T2DM). In the paleo/keto/carnivore camp, people will often claim that T2DM is caused by chronic exposure to refined sugar, with some even going so far as to claim that it is caused by exposure to carbohydrates (CHO) more broadly (including foods like apples and even carrots). However, these days it is more trendy in that group to blame T2DM on vegetable oils, but I have previously debunked this on my blog. Over in the "whole food plant-based" (WFPB) cult, it is routinely remarked that T2DM is caused by intramyocellular lipid (IMCL), and that chronic exposure to the saturated fat (SFA) in animal products is responsible for the condition.
In this article, I'll go over the mechanistic reasoning and experiment and/or observational support for these hypotheses, as well as provide an accounting of the leading hypothesis and its supporting evidence. Let's start off by tackling the fantastical notions dreamed up by our vegan friends, and address the IMCL hypothesis.
## The Intramyocellular Lipid Hypothesis
The core idea with this hypothesis is that IMCL, primarily in the form of triglycerides (TG) stored within lipid droplets in muscle cells, act through various pathways to disrupt insulin signaling. The IMCL hypothesis has drawn attention to the role of diet in modulating IMCL levels. High intakes of certain types of fats, particularly SFAs found abundantly in animal products, have been implicated by the proponents of this hypothesis in elevating IMCL levels and contributing to insulin resistance.
This association is often highlighted in discussions on the benefits of WFPB diets for reducing the risk of T2DM and improving insulin sensitivity. Advocates of WFPB diets suggest that such a diet, which is typically lower in SFA and higher in unsaturated fats like monounsaturated fats (MUFA) and polyunsaturated fats (PUFA), which can purportedly help reduce IMCL accumulation and make traction against insulin resistance.
The dietary focus is on whole grains, legumes, fruits, vegetables, nuts, and seeds, with minimal or no intake of animal products. The concern with animal products stems from their content of SFAs, dietary cholesterol, and perhaps even certain supposed inflammatory mediators (possibly Neu5Gc), which may contribute to increased IMCL levels and insulin resistance. WFPB proponents argue that replacing animal products with plant-based sources of protein and fat can mitigate these risks. But is it true?
The IMCL hypothesis attempts to highlight the potential impact of IMCL accumulation on insulin resistance and physiological markers of T2DM. While WFPB are promoted as strategies to reduce IMCL and improve metabolic health, it's important to consider the broader literature and where this hypothesis lands with respect to epistemic virtues over other, possibly more prevailing hypotheses for which there is more evidence.
The mechanistic case for the IMCL hypothesis was first outlined in the late 1990s with two small studies by Jacob, et al. and Perseghin, et al., which discovered relationships between IMCL and insulin resistance in T2DM-free subjects who were born of parents with T2DM [[1]](https://pubmed.ncbi.nlm.nih.gov/10331418/)[[2]](https://pubmed.ncbi.nlm.nih.gov/10426379/). In these experiments, the offspring of those with T2DM were subjected to the gold-standard measure of whole-body insulin sensitivity, the hyperinsulinemic-euglycemic clamp test (HEC). It was discovered that there was an inverse association between IMCL and insulin sensitivity, which led researchers to suspect that perhaps this biomarker was relevant to the pathophysiology of T2DM.
Fast forward to 2004, and another small study from van Loon, et al. would introduce the hypothesis' first paradox [[3]](https://pubmed.ncbi.nlm.nih.gov/15165998/). In this experiment, muscle biopsies and less precise (but still adequate) measures of insulin sensitivity were deployed in an investigation of subjects who were either sedentary, afflicted with T2DM, or who were trained athletes. The study found that the IMCL concentrations of IMCL were actually statistically significantly higher in athletic subjects compared to either sedentary or T2DM-afflicted subjects. Yet, the athletic subjects did not suffer from impaired insulin sensitivity or the hyperglycemia that is characteristic of T2DM.
Researchers Coen and Goodpaster attempted to reconcile the findings in 2012 [[4]](https://pubmed.ncbi.nlm.nih.gov/22721584/). They hypothesized that IMCL behaves differently in the context of T2DM, and that while IMCL serves as a fuel source in athletic subjects, in sedentary subjects with T2DM the IMCL seems to produce more disruptive mediators like ceramides and diacylglycerols. However, the authors tend to play fast and loose with their causal inferences, often citing animal research to buttress clear implications about what holds true in human beings. In fact, the majority of their supporting evidence is derived from mice, despite mice generally being poor facsimiles for human subjects [[5]](https://pubmed.ncbi.nlm.nih.gov/31307492/).
Some of the only human research they can cite are studies wherein there was an observed association between intramyocellular ceramides (IMCC) and insulin resistance. However, there are many biomarkers that serve as proxies for insulin resistance, and there did not seem to be a clear reason proposed by the authors to favour IMCC as causal or mediating. In fact, they cite research that offered conflicting evidence with a broader sample of human subjects, showing that IMCC has no clear association with insulin sensitivity [[6]](https://pubmed.ncbi.nlm.nih.gov/18458871/).
Additionally, Itani, et al (2002) discovered that the concentrations of IMCC do not differ substantially between subjects with varying degrees of insulin sensitivity [[7]](https://pubmed.ncbi.nlm.nih.gov/12086926/). In fact, these researchers challenged subjects with lipids during a HEC to try to alter lipid states in muscle tissue, and ceramides did not change. However, a legitimate criticism of this study is that the lipid challenge done using Liposyn II, which is an intravenous lipid product consisting of 50% soybean oil and 50% safflower oil, making it over half PUFA in its composition. Coen and Goodpaster also cited research on diacylglycerols, but they themselves admit that the human data isn't particularly conclusive on the matter.
To my knowledge there are no recent landmark human experiments that persuasively show that T2DM pathology can be modulated up or down with varying animal products, or even SFA, in the diet. Altogether, the hypothesis has a lot of failed predictions and phenomena to reconcile before it can be taken seriously and can even begin to be seen as epistemically virtuous compared to some other, more scientifically grounded hypotheses. What we need to see is a study that shows that removing SFA and/or animal products from the diets of those with T2DM actually makes traction against pathophysiological markers of T2DM. Ideally this would be done while also controlling for potential confounders or mediators that other competing hypotheses predict would make an impact. The aim is to demonstrate independent effects, and so far no research on the IMCL hypothesis persuasively does this.
## The Sugar Hypothesis
Even though I have touched on this hypothesis five years ago [[8]](https://thenutrivore.blogspot.com/2019/10/sugar-doesnt-cause-diabetes-and-ketosis.html), it bears repeating, with updated epistemic and philosophical rigour. For a recap, my original article challenges perceptions about T2DM that are common in the low carb (LC) diet sphere. I argue against the notions that sugar causes T2DM and that ketosis can somehow reverse it. But we're going to go a little deeper today. So, what is the hypothesis and how does it work? Basically, the hypothesis supposes that chronic exposure to refined sugar or insulin-stimulating CHO leads to T2DM through prolonged over-stimulation of the pancreas. This hypothesis involves several key mechanisms.
Firstly, regular intake of high-sugar or high-glycemic CHOs prompts frequent blood insulin excursions by via the pancreas. To be clear, insulin is the hormone responsible for signaling cells to absorb glucose from the bloodstream for energy or storage. The idea is that over time, constant demand for more and more insulin can lead to insulin resistance via negative feedback. This is when cells become less responsive to insulin's signals because insulin levels are too high. This requires the pancreas to produce even more insulin to achieve the same effect, placing stress on the pancreatic beta cells (which are responsible for insulin secretion).
Secondly, chronic over-stimulation of the pancreas due to persistent high sugar/CHO intake and supposed, resultant insulin resistance can lead to beta-cell dysfunction (which is characteristic of advanced T2DM). Over time, the beta cells' capacity to produce insulin can diminish due to the increased demand, oxidative stress, and subsequent glucotoxicity (toxicity due to hyperglycemia). This dysfunction contributes to the progression of T2DM, where insulin production eventually becomes insufficient to control blood sugar levels effectively.
Lastly, high levels of circulating glucose (glucotoxicity) and fatty acids (lipotoxicity) are actually detrimental to pancreatic beta cells. High glucose levels can lead to the formation of reactive oxygen species (ROS), causing an inflammatory cascade effect, damaging beta cells and impairing insulin secretion. Similarly, elevated free fatty acids (FFAs) can accumulate in non-adipose tissues, including the pancreas, causing cellular dysfunction.
The mechanisms, epidemiological, and experimental evidence for this hypothesis were most succinctly summarized by Stanhope in 2016 [[9]](https://pubmed.ncbi.nlm.nih.gov/26376619/). This review discusses the evidence and controversies surrounding the impact of sugar consumption on T2DM, including mechanisms by which excess sugar intake may promote the development of T2DM directly and indirectly. It covers the direct metabolic pathways through which fructose, a component of table sugar, sucrose, can lead to intrahepatic lipid (IHL) accumulation and decreased insulin sensitivity, contributing to the pathophysiology of T2DM independent of total caloric intake.
The author first refers to literature they themselves conducted, including three primary human trials demonstrating disturbances to energy expenditure, markers of liver function, as well as measures of IHL accumulation [[10]](https://pubmed.ncbi.nlm.nih.gov/26376619/)[[11]](https://pubmed.ncbi.nlm.nih.gov/21952692/)[[12]](https://pubmed.ncbi.nlm.nih.gov/22828276/). The first trial discovered that isocaloric feeding of fructose compared to glucose over a ten-week period significantly increased hepatic fat.
However, it's unclear what the clinical significance of this finding is, considering that the fructose-based intervention resulted in significant overfeeding and only increased fasting glucose by 5% compared to the glucose-based control. Seems like the authors tried pretty damn hard to induce a T2DM phenotype feeding fructose to subjects, and were ultimately unable to achieve that. In fact, they weren't really able to get close. Even the oral glucose tolerance test results, though far from ideal, showed an altogether normal blood glucose curve for the fructose group.
The second trial was unremarkable, and suggested that fructose consumption may decrease energy expenditure over time when isocalorically compared to glucose. Again, it's interesting, but it's far from demonstrating a cause and effect relationship between T2DM and sugar. The third trial is a bit more complicated to unpack. Basically, subjects were split into two groups, 25% of calories as either fructose or glucose as parts of eucaloric diets over 10 weeks, with the primary endpoints beings measures of liver function. Overall, the results of the trial suggest a significantly detrimental effect of fructose compared to glucose on a number of markers related to liver function. However, it's slightly more complicated than that.
While it's true that the treatment effect showed a benefit of glucose over fructose, it's also true that the marker of liver function that was negatively perturbed was gamma-glutamyl transferase (GTT). The change in GGT was also barely statistically significant compared to baseline, while markers such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT) showed a non-significant decrease. Glucose showed greater reductions that were barely statistically significantly different from that of fructose.
Other than that, fructose did seem to increase uric acid levels to a statistically significant degree, making fructose a potential aggravating factor for conditions such as gout. But again, this is a far cry from causally linking fructose consumption to the development of T2DM, especially since fructose seemed to do nothing particularly interesting to markers of liver function. It is true that sugar intake is severely negatively associated with health outcomes [[13]](https://pubmed.ncbi.nlm.nih.gov/34444794/). However, while this is a consistent finding, clinical trials on sugar consistently fail to demonstrate a connection between sugar intake and the development of T2DM.
We can indirectly test the sugar hypothesis by looking at long-term data in those following ketogenic diets for T2DM remission. If subjects cut nearly all carbohydrates out of their diets, presumably this subsumes sugar, and could present a valid test of the hypothesis. One such study might be the Virta Health trial [[14]](https://pubmed.ncbi.nlm.nih.gov/29417495/). In this trial, a non-randomized, self-selected sample of eager subjects elected to participate in a cutting-edge, individualized dietary intervention program, with the aim of nutritional ketosis, called the Continuous Care Intervention (CCI), utilizing a web-app, ketone-verified adherence monitoring, and constant patient support.
> Other aspects of the diet were individually prescribed to ensure safety, effectiveness, and satisfaction, including consumption of 3–5 servings of non-starchy vegetables and adequate mineral and fluid intake for the ketogenic state. At onset of dietary changes, participants were advised to consume a multivitamin, 1000–2000 IU vitamin D3, and up to 1000 mg omega-3 daily. If participants exhibited signs of magnesium depletion (e.g., muscle twitches or cramps), daily supplementation (500 mg magnesium oxide or 200 mg magnesium chloride) was suggested. If participants exhibited headaches, constipation, or lightheadedness, adequate sodium and fluid intake was recommended.
Suffice it to say, there would be little, if any, room for sugar while on such a diet. These subjects were followed up for one year, and, as expected (given the high potential for bias with such a study design), results were impressive. By the end of the first year, the control group was floundering and the CCI group managed to achieve a massive 1.3% reduction in HbA1c, which effectively pushed the once diabetic group into the non-diabetic range on average. However, this change was commensurate with a 14.3% drop in body weight, which we'll revisit in a later section of this article.
Despite these improvements, recidivism continued to climb. As of two years, the CCI group had crept back into the diabetic range on average [[15]](https://pubmed.ncbi.nlm.nih.gov/31231311/). By, 3.5 years, the CCI group was once again firmly within the diabetic range on average, having regained a significant amount of weight [[16]](https://www.hsrd.research.va.gov/publications/esp/virtual-diet-brief.pdf)[[17]](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7208790/).
To be clear, there was a clear distinction between remission and reversal, as defined by the authors. Remission was a much more robust measure of traction against T2DM than reversal, even though it sounds like the latter is stronger than the former. Remission was defined in two parts; partial remission and complete remission. Partial remission was defined as "sub-diabetic hyperglycemia of at least 1 year duration, HbA1c level between 5.7-6.5%, without any medications (two HbA1c measurements)" and complete remission was defined as "Normoglycemia of at least 1 year duration, HbA1c below 5.7%, without any medications (two HbA1c measurements)". Reversal was defined more loosely, as "sub-diabetic hyperglycemia and normoglycemia (HbA1c below 6.5%), without medications except metformin" (Athinarayanan, et al., (2019), Supplement Table 2).
Unfortunately, all but the second year remission data is either aggregated or ambiguous, so it's difficult to make distinctions between partial and complete remission for years one and 3.5. However, at year two only 6.7% of the cohort had achieved complete remission. It's not clear what percentage of the cohort achieved complete remission by year 3.5. Furthermore, reversal rates, as they're defined, are probably just reflecting attrition rates (which were 26%), as the criteria for reversal is having achieved a sub-diabetic blood glucose at least once throughout the trial. It's actually not clear how meaningful that data even is on that definition.
While a 9% weight reduction over 3.5 years is impressive, I'll reiterate the limitations— the subjects were self-selected, and highly motivated to participate in the CCI. In fact, the patients were paying customers of Virta Health's cutting-edge primary care service. This significantly challenges the external validity of the findings, as impressive as they are, to the general population. What we're seeing are results in the context of what is likely to be extraordinary ambition to succeed, and should be interpreted with caution.
As for how these results relate to the sugar hypothesis, it's difficult to tell, had the subjects managed to control their weight. However, adherence rates to the diet dropped significantly by year two, with nutritional ketosis being achieved in 96% of CCI subjects in year one to only 14.1% by the end of year two. This non-adherence makes it difficult to infer the degree of sugar avoidance actually observed by the cohort on average, and makes cause and effect conclusions difficult to draw. There was no 3.5 year data on ketosis rates, and one can only speculate as to why. But given the poor adherence at two years, it's probably not unreasonable to assume it's because the numbers didn't look very good.
## The Oxidation Hypothesis
The underlying premise is that PUFAs, particularly omega-6 fatty acids found in seed oils, are susceptible to oxidation. When oxidized, these fatty acids can form reactive compounds such as malondialdehyde (MDA) and other harmful products, leading to cellular damage and oxidative stress. In the context of the pancreas and liver, organs that, as previously mentioned, are crucial for glucose metabolism and insulin regulation, such oxidative stress could impair their function, contributing to insulin resistance and β-cell dysfunction— key features of T2DM. A tidy little bundle of sophistry indeed.
Since I've already covered how the human outcome data flies in the face of this hypothesis in a previous article [[18]](https://www.the-nutrivore.com/post/a-comprehensive-rebuttal-to-seed-oil-sophistry), I won't rehash all of it here. But, essentially there is no human outcome data supporting this effect across multiple cohort studies and multiple RCTs. In the epidemiology, tight markers of seed oil consumption show a consistent inverse association with T2DM [[19]](https://pubmed.ncbi.nlm.nih.gov/29032079/).
Additionally, there have been several interventions feeding large amounts of PUFA to subjects, to the exclusion of SFA, and measuring long term effects on insulin sensitivity [[20]](https://www.sciencedirect.com/science/article/abs/pii/0163782781900709)[[21]](https://pubmed.ncbi.nlm.nih.gov/1347091/). In both Houtsmuller, et al. (1979) and Watts, et al. (1992), long term feeding of PUFA was associated with improvements in insulin sensitivity. In the case of the former trial, the insulin sensitivity measure, an oral glucose tolerance test (OGTT), showed improvement to glucose tolerance among diabetics over time. These results were aggregated by Hooper, et al. back in 2020 in an exploratory analysis [[22]](https://pubmed.ncbi.nlm.nih.gov/32428300/).
Additionally, we can also see that Ley, et al. (2004) showed an improvement in OGTT results, but with the substitution of CHO for SFA, rather than PUFA for SFA (which is kinda funny) [[23]](https://pubmed.ncbi.nlm.nih.gov/14739050/).
## The Twin Cycles Hypothesis
The prevailing hypothesis, or the hypothesis that has been given the most credence in this domain, is the twin cycles hypothesis (TCH), which was spearheaded by Dr. Roy Taylor. It is closely interconnected with another concept from Dr. Taylor's work, known as the personal fat threshold (PFT). So what are these things? Let's start with the TCH. The TCH postulates that there are two stages, or "cycles", to T2DM development. The TCH was first discussed in a 2011 paper by Lim, et al. (coauthored by Dr. Taylor) detailing the development of the hypothesis from previous clinical trials performed on patients with T2DM [[24]](https://pubmed.ncbi.nlm.nih.gov/21656330/). This trial would come to be known as the Counteracting Pancreatic Inhibition by Triglyceride (CounterPoint) study, and would be reviewed in greater detail two years later by the same authors [[25]](https://pubmed.ncbi.nlm.nih.gov/23075228/).
The first cycle originates in the liver, where chronic, excess calorie intake leads to ectopic fat accumulation, causing hepatic insulin resistance. The reason for this is because tissues that are energy replete will resist the action of insulin, with is a signalling hormone responsible for facilitating energy deposition in tissues. The second cycle concerns the pancreas, where the continued excess fat spills over to the pancreas (primarily via nonesterified fatty acids (NEFA), leading to lipotoxicity and subsequently impairing β-cell function. Ultimately, this contributes to β-cell dysfunction, rather than outright β-cell death, as the pivotal event in diabetes progression.
In fact, the TCH originally came about by appreciating that the assumptions typically relied upon when inferring β-cell death in T2DM patients may be faulty. Usually, we infer to β-cell death by staining pancreatic tissue for insulin; no insulin, no β-cells. However, what if the β-cells aren't really dead? What if the diabetic pancreas is just so dysfunctional that the β-cells aren't producing as much insulin? Those assumptions would have us believing that the β-cells are dead when in fact they are merely dormant due to lipotoxicity— waiting to be brought back to life upon fat mass loss. Which brings us to the next piece of the puzzle.
Now let's discuss the PFT, and how it ties into the overall picture. Essentially, the PFT posits that hepatic and pancreatic fat deposition are facilitated by accumulating more subcutaneous body fat (SBF) than one's body can tolerate, regardless of whether their body mass index (BMI) categorizes them as overweight or obese [[26]](https://pubmed.ncbi.nlm.nih.gov/25515001/). In basic terms, after non-hepatic, non-pancreatic tissues get too fat, there is a spillover of fat (precipitated by chronic calorie excess) onto the liver and the pancreas, which initiates the T2DM phenotype.
Think about it. There's just nowhere left for the energy substrates to go, be it glucose, triglycerides (TG), or even amino acids. They're all increased with T2DM, because all the tissues are energy replete. The liver and the peripheral tissues essentially play a never-ending game of ping pong with the energy substrates because no tissues are able to take on the extra calories. This hypothesis was tested with vindicating results in a recent trial by Taylor, et al. in 2024 [[27]](https://pubmed.ncbi.nlm.nih.gov/37593846/). Essentially, it seems that T2DM development and remission have very little, if anything, to do with BMI, and BMI may be a very poor risk factor for T2DM, due to the individual variation in the PFT from person to person.
Now that we have a clear understanding of the model, let's discuss the overwhelming evidence in favour of it. The clinical trials that first gave rise to the TCH were human experiments that involved both pharmaceutical and dietary means of reducing hepatic fat [[28]](https://pubmed.ncbi.nlm.nih.gov/18535187/)[[29]](https://pubmed.ncbi.nlm.nih.gov/15734833/).
For the first study by Ravikumar, et al., a single-arm trial of 10 subjects, the drug pioglitazone was investigated for its effects on markers of T2DM, particularly postprandial endogenous glucose production (EGP) using isotope labeled glucose, as well as IHL. After 16 weeks of treatment, the pioglitazone group experienced an increase in total body weight equal to +6.2kg on average. Yet, the pioglitazone group also experienced a decrease in IHL.
However, to be fair, the pioglitazone group also experienced a significant decrease in IMCL as well, however there was no significant correlation between decreases in IMCL and EGP. There was however, a direct association between IHL and EGP. Although this trial was not controlled, it certainly doesn't produce results expected on the IMCL hypothesis, and it lends further credence to the TCH. Additionally, many markers of T2DM subsequently improved, such as plasma glucose, hemoglobin A1c (HbA1c), and even TGs, with the changes being -2.3mmol/L, -1.9%, and 0.4mmol/L, respectively.
It can also be inferred that there was a meaningful increase in insulin sensitivity, given the fact that plasma glucose dropped despite the same amount of insulin being produced by subject. Essentially, glucose disposal per unit insulin went up, implying that insulin signalling had improved.
In the second study by Petersen, et al., eight subjects with T2DM were compared to 10 healthy volunteers in a non-randomized weight loss trial over an average of seven weeks. Essentially, subjects were followed up until normoglycemia was achieved, so not every subject was subjected to the same amount of weight loss for the same time period. In this time, body weight dropped by an average of 8kg in the T2DM group. This was marked with commensurate drops in plasma glucose, plasma insulin, and TG, at -2.4mmol/L, -108pmol/L, and -0.3mmol/L, respectively.
The most interesting and surprising finding was that there was no significant change in IMCL despite weight loss. But, subjects did end up achieving normoglycemia and near normal insulin sensitivity as determined by a HEC. However, much like the previous study, insulin sensitivity was directly associated with IHL reduction. Once again, this flies in the face of the IMCL hypothesis, and offers further support for the TCH as the T2DM approached nearly normal levels of IHL. Although neither of these papers directly test for evidence of the sugar or oxidation hypotheses, it should be noted that both of these trials involve the consumption of both sugar and most likely animal products.
In light of this evidence, Steven and Taylor conducted another preliminary human trial, the CounterBalance study, involving 29 subjects in 2015 to test the effects of the same intervention in those with long- versus short-term T2DM [[30]](https://pubmed.ncbi.nlm.nih.gov/25683066/). Both groups experienced similar weight loss (short-duration: 14.8%, long-duration: 14.4%), indicating that the VLCD was effective for weight reduction regardless of diabetes duration. These results were also durable throughout the six month post-intervention follow-up.
In terms of other T2DM markers, such as plasma glucose, the response to the diet was heterogeneous among participants with long-term T2DM. Some showed similar responses to those in the short-term group and some responded slowly. By the end of the study, 87% of the short-term group and 50% of the long-term group achieved non-T2DM fasting plasma glucose levels. HbA1c levels also decreased in both groups, with a more significant reduction observed in the short-term group. However, there was an unforeseen result— about half of subjects did not respond to the treatment at all, which was not expected given nearly all previous research.
Given these results and Dr. Taylor's previous characterization of the PFT concept, the most likely hypothesis seemed clear— these people just needed to lose more weight, which we'll get to later. For now, there was enough evidence of the effectiveness of weight loss for T2DM treatment that Dr. Taylor and his colleagues decided it was time to test the efficacy of the treatment in a real-world outpatient scenario. A cluster-randomized experiment was designed and undertaken, and would come to be known as the Diabetes Remission Clinical Trial (DiRECT) [[31]](https://pubmed.ncbi.nlm.nih.gov/29221645/).
The DiRECT trial involved 298 subjects across 49 primary care practices (or clusters) randomized two groups, a control group receiving the standard of care for T2DM management, and the treatment group receiving a three stage program: stage one, total diet replacement; stage two, food reintroduction; phase three, weight maintenance. For the first stage, the treatment group received a liquid diet consisting of four packets of meal replacement formula, which totaled around 825-853 kcal/day for three to five months (depending on patient-specific goals). For the second stage, after subjects completed the first weight loss phase of the trial, food was gradually reintroduced over a period of two weeks to two months. During the last stage, patients were followed up over the course of around a year. The results were encouraging.
Over the course of the trial, the treatment group lost an average of 10kg, with over 86% of them achieving T2DM remission by the end of the first year. An interesting finding was that on average, at the end of the first year, the treatment group still technically qualified as obese, despite the vast majority of them achieving T2DM remission. This would come to be the first nail in the coffin with respect to the idea that T2DM was somehow coupled to BMI. Additionally, patients experienced significant improvements to quality of life without serious side effects or complications. Altogether the treatment was successful, well-tolerated, and produced impressive rates of T2DM remission that was durable long-term.
However, Dr. Taylor's group published two follow-up, long term durability studies on the DiRECT trial [[32]](https://pubmed.ncbi.nlm.nih.gov/30852132/)[[33]](https://pubmed.ncbi.nlm.nih.gov/38423026/). The results of these follow-up studies was bitter-sweet. At the two-year follow-up, only 41% of the treatment group remained in remission compared to the previous year, and only 10% at five years of follow-up. These results were not promising for the treatment over time once people were reintroduced to their previous diets and left without practitioner support. Even after the two-year follow-up, 94 or the remaining 101 subjects in the treatment group were given access to extended care, which only resulted in 13% remission rates within the extended care group at five years.
It sounds bleak, but let's think about it. Dr. Taylor's research was essentially testing two things at the end of the day— the conceptual model of T2DM, encompassing the TCH and the PFT, as well as the efficacy of radical weight loss in an outpatient setting. With respect to the former, Taylor's work has been a resounding success, and it buttresses the strongest model of T2DM development and progression that we currently have. In regards to the latter, radical supervised weight loss with the practitioner support did not yield terribly promising results beyond two years. All isn't lost, though.
The important thing is that we now have a firm grasp about what causes T2DM. It isn't sugar, seed oils, animal fat, or any other harebrained dietary boogeyman. It's just energy poisoning, with a simple, easy-to-understand etiology; if you gain more fat than your body can tolerate, you develop the phenotype of T2DM. If at that point you do indeed lose enough body fat to fall back below the maximum your body can withstand, T2DM remission follows. The last piece of the puzzle is figuring out what factors cause over-consumption, and how to durably address excessive body fat.
## Discussion
In conclusion, while a myriad of hypotheses continue to circulate within nutritional and diabetic research spheres regarding the genesis and treatment of T2DM, it becomes increasingly clear that simplicity often guides the best practice. The TCH, underscored by the PFT, offers a cogent framework suggesting that T2DM is not merely a product of specific dietary components like sugars, SFA, or PUFA, but rather a complex interplay of caloric excess leading to dysfunctional energy storage and insulin response. As emerging studies, such as those by Dr. Taylor and his colleagues, indicate, interventions aiming at substantial and sustained weight loss may hold the key to reversing T2DM, provided these interventions are maintained with consistent medical oversight and support.
While the exploration of dietary influence on T2DM remains important, we also have to acknowledge the apparently lack of elasticity of our food culture and the stark tendency toward recidivism with dietary intervenions. Emerging pharmacological interventions, particularly GLP-1 receptor agonists, are presenting promising frontiers in the management and potential reversal of this condition. As we advance, the integration of such pharmaceutical approaches alongside dietary management could revolutionize the treatment landscape of T2DM. Emphasizing the synergy between medication and lifestyle changes will likely be pivotal in crafting effective, personalized treatment plans that address both the biochemical and lifestyle facets of diabetes care.
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[13] Meng, Yantong, et al. “Sugar- and Artificially Sweetened Beverages Consumption Linked to Type 2 Diabetes, Cardiovascular Diseases, and All-Cause Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Cohort Studies.” Nutrients, vol. 13, no. 8, July 2021, p. 2636. PubMed, [https://doi.org/10.3390/nu13082636](https://doi.org/10.3390/nu13082636).
[14] Hallberg, Sarah J., et al. “Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.” Diabetes Therapy: Research, Treatment and Education of Diabetes and Related Disorders, vol. 9, no. 2, Apr. 2018, pp. 583–612. PubMed, [https://doi.org/10.1007/s13300-018-0373-9](https://doi.org/10.1007/s13300-018-0373-9).
[15] Athinarayanan, Shaminie J., et al. “Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-Randomized Clinical Trial.” Frontiers in Endocrinology, vol. 10, 2019, p. 348. PubMed, [https://doi.org/10.3389/fendo.2019.00348](https://doi.org/10.3389/fendo.2019.00348).
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[17] McKenzie, Amy, et al. “SUN-LB113 A Continuous Remote Care Intervention Utilizing Carbohydrate Restriction Including Nutritional Ketosis Improves Markers of Metabolic Risk and Reduces Diabetes Medication Use in Patients With Type 2 Diabetes Over 3.5 Years.” Journal of the Endocrine Society, vol. 4, no. Suppl 1, May 2020, p. SUN-LB113. PubMed Central, [https://doi.org/10.1210/jendso/bvaa046.2302](https://doi.org/10.1210/jendso/bvaa046.2302).
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[31] Lean, Michael Ej, et al. “Primary Care-Led Weight Management for Remission of Type 2 Diabetes (DiRECT): An Open-Label, Cluster-Randomised Trial.” _Lancet (London, England)_, vol. 391, no. 10120, Feb. 2018, pp. 541–51. _PubMed_, [https://doi.org/10.1016/S0140-6736(17)33102-1](https://doi.org/10.1016/S0140-6736(17)33102-1).
[32] Lean, Michael E. J., et al. “Durability of a Primary Care-Led Weight-Management Intervention for Remission of Type 2 Diabetes: 2-Year Results of the DiRECT Open-Label, Cluster-Randomised Trial.” The Lancet. Diabetes & Endocrinology, vol. 7, no. 5, May 2019, pp. 344–55. PubMed, [https://doi.org/10.1016/S2213-8587(19)30068-3](https://doi.org/10.1016/S2213-8587(19)30068-3).
[33] Lean, Michael Ej, et al. “5-Year Follow-up of the Randomised Diabetes Remission Clinical Trial (DiRECT) of Continued Support for Weight Loss Maintenance in the UK: An Extension Study.” The Lancet. Diabetes & Endocrinology, vol. 12, no. 4, Apr. 2024, pp. 233–46. PubMed, [https://doi.org/10.1016/S2213-8587(23)00385-6](https://doi.org/10.1016/S2213-8587(23)00385-6).

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By no stretch of the imagination is there any shortage of quackery on social media. Chances are excellent that if you’ve spent any appreciable amount of time on social media, you have encountered some number of quacks and some sort of quackery that they espouse. You might not even be aware that you’re looking at quackery while you’re being exposed to it. So, the aim of this article will be to attempt to simplify the processes of both identifying quackery and dealing with quackery.
Fundamentally, the issue is not merely that quacks are just interpreting studies incorrectly or affirming crazy beliefs. Those are just symptoms of the problem, rather than being the root cause of the problem. Typically, the problem is occurring within their epistemic framework, and is the very thing that is actually leading them to form their crazy beliefs to begin with. As such, a universally efficacious way to get under a quack’s position and expose them as a raving lunatic is to press them on their epistemic standards in one way or another. That is to say, subject their belief-formation process to a thorough stirring, so that their insanity is allowed to bubble to the surface for all to see.
This means dragging them down to a level that is inferentially prior to their current understanding, and away from the level of research and studies. Just like the scientific method is inferentially prior to studies or study design, scientific epistemology is inferentially prior to the scientific method. If your starting point is on the level of studies and study design, following the inferential lineage backward will eventually bring you to a level where the premises will all be principles, virtues, or axioms. This is the level we need to bring the quack to in order to address the fundamental flaws in their reasoning.
The ultimate aim of this process is to expose errors in the quack’s reasoning, not to necessarily convince them of anything. Of course, the hope is that they correct the complications in their belief-formation process, such that they cease to be a quack by the end of the discussion. However, this isn’t a very likely outcome, but this is nonetheless the outcome that you should be aiming for in order to have the best good faith conversation possible. To explore why this outcome isn’t particularly likely, we’ll have to explore what a quack is, and why they’re typically so immovable. So, let’s get into some definitions.
## Quack
> “A quack is a type of scientific delinquent— one who brandishes the trappings of science, yet whose scientific standards are obstinately in violation of those considered most virtuous within the contemporary philosophy of science.”
It was no easy task to get to the bottom of what is so objectionable about the quack’s behaviour. It took interviewing multiple domain experts and trashing dozens of revisions, but I think I finally have something that is workable and minimally assailable for the time being. Essentially, the trait that quantifies over all quacks is a fundamental lack of respect for the rules of scientific inquiry.
If we were to think of science as a country with laws, a quack would be a contemptuous sort of outlaw within that country. But, quacks are not only rule-breakers by nature, they also actively turn their noses up at the rules— almost relishing in their own intransigence. Despite the commonalities, quacks can usually be categorized in at least one of three distinct ways: **deranged**, **dense**, or **dishonest**.
## Deranged
1. **The Zealot**: one who has assimilated quackery into their identity, and will be emotionally damaged if the quackery is challenged.
2. **The Contrarian**: one who espouses quackery due to strong anti-establishment and/or conspiratorial and/or paranoid tendencies.
3. **The Narcissist**: one who is simply so self-assured of their own infallibility that they cannot fathom that their beliefs could be quackery.
4. **The Aggrieved**: one who feels wronged by some conventional scientific paradigm and is seeking vindication or revenge through quackery.
5. **The JAQ-off**: one who slyly hat-tips to quackery, often in an ostentatious or cheeky manner, but claims to be just asking questions when challenged.
6. **The Circlejerker**: one who is deeply impressionable and merely forms the beliefs of whatever community will accept them.
## Dense
1. **The Zombie**: one who has made little to no effort to form their own beliefs, but rather just recapitulates the beliefs of influential people.
2. **The Imbecile**: one who lacks the requisite intelligence and/or cognitive faculties to form rational beliefs of their own accord.
## Dishonest
1. T**he Grifter**: one who espouses quackery, not necessarily because they believe it to be true, but rather for some ulterior motive such as money or clout.
2. **The Yo-Yo**: one who spouses both quackery and non-quackery, often to the point of self-contradiction, depending on the context.
This probably isn’t an exhaustive list of quack species and subspecies, and will likely be updated in the future. For now, these are the most common types of quacks you’re likely to encounter online or on social media. Most quacks you will encounter will be of the deranged variety, and of them, the majority will be either contrarian or narcissistic. The narcissistic quacks are hardly worth engaging with, unless it is for the benefit of an audience. But other than that, you’ll never convince them of anything because they’re cocksure of their own perfection. Contrarians may be swayed by reason, but it is not particularly likely.
Much like the narcissistic quack, the dishonest quacks are also not likely to be worth engaging with, except for the benefit of onlookers to whom you seek to reveal the quack’s dishonesty. Dishonest quacks, especially grifters, will tend to sway their affirmations in lockstep with the trends of the time. For example, many grifters who were pushing low carbohydrate diets back in 2017 are now pushing raw, grassfed carnivore diets in 2022. It just depends on what’s trending at the moment. It’s a game to them. Engaging is typically pointless and you’re justified in disengaging, in my opinion.
Altogether, you have the best chance of convincing dense quacks, because they’re less likely to be as intransigent as other varieties. These types of quacks don’t typically believe quackery due to some emotional commitment or ulterior motives. Usually they’re just either uneducated or dumb. However, if they’re too dumb to understand the difference between good evidence and bad evidence, convincing them may be ultimately beyond your reach. But it is nonetheless worthwhile to attempt reasoning with them. The best discussions will likely be had with the zombie variety of quack, as they’re usually the closest to just being truly naive, and they’re not necessarily dumb.
Now that we have a bit of a handle on what constitutes a quack, let’s move on to the next definition we need to cover:
## Quackery
> “Any ostensible hypothesis that either fails to satisfy any critical theoretical virtue of a scientific hypothesis (i.e., testability, fruitfulness, scope, parsimony, conservativism) or satisfies fewer theoretical virtues compared to the prevailing scientific hypotheses against which it is intended to compete.”
Given that a proposition is a statement that can be either true or false, a scientific hypothesis can be thought of as basically being an empirically testable proposition. For example, say that we wanted to develop a theory to explain the rising of the sun each morning. We could generate a few different hypotheses. Hypothesis A might suppose that the sun rises because God is pulling it across the sky. Hypothesis B might suppose that the sun rises because it is revolving around the Earth. Hypothesis C might suppose that the sun rises because the Earth is spinning.
Let’s linger on hypothesis A for a moment to discuss some of its issues. Firstly, it’s completely unclear how hypothesis A could be tested, so whether or not it genuinely qualifies as a hypothesis is questionable. Those with a background in science have likely been exposed to the principle that unfalsifiable hypotheses are to be avoided, and hypothesis A is an example of that. Testability is arguably the most important aspect of a scientific hypothesis. Without testability, there is no empirical investigation. Without an empirical investigation, there is no science. The hypothesis ends up being completely ad hoc (which we will discuss later).
On the other hand, hypothesis B certainly has the capacity to make predictions. One could create a model wherein the sun travels around the Earth, and observations can certainly be made that are consistent with that model. Hypothesis C could be tested similarly. One could construct a model wherein the Earth is spinning and the sun is fixed in place, and observations can be made to see if that model pans out.
So far, hypothesis B and hypothesis C don’t seem to underdetermine phenomena differently, and the observations seem equally expected on both hypotheses. However, what if we also made the observation that there are other planets out there in space, and we also observe that those planets seem to move in relationship to the sun in a way that suggests that the sun is a fixed object. This observation is more expected on hypothesis C than hypothesis B. The observed phenomena are underdetermined on hypothesis B, and thus hypothesis C would come out on top until there is a better hypothesis to supplant it.
Great! We have established what it takes for a proposition to be a scientific hypothesis, as well as what it takes for one scientific hypothesis to prevail over another. Now let’s move on to discuss the different criteria that such hypotheses need to satisfy in order for them to be competitive within the domain of science. These are the epistemic virtues we touched on earlier— the standards by which the viability of a tentatively competing scientific hypothesis will be measured. [¹](https://www.oxfordbibliographies.com/display/document/obo-9780195396577/obo-9780195396577-0409.xml) [²](https://books.google.ca/books/about/How_to_Think_About_Weird_Things_Critical.html?id=YR4iAAAAQBAJ&redir_esc=y)
## Criteria of Adequacy
1. **Testability**: A hypothesis is scientific only if it is testable, that is, only if it predicts something more than what is predicted by the background theory alone.
2. **Fruitfulness**: Other things being equal, the best hypothesis is the one that is the most fruitful, that is, makes the most successful novel predictions.
3. **Scope**: Other things being equal, the best hypothesis is the one that has the greatest scope, that is, that explains and predicts the most diverse phenomena.
4. **Parsimony**: Other things being equal, the best hypothesis is the simplest one, that is, the one that makes the fewest assumptions.
5. **Conservatism**: Other things being equal, the best hypothesis is the one that is the most conservative, that is, the one that fits best with established beliefs.
All else equal, if an alternative hypothesis fails to outcompete a prevailing hypothesis on any of these measures, why form the belief that the alternative hypothesis is more likely to be true compared to the prevailing hypothesis? Beyond the testability of a hypothesis, the extent to which a hypothesis fails to satisfy any of these theoretical virtues will determine the “ad-hocness” of that hypothesis. An ad hoc hypothesis is also known as a “just-so story”, which is a phrase you may have heard before.
While it goes without saying that ad-hocness is undesirable in science, it is important to emphasize that this is the crux of the quack’s rhetoric. Quackery is like an artichoke of idiocy, and just-so story-telling is at the heart of it. You have to peel it slowly to expose the fuckery. This sort of delinquent fabulism takes many forms, and it’s not always obvious when a hypothesis is ad-hoc and failing to satisfy one or more theoretical virtues compared to another hypothesis. But, hopefully your intuitions can be adequately primed with a few examples. Let’s examine this scientific hypothesis:
> “Vegetable oils are the cause of heart disease.”
At first glance, this hypothesis appears to be extremely attractive in its parsimony. It appears to be making very few assumptions, as it is reducing the cause of heart disease down to a single variable. However, this is an illusion. This hypothesis must actually bootstrap an enormous number of assumptions in order to compensate for its lack of scope and fruitfulness. Not only does the totality of the empirical evidence weigh heavily against this hypothesis, it’s not clear what novel predictions the hypothesis has generated, if any at all.
The primary issue is that the hypothesis is lacking in scope because it does not account for the majority of our observations regarding vegetable oils and heart disease. Typically, the quack will attempt to compensate for this shortcoming by casting doubt on existing research— “those findings are wrong because epidemiology is pseudoscience”. What the quack doesn’t realize is that this actually decreases the parsimony of their hypothesis. This leaves them with an ad-hoc story that is not particularly unifying, fruitful, or parsimonious. Let’s examine another hypothesis:
> “Ancestral foods protect against all illnesses.”
On the face of it, this hypothesis might appear similar to the first in that it lacks scope and fruitfulness, and in turn compromises its own parsimony. However, it may be even worse than that. If ancestral foods are referring to foods that humans consumed during some prehistoric time period, then the hypothesis is actually untestable. Humans no longer have access to those foods, and as such the hypothesis is almost entirely ad hoc, and the theoretical virtues that it upholds are few to none.
The more sensitive you become to when a hypothesis is failing in its virtuousness, the more straightforward it will be to identify and dispatch quackery. For instance, consider what has been described above in previous examples, and examine these other quack hypotheses carefully:
> “Red meat protects against mental illness.”
> "Sunlight protects against skin cancer.”
> “Blueberries cure Alzheimer’s disease.”
> “Refined carbohydrates cause obesity.”
> “Milk products impair bone health.”
> “Soy products feminize men.”
> “Vegan diets cure cancer.”
Remember that quacks fundamentally don’t care about scientific rigour, and virtually all quackery will follow a similar structure at its core— an utter lack of respect for the rules we just discussed. Thus, there is a virtually universally efficacious way of uprooting quackery. Simply interrogate the quack about how their hypothesis better conforms to the rules compared to other hypotheses, and watch them crumble.
Once you start scrutinizing quackery like this on this basis, you will quickly realize that quacks are just master fabulists— iron chefs of word salads. Mind you, quacks will never admit to this. Even when their bullshit has been revealed to them point blank, the exact lack of rigour that got them to be in their current state will end up keeping them smiling through their humiliation.
At this point it would be worthwhile to discuss the **Quack’s Trichotomy**. This concept has been borrowed from Lance Bush’s anti-realist metaethical thesis. While it was originally a way of categorizing different types of moral realism, it would appear to be highly applicable to categorizing different types of quackery as well.
Basically, quackery will ultimately reduce down into one of three categories: **false**, **trivial**, or **unintelligible**. As discussed above, most quackery will end up being false (or at least more likely to be false than true). But, there are some other common cases to explore. Identifying just what kind of utterances the quack is making will be helpful in figuring out whether or not it’s even worth entertaining their madness. Consider the following three interpretations of this hypothesis:
> “Red meat is healthy.”
## False Interpretation
Perhaps the tentative quack cashes out the term “healthy” into some sort of claim about red meat not increasing the risk of heart disease. This can be tested, and it turns out that when the best available data is aggregated together, across multiple domains, red meat consumption reliably associates with an increased risk of heart disease. This means that this hypothesis would just be false, or more likely false than true.
## Trivial Interpretation
Let’s just say that all the tentative quack means by “healthy” is that they themselves just feel really good on a diet that is high in red meat. In this case, the hypothesis is actually going to be “I feel really good on a diet that is high in red meat.” This is not anything that anyone would contest, as it’s clearly true. However, it’s trivially true, and a pointless proposition to utter. We need not debate this. This claim may not necessarily make them a quack, but we should probably just leave this idiot to their fuzzy feelings and move on.
## Unintelligible Interpretation
In this case, we’ll imagine that the tentative quack doesn’t unpack the utterance any further, and just continues to insist that red meat is “healthy”, over and over. If no further clarification is offered, this interpretation of the hypothesis is just gibberish. What is healthy supposed to mean? To me, “healthy” is a relational concept that joins many relata— X is healthy for Y compared to W relative to standard Z (where healthy is defined as an exposure that increases the lag-time to the onset of illness compared to a different exposure). Unless their meaning is unpacked in an intelligible way, their utterance doesn’t even rise to the level of being a proposition. They’re literally just gibberating, and we need not debate their ramblings. Leave them to their delusions.
In an exceedingly small minority of cases that fall outside of the scope of the **Quack’s Trichotomy**, the tentative quack’s proposition will be true and convincing, rather than being false, trivial, or unintelligible. In this case, the proposition likely isn’t quackery and you likely just mistook the proposition as quackery due to miscommunication. If this happens, you should just accept the proposition and feel good that you learned a new fact today. Enjoy it when it happens. But again, this almost never happens.
There is one final trope we need to explore, though. Every so often, you will encounter someone who is committed to extraordinarily high standards of evidence. For example, quacks in the nutrition blogosphere will sometimes claim the following:
> “Evidence cannot be obtained in nutrition science unless you have studied the effects of a food in a multi-generational, quadruple-blind randomized controlled metabolic ward crossover trial in human clones.”
This is not really a hypothesis. It’s just a claim that directly pertains to scientific epistemology itself, which means we must deal with this in a unique way. In this case, we should simply ask them what theoretical virtue would be either violated or unable to be satisfied unless we had such evidence for our hypothesis? As such, it would be worthwhile to get into a few definitions regarding what constitutes evidence.
## Evidence
> “That which is more expected on a given hypothesis compared to the negation of that hypothesis.”
On this definitions, falling short of achieving a trial design like the one described above does not bar us from making discoveries that are more or less expected on different hypotheses. Thus, failing to achieve such a trial design is not a barrier to discovering any sort of evidence. If a short trial with a limited number of people finds an effect of some intervention, that effect is still going to be expected on a hypothesis that predicts it. So, it’s still evidence.
Now we’re ready to start tackling quackery ourselves. Next up, we’ll go through a universally applicable procedures for smashing quackery. The beauty is that the procedures leave the burden of proof squarely on the quack, and pressure test their epistemic standards. This means that you probably don’t even need to show up with studies of your own if you don’t want to. The ball will mostly be in their court, and the burden of proof will be squarely theirs. By the end they’ll find themselves looking up from within their own grave and they will have nobody but themselves to blame for them being there.
Before we move on to the quack-smashing debate procedure, it's recommended that you download the included [dialogue tree](https://drive.google.com/file/d/1QQaN6HRwzp3kY2DAcnHVBxeX6jBhrvkw/view?usp=share_link) and refer to it while reading.
###### PHASE ONE
###### CLARIFICATION
## Step 1: Ask for a proposition
Essentially, a proposition is what is known as a truth-apt statement. Meaning that it is a statement that can be either true or false. You can think of a proposition like a claim. A common tactic among quacks is to dance around some implied commitment without ever actually explicitly making any claims.
Quacks are notoriously unclear when they communicate. Sometimes quacks will simply gesture in your direction with a series of vague utterances that merely have the appearance of communicating disagreement. For example, a quack might say to you:
> “Read the studies you idiot!”
> “Follow the money to know the truth!”
> “We’ve been lied to for over fifty years!”
Notice how vague these statements are. Quackery thrives on vagueness. You must straightforwardly ask the quack for their position— “I’m sorry, I just want to understand what you mean. What do you think is true that people who believe this study think is false?” Be firm, and stand your ground. Press them until they give you an utterance that at least has the appearance of something propositional.
## Step 2: Evaluate their ostensible proposition
Once you have a proposition, we begin the clarification phase. During this step you are aiming to demystify anything that you find unclear. If there are terms over which there may be disagreement, such as relational terms with missing relata, you must ask for clarification.
If clarification is required, proceed to **step 2.1**. If clarification is not required, proceed to **step 2.2**.
## Step 2.1: Ask for clarification
Essentially what we need from the quack is a clear, contestable proposition. Scrutinize every word in their proposition if necessary. This is not to bog down the debate, but to make sure that there is as close to a complete, unambiguous shared understanding of the terms being used by the quack as possible. In the vast majority of cases, asking the quack simple clarifying questions about their proposition will make it fall apart on the spot.
If the tentative quack’s explanation devolves into bullshit like rambling or gibberish, just walk away from the idiot. If it appears intelligible and it’s just some trivial utterance that isn’t worth discussing, we can start assessing its truth value.
###### PHASE TWO
###### ARGUMENTATION
## Step 2.2: Check for modal claims
If we manage to obtain an intelligible proposition from the quack, we can begin checking for modal language. Modal language typically refers to concepts like impossibility, necessity, possibility, or contingency. Be sensitive to when your interlocutor is using words that function as synonyms for any of these terms. For example, words like “can”, “able”, “may”, “could”, or “capable” should all be taken as synonyms for the modal term “possible”, whereas words like “unable”, “cannot”, “couldn’t”, “unable”, “incapable”, should all be taken as synonyms for the modal term “impossible”.
Additionally, if your interlocutor suggests that something is necessarily the case, that should be taken as just another way of saying that the contrary is impossible. As such, impossibility and necessity are modal terms that can essentially be captured by the same modal operator. Similarly, if your interlocutor suggests that something is possible, all they’re saying is that it's necessarily not impossible, which is to say that it's contingent upon something else. So, much like impossibility and necessity, possibility and contingency can also be interpreted interchangeably, under the same modal operator. At the end of the day the terms can ultimately be cashed out into what is impossible or possible.
To be clear, these terms are just operators, and don’t mean much unless they’re in reference to a given modality. Modalities are just means by which these modal operators can be understood. There are two primary modalities that are commonly discussed in the philosophy literature— physical and logical. For example, something is logically impossible if it entails a contradiction, and something is physically impossible if it violates a law of physics.
Of course there are other modalities. In fact, there are probably infinite numbers of modalities on which an operator like impossible can be understood. For instance, while it’s certainly logically and physically possible to murder someone in any country, it is legally impossible to murder someone in most countries. Though we don’t really use modal language in this way.
Overall, impossibility can be interpreted as something that is incompatible with a given rule/standard or set of rules/standards, and possibility can just be interpreted as something that is compatible with a given rule/standard or rule/standard set.
In most cases, if the modal operator they’re invoking relates to possibility, then it’s probably not even worth continuing the discussion. In the vast majority of cases it’s just trivial to claim something is possible. If the proposition contains a modal operator related to impossibility, proceed to **step 2.3**. If their proposition does not contain a modal operator, proceed to **step 2.4**.
## Step 2.3: Ask which law is broken on their stated modality
This step is pretty straightforward. If your interlocutor is claiming something is impossible, ask them on what modality is it impossible. If necessary, explain to them what modalities and modal operators are, just so they’re both clear on what you’re asking of them and what kind of claim they’ve actually made.
If they cannot unpack the modality and the law that’s violated on that modality first give them the opportunity to amend their claim. If they refuse to amend the claim or are unable to unpack the claim, then proceed to **step 6**. If they actually manage to unpack the modality and the law that’s violated on that modality, and it’s convincing to you, you should probably just concede.
## Step 2.4: Ask for a goalpost
Assuming there were no modal claims in our tentative quack’s proposition, we can proceed to the first step in the actual debate— requesting a goalpost. Basically, you will merely ask them what evidence would be required for them to affirm that their proposition is false. This is different than asking them what evidence it would take for them to reject their proposition. We want to know what it would take for them to affirm their proposition’s negation.
This step isn’t vital, so it’s not a huge concern if our tentative quack doesn’t render a goalpost to you. However, keep in mind that if they can’t tell you their goalpost for affirming their proposition’s negation, they are essentially telling you that they don’t even know why they believe that their proposition is true. So, it’s up to you if you want to proceed further. If you want to stop here, just shame them for being a sophist and disengage.
If you decide to continue, proceed to **step 3**.
## Step 3: Ask for an inference for their proposition
This step is pretty straightforward. You’re just straight up asking for the argument for the proposition. After you’ve obtained a clear, contestable proposition from the quack, you must then ask them what the evidence is for their proposition. Asking the quack for evidence is perfectly fair. Don’t let them try to convince you otherwise. They bear the burden of proof, and the onus is solely on them to demonstrate the merits of their proposition.
If they actually manage to render an argument, you can proceed to **step 3.1**. If they refuse to render an argument, proceed to **step 6**.
## Step 3.1: Identify the type of inference
Basically there are two broad categories of inference someone can make. Either their inference is going to be a posteriori or it is going to be a priori. Both a posteriori and a priori inferences are forms of deductive arguments. However, in contrast to an a priori inference, an a posteriori inference requires synthesizing prior experience of the world. The truth or falsity of an a posteriori inference will rest on empirical evidence.
## A Posteriori
> **P1)** An unmarried person is more likely to be depressed.
> **P2)** Jim is unmarried.
> **C)** Therefore, Jim is more likely to be depressed.
An a priori inference doesn’t require prior experience of the world, and the truth of falsity of the inference will hinge on the definitions or meaning of the terms used.
## A Priori
> **P1)** An unmarried man is a bachelor.
> **P2)** Jim is an unmarried man.
> **C)** Therefore, Jim is a bachelor.
For the purposes of this article, we’ll just be focusing on a posteriori inferences. If you are interested in how to address a priori inference, please refer to the included dialogue tree at the top of this section. Otherwise, proceed to **step 3.2**.
## Step 3.2: Check for modal claims
Generally speaking, if their inference is a posteriori and it contains a modal operator, they’re likely to be referring to a physical modality (but they could be referring to another modality).
If they are invoking an operator that is related to impossibility, proceed to **step 3.3**. Once again, if the invoke a modal operator related to possibility, then it’s probably worthwhile to just agree and disengage, as it’s typically just trivial to claim that things are possible. If there are no modal operators in their claim, proceed to **step 3.4**.
## Step 3.3: Ask which law is broken on their stated modality
The overall procedure is identical to **step 2.3**. If the quack can’t unpack the claim or they refuse to amend the claim, then proceed to **step 6**. If they actually manage to unpack their the modality and the law that’s violated on that modality, and it’s convincing to you, you should probably just concede.
## Step 3.4: Evaluate their empirical evidence
During this step, it pays to have some critical appraisal skills to fall back on, but it’s not necessary. The most important thing to remember is that you have to be honest about what you find convincing and you have to be honest enough to amend your views according to new evidence.
Keep the definitions of evidence that we discussed earlier in mind going forward. After the quack has rendered their evidence, examine it carefully. In the vast majority of cases it will be unclear how this evidence should be more expected on their hypothesis as opposed to some other hypothesis, even another hypothesis that you literally dream up on the spot as a counter explanation (which we will be covered in later steps). Consider the following proposition:
> “Carnivorous diets made humans more intelligent.”
A bold proposition like this certainly requires substantial evidence, which is perfectly reasonable to request of the quack. Let’s say you ask for the evidence, and the quack renders something along the lines of this in response:
> “Because plant agriculture decreased human brain size by 11%.”
Bearing all of the above in mind, critically evaluate their evidence and think hard about the assumptions it makes. If you don’t find anything objectionable, it is perfectly OK to admit that sufficient evidence for the proposition has been rendered, and that you concede the proposition on that basis.
If the quack managed to render a goalpost to you in **step 2.4**, then proceed to **step 3.5**. If they did not render a goalpost to you, and their evidence is not convincing to you, then proceed to **step 5**.
## Step 3.5: Compare their evidence to their goalpost
Check to see if their empirical evidence is actually consistent with the goalpost they described. If their empirical evidence is either consistent or stronger than the sort of evidence described in their goalpost, then simply proceed to **step 5**. However, if their empirical evidence is _weaker_ than the sort of evidence they described in their goalpost, then the quack has just straightforwardly contradicted themselves and you can proceed straight to **step 6**.
## Step 5: Propose an alternative hypothesis
As with **step 3.4**, it pays to have some critical appraisal skills, but it is again not actually necessary. The only thing that you really require to proceed with this step is the creativity to dream up alternative hypotheses. But not just any alternative hypothesis. Your alternative hypothesis has to make the same prediction as their hypothesis, but also be mutually incompatible with their hypothesis.
In reference to the evidence presented in **step 3.4**, while this evidence may sound hilarious to us, it may actually be convincing to some people, so contesting it is probably still a good idea. Don’t dismiss it outright. At this point, it may be true that the quack has already put their foot in their mouth. But continue to be a fair interlocutor, and give the quack an opportunity to either swallow it or pull it out. Hit them back with an alternative hypothesis that makes the same prediction:
> “Perhaps agriculture actually increased the efficiency of the human brain, and there was actually no change in intelligence.”
Remember that it’s not at all clear why plant agriculture decreasing human brain size by 11% would necessarily, or even probably, be evidence for carnivorous diets making humans more intelligent. Perhaps plant agriculture increased the efficiency of our brains, such that our brains could achieve the same level of intelligence using less tissue. So, why would plant agriculture decreasing human brain size by 11% be more expected on the quack’s hypothesis as opposed to your alternative hypothesis?
Now the quack is in a tough position, because he has to actually explain why the evidence in question is more expected on their hypothesis than the one you just cooked up on the spot. In the vast majority of cases, the quack will not be able to produce any compelling reason for why one hypothesis has more explanatory power over the other.
Notice as well that we’re not asking them to substantiate their evidence, and we’re not scrambling to find studies of our own to refute their evidence. We’re just asking the quack why their hypothesis is more virtuous than ours. This is not a strategy that virtually any quacks are going to be prepared to deal with (because if they were, they probably wouldn’t propose stuff as stupid as they typically do).
In the vast majority of cases, merely asking the quack why the evidence in question is more expected on their hypothesis, rather than your own hypothesis, will lead them to fold like a chair, right on the spot.
If your interlocutor actually can demonstrate that the evidence they brought to the table is indeed more expected on their hypothesis than some alternative hypothesis, you have a few options. You retry **step 5**, and attempt to create another alternative hypothesis that will challenge the strength of their evidence even harder. Alternatively, you can concede the proposition for the time being and come back to it later, even if you don’t find it convincing. Just be honest. Conceding the debate doesn’t mean that your interlocutor was correct.
Remember, you can always be agnostic (even about your own alternative hypotheses), and try to remember that you don’t need to affirm the negation of their proposition. The onus is not on you to prove anything in this exchange. Not a goddamn thing. Remember that.
Assuming they’re unable to answer your question, it must be reiterated that it is very important to never allow the quack to flip the burden of proof on you. It’s their proposition, and the burden of proof is theirs and only theirs. A tip for identifying when the quack is trying to flip the burden of proof is when they attempt to ask questions that are not clarifying questions. Any question other than a clarifying question is always a dodge when you hold the line of questioning, and your line of questioning is only over when you’ve obtained all of the answers you require.
If the quack rejects your alternative hypothesis, proceed to **step 5.1**. If the quack accepts your alternative hypothesis and admits that he has no justification for why their evidence is more expected on their hypothesis than your hypothesis, then proceed to **step 6**.
## Step 5.1: Ask what’s wrong with your alternative hypothesis
Rejecting your alternative hypothesis could mean a couple different things. Either they’re calling the alternative hypothesis itself into question, or they are going to explain why their evidence is more expected on their hypothesis than your hypothesis. If they’re rejecting your alternative hypothesis, just ask them for the explanation. If their explanation is convincing to you, there are a couple of different options. You can either concede or return to **step 5** and press them with an even stronger hypothesis. It just depends on how comfortable you are giving it another shot.
Alternatively (and altogether more likely), if they can’t give you a clear explanation as to why their evidence is more expected on your hypothesis, then proceed to **step 6**.
###### PHASE THREE
###### STEAMROLLING
## Step 6: Demand that they concede their proposition
Once you find yourself in a position where you have not conceded the proposition and the quack is unable to render an argument in favour of the proposition, you’ve obtained all you need from the quack to begin steamrolling. Just refuse to proceed until you obtain either an argument for the proposition or a concession on the proposition itself. Anything other than these outcomes is not satisfactory. Don’t accept any “agree to disagree” cop-outs. Hold their feet to the fire and press the issue.
The quack may try to spiral down on some tangent that isn’t germane to any of the previous questions you have asked them. In this event, redirect them immediately after their ramble. If their ramble is excessively long, feel free to cut them off. Tangents waste time, and it’s inappropriate to let tangents go to completion. Most quacks are bad faith actors, so concessions are too optically intolerable for them and rendering an argument for their claim is usually beyond their capabilities. Most will simply just disengage once you’ve gotten this far.
Lastly, we have to talk about an exceptionally rare outcome you will almost never encounter on your quack smashing journey— the quack concedes the proposition. Congratulate and praise the quack for their honesty. In fact, they may not even be a quack anymore. You may have rescued them from utter insanity, and that’s certainly worth a pat on the back for both of you.
Thanks for reading! If you enjoy my writing and want more content like this, consider pledging to either my [Patreon](https://www.patreon.com/thenutrivore) or my [LiberaPay](https://liberapay.com/TheNutrivore/)! Alternatively, I accept crypto as either ETH, MATIC, or BTC at 0xdfcb7e3D00EdC138300E9Ad122dB0ebE85426a65!
## References:
[1] ‘Theoretical Virtues in Science’. Obo, Accessed 24 Dec. 2022. [https://www.oxfordbibliographies.com/display/document/obo-9780195396577/obo-9780195396577-0409.xml](https://www.oxfordbibliographies.com/display/document/obo-9780195396577/obo-9780195396577-0409.xml).
[2] Schick, Theodore, and Lewis Vaughn. How to Think About Weird Things: Critical Thinking for a New Age: Seventh Edition. McGraw-Hill Higher Education, 2013. [https://books.google.ca/books/about/How_to_Think_About_Weird_Things_Critical.html?id=YR4iAAAAQBAJ&redir_esc=y](https://books.google.ca/books/about/How_to_Think_About_Weird_Things_Critical.html?id=YR4iAAAAQBAJ&redir_esc=y)

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[Brian Sanders](https://www.sapien.org/brian) is an entrepreneur and filmmaker who advocates for an "ancestral" diet he has coined the Sapien Diet™. This diet is characterized by high intakes of animal products and considerably strict abstinence from processed food consumption. His diet is supposedly based on the teaching of [Weston Price](https://en.wikipedia.org/wiki/Weston_A._Price), a dentist and nutritional anthropologist of the early 1900s who also advocated for the consumption of animal products. Right off the bat, we can tell that Brian's diet is marinated in quackery, as Price's methods and inferences were [questionable at best](https://quackwatch.org/related/holisticdent/).
Whatever the case, Brian publicly advocated for his diet back in 2020 during a talk at [Low Carb Down Under](https://lowcarbdownunder.com.au) entitled ["Despite what you've been told COWS CAN SAVE THE WORLD"](https://www.youtube.com/watch?v=VYTjwPcNEcw). In this talk, he describes the benefits and virtues of animal food production and consumption, and also touches on the supposed pitfalls and fallacies of veganism and plant-based diets. He structures his talk into three sections, which serve as direct rebuttals to three propositions that he characterizes as mainstream:
- Red meat is harmful to human health.
- Cows are harmful to the environment.
- It's unethical to kill animals for food.
Brian's talk is riddled with half-truths, misunderstandings, bald-faced lies, and other idiocy. To go through everything individually would take far too long, so in this article I will only be addressing the primary points that Brian makes throughout his presentation. Some of the quotes that I will be referencing will be paraphrased to account for Brian's unclear manner of speaking, but I nonetheless believe that I have represented his beliefs fairly. So, let's dive in!
###### Heath Claims
**Claim #1 (**[**4:52**](https://youtu.be/VYTjwPcNEcw?t=292)**):**
> "Hong Kong eats the most amount of meat and animal foods in the world and has the longest life expectancy."
**Post-hoc Fallacy**
This is just a post-hoc fallacy and a misunderstanding of the evidence being presented. Firstly, Brian's argument doesn't even get off the ground unless there is an assessment of what is causing the differences in longevity, and how the mortality stats are calculated. In this case, Brian is suggesting temporal connections that can't be verified to exist based on the data provided. More to the point, differential ecological associations between populations can't really tell us anything about differences in outcomes between individuals consuming the least meat versus individuals consuming the most meat.
For example, there is a positive ecological association between smoking and life expectancy [[1]](http://www.thefunctionalart.com/2018/07/visualizing-amalgamation-paradoxes-and.html). But, we wouldn't infer from this association that cigarette consumption increases longevity. Those sorts of inferences are what prospective cohort studies and randomized controlled trials are for, as they are actually equipped to assess individual-level exposure and outcomes.
**Base Rate Fallacy**
According to Brian's source, Hong Kong's meat intake has been steadily increasing and didn't reach UK-levels of intake in 1972 and US-levels of intake in 1967 [[2]](https://www.nationalgeographic.com/what-the-world-eats/). If the hypothesis is that meat causes higher mortality via chronic disease, then people who started eating that much meat during those time periods would barely even be old enough to contribute substantially higher mortality statistics at the time of this report anyway. So, while it's true that Hong Kong now eats a lot of meat and enjoys longer lifespans, Brian is not appreciating the base rate of historical meat consumption for this population.
As an aside, it is also interesting to note that those in Hong Kong who followed a non-ancestral "Portfolio diet" (which is characterized by low saturated fats, sodium, and dietary cholesterol, as well as higher plant proteins, vegetable oils, high fruits, vegetables, and whole grains) were at a lower risk of dying from all causes, as well as dying of CVD or cancer [[3]](https://pubmed.ncbi.nlm.nih.gov/34959911/). In fact, multiple sensitivity analyses were done to remove the possibility for reverse causality, and the reductions in risk are still apparent.
**Claim #2 (**[**5:13**](https://youtu.be/VYTjwPcNEcw?t=313)**):**
> "There is an inverse association between red meat and total mortality in Asian populations."
**Red Herring**
The aggregated difference in the lowest to highest red meat intake in this pooled analysis was ~60g/day, which is approximately two bites [[4]](https://pubmed.ncbi.nlm.nih.gov/23902788/). It's unclear how this is capable of informing our judgements about the health value of red meat in the context of something like a Sapien Diet™. Not only that, but the contrast is occurring primarily at lower levels of intake.
Generally speaking, contrasts in red meat intake exceeding 80-100g/day are typically required on a per-cohort basis to reveal the increased risk of cardiovascular disease mortality or even all-cause mortality. Contrasts that fall below this threshold often do not provide for the statistical power that is necessary to obtain a statistically significant estimate.
Brian's own reference also confirms that meat intake in Asian populations is generally quite a bit lower than the United States.
> “Per capita beef consumption has decreased to some degree in the past decade in the United States but still remains substantially higher than that in Asian countries. Beef consumption increased in China, Japan, and Korea from 1970 to 2007.”
In actuality, when we select Asian populations with the widest contrasts in red meat intake, with sound multivariable adjustment models, appropriate population ages, and adequate follow-up time, we see the increase in total mortality with red meat very clearly [[5]](https://pubmed.ncbi.nlm.nih.gov/33320898/). Even when diet and lifestyle covariates are balanced between ranges of intake. These results are also consistent with results we see in American cohorts that also balance diet and lifestyle covariates reasonably well, such as the Nurse's Health Study [[6]](https://pubmed.ncbi.nlm.nih.gov/22412075/).
**Potential Contradiction**
Additionally, Brian has [stated publicly](https://twitter.com/FoodLiesOrg/status/1419347985935257601?s=20&t=_2uz8-vTlkgxnFPP4DCqtg) that steak is a good source of iron and can protect against iron deficiency. This claim is in accord with the available evidence on red meat consumption and iron deficiency anemia, with unprocessed red meat associating with a 20% decreased risk of anemia in the UK Biobank cohort [[7]](https://pubmed.ncbi.nlm.nih.gov/33648505/). Interestingly, unprocessed red meat was also associated with a statistically significant increase in the risk of many other diseases as well.
If the methods were sensitive enough to detect the inverse association with iron deficiency anemia, why not also conclude that the methods were also sensitive enough to detect the effect on heart disease as well? Why form differential beliefs about the causal nature of these associations?
Furthermore, the association between red meat intake and heart disease is observable when meta-analyzed as well [[8]](https://pubmed.ncbi.nlm.nih.gov/34284672/). For every 50g/day increase in red meat intake, there was a statistically significant dose-dependent relationship between red meat intake and heart disease.
Almost all of the most highly powered studies found positive associations between heart disease risk and red meat. Altogether, those studies also had the highest contrast in red meat, with Asian countries having the lowest contrast, as mentioned earlier. The majority of the included studies included adjustments for diet quality, used validated food frequency questionnaires, and had adequate follow-up time. The greatest increase in risk was found among studies with follow-up times exceeding 10 years. Removing all of the more poorly powered cohorts leaves us with a remarkably consistent relationship overall.
This one change results in a 38.3% attenuation in the I², going from 41.3% to 13%. Which suggests that of the variance that was attributable to heterogeneity, poor statistical power could explain about 68% of it.
Lastly, when cohort studies from around the world are meta-analyzed, we see the same thing for all cause mortality [[9]](https://pubmed.ncbi.nlm.nih.gov/24148709/). Overall, there is a non-significant increase in all-cause mortality risk when comparing the lowest red meat intakes to the highest red meat intakes. Whiteman, et al. (1999) was the only study that found a statistically significant decrease in risk, and is the sole reason for the non-significant finding.
However, Whiteman, et al. also had one of the shortest follow-up times, one of the youngest populations (and thus one of the lowest death rates), and used a very poor adjustment model (only adjusting for three confounders). If a leave-one-out analysis is performed that excludes Whiteman, et al., a different picture is painted.
Anybody who wishes to complain about this reanalysis is free to try to explain to me why increasing the potential for bias with poor multivariable adjustment is a desirable thing. But, it probably doesn't matter anyway. This meta-analysis was published in 2014, and more cohort studies have been published since then. If we add those results to the original forest plot conducted by Larsson et al., we would still get significant results.
**Claim #3 (**[**5:22**](https://youtu.be/VYTjwPcNEcw?t=322)**):**
> "We cannot use correlational studies to try to say that meat is bad."
**Category Error**
It's unclear what this means. As per the Duhem-Quine thesis, all scientific findings are correlational in one way or another [[10]](https://en.wikipedia.org/wiki/Duhem%E2%80%93Quine_thesis). As such, the state of being "correlational" is not a differential property between any two modes of scientific investigation. For example, intervention studies are a form of observational study, because you're observing what happens when you intervene. So this objection just seems like confusion, because if there ever was a study that showed meat to be "bad", it would be straightforwardly correlational in nature. Assuming that what Brian means by "correlational studies" is actually just nutritional epidemiology, even that would still be wrong.
In 2021, Shwingshakl et al. published an enormous meta-analysis that compared the results of 950 nutritional randomized controlled trials to results from 750 prospective cohort studies [[11]](https://pubmed.ncbi.nlm.nih.gov/34526355/). In the aggregate, results from nutritional epidemiology are consistent with results from nutritional randomized controlled trials approximately 92% of the time when comparing intakes to intakes (omitting supplements).
Across 23 comparisons of meta-analytically summated findings from both bodies of evidence, only 2 comparisons showed discordance. This means that nutritional epidemiology tends to replicate in randomized controlled trials in the supermajority of cases.
If not randomized controlled trials, I have no idea where Brian plants his goalpost for high evidential quality. Nevertheless, current evidence suggests that nutritional epidemiology is highly validated methodology if randomized controlled trials are used as the standard. If one places high credence in randomized controlled trials, it's unclear why they wouldn't also place high credence in nutritional epidemiology.
**Claim #4 (**[**5:36**](https://youtu.be/VYTjwPcNEcw?t=336)**):**
> "73% of hunter gatherers get over 50% of their diet from animal foods."
**Non Sequitur**
I'm not sure why we should care. If this isn't cashing out into some sort of health claim, then it seems very much like a non sequitur. Assuming this is implying something about the health value of hunter-gatherer diets, it is also misleading. I've discussed [here](https://www.the-nutrivore.com/post/should-we-eat-like-hunter-gatherers) why positions like this ultimately fail.
**Claim #5 (**[**5:51**](https://youtu.be/VYTjwPcNEcw?t=351)**):**
> _"We have beef as this highly bioavailable, easily digestible protein, and beans is one example of something that is touted as a pretty high protein food. But this is not the case."_
**False Claim**
This is just whacky, and it seems to be based on data from a 1950s textbook to which I cannot get access. However, we don't really need to in order to address this claim. Let's take a look at this table that Brian has generated.
First of all, if these two foods are weight-standardized, then the protein content of navy beans only makes sense if the navy beans were considered raw. Navy beans can't even be consumed raw because they're hard as fucking rocks. So, immediately this table is potentially misleading, having possibly presented an unrealistic comparison between these two foods. But, that's not the most egregious part of Brian's table. It's actually completely unnecessary to consider digestibility and biological value separately as Brian has [[12]](https://pubmed.ncbi.nlm.nih.gov/26369006/).
> _"The PDCAAS value should predict the overall efficiency of protein utilization based on its two components, digestibility and biological value (BV; nitrogen retained divided by digestible nitrogen). The principle behind this approach is that the utilization of any protein will be first limited by digestibility, which determines the overall amount of dietary amino acid nitrogen absorbed, and BV describes the ability of the absorbed amino acids to meet the metabolic demand."_
Biological value is inherently captured by both of the standard protein quality scores, the protein digestibility-corrected amino acid score (PDCAAS) and the digestible indispensable amino acid score (DIAAS). This means that if you want to represent all the things that matter for a given protein in isolation (such as digestibility, biological value, and limiting amino acids), all you need is either a PDCAAS or DIAAS value for the proteins in question. But, the DIAAS is probably better.
Aggregating DIAAS data across multiple protein foods paints a completely different picture than the one that Brian cobbled together [[13]](https://pubmed.ncbi.nlm.nih.gov/28748078/)[[14]](https://pubmed.ncbi.nlm.nih.gov/33333894/)[[15]](https://pubmed.ncbi.nlm.nih.gov/34476569/)[[16]](https://onlinelibrary.wiley.com/doi/full/10.1002/fsn3.1809). Some plant proteins actually do quite well. But what are these numbers really representing? Ultimately the scores are going to be truncated by limiting amino acids more than any other parameter, and pairing complementary proteins will increase the DIAAS value [[17]](https://pubmed.ncbi.nlm.nih.gov/34685808/). In fact, this is also true of the PDCAAS, as combining different lower-scoring plant proteins will often result in perfect scores [[18]](https://www.2000kcal.cz/lang/en/static/protein_quality_and_combining_pdcaas.php).
If beef is awesome in virtue of it getting a perfect score for protein digestibility, biological value, and limiting amino acids, then navy beans and wild rice must also be awesome too. If not, then I don't know what the hell Brian is talking about, or why he even brings the point up. It's also worth pointing out that certain animal foods, like collagen, actually score a zero on the PDCAAS as well.
As an aside, even if plant protein was generally inferior to animal protein by some evaluative standard (such as the PDCAAS or DIAAS), it would not necessarily mean that it would be more desirable to consume animal protein over plant protein. That would depend on one's goals. In fact, animal protein is associated with a number of chronic diseases in a dose-dependent manner, whereas plant protein is inversely associated, also in a dose-dependent manner [[19]](https://pubmed.ncbi.nlm.nih.gov/32699048/). This also holds true for Japanese populations, by the way [[20]](https://pubmed.ncbi.nlm.nih.gov/31682257/).
**Claim #6 (**[**6:35**](https://youtu.be/VYTjwPcNEcw?t=395)**):**
> "744 studies were excluded from consideration in the WHO's evaluation of meat as a carcinogen."
**Red Herring**
Here, Brian is referring to an analysis on red meat and colorectal cancer risk that was conducted by the International Agency for Research on Cancer (IARC) [[21]](https://pubmed.ncbi.nlm.nih.gov/26514947/). If you dig into the IARC's methods, you can see that they had very specific, sound inclusion-exclusion criteria, which involved selecting cohort studies with the widest contrasts in red meat intake, clear definitions, sufficient event rates and participant numbers, and adequate adjustment models.
> "A meta-analysis including data from 10 cohort studies reported a statistically significant dose-response association between consumption of red meat and/or processed meat and cancer of the colorectum. The relative risks of cancer of the colorectum were 1.17 (95% CI, 1.05-1.31) for an increase in consumption of red meat of 100 g/day and 1.18 (95% CI, 1.10-1.28) for an increase in consumption of processed meat of 50 g/day. Based on the balance of evidence, and taking into account study design, size, quality, control of potential confounding, exposure assessment, and magnitude of risk, an increased risk of cancer of the colorectum was seen in relation to consumption of red meat and of processed meat."
This is very sensible methodology for anyone familiar with epidemiology. Additionally, this is not the only reason Brian's claim is misleading, because there are not 744 cohort studies or RCTs combined on this question. Full stop. I can only imagine that he is referring to mechanistic studies or other weaker forms of evidence. He's never fully unpacked this claim, to my knowledge.
**Claim #6 (**[**7:05**](https://youtu.be/VYTjwPcNEcw?t=425)**):**
> _"There were 15 studies showing that red meat was good and 14 studies showing that red meat was bad. I mean, it's basically a toss-up."_
**Red Herring**
Again, the IARC had very strict inclusion-exclusion criteria, and of the studies that met those criteria, the majority of them found statistically significant associations between red meat and colorectal cancer. This is after multivariable adjustment for known confounders and covariates, in populations that we'd expect to have an increased risk. It's straight up expected that not all of the available studies on a given research question will be included in a meta-analysis.
**Red Herring**
Brian then goes on to claim that the results are a toss-up simply because there were 15 studies ostensibly showing that red meat was "good" and 14 studies ostensibly showing that red meat was "bad". To imply that this is necessarily a "toss up" is just pure confusion. Even if you have double the studies showing that red meat is "good", that doesn't necessarily mean there is a lower probability that red meat is "bad". It depends on the strength of the studies included. Consider this forest plot.
Here we see that despite the fact that there is a 2:1 ratio of studies that show a decreased risk with red meat to studies that show an increased risk with red meat, the summary effect measure still points toward a statistically significant increase in risk. This is because not every study has equal power or precision. Some findings are just less certain than others.
**Claim #7 (**[**7:22**](https://youtu.be/VYTjwPcNEcw?t=442)**):**
> "The risk factor of cancer from meat is 0.18%, whereas the risk factor of cancer from smoking is 10-30%."
**Unintelligible**
This is truly bizarre. It's incredibly unclear what Brian is trying to say here, and he was unable to unpack it to me in [our verbal debate](https://www.youtube.com/watch?v=S8p39Gwct1Y), so I'm not even sure he knowns what the fuck he means. His use of the term "risk factor" here makes the utterance appear like a category error. However, if I really stretch my imagination, I may be able to cobble together an interpretation that isn't gibberish.
**Equivocation**
Firstly, this appears to be just a straight up equivocation of cancer types. Colorectal cancer and lung cancer are two different diseases, and the prevalence of these diseases are different in the general population. If Brian's criticism is that the relative risk of lung cancer from smoking is higher than the relative risk of colorectal cancer from red meat, then he's just confused. Massive differences in the magnitude of those effect estimates are expected, as the prevalence of a given disease will determine the maximum possible relative risk [[22]](https://pubmed.ncbi.nlm.nih.gov/21402371/).
Let's take a look at the prevalence of these diseases in Canada [[23]](https://cancer.ca/en/cancer-information/cancer-types.). The prevalence of lung cancer among Canadian non-smokers is 1 in 84 (1.19% prevalence). Prevalence of colorectal cancer, assuming red meat has nothing to do with colorectal cancer, is 1 in 16 (6.25% prevalence). The baseline prevalence of lung cancer is much smaller than the baseline prevalence of colorectal cancer, so comparing the two is dubious.
In the case of lung cancer and colorectal cancer, the maximum possible relative risks would be ~53 and ~16, respectively. So it's not even mathematically possible for the relative risk of colorectal cancer from red meat to even approach the upper bounds for the relative risk of lung cancer from smoking that Brian submitted (assuming he meant 30x and not 30%).
For this reason, it's best that we do an apples to apples comparison. In a massive 2009 analysis by Huxley, et al., which helped inform the IARC's analysis on meat and cancer, 26 cohort studies were included in their meta-analytic summation [[24]](https://pubmed.ncbi.nlm.nih.gov/19350627/). Overall they showed a statistically significant 21% increase in risk of colorectal cancer with unprocessed red meat.
However, they also included an analysis on smoking, which found a statistically significant 16% increase in the risk of colorectal cancer with smoking as well. Yes, that is right— there was a slightly stronger association between red meat and colorectal cancer than there was between smoking and colorectal cancer. But the two were likely non-inferior. Huxley et al. also found around the same magnitude of effect for many other exposures.
What's the symmetry breaker? Why form a causal belief with regards to smoking or physical inactivity or obesity and not red meat? If Brian argues that he doesn't infer causality for any of the exposures with non-inferior effect sizes to red meat, then the appropriate thing to do is honestly just to laugh at his absurdity and move on.
If Brian argues that red meat has never been studied in the context of a junk-free diet, then we could just argue it in the opposite direction. For example, the smoking literature is also notoriously unadjusted for dietary covariates (which is something not many people appreciate about that body of evidence). As such, smoking arguably has never been studied in the context of a meat-free diet either, so perhaps the data on smoking is simply biased by red meat. Again, we need symmetry breakers.
**Claim #8 (**[**7:37**](https://youtu.be/VYTjwPcNEcw?t=457)**):**
> _"Ancestral foods are better than processed foods."_
**Appeal to Nature**
Why should we be using anthropological data about ancestral diets to inform best practice in terms of modern diets for modern humans? And why is the property of being ancestral a reasonable sufficiency criteria for a food to be "better" than processed foods? This seems like a non sequitur.
Favouring whole foods is heuristic, and not a rule. There are plenty of examples of processed foods being superior to whole foods, even foods that we could identify as ancestral. In fact, there are been specific analyses investigating the differential contributions of animal-based foods (red meat, poultry, fish, dairy, and eggs) and ultra-processed foods to disease risk within the context of a health-conscious population [[25]](https://pubmed.ncbi.nlm.nih.gov/35199827/).
Overall, ultra-processed foods and animal foods are non-inferior to one another for CVD mortality and cancer mortality risk. Animal based foods also seem to associate with the risk of endocrine disorders like T2DM, whereas ultra-processed foods did not. Once again, we require symmetry-breakers. Why form the belief that ultra-processed foods increase the risk of these diseases and not animal foods?
###### Environmental Claims
**Claim #9 (**[**10:13**](https://youtu.be/VYTjwPcNEcw?t=613)**):**
> "Grazing agricultural systems are better for the environment and sequester more carbon."
**False Claim**
This claim is as hilarious as it is vague. Firstly, better compared to what? According to Brian's reference (which was an analyses of the association between White Oak Pastures' regenerative grazing methodology and carbon balance) it was assumed that carbon sequestration estimates were exclusively from beef, yet poultry accounted for almost half of the carcass weight (46.5%) of the entire system [[26]](https://www.frontiersin.org/articles/10.3389/fsufs.2020.544984/full). They also can’t even attribute the sequestration to cows because the study was cross-sectional in design.
This study isn't actually investigating temporal changes in soil carbon at all. To make matters worse, the author's darling figure, −4.4kg CO₂-e kg carcass weight−1 per year, was actually just produced from thin air, and the cross-sectional association between years of grazing and soil carbon stocks between pasturelands was just assumed to be reflecting grazing-mediated soil carbon sequestration. Utterly misleading sophistry.
> _"Importantly, if we were to attribute the soil C sequestration across the chronosequence to only cattle, MSPR beef produced in this system would be a net sink of −4.4 kg CO2-e kg CW−1 annually."_
Even just ignoring the fact that this methodology creates mathematically atrocious pigs and chickens in terms of carbon balance in their model, the data provided suggests that 20 years worth of carbon sequestration are roughly equal to three years of plant composting. In second figure of the publication, they show a cross-sectional analysis of seven different degraded lands (previously used for crops) that are in the process of being restored over a varied number of years.
> _"In years 1–3, these fields are minimally grazed and receive 1 cm of compost ha−1 yr−1. After year 3, exogenous inputs (hay and compost) were ceased, and the regeneration strategy shifted toward an animal-only approach, whereby animals were the primary mechanism of improving the land."_
The third dot is roughly equal to that of the seventh dot on the chart, which represents three years of plant composting and 20 years of grazing, respectively. If we're assuming a causal relationship between grazing and soil carbon stock, why not also assume a causal relationship between composting and soil carbon stock?
If composting can increase soil carbon sequestration that much, why are they even trying to argue for grazing agriculture as a solution? It would appear that plant agriculture waste could be a viable solution for restoring these degraded lands as well. This is also just granting that these associations are reflective of soil carbon sequestration over time at all, which they may not be. Again, this analysis is cross-sectional.
It's convenient that the time scale of the investigation by Rowntree, et al. caps out at 20 years, because current literature suggests that there is a soil carbon saturation point at around 20 years, after which pasture grazing systems will yield diminishing returns.
Here we see three different scenarios for soil carbon sequestration rates from grazing agriculture. Even under the most generous estimates (the larger black hashed line), soil carbon sequestration plateaus at around 20 years.
However, current estimates suggest that if we switch to more plant-predominant diets by the year 2050, we could reforest a large proportion of current pastureland, which acts as a substantial carbon sink (~547GtCO2) [[27]](https://www.nature.com/articles/s41893-020-00603-4). The effect of that over 30 years is to neutralize about 15 years of fossil fuel emissions and 12 years of total world GHG emissions.
If we switch to plant-predominant diets by 2050 we could sequester -14.7 GtCO2 per year by reforesting pasture land, compared to other agricultural methods that make use of grazing land for pasture. Merely the introduction of pasture grazing increases land use by almost double compared to a vegan agricultural system [[28]](https://experts.syr.edu/en/publications/carrying-capacity-of-us-agricultural-land-ten-diet-scenarios).
In fact, there are stepwise decreases in the per-person carrying capacity of different agricultural scenarios as more pastureland is included in the model. However, vegan agricultural scenarios were largely comparable to both dairy-inclusive and egg-inclusive vegetarian models.
As mentioned earlier in this article, there are plant agriculture methods that are also touted as "regenerative", that also may have greater soil carbon sequestration potential per hectare than current "regenerative" grazing livestock methods [[29]](https://www.nature.com/articles/ncomms6012). It would be interesting to see a head-to-head comparison of wheat versus meat, using "regenerative" methodology, on soil carbon sequestration overall.
**Claim #10 (**[**13:15**](https://youtu.be/VYTjwPcNEcw?t=795)**):**
> "We have enough land for grazing agricultural systems."
**False Claim**
It has been calculated that even if all grasslands were repurposed for grazing, this could provide everyone on earth with 7-18g/day of animal protein per person on Earth [[30]](https://www.oxfordmartin.ox.ac.uk/publications/grazed-and-confused/). The authors also provided a hyper-idealized, candy-land scenario they also calculated that 80g/day of animal protein per person on Earth. However, this would require all pasturable land on Earth being used. As an aside, the authors also calculated an additional scenario that included waste from plant agriculture, but it probably won't be very relevant to Brian's idealized world, because plant agriculture would be extremely minimal on the Sapien Diet™.
The remaining two scenarios encounter some issues when we think of what would be required to sustain people on meat-heavy diets, because 80g of protein from the fattiest beef still would not provide enough calories per person. We would appear to need multiple planets. But we should use a grass-fed example to do the calculations, so I've chosen White Oak Pastures' ground beef as the example meat. We'll also be multiplying the results by 2.5 to account for the extra land used by rotational grazing and/or holistic management [[26]](https://www.frontiersin.org/articles/10.3389/fsufs.2020.544984/full).
Under no plausible scenario (calculable from the 'Grazed and Confused?' report) would either continuous grazing or rotational grazing be tenable on a global scale. Even if the calorie allotment for animal foods in the EAT Lancet diet was occupied only by grass-fed beef, we'd still be exceeding the carrying capacity of the Earth by 70% for continuous grazing and 325% for rotational grazing. As for Brian's pet diet, the Sapien Diet™, we'd need over 10 Earths in the optimistic plausible scenario.
Essentially, we would need to figure out a way to extend the pasturable land beyond the available land on Earth. Perhaps we could do this by terraforming Mars or ascending to a type 2 civilization on the Kardashev scale by building a megastructure in space, such as a Dyson sphere or an O'Neill cylinder. But, those options don't sound very ancestral at all.
We're not even scratching the surface, though. The authors of 'Grazed and Confused?' likely did not consider the suitability of each grassland in their calculation, because current suitability thresholds are set for crop production, rather than livestock. The issue is that grass itself could be considered a crop, so it's unclear why suitability considerations that have been established for crop production wouldn't also apply to pasture-raised animal production.
The IIASA/FAO define the suitability of a given grassland as a threshold of a 25% ratio of actual yield per acre and potential yield per acre [[31]](https://pure.iiasa.ac.at/id/eprint/13290/). Had these suitability criteria been considered by the authors of 'Grazed and Confused?', their models likely would have produced much smaller estimates. This is because much of the available grassland is either unsuitable or poorly suitable to begin with.
These suitability criteria have been used by livestock agriculture advocates to argue against the scalability of crop agriculture and for the scalability of grazing-based livestock agriculture [[32]](https://www.sciencedirect.com/science/article/abs/pii/S2211912416300013). However, [Avi Bitterman](https://twitter.com/AviBittMD) demonstrated on his [Discord server](https://discord.gg/YtfQNPnk) that these individuals are not symmetrically applying this standard and it would actually turn out that current "regenerative" grazing systems wouldn't be likely to even meet the suitability standards themselves.
According to figures produced by White Oak Pastures, their "regenerative" grazing system is far less efficient than conventional feedlot approaches [[33]](https://blog.whiteoakpastures.com/hubfs/WOP-LCA-Quantis-2019.pdf). Overall, White Oak Pastures uses 150% more land than conventional approaches to yield only about 20% of what a conventional farm can produce, and only 90% of the average slaughter weight.
This would give us a "suitability" estimate of around 7%, which would likely drastically reduce the amount of grassland that would be considered suitable for "regenerative" grazing agriculture as well. It would be doubly important to adhere to this standard when critiquing "regenerative" plant agricultural methods, in order to ensure an apples-to-apples comparison [[29]](https://www.nature.com/articles/ncomms6012).
**Claim #11 (**[**13:54**](https://youtu.be/VYTjwPcNEcw?t=834)**):**
> _"If we don't use all this cropland for corn, wheat, and soy...we can use some of this land for cows."_
**False Claim**
Here, Brian presents us a with figure from the USDA showing the available cropland in the United States as of 2007, and suggests that we simply have enough land for "regenerative" grazing. No analysis or even conceptual model of how this could be done was actually provided. He just expects us to take it for granted that the claim is true. But is it actually true?
As with the issues for this narrative that were entailed from the land requirement estimates detailed in the 'Grazed and Confused?' report, this narrative again encounters similar issues here. Firstly, a complete grazing agriculture scenario has been modeled, and the results suggest that the United States wouldn't get anywhere close to plausibly being able to meet their current demand for beef with grazing agriculture [[34]](https://iopscience.iop.org/article/10.1088/1748-9326/aad401). We'd simply need more land. About 30% more land.
> _"Increases in cattle population, placements, and slaughter rates are demonstrated in figure 2. The increased slaughtering and placement numbers would also require a 24% increase in the size of the national beef cow-calf herd, proportional to the increased annual grass-finishing placement rate, in order to provide additional cattle to stock the grass-finishing stage. Increases in both the cow-calf herd and the grass-finishing population together would result in a total increase to the US cattle population of an additional 23 million cattle, or 30% more than the current US beef cattle population as a whole"_
If Brian wants to criticize vegans for indulging idealized pie-in-the-sky fantasies, what in the sweet holy blue fuck is this shit? The United States can't maintain their current demands for beef with the system that Brian is proposing. This is doubly problematic if you consider that the White Oak Pastures model for which Brian advocates probably requires even more land than the conventional grazing methods included in the above model. This means that 30% could very well be an underestimate.
###### Ethical Claims
**Claim #12 (**[**19:11**](https://youtu.be/VYTjwPcNEcw?t=1151)**):**
> _"Vegans kill animals too. It's death on a plate, there's just no blood."_
**Appeal to Hypocrisy**
It's not clear what point this is trying to make. It seems like a failed appeal to hypocrisy to me. But, let's try to tackle the proposition in the most charitable way possible. Let's assume that Brian means to say that the Sapien Diet™ leads to fewer animal deaths than vegan diets that rely on plant agriculture (which is a claim that he has made before). In this case, this is just an empirical claim and needs to be supported by some sort of evidence.
In Brian's presentation, he supports this claim with a study of wood mouse predation after harvest, which showed that up to 80% of mice were preyed upon by predators upon the harvesting of cereal crops [[35]](https://www.sciencedirect.com/science/article/abs/pii/000632079390060E?via%3Dihub). What Brian isn't taking into account is that this can actually be used to are for less mouse predation on cropland as opposed to pastureland. Let me explain.
If you cut down your crop, you will expose the mice to predation. This is true. However, this also applies to pastureland. On pastureland, there is no substantial amount of tall forage that mice can use for shelter. The mice are exposed all year round. Which actually allows for the possibility that cropland could temporarily shelter mice from predators in a way that pastureland can't.
Furthermore, during [my debate](https://www.youtube.com/watch?v=S8p39Gwct1Y) with Brian, his cited evidence was the single cow that was killed when he paid a visit to his friend's cattle farm. Needless to say, this is not very good evidence, and this is not the evidence we will be using to steelman Brian's position. Instead, let's actually look at literature that compares the wildlife carrying capacity of plant verses grazing agricultural scenarios.
In 2020, Tucker et al. published a comprehensive comparative analysis of mammalian populations across a number of human-modified areas, such as cropland and pastureland [[36]](https://onlinelibrary.wiley.com/doi/full/10.1111/ecog.05126). Overall, their findings suggest that there is higher taxonomic diversity with increasing pastureland as opposed to increasing cropland.
In the absence of countervailing data, this actually counts against the hypothesis that pastureland entails less animal death than cropland. This is because increasing taxonomic diversity implies a higher number of trophic strata. A higher number of trophic strata implies higher levels of predation. Higher levels of predation thus imply higher levels of animal death. The land with the lesser carrying capacity should probably be assumed to entail less death.
**Red Herring**
Even if we granted Brian that pastureland entailed fewer animal deaths than cropland, it's not clear why vegans should necessarily care. If veganism is understood to be a social and politic movement that aims to extend human rights to animals when appropriate, it's not clear how the deaths entailed from cropland would be incompatible to those goals. In fact, we'd likely tolerate the killing of people who threatened our food supply in comparable ways as well.
For example, if our food security was threatened by endless armies of humans with the intelligence of fieldmice or insects and we had no practical means of separating them from our food without killing them, I don't think we'd consider killing them to be a rights violation. In fact, we'd likely assume a similar defensive posture and similarly tolerate the loss of human life if a foreign country was also threatening to destroy our food. I doubt we'd even consider the enemy deaths entailed from such a defensive posture to constitute a rights violation. We have the right to defend our property against assailants, and I doubt Brian would even deny this himself.
**Claim #13 (**[**19:19**](https://youtu.be/VYTjwPcNEcw?t=1159)**):**
> _"There is no life without death. This is how nature works...animals in nature either starve to death or are eaten alive...the animals are going to die either way, and it's not a good death...billions of people rely on animals for their livelihood."_
**Potential Contradiction**
This proposition is simple to address. If Brian believes that we are ethically justified in breeding sentient animals into existence for the explicit purpose of slaughtering them for food, but we would not be justified in condemning humans to likewise treatment, he must explain why. This same question can be asked of him regardless of the justification he uses for animal agriculture.
During my debate with Brian, I submitted to him an argument for the non-exploitation of animals, which is essentially just a rephrasing of [Isaac Brown](https://twitter.com/askyourself92)'s [Name the Trait](https://drive.google.com/drive/folders/1tAjU2Bv1tsGbNLA2TfJesgbIh8JKh9zc) argument.
**Definitions:**
**W** := Moral worth
**N** := Exploit it unnecessarily any more than we would for humans
**A** := Absent
**a** := animal
**h** := human
**t** := property
**P1)** For all things, if something has moral worth we should not exploit it unnecessarily any more than we would for humans.
**(∀x(Wx→¬Nx))**
**P2)** If animals don’t have moral worth, then there exists a property that is absent in animals such that if it were absent in humans, humans wouldn’t have moral worth.
**(¬Wa→∃t(Ata→(Ath→¬Wh)))**
**P3)** There doesn’t exist a property that is absent in animals such that if it were absent in humans, humans wouldn’t have moral worth.
**(¬∃t(Ata→(Ath→¬Wh)))**
**C)** Therefore, we should not exploit animals unnecessarily any more than we would for humans.
**(∴¬Na)**
This argument for non-exploitation simply requires one to identify the property that is true of humans that also is untrue of animals, that if true of humans, would cause humans to lose sufficient moral value, such that we’d be justified in slaughtering them for food as well. Brian rejected P3, stating that "consciousness" was the property true of humans, but untrue of animals, such that animals were ethical to exploit for food but humans were not. This fails and entails a contradiction on Brian's part, because consciousness is not a differential property between humans and the animals he advocates farming for food.
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[34] Hayek, Matthew N., and Rachael D. Garrett. ‘Nationwide Shift to Grass-Fed Beef Requires Larger Cattle Population’. _Environmental Research Letters_, vol. 13, no. 8, July 2018, p. 084005. _DOI.org (Crossref)_, [https://doi.org/10.1088/1748-9326/aad401](https://doi.org/10.1088/1748-9326/aad401).
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# Coronary Heart Disease
Coronary heart disease (CHD) is a condition where the coronary arteries, which supply oxygen-rich blood to the heart muscle, become narrowed or blocked due to the buildup of plaque, known as [[atherosclerosis]]. This reduction in blood flow can cause chest pain (angina), shortness of breath, and other symptoms. This can be caused by various factors including genetic predisposition, poor [[lifestyle]] habits, such as following a [[standard american diet]], and underlying medical conditions.****
Coronary heart disease (CHD) is a condition where the coronary arteries, which supply oxygen-rich blood to the heart muscle, become narrowed or blocked due to the buildup of plaque, known as [[atherosclerosis]]. This reduction in blood flow can cause chest pain (angina), shortness of breath, and other symptoms. This can be caused by various factors including genetic predisposition, poor [[lifestyle]] habits, such as following a [[standard american diet]], and underlying medical conditions.
**Key features of coronary heart disease:**

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## Rebuttal
While partially true, this claim counts as a [[red herring]], because it's not actually seed oils simpliciter that causes [[cholestasis]]. In the [[LA Veterans Administration Hospital Study]], the seed oil group had a dose-dependent increase in gallstones [(1)](https://pubmed.ncbi.nlm.nih.gov/4681896/). However, the most parsimonious way of explaining the effect is through hepatic [[phytosterol]] elimination leading to gallstones, not [[linoleic acid]] [(2)](https://pubmed.ncbi.nlm.nih.gov/9437703/)[(3)](https://pubmed.ncbi.nlm.nih.gov/27812789/).
While partially true, this claim counts as a [[red herring]], because it's not actually seed oils simpliciter that causes [[cholestasis]]. In the [[LA Veterans Administration Hospital Study]], the seed oil group had a dose-dependent increase in gallstones [(1)](https://pubmed.ncbi.nlm.nih.gov/4681896/). However, the most parsimonious way of explaining the effect is through the elimination of hepatic [[phytosterols]], leading to gallstones, not [[linoleic acid]] [(2)](https://pubmed.ncbi.nlm.nih.gov/9437703/)[(3)](https://pubmed.ncbi.nlm.nih.gov/27812789/).
Some seed oils, such as corn oil (the primary seed oil investigated in the LA Veterans trial), have extremely high concentrations of [[phytosterols]] [(4)](https://pubmed.ncbi.nlm.nih.gov/31404986/). At the doses investigated, this may be expected to cause issues, but these are not doses that people typically consume, even on the [[standard american diet]].
Some seed oils, such as corn oil (the primary seed oil investigated in the LA Veterans trial), have extremely high concentrations of phytosterols [(4)](https://pubmed.ncbi.nlm.nih.gov/31404986/). At the doses investigated, this may be expected to cause issues, but these are not doses that people typically consume, even on the [[standard american diet]].
---