diff --git a/frontend/src/Config/Helpers/CardFormat.elm b/frontend/src/Config/Helpers/CardFormat.elm index fd9db9f..500632d 100755 --- a/frontend/src/Config/Helpers/CardFormat.elm +++ b/frontend/src/Config/Helpers/CardFormat.elm @@ -170,6 +170,12 @@ cardImageMaker size1 size2 image urlLink = || urlLink == Path.toString Path.Blog_Seedoils || urlLink + == Path.toString Path.Blog_Huntergatherers + || urlLink + == Path.toString Path.Blog_Sapiendiet + || urlLink + == Path.toString Path.Blog_Nagragoodrich + || urlLink == Path.toString Path.Interviews || urlLink == Path.toString Path.Nutridex diff --git a/frontend/src/Config/Helpers/Converters.elm b/frontend/src/Config/Helpers/Converters.elm index 6791f93..b38fb36 100755 --- a/frontend/src/Config/Helpers/Converters.elm +++ b/frontend/src/Config/Helpers/Converters.elm @@ -26,3 +26,35 @@ wordCount text = text |> String.words |> List.length + + +toTitleCase : String -> String +toTitleCase input = + let + lowercaseWords = + [ "a", "an", "the", "and", "but", "or", "for", "nor", "on", "at", "to", "in", "of", "with", "by" ] + + words = + String.words input + + capitalizeFirst word = + case String.uncons word of + Just ( first, rest ) -> + String.toUpper (String.fromChar first) ++ String.toLower rest + + Nothing -> + "" + + capitalizeWord index word = + if index == 0 then + capitalizeFirst word + + else if not (List.member (String.toLower word) lowercaseWords) then + capitalizeFirst word + + else + String.toLower word + in + words + |> List.indexedMap capitalizeWord + |> String.join " " diff --git a/frontend/src/Config/Helpers/Markdown.elm b/frontend/src/Config/Helpers/Markdown.elm old mode 100644 new mode 100755 index 82a8427..e4a5de9 --- a/frontend/src/Config/Helpers/Markdown.elm +++ b/frontend/src/Config/Helpers/Markdown.elm @@ -1,6 +1,7 @@ module Config.Helpers.Markdown exposing (..) import Browser +import Config.Helpers.Converters exposing (toTitleCase) import Config.Helpers.Format exposing ( headerFontSizeBig @@ -56,24 +57,162 @@ articleImage pic = renderDeviceMarkdown : String -> Element msg renderDeviceMarkdown markdown = case renderMarkdown markdown of - Ok renderedMarkdown -> + Ok ( toc, renderedMarkdown ) -> column [ width fill , centerX , spacing 10 ] - renderedMarkdown + (tocView toc :: renderedMarkdown) Err error -> E.text error -renderMarkdown : String -> Result String (List (Element msg)) +renderMarkdown : String -> Result String ( TableOfContents, List (Element msg) ) renderMarkdown markdown = - markdown - |> Markdown.Parser.parse - |> Result.mapError (\error -> error |> List.map Markdown.Parser.deadEndToString |> String.join "\n") - |> Result.andThen (Markdown.Renderer.render elmUiRenderer) + case + markdown + |> Markdown.Parser.parse + of + Ok okAst -> + case Markdown.Renderer.render elmUiRenderer okAst of + Ok rendered -> + Ok ( buildToc okAst, rendered ) + + Err errors -> + Err errors + + Err error -> + Err (error |> List.map Markdown.Parser.deadEndToString |> String.join "\n") + + +tocView : TableOfContents -> Element msg +tocView toc = + column + [ alignTop + , width fill + , spacing 10 + ] + [ paragraph + [ F.bold + , F.size 23 + , F.center + , width fill + , F.color colourTheme.textLightOrange + ] + [ text "TABLE OF CONTENTS" ] + , column + [ E.spacing 3 + , paragraphFontSize + , E.width fill + ] + (toc + |> List.indexedMap + (\index headingBlock -> + row + [ E.width fill ] + [ el + [ E.alignTop + , width <| px 30 + , F.bold + , alignRight + , alignBottom + ] + (text (String.fromInt (index + 1) ++ ".")) + , el + [ F.alignLeft + , E.width fill + , F.size 18 + , alignTop + ] + <| + newTabLink + [] + { url = "#" ++ headingBlock.anchorId + , label = + el + [ F.color colourTheme.textLightOrange + , transitionStyleFast + , hoverFontDarkOrange + ] + <| + text (toTitleCase headingBlock.name) + } + ] + ) + ) + , el + [ width fill + , height fill + , spacing 20 + , paddingEach + { top = 0 + , bottom = 0 + , left = 100 + , right = 100 + } + ] + <| + row + [ centerX + , D.widthEach + { bottom = 1 + , top = 0 + , left = 0 + , right = 0 + } + , D.color colourTheme.textLightOrange + , paddingEach + { top = 10 + , bottom = 0 + , left = 0 + , right = 0 + } + ] + [] + , el + [] + <| + text "" + ] + + +buildToc : List Block -> TableOfContents +buildToc blocks = + let + headings = + gatherHeadings blocks + in + headings + |> List.map Tuple.second + |> List.map + (\styledList -> + { anchorId = styledList |> Block.extractInlineText |> rawTextToId + , name = styledToString styledList + , level = 1 + } + ) + + +styledToString : List Inline -> String +styledToString list = + list + |> Block.extractInlineText + + +gatherHeadings : List Block -> List ( Block.HeadingLevel, List Inline ) +gatherHeadings blocks = + List.filterMap + (\block -> + case block of + Block.Heading level content -> + Just ( level, content ) + + _ -> + Nothing + ) + blocks elmUiRenderer : Markdown.Renderer.Renderer (Element msg) @@ -312,29 +451,54 @@ codeBlock details = heading : { level : Block.HeadingLevel, rawText : String, children : List (Element msg) } -> Element msg heading { level, rawText, children } = - E.paragraph - [ F.size - (case level of - Block.H1 -> - headerFontSizeBig + column [ width fill ] + [ el + [ width fill + , height fill + , spacing 20 + , paddingEach + { top = 10 + , bottom = 20 + , left = 100 + , right = 100 + } + ] + <| + row + [ centerX + , D.widthEach + { bottom = 1 + , top = 0 + , left = 0 + , right = 0 + } + , D.color colourTheme.textLightOrange + ] + [] + , E.paragraph + [ F.size + (case level of + Block.H1 -> + headerFontSizeBig - Block.H2 -> - headerFontSizeMedium + Block.H2 -> + headerFontSizeMedium - _ -> - headerFontSizeSmall - ) - , F.bold - , F.center - , width fill - , F.color colourTheme.textLightOrange - , Region.heading (Block.headingLevelToInt level) - , E.htmlAttribute - (Html.Attributes.attribute "name" (rawTextToId rawText)) - , E.htmlAttribute - (Html.Attributes.id (rawTextToId rawText)) + _ -> + headerFontSizeSmall + ) + , F.bold + , F.center + , width fill + , F.color colourTheme.textLightOrange + , Region.heading (Block.headingLevelToInt level) + , E.htmlAttribute + (Html.Attributes.attribute "name" (rawTextToId rawText)) + , E.htmlAttribute + (Html.Attributes.id (rawTextToId rawText)) + ] + children ] - children rawTextToId rawText = @@ -344,3 +508,11 @@ rawTextToId rawText = |> String.join "-" |> Debug.log "joined" |> String.toLower + + + +-- Types + + +type alias TableOfContents = + List { anchorId : String, name : String, level : Int } diff --git a/frontend/src/Config/Helpers/References.elm b/frontend/src/Config/Helpers/References.elm new file mode 100755 index 0000000..c2c86a6 --- /dev/null +++ b/frontend/src/Config/Helpers/References.elm @@ -0,0 +1,46 @@ +module Config.Helpers.References exposing (..) + +import Config.Style.Colour exposing (colourTheme) +import Config.Style.Transitions + exposing + ( hoverFontDarkOrange + , transitionStyleFast + ) +import Element as E exposing (..) +import Element.Font as F + exposing + ( alignLeft + , color + , regular + ) + + +makeReference : References -> Int -> Element msg +makeReference references index = + paragraph + [ F.regular + , F.alignLeft + ] + [ row [] + [ newTabLink + [ F.bold + , F.color colourTheme.textLightOrange + , hoverFontDarkOrange + , transitionStyleFast + ] + { url = references.link, label = text (String.fromInt index ++ ". ") } + , text (references.author ++ ", ") + , text (references.title ++ ", ") + , text (references.journal ++ ", ") + , text references.year + ] + ] + + +type alias References = + { author : String + , title : String + , link : String + , year : String + , journal : String + } diff --git a/frontend/src/Config/Pages/Blog/Records/HunterGatherers.elm b/frontend/src/Config/Pages/Blog/Records/HunterGatherers.elm new file mode 100755 index 0000000..8cb01ca --- /dev/null +++ b/frontend/src/Config/Pages/Blog/Records/HunterGatherers.elm @@ -0,0 +1,245 @@ +module Config.Pages.Blog.Records.HunterGatherers exposing (..) + +import Config.Pages.Blog.Types exposing (..) +import Route.Path as Path + + +articleHunterGatherers : BlogArticle +articleHunterGatherers = + { articleName = "Should Modern Humans Eat Like Hunter-Gatherers?" + , articleDescription = "This article presents a philosophical critique of the belief that a diet consisting solely of natural or ancestral foods is the best way for modern humans to achieve optimal health. I argue that even if a hunter-gatherer diet may be superior to a Western diet, it is still not necessarily the healthiest choice due to factors like the potential risks of ancestral foods and the ability to improve food quality through scientific manipulation." + , articleLink = Path.toString Path.Blog_Huntergatherers + , articleAuthor = "Nick Hiebert" + , isNewTabLink = False + , articleImage = "huntergatherers" + , articlePublished = "May 14, 2021" + , articleBody = """ +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. + +# SURVIVORSHIP BIAS + +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)]. + +![][image1] +[image1]: /blog/huntergatherers/image1.png + +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. + +![][image2] +[image2]: /blog/huntergatherers/image2.png + +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. + +![][image3] +[image3]: /blog/huntergatherers/image3.png + +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. + +# SELECTION SHADOW + +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/)]. + +![][image4] +[image4]: /blog/huntergatherers/image4.png + +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/)]. + +![][image5] +[image5]: /blog/huntergatherers/image5.png + +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://pubmed.ncbi.nlm.nih.gov/28320601/)]. + +![][image6] +[image6]: /blog/huntergatherers/image6.png + +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. + +# ANTAGONISTIC PLEIOTROPY + +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. + +![][image7] +[image7]: /blog/huntergatherers/image7.png + +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: + +![][argument1] +[argument1]: /blog/huntergatherers/argument1.png + +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. + +# OPTIMAL DIETS + +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. + +![][argument2] +[argument2]: /blog/huntergatherers/argument2.png + +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 me create more content like this, consider pledging your [Support](https://www.uprootnutrition.com/donate). Every little bit helps! I hope you found the content interesting! + +# BIBLIOGRAPHY""" + , articleReferences = + [ { author = "Anthony A. Volka and Jeremy A. Atkinson" + , title = "Infant and child death in the human environment of evolutionary adaptation" + , journal = "Evolution and Human Behavior" + , year = "2013" + , link = "https://www.sciencedirect.com/science/article/abs/pii/S1090513812001237" + } + , { author = "Lee Hooper, et al." + , title = "Reduction in saturated fat intake for cardiovascular disease" + , journal = "Cochrane Database Syst Rev" + , year = "2020" + , link = "https://pubmed.ncbi.nlm.nih.gov/32428300/" + } + , { author = "Arash Etemadi, et al." + , title = "Mortality from different causes associated with meat, heme iron, nitrates, and nitrites in the NIH-AARP Diet and Health Study: population based cohort study" + , journal = "BMJ" + , year = "2017" + , link = "https://pubmed.ncbi.nlm.nih.gov/28487287/" + } + , { author = "Andrew Mente, et al." + , title = "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies" + , journal = "Lancet" + , year = "2016" + , link = "https://pubmed.ncbi.nlm.nih.gov/27216139/" + } + , { author = "Rik H G Olde Engberink, et al." + , title = "Use of a Single Baseline Versus Multiyear 24-Hour Urine Collection for Estimation of Long-Term Sodium Intake and Associated Cardiovascular and Renal Risk" + , journal = "Circulation" + , year = "2017" + , link = "https://pubmed.ncbi.nlm.nih.gov/28655835/" + } + , { author = "Thomas Flatt and Linda Partridge" + , title = "Horizons in the evolution of aging" + , journal = "BMC Biol" + , year = "2018" + , link = "https://pubmed.ncbi.nlm.nih.gov/30124168/" + } + , { author = "Ryan McCready" + , title = "For Olympic Athletes, Is 30 the New 20?" + , journal = "" + , year = "2016" + , link = "https://venngage.com/blog/olympics/" + } + , { author = "Hillard Kaplan, et al." + , title = "Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study" + , journal = "Lancet" + , year = "2017" + , link = "https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)30752-3/fulltext" + } + , { author = "Mahesh V Madhavan, et al." + , title = "Coronary artery calcification: pathogenesis and prognostic implications" + , journal = "J Am Coll Cardiol" + , year = "2014" + , link = "https://pubmed.ncbi.nlm.nih.gov/24530667/" + } + , { author = "Michael Gurven" + , title = "Infant and fetal mortality among a high fertility and mortality population in the Bolivian Amazon" + , journal = "Soc Sci Med" + , year = "2012" + , link = "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502712/" + } + , { author = "Horvath et al." + , title = "An epigenetic clock analysis of race/ethnicity, sex, and coronary heart disease" + , journal = "Genome Biol" + , year = "2016" + , link = "https://pubmed.ncbi.nlm.nih.gov/27511193/" + } + , { author = "J Mitteldorf" + , title = "What Is Antagonistic Pleiotropy?" + , journal = "Biochemistry (Mosc)" + , year = "2019" + , link = "https://pubmed.ncbi.nlm.nih.gov/31870250/" + } + , { author = "He and Zhang" + , title = "Toward a molecular understanding of pleiotropy" + , journal = "Genetics" + , year = "2006" + , link = "https://pubmed.ncbi.nlm.nih.gov/16702416/" + } + , { author = "J M Stanhope and I A Prior" + , title = "The Tokelau island migrant study: prevalence and incidence of diabetes mellitus" + , journal = "N Z Med J" + , year = "1980" + , link = "https://pubmed.ncbi.nlm.nih.gov/6937778/" + } + , { author = "J M Stanhope and I A Prior" + , title = "The Tokelau Island Migrant Study: serum lipid concentration in two environments" + , journal = "J Chronic Dis" + , year = "1981" + , link = "https://pubmed.ncbi.nlm.nih.gov/7462380/" + } + ] + } diff --git a/frontend/src/Config/Pages/Blog/Records/NagraGoodrich.elm b/frontend/src/Config/Pages/Blog/Records/NagraGoodrich.elm new file mode 100644 index 0000000..23ae0e9 --- /dev/null +++ b/frontend/src/Config/Pages/Blog/Records/NagraGoodrich.elm @@ -0,0 +1,331 @@ +module Config.Pages.Blog.Records.NagraGoodrich exposing (..) + +import Config.Pages.Blog.Types exposing (..) +import Route.Path as Path + + +articleNagraGoodrich : BlogArticle +articleNagraGoodrich = + { articleName = "Grading Tucker Goodrich: A Lesson in Debate Etiquette" + , articleDescription = "" + , articleLink = Path.toString Path.Blog_Nagragoodrich + , articleAuthor = "Nick Hiebert" + , isNewTabLink = False + , articleImage = "nagragoodrich" + , articlePublished = "May 12, 2022" + , articleBody = """ +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! + +# DEBATE + +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._ + +# NUTRITIONAL EPIDEMIOLOGY + +**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. + +# MINNESOTA CORONARY EXPERIMENT + +**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: + +![][argument1] +[argument1]: /blog/nagragoodrich/argument1.png + +# LA VETERANS ADMINISTRATION HOSPITAL STUDY + +**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: + +![][argument2] +[argument2]: /blog/nagragoodrich/argument2.png + +# LYON DIET-HEART STUDY + +**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. + +# LOW DENSITY LIPOPROTEINS + +**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: + +![][argument3] +[argument3]: /blog/nagragoodrich/argument3.png + +**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. + +![][argument4] +[argument4]: /blog/nagragoodrich/argument4.png + +# TUCKER CONCEDES + +**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: + +![][argument5] +[argument5]: /blog/nagragoodrich/argument5.png + +**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. + +# HOOPER 2020 META-ANALYSIS + +**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: + +![][argument6] +[argument6]: /blog/nagragoodrich/argument6.png + +**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. + +# ECOLOGICAL STUDIES + +**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: + +![][argument7] +[argument7]: /blog/nagragoodrich/argument7.png + +# SYDNEY DIET-HEART STUDY + +**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: + +![][argument8] +[argument8]: /blog/nagragoodrich/argument8.png + + +**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. + +# OLIVE OIL SUBSTITUTION ANALYSIS + +**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. + +![][argument9] +[argument9]: /blog/nagragoodrich/argument9.png + +# DISCUSSION + +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. + +Thank you for reading! If you like what you've read and want help me create more content like this, consider pledging your [Support](https://www.uprootnutrition.com/donate). Every little bit helps! I hope you found the content interesting!""" + , articleReferences = + [ { author = "" + , title = "" + , journal = "" + , year = "" + , link = "" + } + ] + } diff --git a/frontend/src/Config/Pages/Blog/Records/SapienDiet.elm b/frontend/src/Config/Pages/Blog/Records/SapienDiet.elm new file mode 100755 index 0000000..f95ac3f --- /dev/null +++ b/frontend/src/Config/Pages/Blog/Records/SapienDiet.elm @@ -0,0 +1,597 @@ +module Config.Pages.Blog.Records.SapienDiet exposing (..) + +import Config.Pages.Blog.Types exposing (..) +import Route.Path as Path + + +articleSapienDiet : BlogArticle +articleSapienDiet = + { articleName = "The Sapien Diet: Peak Human or Food Lies?" + , articleDescription = "This article tackles many of the dubious claims made by ancestral diet advocate, Brian Sanders, during his popular 2020 talk, \"Despite what you've been told COWS CAN SAVE THE WORLD\". In this talk, Brian makes a number of baseless claims related to health, nutrition, argiculture, environmental science, and ethical philsophy. Make no mistake— virtually every listener was likely rendered slightly dumber for each word they heard leave Brian's mouth during his 26 minute presentation." + , articleLink = Path.toString Path.Blog_Sapiendiet + , articleAuthor = "Nick Hiebert" + , isNewTabLink = False + , articleImage = "sapiendiet" + , articlePublished = "Aug 24, 2022" + , articleBody = """ +[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! + +# HEALTH 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. + +![][image1] +[image1]: /blog/sapiendiet/image1.png + +**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. + +![][image2] +[image2]: /blog/sapiendiet/image2.png + +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. + +![][image3] +[image3]: /blog/sapiendiet/image3.png + +>_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. + +![][image4] +[image4]: /blog/sapiendiet/image4.png + +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. + +![][image5] +[image5]: /blog/sapiendiet/image5.png + +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. + +![][image6] +[image6]: /blog/sapiendiet/image6.png + +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. + +![][image7] +[image7]: /blog/sapiendiet/image7.png + +**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). + +![][image8] +[image8]: /blog/sapiendiet/image8.png + +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. + +![][image9] +[image9]: /blog/sapiendiet/image9.png + +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. + +![][image10] +[image10]: /blog/sapiendiet/image10.png + +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). + +![][image11] +[image11]: /blog/sapiendiet/image11.png + +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. + +![][image12] +[image12]: /blog/sapiendiet/image12.png + +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/). + +![][image13] +[image13]: /blog/sapiendiet/image13.png + +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. + +![][image14] +[image14]: /blog/sapiendiet/image14.png + +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/). + +![][image15] +[image15]: /blog/sapiendiet/image15.png + +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. + +![][image16] +[image16]: /blog/sapiendiet/image16.png + +>_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. + +![][image17] +[image17]: /blog/sapiendiet/image17.png + +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). + +![][image18] +[image18]: /blog/sapiendiet/image18.png + +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. + +![][image19] +[image19]: /blog/sapiendiet/image19.png + + +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). + +![][image20] +[image20]: /blog/sapiendiet/image20.png + + +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. + +![][image21] +[image21]: /blog/sapiendiet/image21.png + +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. + +![][image22] +[image22]: /blog/sapiendiet/image22.png + +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. + +![][image23] +[image23]: /blog/sapiendiet/image23.png + +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"_ + +![][image24] +[image24]: /blog/sapiendiet/image24.png + +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. + +![][image25] +[image25]: /blog/sapiendiet/image25.png + +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. + +![][argument1] +[argument1]: /blog/sapiendiet/argument1.png + +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. + +Thank you for reading! If you like what you've read and want help me create more content like this, consider pledging your [Support](https://www.uprootnutrition.com/donate). Every little bit helps! 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A New Analysis of the Feed/Food Debate" + , journal = "Global Food Security" + , year = "2017" + , link = "https://doi.org/10.1016/j.gfs.2017.01.001" + } + , { author = "" + , title = "Carbon Footprint Evaluation of Regenerative Grazing At White Oak Pastures: Results Presentation" + , journal = "Quantis - Environmental Sustainability Consultancy" + , year = "" + , link = "https://blog.whiteoakpastures.com/hubfs/WOP-LCA-Quantis-2019.pdf" + } + , { author = "Hayek, Matthew N., and Rachael D. Garrett" + , title = "Nationwide Shift to Grass-Fed Beef Requires Larger Cattle Population" + , journal = "Environmental Research Letters" + , year = "2018" + , link = "https://doi.org/10.1088/1748-9326/aad401" + } + , { author = "Tew, T. E., and D. W. Macdonald" + , title = "The Effects of Harvest on Arable Wood Mice Apodemus Sylvaticus" + , journal = "Biological Conservation" + , year = "1993" + , link = "https://doi.org/10.1016/0006-3207(93)90060-E" + } + , { author = "Tucker, Marlee A., et al." + , title = "Mammal Population Densities at a Global Scale Are Higher in Human‐modified Areas" + , journal = "Ecography" + , year = "2021" + , link = "https://doi.org/10.1111/ecog.05126" + } + ] + } diff --git a/frontend/src/Config/Pages/Blog/Records/SeedOils.elm b/frontend/src/Config/Pages/Blog/Records/SeedOils.elm old mode 100644 new mode 100755 index bfe3585..5b91095 --- a/frontend/src/Config/Pages/Blog/Records/SeedOils.elm +++ b/frontend/src/Config/Pages/Blog/Records/SeedOils.elm @@ -7,7 +7,7 @@ import Route.Path as Path articleSeedOils : BlogArticle articleSeedOils = { articleName = "A Comprehensive Rebuttal to Seed Oil Sophistry" - , articleDescription = "The article argues that vegetable oils, often criticized in recent years, are not harmful and may even offer health benefits, such as preventing heart disease and type 2 diabetes. It challenges claims based on mechanistic or ecological research, which lack strong evidence linking vegetable oils to chronic diseases. Instead, the article supports their inclusion in a balanced diet, cautioning against overconsumption, and debunking myths based on speculative studies." + , articleDescription = "This article argues that vegetable oils, often criticized in recent years, are not harmful and may even offer health benefits, such as preventing heart disease and type 2 diabetes. It challenges claims based on mechanistic or ecological research, which lack strong evidence linking vegetable oils to chronic diseases. Instead, the article supports their inclusion in a balanced diet, cautioning against overconsumption, and debunking myths based on speculative studies." , articleLink = Path.toString Path.Blog_Seedoils , articleAuthor = "Nick Hiebert" , isNewTabLink = False @@ -38,24 +38,24 @@ It is also suggested that saturated fatty acids (SFA) are resistant to this sort As it turns out, we've thoroughly investigated the effects of altering the fatty acid composition of the diet on LDL oxidation rates in humans. For example, Mata et al. (1996) explored this question with one of the most rigorous studies of its kind. No statistically significant differences between the effects of high-SFA diets and high-PUFA diets on the lag time to LDL oxidation were observed [[2](https://pubmed.ncbi.nlm.nih.gov/8911273/)]. ![][image1] -[image1]: /blog/image1.png +[image1]: /blog/seedoils/image1.png However, diets high in monounsaturated fat (MUFA) diets might actually increase the lag time to LDL oxidation more than either SFA-rich or PUFA-rich diets. It would appear as though this effect could be explained due to the fact that MUFA might be better than SFA at replacing LA in LDL particles. So, it seems as though the implication that SFA could offer unique protection against LDL oxidation is less straightforward than originally suggested. ![][image2] -[image2]: /blog/image2.png +[image2]: /blog/seedoils/image2.png When comparing LDL that were enriched with PUFA to LDL that were enriched with MUFA, Kratz et al. (2002) observed a stepwise decrease in LDL lag time to oxidation with increasing PUFA, specifically linoleic acid (LA) [[3](https://pubmed.ncbi.nlm.nih.gov/11840183/)]. These results cohere with the results of Mata el al., suggesting that MUFA increases the lag time to LDL oxidation more than SFA or PUFA. ![][image3] -[image3]: /blog/image3.png +[image3]: /blog/seedoils/image3.png In short, it would at least seem to be true that vegetable oil consumption, when investigated in isolation, increases the susceptibility of LDL to oxidize. But, don't get too excited. As we will discuss, these are paltry changes compared to what can be accomplished with antioxidants. Despite Kratz et al. claiming that vitamin E doesn't mask the effects of dietary fatty acids on LDL susceptibility to oxidation, their reference for this claim does not clearly support this conclusion. The work of Reaven et al. (1994) was their supporting reference for this claim and it actually paints a slightly different picture [[4](https://pubmed.ncbi.nlm.nih.gov/8148354/)]. The Lag time to LDL oxidation with vitamin E supplementation was more than double that which was observed in the previous study (or nearly any other random population sample from any other study that I've seen for that matter). ![][image4] -[image4]: /blog/image4.png +[image4]: /blog/seedoils/image4.png Reaven et al. discovered that the lag time to LDL oxidation was enormously high in all groups after a run-in diet that included 1200mg/day of vitamin E for three months before randomization. Compared to the previous study by Kratz et al. (2002), the LDL lag time to oxidation was 150% higher (~60 minutes to ~150 minutes). This is consistent with other research showing that the vitamin E content of LDL particles linearly increases the lag-time to LDL oxidation [[5](https://pubmed.ncbi.nlm.nih.gov/1985404/)]. @@ -66,23 +66,23 @@ All three studies used the same copper sulfate solution methodology to measure t Which brings me back to the trial by Kratz et al. (2002), which compared olive oil (OO) versus sunflower oil (SU). Despite the fact that all diet groups were receiving roughly the same amount of vitamin E, the OO group ended up with significantly higher vitamin E status compared to the SU group. This is consistent with the observations that MUFA increases the lag time to LDL oxidation to a greater degree than SFA or PUFA. Which leads to higher vitamin E representation in the end. ![][image5] -[image5]: /blog/image5.png +[image5]: /blog/seedoils/image5.png It is well understood that higher PUFA intakes increase vitamin E requirements in humans [[7](https://pubmed.ncbi.nlm.nih.gov/26291567/)]. However, the OO group also started with much higher status to begin with, which likely contributed to the effect. Lastly, the run-in diet was high in SFA. Such a diet is almost assuredly to be lower in vitamin E, which could exaggerate the effects of high-PUFA diets. As discussed earlier, SFA is not vulnerable to lipid peroxidation in any way similar to that of PUFA. However, SFA being less vulnerable to lipid peroxidation typically means that sources of SFA contain very low amounts of antioxidants [[8](https://pubmed.ncbi.nlm.nih.gov/14100992/)]. For example, both coconut oil and butter contain negligible vitamin E and have minimal polyphenols. The potential importance of polyphenol antioxidants in protecting LDL from oxidation has been demonstrated in research investigating OO [[9](https://pubmed.ncbi.nlm.nih.gov/15168036/)]. ![][image6] -[image6]: /blog/image6.png +[image6]: /blog/seedoils/image6.png Figure 2 from Marrugat et al. (2004) shows that virgin OO increases the lag time to oxidation to a greater degree than that of refined OO, with the primary differences between these different OOs being their polyphenol content. Many polyphenols act as antioxidants once they're inside our bodies, so these results are not particularly surprising. -It is likely that the overall dietary pattern matters more than PUFA, or even LA, in altering the susceptibility of LDL to oxidation. This principle has been demonstrated multiple times [[1](https://pubmed.ncbi.nlm.nih.gov/28371298/)0-[1](https://pubmed.ncbi.nlm.nih.gov/30282925/)3]. +It is likely that the overall dietary pattern matters more than PUFA, or even LA, in altering the susceptibility of LDL to oxidation. This principle has been demonstrated multiple times [[10](https://pubmed.ncbi.nlm.nih.gov/28371298/)][[11](https://pubmed.ncbi.nlm.nih.gov/17563030/)][[12](https://pubmed.ncbi.nlm.nih.gov/17887946/)][[13](https://pubmed.ncbi.nlm.nih.gov/30282925/)]. For example, in a trial by Aronis et al. (2007), diabetic subjects were placed on either a fast food diet that was formulated to be "Mediterranean diet-like" or assigned to follow their usual diet. There was also a third arm of non-diabetics placed on the Mediterranean-style fast food diet. Lag time to LDL oxidation was measured according to the same methodology as described above, with a copper sulfate solution. ![][image7] -[image7]: /blog/image7.png +[image7]: /blog/seedoils/image7.png It should be noted that the foods were specifically formulated to increase the lag time to LDL oxidation. However, what makes these results more impressive is that the fast food groups (groups A and B) were consuming twice as much PUFA than they were at baseline. Despite this we see some of the longest lag times to LDL oxidation observed in the literature in a population that has not been primed with megadoses of vitamin E for three months. @@ -94,27 +94,27 @@ A marker like oxLDL can give us a better sense of just how many oxidized LDL are For example, it may be the case that when you expose LDL particles to copper sulfate, they oxidize in under an hour. But under physiological conditions, that same oxidation could potentially take days. If the LDL are cleared from the blood before oxidation can occur, then the results of the copper sulfate test are probably not very informative. -One particularly long crossover-style RCT by Palomäki et al. (2010) compared the effects of butter to that of canola oil (CAO) on oxLDL [[1](https://pubmed.ncbi.nlm.nih.gov/21122147/)4]. Overall the butter diet resulted in higher LDL and higher oxLDL. I wasn't able to find many PUFA-SFA substitution trials that measured oxLDL beyond this one study, unfortunately. +One particularly long crossover-style RCT by Palomäki et al. (2010) compared the effects of butter to that of canola oil (CAO) on oxLDL [[14](https://pubmed.ncbi.nlm.nih.gov/21122147/)]. Overall the butter diet resulted in higher LDL and higher oxLDL. I wasn't able to find many PUFA-SFA substitution trials that measured oxLDL beyond this one study, unfortunately. ![][image8] -[image8]: /blog/image8.png +[image8]: /blog/seedoils/image8.png Again, I speculate that this is likely the result of SFA being a poor source of antioxidants. Or perhaps it's because baseline diets could have been higher in PUFA, and reducing vegetable oil intakes might just be cutting off robust sources of antioxidants and increasing LDL oxidation. There are not many studies investigating this, so it's not clear at the moment. -But, just for the sake of argument let's assume that high-PUFA diets do increase LDL oxidation relative to high-SFA diets. Would that actually be a bad thing? Perhaps not. One study by Oörni et al. (1997) has identified that oxidized LDL are less likely to be retained within the arterial intima when compared to native LDL [[1](https://pubmed.ncbi.nlm.nih.gov/9261142/)5]. If the LDL are oxidizing in the serum, perhaps this just opens up more disposal pathways for LDL and lowers its chances of getting retained in the subendothelial space to begin with. +But, just for the sake of argument let's assume that high-PUFA diets do increase LDL oxidation relative to high-SFA diets. Would that actually be a bad thing? Perhaps not. One study by Oörni et al. (1997) has identified that oxidized LDL are less likely to be retained within the arterial intima when compared to native LDL [[15](https://pubmed.ncbi.nlm.nih.gov/9261142/)]. If the LDL are oxidizing in the serum, perhaps this just opens up more disposal pathways for LDL and lowers its chances of getting retained in the subendothelial space to begin with. -Lastly, while we have established that vegetable oil consumption does appear to have an independent impact on LDL oxidation (though the effect is dwarfed by the effect of antioxidants), it is also true that oxLDL isn't actually a robust risk factor for CHD. Wu et al. (2006) discovered that the association between oxLDL and CHD does not survive adjustment for traditional risk factors like apolipoprotein (ApoB) or TC/high density lipoprotein cholesterol (HDL-C) [[1](https://pubmed.ncbi.nlm.nih.gov/16949489/)6]. +Lastly, while we have established that vegetable oil consumption does appear to have an independent impact on LDL oxidation (though the effect is dwarfed by the effect of antioxidants), it is also true that oxLDL isn't actually a robust risk factor for CHD. Wu et al. (2006) discovered that the association between oxLDL and CHD does not survive adjustment for traditional risk factors like apolipoprotein (ApoB) or TC/high density lipoprotein cholesterol (HDL-C) [[16](https://pubmed.ncbi.nlm.nih.gov/16949489/)]. ![][image9] -[image9]: /blog/image9.png +[image9]: /blog/seedoils/image9.png Essentially this means that after accounting for ApoB or TC/HDL, risk is more closely tracking ApoB or TC/HDL-C, and is not particularly likely to be tracking oxLDL at all. So even if it were the case that diets high in vegetable oils simply increased oxLDL, it wouldn't appear that it moves the needle for risk in the real world. It would also suggest that the hypothetical detriments of increasing LDL oxidation aren't significant enough to offset the LDL-lowering benefits of a high-PUFA diet. As we will discuss later in this section. -In the above study by Wu et al. (2006), the Mercodia 4E6 antibody assay was used to measure oxLDL. Some have argued that this assay is invalid due to supposedly making poor distinctions between native LDL and oxLDL [[1](https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000164264.00913.6D?related-urls=yes&legid=circulationaha%3B111%2F18%2Fe284)7]. However, if the 4E6 assay was truly making poor distinctions between oxLDL and native LDL, the two biomarkers would essentially be proxying for one another to the point of being either interchangeable or even being the same thing. In this scenario, the results of the model would suggest extreme multicollinearity as indicated by similarly (extremely) wide confidence intervals for both results. +In the above study by Wu et al. (2006), the Mercodia 4E6 antibody assay was used to measure oxLDL. Some have argued that this assay is invalid due to supposedly making poor distinctions between native LDL and oxLDL [[17](https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000164264.00913.6D?related-urls=yes&legid=circulationaha%3B111%2F18%2Fe284)]. However, if the 4E6 assay was truly making poor distinctions between oxLDL and native LDL, the two biomarkers would essentially be proxying for one another to the point of being either interchangeable or even being the same thing. In this scenario, the results of the model would suggest extreme multicollinearity as indicated by similarly (extremely) wide confidence intervals for both results. If oxLDL and native LDL were truly proxying for one another in the model in this fashion, we'd expect the confidence intervals for each relative risk to be inflated and more likely non-significant. But, there is no evidence of extreme multicollinearity in the results. Therefore, it is unlikely that the 4E6 antibody assay is actually making poor distinctions between oxLDL and native LDL. This is important to consider, because the argument for extreme multicollinearity is the primary criticism used against the 4E6 antibody assay's usefulness. But the argument doesn't actually pan out. -It is instead suggested by skeptics of the 4E6 antibody assay that measures of oxidized phospholipids, such as the E06 antibody assay, are more robust measures of oxLDL than the 4E6 antibody assay. However, the E06 antibody assay is actually more vulnerable to the exact type of confounding that has been suggested for the 4E6 antibody assay. This is explained on Mercodia's website [[1](https://www.mercodia.com/product/oxidized-ldl-elisa/#:~:text=Mercodia%20Oxidized%20LDL%20ELISA%20is,epitope%20in%20oxidized%20ApoB%2D100.&text=Substituting%20aldehydes%20can%20be%20produced,the%20generation%20of%20oxidized%20LDL)8]. +It is instead suggested by skeptics of the 4E6 antibody assay that measures of oxidized phospholipids, such as the E06 antibody assay, are more robust measures of oxLDL than the 4E6 antibody assay. However, the E06 antibody assay is actually more vulnerable to the exact type of confounding that has been suggested for the 4E6 antibody assay. This is explained on Mercodia's website [[18](https://www.mercodia.com/product/oxidized-ldl-elisa/#:~:text=Mercodia%20Oxidized%20LDL%20ELISA%20is,epitope%20in%20oxidized%20ApoB%2D100.&text=Substituting%20aldehydes%20can%20be%20produced,the%20generation%20of%20oxidized%20LDL)]. >_The proprietary mouse monoclonal antibody 4E6 is developed by professors Holvoet and Collen at the University of Leuven in Belgium. It is directed against a conformational epitope in the ApoB100 moiety of LDL that is generated as a consequence of substitution of at least 60 lysine residues of Apo B100 with aldehydes (Holvoet 2006). This number of substituted lysines corresponds to the minimal number required for scavenger-mediated uptake of oxidized LDL._ @@ -124,25 +124,25 @@ Mercodia goes on to discuss the reasons for why the E06 antibody assay could be >_Substituting aldehydes can be produced by peroxidation of lipids of LDL, resulting in the generation of oxidized LDL. However, lipid peroxidation is not required. Indeed, aldehydes that are released by endothelial cells under oxidative stress or by activated platelets may also induce the oxidative modification of Apo B100 in the absence of lipid peroxidation of LDL._ -Because lipid peroxidation of the LDL particle's phospholipid membrane is not required for an LDL particle to oxidize, a measurement of oxPL could easily mistake a minimally oxidized LDL particle as an oxLDL. For this reason, it is likely that the 4E6 antibody assay is likely to better reflect the actual number of oxLDL [[1](https://cms.mercodia.com/wp-content/uploads/2019/06/poster-oxldl-know-what-you-measure.pdf)9]. +Because lipid peroxidation of the LDL particle's phospholipid membrane is not required for an LDL particle to oxidize, a measurement of oxPL could easily mistake a minimally oxidized LDL particle as an oxLDL. For this reason, it is likely that the 4E6 antibody assay is likely to better reflect the actual number of oxLDL [[19](https://cms.mercodia.com/wp-content/uploads/2019/06/poster-oxldl-know-what-you-measure.pdf)]. -This is relevant because the immune cells that mediate the formation of atherosclerotic plaques only tend to take up maximally oxidized LDL particles, not minimally oxidized LDL particles [[2](https://pubmed.ncbi.nlm.nih.gov/6838433/)0][[2](https://pubmed.ncbi.nlm.nih.gov/24891335/)1]. Maximally oxidized LDL have to be disposed of through scavenger receptor-mediated pathways, rather than LDL receptor-mediated pathways. +This is relevant because the immune cells that mediate the formation of atherosclerotic plaques only tend to take up maximally oxidized LDL particles, not minimally oxidized LDL particles [[20](https://pubmed.ncbi.nlm.nih.gov/6838433/)][[21](https://pubmed.ncbi.nlm.nih.gov/24891335/)]. Maximally oxidized LDL have to be disposed of through scavenger receptor-mediated pathways, rather than LDL receptor-mediated pathways. ![][image10] -[image10]: /blog/image10.png +[image10]: /blog/seedoils/image10.png If minimally oxidized LDL likely contribute as little to foam cell formation as native LDL, why favour measures of minimally oxidized LDL such as the E06 antibody assay over measures of maximally oxidized LDL such as the 4E6 antibody assay? -Unfortunately, so far no studies have attempted to explore the relationship between oxLDL, as measured by the E06 antibody assay, and CHD outcomes after adjustment for total ApoB. The closest we have is a single study by Tsimikas et al. (2006) that found no correlation between oxPL/ApoB and ApoB [[2](https://pubmed.ncbi.nlm.nih.gov/16750687/)2]. +Unfortunately, so far no studies have attempted to explore the relationship between oxLDL, as measured by the E06 antibody assay, and CHD outcomes after adjustment for total ApoB. The closest we have is a single study by Tsimikas et al. (2006) that found no correlation between oxPL/ApoB and ApoB [[22](https://pubmed.ncbi.nlm.nih.gov/16750687/)]. However, if ApoB and oxPL tend to vary in tandem, the oxPL/ApoB ratio might not be expected to change very much from subject to subject. If that is the case, then we would not expect oxPL/ApoB to correlate very well at all. It would be nice to see univariable and multivariable models presented that test for independent effects of these biomarkers. -Nevertheless, if merely having more LA in your body meant that you would increase lipoprotein oxidation and thus get more CHD, we would not expect results like those of the meta-analysis conducted by Marklund et al. (2019) [[2](https://pubmed.ncbi.nlm.nih.gov/30971107/)3]. When investigated closely, the higher your tissue representation, the lower your risk of both CHD and ischemic stroke. +Nevertheless, if merely having more LA in your body meant that you would increase lipoprotein oxidation and thus get more CHD, we would not expect results like those of the meta-analysis conducted by Marklund et al. (2019) [[23](https://pubmed.ncbi.nlm.nih.gov/30971107/)]. When investigated closely, the higher your tissue representation, the lower your risk of both CHD and ischemic stroke. -It’s important to note that there was not a single statistically significant increase in risk observed in any of the included cohorts when comparing the lowest tissue LA to the highest tissue LA. One of the more interesting findings was from a regression analysis of the Scottish Heart Health Extended Cohort by Wood et al. (1984), which found a strong inverse correlation between adipose LA and CHD incidence [[2](https://pubmed.ncbi.nlm.nih.gov/6146032/)4]. +It’s important to note that there was not a single statistically significant increase in risk observed in any of the included cohorts when comparing the lowest tissue LA to the highest tissue LA. One of the more interesting findings was from a regression analysis of the Scottish Heart Health Extended Cohort by Wood et al. (1984), which found a strong inverse correlation between adipose LA and CHD incidence [[24](https://pubmed.ncbi.nlm.nih.gov/6146032/)]. ![][image11] -[image11]: /blog/image11.png +[image11]: /blog/seedoils/image11.png This certainly isn't what we would expect if the chain of causality is LA -> OxLDL -> CHD. However, as we'll discuss in the next section, this is what we'd expect if the chain of causality is SFA -> LDL -> CHD. So, let's go ahead and dive into that data next. @@ -152,29 +152,29 @@ Now that we've established that there is scant evidence validating oxLDL as a ro Let's start with the epidemiological evidence, being sure to keep the original question in mind— does substituting PUFA for SFA lower CVD rates? There have been multiple meta-analyses that have aimed to answer this question, however the application of meta-analysis methods in this context can produce some significant interpretative challenges. Let me explain why. -The relationship between SFA and CVD is nonlinear, and significantly influenced by the degree of replacement with PUFA. As such, the linear summation of prospective cohort studies can hide the nonlinear effect. For example, let's have a look at one of the most heavily-cited meta-analyses by Siri-Tarino et al. (2010), which investigated the relationship between SFA and CVD in prospective cohort studies [[2](https://pubmed.ncbi.nlm.nih.gov/20071648/)5]. +The relationship between SFA and CVD is nonlinear, and significantly influenced by the degree of replacement with PUFA. As such, the linear summation of prospective cohort studies can hide the nonlinear effect. For example, let's have a look at one of the most heavily-cited meta-analyses by Siri-Tarino et al. (2010), which investigated the relationship between SFA and CVD in prospective cohort studies [[25](https://pubmed.ncbi.nlm.nih.gov/20071648/)]. ![][image12] -[image12]: /blog/image12.png +[image12]: /blog/seedoils/image12.png As we can see, the aggregated results are null (P = 0.22). However, the I² (a measure of heterogeneity) is 41%, and no attempt was made to investigate the source of that heterogeneity. If we take the time to calculate the intake ranges of each cohort study (when possible), we can test for nonlinearity. ![][image13] -[image13]: /blog/image13.png +[image13]: /blog/seedoils/image13.png After stratifying the included studies by intake range, we see a statistically significant 30% increase in risk in subgroup one (~25±15g/day) and null results for subgroups two and three (35±15g/day and 45±15g/day, respectively). This is precisely what we'd expect to see if the risk threshold presupposed by the Dietary Guidelines was correct. McGee et al. (1984) needed to be removed for this analysis because SFA intake ranges could not be determined from the provided data. -But perhaps this is an isolated finding. There are many other meta-analyses on this subject [[2](https://pubmed.ncbi.nlm.nih.gov/27697938/)6-[2](https://pubmed.ncbi.nlm.nih.gov/19752542/)9]. Maybe the other meta-analyses on this subject would find something different? Let's find out. +But perhaps this is an isolated finding. There are many other meta-analyses on this subject [[26](https://pubmed.ncbi.nlm.nih.gov/27697938/)][[27](https://pubmed.ncbi.nlm.nih.gov/30954077/)][[28](https://pubmed.ncbi.nlm.nih.gov/32307197/)][29](https://pubmed.ncbi.nlm.nih.gov/19752542/)]. Maybe the other meta-analyses on this subject would find something different? Let's find out. ![][image14] -[image14]: /blog/image14.png +[image14]: /blog/seedoils/image14.png Applying the same methodology to all of the available meta-analyses yields the same result. This time subgroup two is representing the intake threshold presupposed by the Dietary Guidelines (~25±15g/day). We see similar increases in risk in the same subgroup across all published meta-analyses investigating the relationship between SFA and CVD (RR 1.14 [1.07-1.22], P<0.0001). You may be asking why subgroups one, three, and four are null, whereas subgroup two is not. The answer is quite simple. It's because those ranges are not crossing the threshold of effect. The range of intake represented in subgroup one exists below the threshold of effect, whereas subgroups three and four exist above the threshold of effect. As such, comparing lower intakes to higher intakes within those ranges does not show an additional increase in risk. The relationship between SFA and CVD is sigmoidal. ![][image15] -[image15]: /blog/image15.png +[image15]: /blog/seedoils/image15.png Comparing intakes that exist on either the floor or ceiling of the risk curve will typically produce null results. Only when the middle intake range is investigated is the increase in risk observable. @@ -215,10 +215,10 @@ Drag-netting the literature yielded a total of 74 studies. 20 studies were exclu **Results for Saturated Fat:** -Altogether there were 21 studies that met all of the inclusion criteria [[3](https://pubmed.ncbi.nlm.nih.gov/15668366/)0-[5](https://pubmed.ncbi.nlm.nih.gov/15668366/)0]. Cohorts were stratified across four subgroups, based on absolute grams-per-day intakes of SFA. Total pooled results across all subgroups showed a non-significant increase in risk (RR 1.07 [0.97-1.18], P=0.16). Subgroup two was the only subgroup to reach statistical significance (RR 1.24 [1.10-1.40], P=0.0005). +Altogether there were 21 studies that met all of the inclusion criteria [[30](https://doi.org/10.1161/01.atv.3.2.149)][[31](https://doi.org/10.1194/jlr.M044644)][[32](https://doi.org/10.1016/j.jacc.2006.03.001)][[33](https://doi.org/10.1161/CIRCULATIONAHA.118.038908)][[34](https://doi.org/10.3945/ajcn.115.116046)][[35](https://doi.org/10.3945/ajcn.2009.27725)][[36](https://doi.org/10.1136/bjsports-2016-096550)][[37](https://doi.org/10.1186/s12944-019-1035-2)][[38](https://doi.org/10.1016/j.clnu.2020.03.028)][[39](https://doi.org/10.1159/000229002)][[40](https://doi.org/10.1371/journal.pone.0000377)][[41](https://doi.org/10.3945/jn.112.161661)][[42](https://doi.org/10.1161/CIRCRESAHA.118.314038)][[43](https://doi.org/10.1159/000175862)][[44](https://doi.org/10.3945/ajcn.115.116046)][[45](https://doi.org/10.1093/aje/kwh193)][[46](https://doi.org/10.1136/bmj.i5796)][[47](https://doi.org/10.1136/hrt.78.5.450)][[48](https://doi.org/10.1017/S0007114517003889)][[49](https://doi.org/10.1097/HJR.0b013e3282a56c45)][[50](https://doi.org/10.1093/oxfordjournals.aje.a009047)]. Cohorts were stratified across four subgroups, based on absolute grams-per-day intakes of SFA. Total pooled results across all subgroups showed a non-significant increase in risk (RR 1.07 [0.97-1.18], P=0.16). Subgroup two was the only subgroup to reach statistical significance (RR 1.24 [1.10-1.40], P=0.0005). ![][image16] -[image16]: /blog/image16.png +[image16]: /blog/seedoils/image16.png Again, we see the exact same thing. The increase in risk occurs in the same subgroup, in the same intake range— the same intake range presupposed by the Dietary Guidelines to increase risk. @@ -227,84 +227,84 @@ Again, we see the exact same thing. The increase in risk occurs in the same subg Altogether there were 10 studies that met all of the inclusion criteria. In order to preserve the PUFA to SFA ratio, cohorts were stratified across four subgroups, based on absolute grams-per-day intakes of SFA. Total pooled results across all subgroups showed a statistically significant reduction in CVD risk (RR 0.91 [0.83-1.00], P=0.04). Subgroup two was the only subgroup to reach statistical significance (RR 0.87 [0.80-0.93], P=0.0002). ![][image17] -[image17]: /blog/image17.png +[image17]: /blog/seedoils/image17.png This second forest plot was not stratified by PUFA intake. As mentioned above, it was instead stratified by SFA intake. This way the ratio of SFA to PUFA would be better preserved. This is important for understanding the relationship between these two dietary fats. ![][image18] -[image18]: /blog/image18.png +[image18]: /blog/seedoils/image18.png Both SFA and PUFA have inverse sigmoidal relationships with CVD. The more PUFA you replace with SFA, the higher your risk. The more SFA you replace with PUFA, the lower your risk. -This is exactly the same relationship we see in the RCTs as well [[5](https://pubmed.ncbi.nlm.nih.gov/32827219/)1]. Recently, Hooper et al. (2020) published an enormous meta-analysis and meta-regression analysis for the Cochrane Collaboration, which investigated CVD-related outcomes of many PUFA-SFA substitution RCTs. +This is exactly the same relationship we see in the RCTs as well [[51](https://pubmed.ncbi.nlm.nih.gov/32827219/)]. Recently, Hooper et al. (2020) published an enormous meta-analysis and meta-regression analysis for the Cochrane Collaboration, which investigated CVD-related outcomes of many PUFA-SFA substitution RCTs. ![][image19] -[image19]: /blog/image19.png +[image19]: /blog/seedoils/image19.png Their analysis shows that substituting SFA for PUFA, and crossing the 10% of energy threshold as SFA, increases CVD risk in the aggregate. Especially for CVD events, CVD mortality, CHD mortality, and non-fatal acute myocardial infarction (AMI). Cochrane also performed multiple meta-regression analyses on the included data. Meta-regression is a tool used to investigate the relationship between two variables when they are controlled by a moderator variable. In this case, the two variables in question are SFA intakes (or PUFA-SFA substitution) and CVD. Multiple moderator variables were modeled. ![][image20] -[image20]: /blog/image20.png +[image20]: /blog/seedoils/image20.png The only statistically significant moderator variable was total cholesterol (TC) (P=0.04). This suggests that the chain of causality is SFA -> TC -> CVD. This therefore suggests that to the extent that a dietary modification reduces TC, reductions in CVD should follow. This is confirmed in their exploratory analysis later on in the paper. Additional exploratory meta-analyses by Hooper et al. (2020) also further divulge that SFA reduction lowers total CVD events (analysis 1.35), the best replacement for SFA is PUFA from vegetable oils (analysis 1.44), and the effect is likely via lowering TC (analysis 1.51). This evidence dovetails perfectly with the epidemiological evidence discussed above. -Not included in many of Cochrane's analyses were two studies that are often offered up as damning counterevidence, and often cited in support the notion that vegetable oils increase CVD risk. These two trials are the Sydney Diet Heart Study (SDHS) by Woodhill et al. (1978) and the Minnesota Coronary Experiment (MCE) by Frantz et al. (1989) [[5](https://pubmed.ncbi.nlm.nih.gov/727035/)2-[5](https://pubmed.ncbi.nlm.nih.gov/2643423/)3]. These trials were both designed such that SFA was to be replaced with PUFA in the intervention groups in the form of vegetable oil-based margarines, and PUFA was to be replaced with SFA in the control groups. +Not included in many of Cochrane's analyses were two studies that are often offered up as damning counterevidence, and often cited in support the notion that vegetable oils increase CVD risk. These two trials are the Sydney Diet Heart Study (SDHS) by Woodhill et al. (1978) and the Minnesota Coronary Experiment (MCE) by Frantz et al. (1989) [[52](https://pubmed.ncbi.nlm.nih.gov/727035/)][[53](https://pubmed.ncbi.nlm.nih.gov/2643423/)]. These trials were both designed such that SFA was to be replaced with PUFA in the intervention groups in the form of vegetable oil-based margarines, and PUFA was to be replaced with SFA in the control groups. Both trials achieved significant differences in TC during the course of both of the trials. However, the SDHS did not achieve a significant difference in the magnitude of the reduction, and the final difference in TC was only around 12mg/dL. While statistically significant, it is questionable whether or not either of these changes in TC were clinically significant. On the other hand, the MCE saw significant reductions in TC. Neither trial saw a statistically significant difference in either CVD mortality or total mortality. ![][image21] -[image21]: /blog/image21.png +[image21]: /blog/seedoils/image21.png -However, in the aggregate, there is a significant increase in CVD mortality between the two trials. This is concerning, seeing as though these two trials are often touted as the best designed trials that have been conducted in the investigation of this research question, aside from the LA Veterans Administration Hospital Study (LAVAT) by Dayton et al. (1969) [[5](https://www.ahajournals.org/doi/10.1161/01.CIR.40.1S2.II-1)4]. However, the MCE's design ended up allowing participants to enter in and exit out of the trial at their leisure, and this ended up resulting in a mean follow-up time of around 1.5 years. Which is abysmal. +However, in the aggregate, there is a significant increase in CVD mortality between the two trials. This is concerning, seeing as though these two trials are often touted as the best designed trials that have been conducted in the investigation of this research question, aside from the LA Veterans Administration Hospital Study (LAVAT) by Dayton et al. (1969) [[54](https://www.ahajournals.org/doi/10.1161/01.CIR.40.1S2.II-1)]. However, the MCE's design ended up allowing participants to enter in and exit out of the trial at their leisure, and this ended up resulting in a mean follow-up time of around 1.5 years. Which is abysmal. -It should be noted that the SDHS was a secondary prevention trial, which means that the subjects had already had a single CVD event at the time of enrollment. Given the questionable clinical relevance of the final differences in TC, it is even more ambiguous how meaningful the findings were. It has been observed that differences in SFA intake don't always change CVD outcomes in high-risk populations [[5](https://www.nature.com/articles/s41598-021-86324-w)5]. +It should be noted that the SDHS was a secondary prevention trial, which means that the subjects had already had a single CVD event at the time of enrollment. Given the questionable clinical relevance of the final differences in TC, it is even more ambiguous how meaningful the findings were. It has been observed that differences in SFA intake don't always change CVD outcomes in high-risk populations [[55](https://www.nature.com/articles/s41598-021-86324-w)]. Nevertheless, we're left wondering precisely why we didn't see the predicted effect in either of these trials. Aside from the revolving door protocol that was used in the MCE, the designs were not particularly terrible as far as large-scale RCTs go. So, why didn't we see the effect that we see in nearly every other trial of similar design and quality, as mentioned above? The answer likely lies in the types of fat-based products that were provided to the vegetable oil groups in these two trials. The vegetable oil groups were the groups that were meant to increase PUFA intake. PUFA was provided to subjects primarily in the form of corn oil (CO) based margarines. This is a problem. Margarines are typically made primarily from unsaturated fats, which are liquid at room temperature. In order to make the product solid and spreadable, the oils need to be hardened. There are essentially two standard ways to achieve this effect. -First, we can harden oils through hydrogenation or through emulsification. However, non-hydrogenated margarines were not commonplace on the market prior to the 1970s [[5](https://www.soyinfocenter.com/HSS/margarine2.php)6]. Both the SDHS and the MCE were conducted during the 1960s. At the time, hydrogenation was the preferred method to harden margarines. However, this has the secondary effect of generating trans fatty acids (TFA). +First, we can harden oils through hydrogenation or through emulsification. However, non-hydrogenated margarines were not commonplace on the market prior to the 1970s [[56](https://www.soyinfocenter.com/HSS/margarine2.php)]. Both the SDHS and the MCE were conducted during the 1960s. At the time, hydrogenation was the preferred method to harden margarines. However, this has the secondary effect of generating trans fatty acids (TFA). -TFAs are associated with an increased risk of many diseases, including CVD. However, TFAs are the only known fatty acid subtypes that have been associated with increased CVD mortality when replacing SFA on a population-level [[5](https://pubmed.ncbi.nlm.nih.gov/30636521/)7]. +TFAs are associated with an increased risk of many diseases, including CVD. However, TFAs are the only known fatty acid subtypes that have been associated with increased CVD mortality when replacing SFA on a population-level [[57](https://pubmed.ncbi.nlm.nih.gov/30636521/)]. ![][image22] -[image22]: /blog/image22.png +[image22]: /blog/seedoils/image22.png -Basically, TFAs are fucking dangerous— more dangerous than SFA. The CO-based margarine used in the SDHS was "Miracle" brand margarine [[5](https://pubmed.ncbi.nlm.nih.gov/23386268/)8]. According to Dr. Robert Grenfell of the National Cardiovascular Health Director at the Australian Heart Foundation and the Deputy Chairman of the Sydney University Nutrition Research Foundation, Bill Shrapnel, Miracle brand margarine was up to 15% TFA at the time the study was conducted [[5](https://www.ausfoodnews.com.au/2013/02/11/heart-foundation-takes-swipe-at-butter-and-new-study-on-margarine.html)9]. +Basically, TFAs are fucking dangerous— more dangerous than SFA. The CO-based margarine used in the SDHS was "Miracle" brand margarine [[58](https://pubmed.ncbi.nlm.nih.gov/23386268/)]. According to Dr. Robert Grenfell of the National Cardiovascular Health Director at the Australian Heart Foundation and the Deputy Chairman of the Sydney University Nutrition Research Foundation, Bill Shrapnel, Miracle brand margarine was up to 15% TFA at the time the study was conducted [[59](https://www.ausfoodnews.com.au/2013/02/11/heart-foundation-takes-swipe-at-butter-and-new-study-on-margarine.html)]. >_When this study began, Miracle margarine contained approximately 15 per cent trans fatty acids, which have the worst effect on heart disease risk of any fat. The adverse effect of the intervention in this study was almost certainly due to the increase in trans fatty acids in the diet_ If Woodhill et al. (1978) truly fed the subjects in the vegetable oil group (group F) as much of that margarine as they seem to be claiming to in their publication, that could be around 5.7g/day of TFA. ![][image23] -[image23]: /blog/image23.png +[image23]: /blog/seedoils/image23.png The margarine used in the MCE was likely to be Fleischmann's Original, due to the availability and popularity at the time of the intervention. As well as the fact that the product was developed in direct response to pro-PUFA research that was being conducted at the time. ![][image24] -[image24]: /blog/image24.png +[image24]: /blog/seedoils/image24.png -The only other two margarines that were potentially available in the region at the time the MCE was conducted were Imperial margarine and Mazola margarine. Some Imperial products remained high in TFA until very recently [[6](https://abcnews.go.com/Business/story?id=8182555&page=1)0]. Mazola was pretty much the only non-hydrogenated margarine on the market at the time. +The only other two margarines that were potentially available in the region at the time the MCE was conducted were Imperial margarine and Mazola margarine. Some Imperial products remained high in TFA until very recently [[60](https://abcnews.go.com/Business/story?id=8182555&page=1)]. Mazola was pretty much the only non-hydrogenated margarine on the market at the time. ![][image25] -[image25]: /blog/image25.png +[image25]: /blog/seedoils/image25.png -The answer to the question of which margarine was used in the MCE is anybody's guess at this point. But if I were generous, I'd say that based on the margarines that were available (and most likely to be used) at the time the MCE was conducted, there is roughly a 67% chance that the trial was potentially confounded by TFA in the vegetable oil diet. Though Ramsden et al. (2016) remain skeptical that confounding such as this was likely [[6](https://pubmed.ncbi.nlm.nih.gov/27071971/)1]. +The answer to the question of which margarine was used in the MCE is anybody's guess at this point. But if I were generous, I'd say that based on the margarines that were available (and most likely to be used) at the time the MCE was conducted, there is roughly a 67% chance that the trial was potentially confounded by TFA in the vegetable oil diet. Though Ramsden et al. (2016) remain skeptical that confounding such as this was likely [[61](https://pubmed.ncbi.nlm.nih.gov/27071971/)]. However, even if the MCE was not confounded by TFA, we would still have a good reason to exclude it from consideration. Like I mentioned earlier, the trial was designed in such a way that the participants had the liberty to enter and exit the trial at their leisure. In the aggregate, there was only a 12-18 month follow-up time. As such, the trial has significantly less power than all other trials that investigated this particular sort of dietary substitution. Ramsden et al. have argued at length that the control group was likely confounded by TFA to a greater degree than the vegetable oil group. In their view, this could indicate that LA is actually worse for you than TFA. Essentially they claim that vegetable shortening was added to the control group in order to boost the SFA content of the diet, and because vegetable shortening is hydrogenated, it must have contained a large amount of TFA. This is dubious. -Fully hydrogenated oils contain very little TFA [[6](https://pubmed.ncbi.nlm.nih.gov/26048727/)2]. However, partially hydrogenated oils such as most soft margarines of the period contain high levels of TFA. Here is a selection of SOs taken from the USDA's SR28 Nutrient Database [[6](https://www.ars.usda.gov/northeast-area/beltsville-md-bhnrc/beltsville-human-nutrition-research-center/methods-and-application-of-food-composition-laboratory/mafcl-site-pages/sr11-sr28/)3]. +Fully hydrogenated oils contain very little TFA [[62](https://pubmed.ncbi.nlm.nih.gov/26048727/)]. However, partially hydrogenated oils such as most soft margarines of the period contain high levels of TFA. Here is a selection of SOs taken from the USDA's SR28 Nutrient Database [[63](https://www.ars.usda.gov/northeast-area/beltsville-md-bhnrc/beltsville-human-nutrition-research-center/methods-and-application-of-food-composition-laboratory/mafcl-site-pages/sr11-sr28/)]. ![][image26] -[image26]: /blog/image26.png +[image26]: /blog/seedoils/image26.png As you can see, a tablespoon of partially hydrogenated SO margarine contains 2200% more TFA than a tablespoon of fully hydrogenated SO shortening. @@ -314,14 +314,14 @@ Ramsden et al. (2016) also acknowledge that the vegetable oil group's diet used Given that we can soundly infer that the SDHS study was confounded by TFA, and the MCE was likely to be confounded by TFA, the results of these trials start to make a lot more sense. The effect sizes, and the direction of effect, mirror what we see in epidemiological research, as well. When TFA replaces SFA, risk goes up. When PUFA replaces SFA, risk goes down. If it is still to be maintained by skeptics that vegetable oils increase the risk of CVD, rather than lowering it, they must satisfy the burden of proof with extraordinary evidence. -I would surely be remiss if I did not briefly acknowledge one trial that was left out of the analysis by Hooper et al. (2020), which was the Lyon Diet Heart Study [[6](https://pubmed.ncbi.nlm.nih.gov/7911176/)4]. The reason this trial is noteworthy is due to it being the only experimental investigation of the diet-heart hypothesis that actually made an effort to reduce LA alongside SFA. The trial also saw one of the largest reductions in CVD risk ever recorded in this body of literature, with a massive 73% reduction in CVD risk over four years. Skeptics of vegetable oils would like to attribute this effect to the lowering of LA in the diet, but is there any merit to this? +I would surely be remiss if I did not briefly acknowledge one trial that was left out of the analysis by Hooper et al. (2020), which was the Lyon Diet Heart Study [[64](https://pubmed.ncbi.nlm.nih.gov/7911176/)]. The reason this trial is noteworthy is due to it being the only experimental investigation of the diet-heart hypothesis that actually made an effort to reduce LA alongside SFA. The trial also saw one of the largest reductions in CVD risk ever recorded in this body of literature, with a massive 73% reduction in CVD risk over four years. Skeptics of vegetable oils would like to attribute this effect to the lowering of LA in the diet, but is there any merit to this? -The trial did achieve statistically significant differences in LA intake between groups, with 5.3% of energy as LA in the control group and only 3.6% of energy as LA in the intervention group [[6](https://pubmed.ncbi.nlm.nih.gov/9989963/)5]. However, if we calculate the absolute intakes of LA for both groups using each group’s total daily calories, we discover that the absolute differences in LA intake between groups amounted to about 4.5g/day— equal to approximately 1.5 teaspoons of SO. In the most clinical, scientific vernacular, this would be referred to as sweet fuck all. +The trial did achieve statistically significant differences in LA intake between groups, with 5.3% of energy as LA in the control group and only 3.6% of energy as LA in the intervention group [[65](https://pubmed.ncbi.nlm.nih.gov/9989963/)]. However, if we calculate the absolute intakes of LA for both groups using each group’s total daily calories, we discover that the absolute differences in LA intake between groups amounted to about 4.5g/day— equal to approximately 1.5 teaspoons of SO. In the most clinical, scientific vernacular, this would be referred to as sweet fuck all. So, why did the trial see such a massive reduction in risk? Likely because, as far as multifactorial interventions go, this trial did its best to knock the ball out of the park. Just take a look at the diets. ![][image27] -[image27]: /blog/image27.png +[image27]: /blog/seedoils/image27.png Firstly, the groups achieved a difference of 10g/day in SFA and the between-group differences in SFA cross the 25g/day threshold that we discussed earlier. Secondly, the intervention group was consuming significantly fewer foods that are positively associated with CVD, such as whole meat, processed meat, and butter. Lastly, the intervention group was consuming significantly higher amounts of fruit and vegetables (considered together), as well as unsaturated fats, which are strongly inversely associated with CVD. @@ -331,14 +331,14 @@ Lastly, the relationship between LA and CVD has been investigated using Mendelia The study methods of MR also assume that genes are randomly distributed in the population, and this should significantly mitigate the potential for certain types of confounding like the healthy-user bias (HUB). It is generally accepted that this methodology offers superior internal validity for these sorts of research questions than typical methods used in the field of epidemiology. It's essentially giving you the best idea of the magnitude of the effect, independent of confounding, that is achievable without lifelong RCTs. -Even though MR data doesn't really need to be mentioned, because we have actual RCT data on this subject. However, it's worthwhile to add it in here just to hammer home how utterly consistent this evidence actually is. This time the data is being sourced from the UK Biobank, which is a massive prospective cohort study that also leverages a repository of biological samples from over 500,000 subjects [[6](https://pubmed.ncbi.nlm.nih.gov/33924952/)6]. +Even though MR data doesn't really need to be mentioned, because we have actual RCT data on this subject. However, it's worthwhile to add it in here just to hammer home how utterly consistent this evidence actually is. This time the data is being sourced from the UK Biobank, which is a massive prospective cohort study that also leverages a repository of biological samples from over 500,000 subjects [[66](https://pubmed.ncbi.nlm.nih.gov/33924952/)]. ![][image28] -[image28]: /blog/image28.png +[image28]: /blog/seedoils/image28.png Here we see that Park et al. (2021) observed the same relationship yet again. Genetically elevated serum LA was inversely associated with AMI, whereas genetically elevated serum AA was positively associated with AMI. The gene variants that were investigated were related to the function of fatty acid desaturase (FADS) enzymes. -It would seem that those who are less able to convert LA to AA have a decreased risk of AMD, whereas those who are more able to convert LA to AA have an increased risk. Considering the fact that AA conversion is highly regulated, as well as the fact that dietary LA is virtually unavoidable, it seems unlikely that modulating dietary LA would be a reliable way to modulate the conversion of LA into AA [[6](https://pubmed.ncbi.nlm.nih.gov/21663641/)7]. On balance, these findings support increasing dietary LA for CVD prevention. +It would seem that those who are less able to convert LA to AA have a decreased risk of AMD, whereas those who are more able to convert LA to AA have an increased risk. Considering the fact that AA conversion is highly regulated, as well as the fact that dietary LA is virtually unavoidable, it seems unlikely that modulating dietary LA would be a reliable way to modulate the conversion of LA into AA [[67](https://pubmed.ncbi.nlm.nih.gov/21663641/)]. On balance, these findings support increasing dietary LA for CVD prevention. Overall, the available evidence overwhelmingly favours the inclusion of vegetable oils in the diet, especially if consumed to the exclusion of SFA, for reducing CVD risk. The evidence that would need to be bought forward to topple this paradigm would need to be truly extraordinary. @@ -346,7 +346,7 @@ Overall, the available evidence overwhelmingly favours the inclusion of vegetabl ###### **TOTAL CANCER** -The data most often cited in support of the notion that vegetable oils increase the risk of cancer comes from a post-hoc analysis of the aforementioned study, the LAVAT, by Pearce et al. (1971) [[6](https://pubmed.ncbi.nlm.nih.gov/4100347/)8]. This is likely because this is some of the only randomized controlled trial (RCT) data that actually shows this increase in risk [[6](https://pubmed.ncbi.nlm.nih.gov/21090384/)9]. As we will discuss, this is quite easy to cherry-pick. +The data most often cited in support of the notion that vegetable oils increase the risk of cancer comes from a post-hoc analysis of the aforementioned study, the LAVAT, by Pearce et al. (1971) [[68](https://pubmed.ncbi.nlm.nih.gov/4100347/)]. This is likely because this is some of the only randomized controlled trial (RCT) data that actually shows this increase in risk [[69](https://pubmed.ncbi.nlm.nih.gov/21090384/)]. As we will discuss, this is quite easy to cherry-pick. The LAVAT was a double-blind RCT was first reported on by Dayton et al. (1969), and aimed to investigate the effects of substituting vegetable oils for animal fat on the risk of CVD. However, cancer was among their secondary endpoints. The researchers actually took enormous care to ensure that the substitution of vegetable oil for animal fat was the only substitution the subjects were making. Even going so far as providing ice cream made out of vegetable oils rather than dairy fat. @@ -355,7 +355,7 @@ It's important to preface this discussion with an acknowledgment that the trial Essentially, the concern that increasing vegetable oils in the diet increases cancer risk originates from the following figure. Figure 1 from the original analysis by Pearce at al (1971) clearly shows that the cumulative deaths due to carcinoma rise faster in the vegetable oil group than in the control group after around two years into the study. ![][image29] -[image29]: /blog/image29.png +[image29]: /blog/seedoils/image29.png I must admit that the graph looks pretty scary, and narratives surrounding the findings of this study had me convinced for a while too. However, this graph is incredibly misleading when taken out of context. @@ -372,92 +372,92 @@ This basically means that the excess cancer deaths seen in the vegetable oil gro Pearce et al. also included a table that stratifies cancer outcomes by the degree of adherence per group. ![][image30] -[image30]: /blog/image30.png +[image30]: /blog/seedoils/image30.png As mentioned above, the vegetable oil group had significantly more low adherers. As we can see, about 33% of the excess cancer was occurring among low adherers in the vegetable oil group. Let's see what happens when we not only remove the low adherer subgroup, but also compare the between-group difference in carcinoma risk among the highest adherers. ![][image31] -[image31]: /blog/image31.png +[image31]: /blog/seedoils/image31.png Removing the low adherers nullifies the effect of the vegetable oil diet on cancer outcomes. There are also other plausible explanations for the effect as well. For example, the vegetable oil group contained many more moderate smokers than the animal fat group. Moderate smokers were defined as those smoking 0.5-1 packs of cigarettes per day. As you can see, observed cancer among moderate smokers was 3x higher in the vegetable oil group, and this is where all the excess cancer risk is accumulating. ![][image32] -[image32]: /blog/image32.png +[image32]: /blog/seedoils/image32.png -This means that low adherers in the vegetable oil group were likely to be smokers, and the smokers were likely to get more cancer. As we would expect [[7](https://pubmed.ncbi.nlm.nih.gov/22943444/)0]. +This means that low adherers in the vegetable oil group were likely to be smokers, and the smokers were likely to get more cancer. As we would expect [[70](https://pubmed.ncbi.nlm.nih.gov/22943444/)]. To suggest that the results of the LAVAT demonstrate a higher cancer risk for those consuming vegetable oils is just to misunderstand or misrepresent the data that Pearce et al. reported. The study did not actually divulge an independent effect of vegetable oil intake on cancer mortality. In fact, if we only look at high adherers, there are no statistically significant differences in cancer. ![][image33] -[image33]: /blog/image33.png +[image33]: /blog/seedoils/image33.png As the authors reported, if the increase in cancer risk was actually a consequence of the vegetable oil diet, we would see more cancer risk among higher adherers. But we don't. We see no statistically significant differences. Overall, there is insufficient evidence to declare higher vegetable oil intakes to be an independent risk factor for cancer. The available data suggests that, at worst, higher vegetable oil intakes likely have a neutral effect compared to high animal fat intakes. But, the LAVAT was not the only trial to report cancer as a secondary endpoint. Three other trials that substituted vegetable oils for SFA also reported cancer outcomes. ![][image34] -[image34]: /blog/image34.png +[image34]: /blog/seedoils/image34.png When considering all of the studies in the aggregate (subgroup 2.1.1), we see that the effect of substituting vegetable oils for SFA on cancer is null. But, the LAVAT is still boasting its (dubiously) large effect size. When we remove the moderate smokers, the increased risk is nullified (subgroup 2.1.2). However, further excluding all regular smokers pushes the aggregated results to a non-significant decrease in cancer risk with substituting vegetable oils for SFA (subgroup 2.1.3). -The direction of effect that we see is actually consistent with the wider epidemiology investigating the relationship between LA biomarkers and cancer mortality. Here we see a strong inverse association between tissue LA representation and cancer risk overall [[7](https://pubmed.ncbi.nlm.nih.gov/32020162/)1]. +The direction of effect that we see is actually consistent with the wider epidemiology investigating the relationship between LA biomarkers and cancer mortality. Here we see a strong inverse association between tissue LA representation and cancer risk overall [[71](https://pubmed.ncbi.nlm.nih.gov/32020162/)]. ![][image35] -[image35]: /blog/image35.png +[image35]: /blog/seedoils/image35.png However, this is total cancer. There is still some controversy surrounding whether or not vegetable oils may increase the risk of other cancers. So, let's dive into that literature next. ###### **SKIN CANCER** -There is a meta-analysis by Ruan et al. (2020) investigating the limited epidemiological research on the subject. The results suggest that higher intakes of PUFA could also increase the risk of skin cancer in prospective cohort studies [[7](https://pubmed.ncbi.nlm.nih.gov/31298947/)2]. However, if we take a look at the author's data, we have some troubling findings. +There is a meta-analysis by Ruan et al. (2020) investigating the limited epidemiological research on the subject. The results suggest that higher intakes of PUFA could also increase the risk of skin cancer in prospective cohort studies [[72](https://pubmed.ncbi.nlm.nih.gov/31298947/)]. However, if we take a look at the author's data, we have some troubling findings. ![][image36] -[image36]: /blog/image36.png +[image36]: /blog/seedoils/image36.png -Increasing PUFA intake seems to increase the risk of squamous cell carcinoma (SCC). However, a single study by Park et al. (2018) is contributing 92.6% of the weight [[7](https://pubmed.ncbi.nlm.nih.gov/29636341/)3]. +Increasing PUFA intake seems to increase the risk of squamous cell carcinoma (SCC). However, a single study by Park et al. (2018) is contributing 92.6% of the weight [[73](https://pubmed.ncbi.nlm.nih.gov/29636341/)]. ![][image37] -[image37]: /blog/image37.png +[image37]: /blog/seedoils/image37.png -This could be due to the fact that the study's adjustment model lacked several important covariates that may have plausibly changed the association. For example, the multivariate adjustment model adjusted for hair colour rather than skin tone. This is problematic because hair colour does not sufficiently capture the differential effects of skin tone on skin cancer [[7](https://pubmed.ncbi.nlm.nih.gov/23107311/)4]. +This could be due to the fact that the study's adjustment model lacked several important covariates that may have plausibly changed the association. For example, the multivariate adjustment model adjusted for hair colour rather than skin tone. This is problematic because hair colour does not sufficiently capture the differential effects of skin tone on skin cancer [[74](https://pubmed.ncbi.nlm.nih.gov/23107311/)]. ![][image38] -[image38]: /blog/image38.png +[image38]: /blog/seedoils/image38.png -In at least one of the included prospective cohort studies by Ibiebele et al. (2009) that investigated the relationship between LA and skin cancer included adjustments for skin colour, and their results were null [[7](https://pubmed.ncbi.nlm.nih.gov/19462452/)5]. This further casts doubt on the veracity of the findings reported by Park et al. (2018). +In at least one of the included prospective cohort studies by Ibiebele et al. (2009) that investigated the relationship between LA and skin cancer included adjustments for skin colour, and their results were null [[75](https://pubmed.ncbi.nlm.nih.gov/19462452/)]. This further casts doubt on the veracity of the findings reported by Park et al. (2018). -In fact, when tissue representation of LA was investigated by Wallingford et al. (2013) in a separate cohort study, non-significant reduction in the risk of basal cell carcinoma (BCC) can be observed [[7](https://pubmed.ncbi.nlm.nih.gov/23885039/)6]. Additionally, among those with previous skin cancers, higher tissue representation of LA was associated with a statistically significant decrease in risk of re-occurrence (RR 0.54 [0.35-0.82]) A very odd finding if having more LA inside your body is supposed to predispose you to developing skin cancer. +In fact, when tissue representation of LA was investigated by Wallingford et al. (2013) in a separate cohort study, non-significant reduction in the risk of basal cell carcinoma (BCC) can be observed [[76](https://pubmed.ncbi.nlm.nih.gov/23885039/)]. Additionally, among those with previous skin cancers, higher tissue representation of LA was associated with a statistically significant decrease in risk of re-occurrence (RR 0.54 [0.35-0.82]) A very odd finding if having more LA inside your body is supposed to predispose you to developing skin cancer. -There is also one study by Harris et al. (2005) that investigates the relationship between red blood cell cis-LA content and squamous cell carcinoma [[7](https://pubmed.ncbi.nlm.nih.gov/15824162/)7]. While it is a case-control study and lacks the temporal component that is necessary to establish causality, it is some of the only human outcome data we have on the subject, and the results are null. +There is also one study by Harris et al. (2005) that investigates the relationship between red blood cell cis-LA content and squamous cell carcinoma [[77](https://pubmed.ncbi.nlm.nih.gov/15824162/)]. While it is a case-control study and lacks the temporal component that is necessary to establish causality, it is some of the only human outcome data we have on the subject, and the results are null. ![][image39] -[image39]: /blog/image39.png +[image39]: /blog/seedoils/image39.png If one still believes that higher intakes of LA increases the risk of skin cancer, I have a treat for them. Do you remember the LAVAT we mentioned in the cancer section? It turns out that skin cancer was actually one of their secondary endpoints. ![][image40] -[image40]: /blog/image40.png +[image40]: /blog/seedoils/image40.png In table II from the post-hoc analysis by Pearce et al. (1971), we see that in the vegetable oil group, there were ten cases of skin cancer, whereas in the animal fat group there were 21. This produces a statistically significant increase in skin cancer risk for the animal fat group, whether or not we exclude or include the post-diet period (RR: 2.11 [1.01-4.43] and 2.09 [1.07-4.11], respectively). ![][image41] -[image41]: /blog/image41.png +[image41]: /blog/seedoils/image41.png As we discussed earlier, there were no statistically significant differences in cancer risk among heavy smokers, of which there were only two cases in the animal fat group. However, there was a non-significant increase in cancer risk among moderate smokers, of which there were 19 cases in the vegetable oil group. This suggests that the increase in skin cancer seen in the animal fat group is not due to heavy smoking, as there were only two cases of cancer among heavy smokers in the animal fat group, and we have 21 cases of skin cancer. The vegetable oil group had lower rates of skin cancer despite the fact that there were more moderate smokers, and more cancer risk among moderate smokers, in the vegetable oil group. This increase in risk seen in the animal fat group can't be explained by differences in smoking habits. -Additionally, the methods of MR have also been used by Seviiri et al. (2021) to investigate the relationship between elevated plasma LA and skin cancer [[7](https://pubmed.ncbi.nlm.nih.gov/34088753/)8]. Data was collected for two different keratinocyte cancers, which were BCC and SCC, and the results are consistent with those found in the LAVAT. +Additionally, the methods of MR have also been used by Seviiri et al. (2021) to investigate the relationship between elevated plasma LA and skin cancer [[78](https://pubmed.ncbi.nlm.nih.gov/34088753/)]. Data was collected for two different keratinocyte cancers, which were BCC and SCC, and the results are consistent with those found in the LAVAT. ![][image42] -[image42]: /blog/image42.png +[image42]: /blog/seedoils/image42.png -There was a statistically significant 6% reduction in BCC risk with genetically elevated plasma LA, whereas AA showed a statistically significant 4% increase in risk. Oddly, the effect size of eicosapentaenoic acid (EPA) was actually larger than that of AA, which would seem to be at odds with the RCT data on the subject [[7](https://pubmed.ncbi.nlm.nih.gov/24265065/)9]. +There was a statistically significant 6% reduction in BCC risk with genetically elevated plasma LA, whereas AA showed a statistically significant 4% increase in risk. Oddly, the effect size of eicosapentaenoic acid (EPA) was actually larger than that of AA, which would seem to be at odds with the RCT data on the subject [[79](https://pubmed.ncbi.nlm.nih.gov/24265065/)]. ![][image43] -[image43]: /blog/image43.png +[image43]: /blog/seedoils/image43.png For SCC, the only statistically significant relationship between genetically elevated plasma PUFA was a 4% increased risk with plasma AA. The results for all other PUFA were null. @@ -467,19 +467,19 @@ In conclusion, it is true that there are some cohort studies suggesting that hig ###### **2-ARACHIDONOYLGLYCEROL** -The notion that vegetable oils are responsible for the obesity epidemic is extremely pervasive across a wide variety of niche diet communities. The hypothesis that dietary LA increases hunger through the passive production of an endocannabinoid known as 2-arachidonoylglycerol (2-AG) has been articulated by Watkins et al. (2015) [[8](https://pubmed.ncbi.nlm.nih.gov/25610411/)0]. They suggest that this endocannabinoid interacts with cannabinoid receptor type 1 (CB1) and facilitates obesity by stimulating appetite. Essentially, vegetable oils supposedly give us "the munchies" similarly to marijuana, as the story goes. But, does this mechanism actually work? +The notion that vegetable oils are responsible for the obesity epidemic is extremely pervasive across a wide variety of niche diet communities. The hypothesis that dietary LA increases hunger through the passive production of an endocannabinoid known as 2-arachidonoylglycerol (2-AG) has been articulated by Watkins et al. (2015) [[80](https://pubmed.ncbi.nlm.nih.gov/25610411/)]. They suggest that this endocannabinoid interacts with cannabinoid receptor type 1 (CB1) and facilitates obesity by stimulating appetite. Essentially, vegetable oils supposedly give us "the munchies" similarly to marijuana, as the story goes. But, does this mechanism actually work? -Indeed, this mechanism does appear to work— in mice [[8](https://pubmed.ncbi.nlm.nih.gov/22334255/)1]. In this study by Alvheim et al. (2012), mice were fed two different diets with varying fatty acid compositions. Essentially, mice were randomized to two diets that contained either moderate fat (35% of energy) or high fat (60% of energy). Within each diet group there were three distinct diet conditions. One of the diet conditions was low in LA (1% of energy), and the two remaining diet conditions were "high" in LA (8% of energy), with one of which also being supplemented with long-chain omega-3s. +Indeed, this mechanism does appear to work— in mice [[81](https://pubmed.ncbi.nlm.nih.gov/22334255/)]. In this study by Alvheim et al. (2012), mice were fed two different diets with varying fatty acid compositions. Essentially, mice were randomized to two diets that contained either moderate fat (35% of energy) or high fat (60% of energy). Within each diet group there were three distinct diet conditions. One of the diet conditions was low in LA (1% of energy), and the two remaining diet conditions were "high" in LA (8% of energy), with one of which also being supplemented with long-chain omega-3s. ![][image44] -[image44]: /blog/image44.png +[image44]: /blog/seedoils/image44.png By the end of the study, the mice receiving 8% of their energy from LA had consistently higher body weight, with a slightly mitigating effect of supplemented omega-3s in the mice fed a high-fat diet (chart e). The increases in body weight in the mice that were fed high-LA diets was commensurate with increases in 2-AG. Ergo, consuming a high-LA diet will increase 2-AG and facilitate obesity— in mice. But what about humans? -A study by Blüher et al. (2006) involving 60 subjects explored the correlation between body fatness and a number of markers related to the endocannabinoid system. There ended up being significant correlations between circulating 2-AG and obesity [[8](https://pubmed.ncbi.nlm.nih.gov/17065342/)2]. +A study by Blüher et al. (2006) involving 60 subjects explored the correlation between body fatness and a number of markers related to the endocannabinoid system. There ended up being significant correlations between circulating 2-AG and obesity [[82](https://pubmed.ncbi.nlm.nih.gov/17065342/)]. ![][image45] -[image45]: /blog/image45.png +[image45]: /blog/seedoils/image45.png However, there is an issue. Unlike mice, circulating levels of the 2-AG precursor, ARA, did not differ between lean and obese subjects. For this reason, the authors go on to express skepticism toward the hypothesis that 2-AG synthesis is driven passively by the supply of precursors in humans. Instead, they point out that there is more evidence that obesity itself acts to inhibit the degradation of 2-AG. @@ -487,30 +487,30 @@ However, there is an issue. Unlike mice, circulating levels of the 2-AG precurso > >_Thus, decreased endocannabinoid degradation must be considered as a second possibility. Given the overwhelming mass of adipose tissue compared with other organs, a contribution of adipocytes to endocannabinoid inactivation, which may be disturbed in visceral obese subjects, is an attractive hypothesis._ -This would not be surprising, considering that the impaired clearance and/or degradation of metabolic substrates is a well-characterized phenomenon in human obesity. Not only that, but there is also a large body of research divulging that the production of 2-AG from its precursors is regulated, not passive [[8](https://pubmed.ncbi.nlm.nih.gov/14595399/)3]. +This would not be surprising, considering that the impaired clearance and/or degradation of metabolic substrates is a well-characterized phenomenon in human obesity. Not only that, but there is also a large body of research divulging that the production of 2-AG from its precursors is regulated, not passive [[83](https://pubmed.ncbi.nlm.nih.gov/14595399/)]. -While somewhat tangential to the point, it is interesting to note that we have tested the effects of selective CB1-antagonism in humans with a pharmaceutical called Rimonabant [[8](https://pubmed.ncbi.nlm.nih.gov/17054276/)4]. Overall, this drug does appear to reduce energy intake and result in weight loss that is equal to just over a quarter-pound per week. +While somewhat tangential to the point, it is interesting to note that we have tested the effects of selective CB1-antagonism in humans with a pharmaceutical called Rimonabant [[84](https://pubmed.ncbi.nlm.nih.gov/17054276/)]. Overall, this drug does appear to reduce energy intake and result in weight loss that is equal to just over a quarter-pound per week. ![][image46] -[image46]: /blog/image46.png +[image46]: /blog/seedoils/image46.png The reason this is tangential is because CB-antagonists such as Rimonabant are not specifically targeting LA metabolism. All this research tells us is that the endocannabinoid system is involved with the regulation of body weight in humans, but it does not tell us what independent contributions are being made by 2-AG, or even dietary LA for that matter. ###### **ENERGY INTAKE** -If we wish to explore the effects of dietary LA on appetite, there have been a number of short-term fatty acid substitution trials investigating this question. One trial by Naughton et al. (2018) showed an effect of LA on hunger hormones, and a non-significant reduction in prospective energy intake compared to control and high-oleate diets [[8](https://www.ncbi.nlm.nih.gov/pubmed/30261617)5]. However, the authors spuriously claim that there was no effect of the high-LA diet in reducing prospective energy intake. This is an example of the interaction fallacy, because there was actually non-inferiority between the high-LA diet and the other diet conditions. +If we wish to explore the effects of dietary LA on appetite, there have been a number of short-term fatty acid substitution trials investigating this question. One trial by Naughton et al. (2018) showed an effect of LA on hunger hormones, and a non-significant reduction in prospective energy intake compared to control and high-oleate diets [[85](https://www.ncbi.nlm.nih.gov/pubmed/30261617)]. However, the authors spuriously claim that there was no effect of the high-LA diet in reducing prospective energy intake. This is an example of the interaction fallacy, because there was actually non-inferiority between the high-LA diet and the other diet conditions. -Of the trials that actually reported ad libitum energy intake in response to diets of varying fatty acid composition, no consistent effects are observed [[8](https://www.ncbi.nlm.nih.gov/pubmed/14694208)6-[9](https://pubmed.ncbi.nlm.nih.gov/28760423/)1]. All together, the short-term evidence is largely a wash. In fact, this was remarked upon by Strik et al. (2010) in table 4 of one such publication, and they included the aggregated findings across a number of different trials investigating the relationship between fatty acid saturation, satiety, and energy intake [[9](https://pubmed.ncbi.nlm.nih.gov/20492735/)2]. Overall, when there was an effect of LA, it tended to decrease energy intake. +Of the trials that actually reported ad libitum energy intake in response to diets of varying fatty acid composition, no consistent effects are observed [[86](https://www.ncbi.nlm.nih.gov/pubmed/14694208)][[87](https://pubmed.ncbi.nlm.nih.gov/26331956/)][[88](https://pubmed.ncbi.nlm.nih.gov/10953671/)][[89](https://pubmed.ncbi.nlm.nih.gov/11040181/)][[90](https://pubmed.ncbi.nlm.nih.gov/23328113/)][[91](https://pubmed.ncbi.nlm.nih.gov/28760423/)]. All together, the short-term evidence is largely a wash. In fact, this was remarked upon by Strik et al. (2010) in table 4 of one such publication, and they included the aggregated findings across a number of different trials investigating the relationship between fatty acid saturation, satiety, and energy intake [[92](https://pubmed.ncbi.nlm.nih.gov/20492735/)]. Overall, when there was an effect of LA, it tended to decrease energy intake. ![][image47] -[image47]: /blog/image47.png +[image47]: /blog/seedoils/image47.png In one particularly well-done trial by Strik et al., participants in the three groups were given unlimited access to muffins made using either SFA, MUFA, or PUFA. They would consume these muffins ad libitum one variety at a time, with a washout period between different muffin types. By the end, all three groups experienced all three muffin types. Each time researchers collected subjective data on satiety and the general satisfaction of the food experience. No differences in any parameters reached statistical significance. ![][image48] -[image48]: /blog/image48.png +[image48]: /blog/seedoils/image48.png There were no statistically significant differences in hunger, fullness, satisfaction, or prospective consumption (how much more subjects suspected they could eat at that moment). It appeared as though SFA trended toward a decrease in fullness, perhaps. There were also no observed differences in ad libitum energy intake. @@ -523,51 +523,51 @@ I have also heard it proposed that in order to study this effect, researchers ma This difference in LA intake produced an enormous increase in adipose LA in the vegetable oil group. It's probably safe to say that these people reached a maximal saturation point, as evidenced by the hyperbolic curve in adipose LA representation over time. ![][image49] -[image49]: /blog/image49.png +[image49]: /blog/seedoils/image49.png -The median LA representation in adipose tissue increased from around 8-11% of total fatty acids to over 30% of total fatty acids across the eight year study. The baseline levels are consistent with levels found in traditional populations like the Tsimane, Inuit, and the Navajo aboriginals [[9](https://pubmed.ncbi.nlm.nih.gov/22624983/)3-[9](https://onlinelibrary.wiley.com/doi/10.1002/cphy.cp050117)5]. While the data published by Martin et al. (2012) is representing the fatty acid composition of breast milk in the Tsimane, it is also true that the LA contents of both breast milk and adipose tissue correlate extremely tightly [[9](https://pubmed.ncbi.nlm.nih.gov/16829413/)6-[9](https://pubmed.ncbi.nlm.nih.gov/9684741/)8]. +The median LA representation in adipose tissue increased from around 8-11% of total fatty acids to over 30% of total fatty acids across the eight year study. The baseline levels are consistent with levels found in traditional populations like the Tsimane, Inuit, and the Navajo aboriginals [[93](https://pubmed.ncbi.nlm.nih.gov/22624983/)][[95](https://onlinelibrary.wiley.com/doi/10.1002/cphy.cp050117)]. While the data published by Martin et al. (2012) is representing the fatty acid composition of breast milk in the Tsimane, it is also true that the LA contents of both breast milk and adipose tissue correlate extremely tightly [[96](https://pubmed.ncbi.nlm.nih.gov/16829413/)][[97](https://pubmed.ncbi.nlm.nih.gov/8237871/)][[98](https://pubmed.ncbi.nlm.nih.gov/9684741/)]. ![][image50] -[image50]: /blog/image50.png +[image50]: /blog/seedoils/image50.png There were no statistically significant differences between the baseline tissue LA presentation in the LAVAT and measurements taken from either the Navajo or Tsimane (SD estimated for Navajo). However, tissue LA was statistically significantly higher among Inuit when compared to the baseline measurements observed in the LAVAT. From this, we can likely infer that the subjects in the LAVAT were largely starting from ancestral levels of tissue LA, and increasing tissue LA to approximately threefold higher levels over the eight year trial period. So how did this threefold increase in tissue LA affect their body weight over time? Long story short, it didn't. ![][image51] -[image51]: /blog/image51.png +[image51]: /blog/seedoils/image51.png -Some may speculate that perhaps the 10.8g of LA being consumed in the control group was simply too high, and that the hyperphagic effects of the LA could have been masked by both groups exceeding a particular threshold. This is difficult to reconcile with the fact that the LA intake of the animal fat group was perfectly within bounds when compared to all known estimates of preagricultural LA intakes, as mentioned above [[9](https://pubmed.ncbi.nlm.nih.gov/20860883/)9]. Also, this was an ad libitum trial in normal weight subjects and body weight remained within 2% of baseline. +Some may speculate that perhaps the 10.8g of LA being consumed in the control group was simply too high, and that the hyperphagic effects of the LA could have been masked by both groups exceeding a particular threshold. This is difficult to reconcile with the fact that the LA intake of the animal fat group was perfectly within bounds when compared to all known estimates of preagricultural LA intakes, as mentioned above [[99](https://pubmed.ncbi.nlm.nih.gov/20860883/)]. Also, this was an ad libitum trial in normal weight subjects and body weight remained within 2% of baseline. The LA intakes in the vegetable oil group universally overshoot the upper bounds of all of those same estimates of preagricultural LA intakes. This means that the animal fat group was consuming levels of LA that were consistent with those consumed before the obesity epidemic occurred. However, the vegetable oil group was consuming a level of LA that far surpassed all known preagricultural estimates of LA consumption. -This wasn't the only RCT that substituted vegetable oils for animal fat to measure body weight over time. According to the secondary endpoint analysis done by Hooper et al. 2020 with the Cochrane Collaboration, Olso Diet-Heart saw a 2.5kg reduction in body weight during their study period, whereas the Medical Research Council saw no change in body weight as well [[1](https://pubmed.ncbi.nlm.nih.gov/2607071/)00-[1](https://pubmed.ncbi.nlm.nih.gov/4175085/)01]. +This wasn't the only RCT that substituted vegetable oils for animal fat to measure body weight over time. According to the secondary endpoint analysis done by Hooper et al. 2020 with the Cochrane Collaboration, Olso Diet-Heart saw a 2.5kg reduction in body weight during their study period, whereas the Medical Research Council saw no change in body weight as well [[100](https://pubmed.ncbi.nlm.nih.gov/2607071/)][[101](https://pubmed.ncbi.nlm.nih.gov/4175085/)]. ![][image52] -[image52]: /blog/image52.png +[image52]: /blog/seedoils/image52.png Altogether, it does not appear as though vegetable oils uniquely increase body weight in humans. So, while vegetable oils may increase 2-AG and induce obesity in mice, this does not appear to pan out in humans. Large scale RCTs in humans do not support the hypothesis that vegetable oils lead to weight gain over time in humans. ###### **THERMOGENESIS** -The effect of varying PUFA and SFA in the diet on measures of energy expenditure (EE) have been tested numerous times and show unambiguously consistent results [[1](https://pubmed.ncbi.nlm.nih.gov/24363161/)02]. Overall, diets higher in PUFA and lower in SFA tend to increase EE in humans [[1](https://pubmed.ncbi.nlm.nih.gov/1556946/)03-[1](https://pubmed.ncbi.nlm.nih.gov/9467221/)04]. +The effect of varying PUFA and SFA in the diet on measures of energy expenditure (EE) have been tested numerous times and show unambiguously consistent results [[102](https://pubmed.ncbi.nlm.nih.gov/24363161/)]. Overall, diets higher in PUFA and lower in SFA tend to increase EE in humans [[103](https://pubmed.ncbi.nlm.nih.gov/1556946/)][[104](https://pubmed.ncbi.nlm.nih.gov/9467221/)]. ![][image53] -[image53]: /blog/image53.png +[image53]: /blog/seedoils/image53.png Here is an example from that body of literature. In this study by Lichtenbelt et al. (1997), we can clearly see a consistent effect across all six subjects with higher PUFA intakes increasing postprandial EE. The same trend was also observed for resting metabolic rate (RMR). Ultimately, high-SFA, low-PUFA diets tend to lower EE and RMR compared to high-PUFA, low-SFA diets. This finding is incredibly consistent, though PUFA and MUFA seem to trade blows in some studies, the overall trend of SFA being least thermogenic is clear. -The effects of high-PUFA feeding on fat oxidation have also been studied by Casas-Agustench et al. (2009) as well [[1](https://pubmed.ncbi.nlm.nih.gov/19010571/)05]. When using the respiratory quotient to compare the effects of diets that are high in PUFA, MUFA, and SFA on EE and fat oxidation, we see a similar trend emerge once again. +The effects of high-PUFA feeding on fat oxidation have also been studied by Casas-Agustench et al. (2009) as well [[105](https://pubmed.ncbi.nlm.nih.gov/19010571/)]. When using the respiratory quotient to compare the effects of diets that are high in PUFA, MUFA, and SFA on EE and fat oxidation, we see a similar trend emerge once again. ![][image54] -[image54]: /blog/image54.png +[image54]: /blog/seedoils/image54.png High-PUFA feeding resulted in higher postprandial EE as well as a higher thermic effect of feeding (TEF). Though the differences in the rate of fat oxidation did not reach significance between groups, there was an obvious trend that reflected the degree of fatty acid saturation. PUFA was the most thermogenic, SFA was the least thermogenic, and MUFA was somewhere in between. -The same results were observed by DeLany et al. (2000), only this time different dietary fats containing labeled carbon isotopes are used [[1](https://pubmed.ncbi.nlm.nih.gov/11010930/)06]. You can measure these isotopes in the breath in order to measure how much of the dietary fat a subject has consumed was burned in the time after a meal. +The same results were observed by DeLany et al. (2000), only this time different dietary fats containing labeled carbon isotopes are used [[106](https://pubmed.ncbi.nlm.nih.gov/11010930/)]. You can measure these isotopes in the breath in order to measure how much of the dietary fat a subject has consumed was burned in the time after a meal. ![][image55] -[image55]: /blog/image55.png +[image55]: /blog/seedoils/image55.png Using this methodology, we see that there is one type of SFA that is preferentially oxidized over all other FAs that were tested, and that is lauric acid. However, lauric acid might have ketogenic properties, so interpret with caution. Looking over the rest of the tested FAs, we see that PUFA once again has the highest oxidation rate, followed by MUFA, and SFA once again comes in last place. @@ -578,41 +578,41 @@ Vegetable oils don't appear to make you fat. But even if they did, it does not a The idea that vegetable oils are the primary driver of obesity and/or type 2 diabetes mellitus (T2DM) has deep roots in many diet communities. However, the evidence cited to support this assertion is typically animal research investigating the effects of LA on hypothalamic function and energy intake. Not to mention that, as we discussed earlier, altering the fatty acid saturation of the diet has no discernable effect on ad libitum energy intake. So, let's investigate the effects on insulin sensitivity. ![][image56] -[image56]: /blog/image56.png +[image56]: /blog/seedoils/image56.png -When the relationship between tissue LA and insulin sensitivity was investigated by Iggman et al. (2010), the results are null for leaner individuals. However for overweight individuals, adipose LA is associated with a statistically significant increase in insulin sensitivity [[1](https://pubmed.ncbi.nlm.nih.gov/20127308/)07]. +When the relationship between tissue LA and insulin sensitivity was investigated by Iggman et al. (2010), the results are null for leaner individuals. However for overweight individuals, adipose LA is associated with a statistically significant increase in insulin sensitivity [[107](https://pubmed.ncbi.nlm.nih.gov/20127308/)]. This study into T2DM incidence is the closest thing I've been able to find investigating the association between adipose tissue fatty acids and insulin sensitivity that also adjusts for the fewest mediators of T2DM, such as energy intake. -Again, we can turn our attention to well-conducted crossover RCTs for clearer answers to these sorts of questions. Fortunately, we have one such trial by Heine et al. (1989), investigating the effects of altering fatty acid saturation on measures of insulin sensitivity and glucose homeostasis [[1](https://pubmed.ncbi.nlm.nih.gov/2923077/)08]. Subjects were placed on either a high-LA diet (10.9% of energy) or a low-LA diet (4.2% of energy) for 30 weeks, after which measures of plasma insulin and glucose clearance were taken. +Again, we can turn our attention to well-conducted crossover RCTs for clearer answers to these sorts of questions. Fortunately, we have one such trial by Heine et al. (1989), investigating the effects of altering fatty acid saturation on measures of insulin sensitivity and glucose homeostasis [[108](https://pubmed.ncbi.nlm.nih.gov/2923077/)]. Subjects were placed on either a high-LA diet (10.9% of energy) or a low-LA diet (4.2% of energy) for 30 weeks, after which measures of plasma insulin and glucose clearance were taken. ![][image57] -[image57]: /blog/image57.png +[image57]: /blog/seedoils/image57.png While there were no statistically significant differences between groups in most ways, the high-LA group has a significantly higher glucose clearance rate during the first infusion test. Overall, there was an obvious trend toward a benefit with the high-LA diet. -Another trial by Zibaeenezhad et al. (2016) compared 15g of walnut oil (containing approximately 8g of LA) to no intervention, and measured a number of endpoints relevant to T2DM [[1](https://pubmed.ncbi.nlm.nih.gov/28115966/)09]. Presumably, randomization balanced baseline LA between groups, so we can assume that the trial is effectively testing the effects of adding a tablespoon of walnut oil to the diet. +Another trial by Zibaeenezhad et al. (2016) compared 15g of walnut oil (containing approximately 8g of LA) to no intervention, and measured a number of endpoints relevant to T2DM [[109](https://pubmed.ncbi.nlm.nih.gov/28115966/)]. Presumably, randomization balanced baseline LA between groups, so we can assume that the trial is effectively testing the effects of adding a tablespoon of walnut oil to the diet. ![][image58] -[image58]: /blog/image58.png +[image58]: /blog/seedoils/image58.png By the end of the trial, the walnut oil diet improved both HbA1C and fasting blood glucose. There were also no statistically significant changes in body weight or BMI. Which suggests that these effects were independent of weight loss. This is not what we'd expect if the vegetable oils were increasing the risk of developing T2DM. -We also have at least one study by Pertiwi et al. (2020) investigating the relationship between LA and both glycemic control and liver function [[1](https://pubmed.ncbi.nlm.nih.gov/32546275/)10]. LA seems to have no association with glycemic control, and is associated with better liver function in the minimally adjusted model. The association is then null in model 2, which adjusts for a few T2D mediators. Lastly, after a better adjustment for diet quality, many of the associations gain significance again. +We also have at least one study by Pertiwi et al. (2020) investigating the relationship between LA and both glycemic control and liver function [[110](https://pubmed.ncbi.nlm.nih.gov/32546275/)]. LA seems to have no association with glycemic control, and is associated with better liver function in the minimally adjusted model. The association is then null in model 2, which adjusts for a few T2D mediators. Lastly, after a better adjustment for diet quality, many of the associations gain significance again. -There are a few more studies that do not adjust for many T2D mediators. In this study by Kröger et al. (2011), the relationship between red blood cell LA and T2D incidence in the EPIC-Potsdam cohort was investigated [[1](https://pubmed.ncbi.nlm.nih.gov/20980488/)11]. We see that the minimally adjusted model (which did not adjust for any T2D mediators) shows a statistically significant reduction in the risk of T2D. Whereas in the fully adjusted model the association is null, as we would expect. However, the trend toward a benefit of LA reached statistical significance. +There are a few more studies that do not adjust for many T2D mediators. In this study by Kröger et al. (2011), the relationship between red blood cell LA and T2D incidence in the EPIC-Potsdam cohort was investigated [[111](https://pubmed.ncbi.nlm.nih.gov/20980488/)]. We see that the minimally adjusted model (which did not adjust for any T2D mediators) shows a statistically significant reduction in the risk of T2D. Whereas in the fully adjusted model the association is null, as we would expect. However, the trend toward a benefit of LA reached statistical significance. Ultimately, it appears that neither LA biomarkers nor intake associate with negative outcomes with regards to insulin sensitivity, obesity, T2D, or liver function. These results are pretty consistent with existing meta-analyses on this question (which I combed through to find minimally adjusted data) [[112](https://pubmed.ncbi.nlm.nih.gov/29032079/)]. ![][image59] -[image59]: /blog/image59.png +[image59]: /blog/seedoils/image59.png These are not at all the results that we would expect to see if merely having more LA in either your body or your diet increased the risk of T2DM. Although, there are some who would claim that associations between LA biomarkers and diseases are unreliable. Essentially, the idea is that LA can oxidize for various reasons and potentially skew the biomarker in different directions. For example, if higher tissue representation of LA is inversely associated with a disease, but the disease itself predisposes LA to oxidation (and thus creates the potential for the LA biomarker to appear artificially lower), the data could be confounded. However, there is fascinating data that would seem to contradict this [[113](https://pubmed.ncbi.nlm.nih.gov/30987358/)]. ![][image60] -[image60]: /blog/image60.png +[image60]: /blog/seedoils/image60.png In analysis of a prospective cohort study by Yepes-Calderón et al. (2019), levels of the LA peroxidation products, malondialdehyde (MDA), was strongly and inversely associated with new onset T2DM after kidney transplant. Even after applying seven different multivariate adjustment models, no adjustment succeeded in nullifying the effect. @@ -621,12 +621,12 @@ Perhaps the reason LA is inversely associated with T2DM is _because_ it undergoe Lastly, in a multinational MR study of almost a million participants by Chen et al. (2017), there was an inverse association between elevated plasma LA levels and incidence of T2DM [[114](https://pubmed.ncbi.nlm.nih.gov/28032469/)]. ![][image61] -[image61]: /blog/image61.png +[image61]: /blog/seedoils/image61.png Once again, we see the same thing that we saw in the MR studies investigating CVD. Genetically higher plasma LA is inversely associated with lower fasting blood glucose and T2DM incidence, whereas genetically higher plasma AA is positively associated with both higher fasting blood glucose and T2DM incidence. We also see in their subgroup analysis that the conversion of LA to AA through FADS is once again mediating. ![][image62] -[image62]: /blog/image62.png +[image62]: /blog/seedoils/image62.png When excluding gene variants affecting the function of FADS, the association between genetically elevated plasma LA and T2DM is null. However, when FADS gene variants are considered, the association is statistically significant. This once again suggests a causal relationship between the conversion of LA to AA and disease incidence. Strangely, long chain omega-3s are positively associated as well, which is in contrast to the RCT data on the subject [[115](https://pubmed.ncbi.nlm.nih.gov/31434641/)]. @@ -638,14 +638,14 @@ Overall it would appear that higher intakes of LA are inversely associated with Increased intakes of LA have been proposed by Santoro et al. (2013) as a mechanism by which non-alcoholic fatty liver disease (NALFD) may occur [[116](https://pubmed.ncbi.nlm.nih.gov/26405460/)]. The most direct evidence cited in support of this hypothesis comes from parenteral feeding studies. Typically these studies divulge that soybean oil (SO) based intravenous lipid emulsions (IVLE) have a tendency to produce a particular liver pathology called cholestasis in children on total parenteral nutrition (TPN) under certain conditions [[117](https://pubmed.ncbi.nlm.nih.gov/23520135/)]. On the other hand, Gura and Puder (2010) discovered that fish oil (FO) based IVLEs tend to prevent and/or abolish cholestasis during parenteral feeding [[118](https://pubmed.ncbi.nlm.nih.gov/20702846/)]. -However, within this body of literature, the primary hypothesis that has been put forth to explain the cholestasis observed with SO-IVLEs implicates phytosterols as the primary driver [[119](https://pubmed.ncbi.nlm.nih.gov/26374182/)-[120](https://pubmed.ncbi.nlm.nih.gov/9437703/)]. Overall the evidence does not seem to strongly support LA as uniquely pathological in this regard, and most authors seem to reject this hypothesis. +However, within this body of literature, the primary hypothesis that has been put forth to explain the cholestasis observed with SO-IVLEs implicates phytosterols as the primary driver [[119](https://pubmed.ncbi.nlm.nih.gov/26374182/)][[120](https://pubmed.ncbi.nlm.nih.gov/9437703/)]. Overall the evidence does not seem to strongly support LA as uniquely pathological in this regard, and most authors seem to reject this hypothesis. Because it would be unethical to truly test the effects of IVLE overfeeding in humans, we have to rely on animal models to provide us with insights. In one well-designed mouse study by Ksami et al. (2013), both SO- and FO-IVLEs were fed to mice with intestinal injuries [[121](https://pubmed.ncbi.nlm.nih.gov/24107776/)]. Except there were additional groups that were fed FO-IVLEs that also contained SO-derived phytosterols. Markers of liver pathology were comparable between phytosterol-containing FO-IVLEs and controls fed SO-IVLEs. ![][image63] -[image63]: /blog/image63.png +[image63]: /blog/seedoils/image63.png -When tested in humans at matched, eucaloric dosages, there are no clinically meaningful differences between SO-IVLEs and FO-IVLEs [[122](https://pubmed.ncbi.nlm.nih.gov/23770843/)-[123](https://pubmed.ncbi.nlm.nih.gov/22796064/)]. Across all of the markers investigated by Nehra et al. (2014), the only significant changes were increases in alkaline phosphatase, but they occurred in both groups. +When tested in humans at matched, eucaloric dosages, there are no clinically meaningful differences between SO-IVLEs and FO-IVLEs [[122](https://pubmed.ncbi.nlm.nih.gov/23770843/)][[123](https://pubmed.ncbi.nlm.nih.gov/22796064/)]. Across all of the markers investigated by Nehra et al. (2014), the only significant changes were increases in alkaline phosphatase, but they occurred in both groups. Since FO-IVLEs are extremely low in LA, it is unlikely that LA is the mediator of this change. Despite the fact that dosages were titrated down to tolerable levels, such to be compliant with current standards of care for IVLEs, tissue LA increased significantly in subjects receiving SO-IVLEs. @@ -660,21 +660,21 @@ There is just a tiny little problem, though. They actually weren't testing the e Ultimately, they likely did not significantly alter the LA content of the diet itself, as evidenced by the fact that tissue LA went largely unchanged throughout the duration of the trial. ![][image64] -[image64]: /blog/image64.png +[image64]: /blog/seedoils/image64.png Fortunately, we do have better, more direct experiments investigating the effects of dietary fatty acid composition and fatty acid saturation on measures of liver fat in humans [[126](https://pubmed.ncbi.nlm.nih.gov/22492369/)]. First is an isocaloric feeding study by Bjermo et al. (2012) that largely found non-inferiority between LA and SFA on measures of visceral adipose tissue (VAT). However, the high-LA diet resulted in a greater overall improvement in the subjects' metabolic profile. The high-LA diet did result in lower waist circumference, PCSK9, cholesterol, serum insulin, and ALT, though it did not necessarily result in a difference in VAT compared to the high-SFA diet. The results are slightly different when looking at human overfeeding [[127](https://pubmed.ncbi.nlm.nih.gov/24550191/)]. In this trial by Rosqvist et al. (2014), which compared hypercaloric diets that were either high-LA or high-SFA, the high-LA diet did appear to be protective against VAT accumulation. ![][image65] -[image65]: /blog/image65.png +[image65]: /blog/seedoils/image65.png The high-LA diet seemed to be uniquely protective against liver fat accumulation in particular. Additionally, the high-LA diet seemed to be associated with a greater increase in lean body mass (LBM) when compared to the high-SFA diet. But not only that, the high-LA diet seemed more resistant to fat gain overall compared to the high-SFA diet. These are not the results we'd expect if LA was uniquely causal in NAFLD. -These human experimental finding are perfectly consistent with the observational evidence on the subject as well, which typically shows that either high-PUFA or high-LA diets protect against NAFLD at the population level as well [[128](https://pubmed.ncbi.nlm.nih.gov/22209679/)-[129](https://pubmed.ncbi.nlm.nih.gov/27618908/)]. +These human experimental finding are perfectly consistent with the observational evidence on the subject as well, which typically shows that either high-PUFA or high-LA diets protect against NAFLD at the population level as well [[128](https://pubmed.ncbi.nlm.nih.gov/22209679/)][[129](https://pubmed.ncbi.nlm.nih.gov/27618908/)]. ![][image66] -[image66]: /blog/image66.png +[image66]: /blog/seedoils/image66.png Overall there is an inverse association between high-PUFA intake and measures of hepatic lipid concentrations. There is, however, an association between high-SFA diets, just like the experimental literature. There is also evidence from Wehmeyer et al. (2016) that suggests that the effect of total energy intake on NAFLD is greater than either high-PUFA or high-SFA diets [[130](https://pubmed.ncbi.nlm.nih.gov/27281105/)]. Regardless, there does not appear to be any clear or persuasive evidence that LA is uniquely causal of NAFLD. @@ -687,18 +687,18 @@ If you've spent any amount of time in any low carb or vegan diet community or bl There is an analysis of the Epidemiological Investigation of Rheumatoid Arthritis cohort by Lourdudoss et al. (2018) that investigated the relationship between dietary fatty acids and RA pain [[131](https://pubmed.ncbi.nlm.nih.gov/28371257/)]. As per the recurring theme throughout much of the dietary fat literature, a high O6:O3 ratio is associated with an increased risk of both unacceptable pain and refractory pain (RR 1.70 [1.03-2.82] and 2.33 [1.28-4.24], respectively. ![][image67] -[image67]: /blog/image67.png +[image67]: /blog/seedoils/image67.png However, if we look at omega-3 we see that there is a statistically significant decrease in both unacceptable pain and refractory pain (RR 0.57 [0.35-0.95] and 0.47 [0.26-0.84], respectively). Whereas for omega-6, results for all three endpoints are null. If we do a little math (1/0.54 and 1/0.47), we see that the risk increase when going from the highest to lowest intakes of omega-3 for both unacceptable pain and refractory pain are pretty much the same as the risk ratios for the lowest to highest O6:O3 ratio. Which are 1.75 and 2.12, respectively. -When considered together, this likely means that the effect of a high O6:O3 ratio has more to do with insufficient omega-3 than it has to do with excessive omega-6, which is consistent with the experimental literature on the subject [[132](https://pubmed.ncbi.nlm.nih.gov/29017507/)-[133](https://pubmed.ncbi.nlm.nih.gov/28067815/)]. However, these results are not consistent across all measures of RA, such as bone marrow lesions in those without RA at baseline [[134](https://pubmed.ncbi.nlm.nih.gov/19426478/)]. +When considered together, this likely means that the effect of a high O6:O3 ratio has more to do with insufficient omega-3 than it has to do with excessive omega-6, which is consistent with the experimental literature on the subject [[132](https://pubmed.ncbi.nlm.nih.gov/29017507/)][[133](https://pubmed.ncbi.nlm.nih.gov/28067815/)]. However, these results are not consistent across all measures of RA, such as bone marrow lesions in those without RA at baseline [[134](https://pubmed.ncbi.nlm.nih.gov/19426478/)]. ![][image68] -[image68]: /blog/image68.png +[image68]: /blog/seedoils/image68.png In an analysis of this Australian cohort by Wang et al. (2009), neither omega-3, omega-6, nor the O6:O3 ratio had a statistically significant effect on the incidence of bone marrow lesions. However, intakes of saturated fat were associated with a statistically significant increase in risk in both multivariate models (RR 2.62 [1.11-6.17] and 2.56 [1.03-6.37], respectively). -As far as experimental evidence goes, the effects of all sorts of high-LA oils on RA-related endpoints have been investigated over the years. First we have 3-10.5g/day of blackcurrant seed oil (BCSO) [[135](https://pubmed.ncbi.nlm.nih.gov/8081671/)-[136](https://pubmed.ncbi.nlm.nih.gov/1397534/)]. BCSO has an LA content in excess of 40% by weight [[137](https://pubmed.ncbi.nlm.nih.gov/23341215/)]. Though most of these findings were null, there is one trial by Watson et al. (1993) that did have interesting results [[138](https://pubmed.ncbi.nlm.nih.gov/8252313/)]. +As far as experimental evidence goes, the effects of all sorts of high-LA oils on RA-related endpoints have been investigated over the years. First we have 3-10.5g/day of blackcurrant seed oil (BCSO) [[135](https://pubmed.ncbi.nlm.nih.gov/8081671/)][[136](https://pubmed.ncbi.nlm.nih.gov/1397534/)]. BCSO has an LA content in excess of 40% by weight [[137](https://pubmed.ncbi.nlm.nih.gov/23341215/)]. Though most of these findings were null, there is one trial by Watson et al. (1993) that did have interesting results [[138](https://pubmed.ncbi.nlm.nih.gov/8252313/)]. Patients with RA were divided into two groups that received either 3g of BCSO or 3g of SO, and were compared to two healthy control groups consuming the same oils at the same dosages. The BCSO group, including both healthy subjects as well as those with RA saw a statistically significant decrease in tumor necrosis factor (TNF), whereas the SU group didn't. @@ -709,11 +709,11 @@ Next up is evening primrose oil (EPO), which contains approximately 72% LA by we However, EPO trials using this design have been criticized by Horrobin (1989) for having a number of potential methodological errors [[141](https://pubmed.ncbi.nlm.nih.gov/2688567/)]. In another trial by Belch et al. (1988) using more robust methodology and more complex comparisons, EPO seems to do quite well in moderate doses [[142](https://pubmed.ncbi.nlm.nih.gov/2833184/)]. In this trial, 49 subjects with RA, managed with nonsteroidal anti-inflammatory drugs (NSAID), were randomized to three groups. One group had 12g/day of EPO, another group received 12g/day of EPO+FO, and the final group was placed on a placebo. ![][image69] -[image69]: /blog/image69.png +[image69]: /blog/seedoils/image69.png While EPO alone resulted in significant reduction in the use of NSAIDs, the largest reductions in NSAID usage was seen when EPO was paired with FO. Not only does this detract from the notion that LA increases RA, this also lends further credibility to the beneficial effects of increasing dietary omega-3. -However, the double blind RCT conducted by Volker et al. (2000) would seem to contradict this finding [[143](https://pubmed.ncbi.nlm.nih.gov/11036827/)]. In this trial, it is claimed that FO may improve symptoms as long as the background diet is low in omega-6. However, it is unclear if these results are actually compared to a high omega-6 diet, or if all of the study subjects were on low omega-6 diets. These results seem odd, as there are plenty of studies using high omega-6 oils that show positive results [[144](https://pubmed.ncbi.nlm.nih.gov/28699499/)-[146](https://pubmed.ncbi.nlm.nih.gov/29705470/)]. +However, the double blind RCT conducted by Volker et al. (2000) would seem to contradict this finding [[143](https://pubmed.ncbi.nlm.nih.gov/11036827/)]. In this trial, it is claimed that FO may improve symptoms as long as the background diet is low in omega-6. However, it is unclear if these results are actually compared to a high omega-6 diet, or if all of the study subjects were on low omega-6 diets. These results seem odd, as there are plenty of studies using high omega-6 oils that show positive results [[144](https://pubmed.ncbi.nlm.nih.gov/28699499/)][[145](https://pubmed.ncbi.nlm.nih.gov/12548113/)][[146](https://pubmed.ncbi.nlm.nih.gov/29705470/)]. Bear in mind that most of these trials discussed in this section were small in size and relatively short in duration, and are plagued by a number of challenges that are common in nutrient supplement studies. However, one thing that seems clear is that omega-6 is not associated with the development of RA, nor is it associated with worsening RA symptoms. In clinical trials, high omega-6 oils do not uniquely increase the prevalence of RA symptoms, and may even be useful for RA management. @@ -733,10 +733,10 @@ While ANA is an important part of the diagnostic criteria for SLE, I would take Not only that, but there was no multivariable adjustment to ascertain whether or not high serum LA was merely a correlate for other dietary habits that actually do increase risk. It's impossible to tell from this data alone. -Puzzlingly, in stark contrast to these findings, other cross-sectional data seems to suggest that LA has either a neutral or beneficial effect on SLE, at least once people are diagnosed [[148](https://pubmed.ncbi.nlm.nih.gov/31074595/)-[149](https://pubmed.ncbi.nlm.nih.gov/26848399/)]. In the first paper by Charoenwoodhipong et al. (2020), it was observed that LA had no association with worsening SLE-related symptoms. +Puzzlingly, in stark contrast to these findings, other cross-sectional data seems to suggest that LA has either a neutral or beneficial effect on SLE, at least once people are diagnosed [[148](https://pubmed.ncbi.nlm.nih.gov/31074595/)][[149](https://pubmed.ncbi.nlm.nih.gov/26848399/)]. In the first paper by Charoenwoodhipong et al. (2020), it was observed that LA had no association with worsening SLE-related symptoms. ![][image70] -[image70]: /blog/image70.png +[image70]: /blog/seedoils/image70.png As you can see in Figure 3, there is no consistent relationship between LA and SLE-related symptoms in either direction. However, a consistent trend toward favourable outcomes was observed with higher omega-3, and the inverse of which was observed with a high O6:O3. This suggests that while a high O6:O3 is a correlate for worse outcomes, it does not appear to be a function of LA, but rather a function of insufficient omega-3. This is a consistent trend in the literature so far. @@ -747,27 +747,27 @@ However, this correlation may be spurious considering that people diagnosed with Again, at the risk of sounding like a broken record, the inverse of this has been suggested in additional research by Lourdudoss et al. (2016) investigating the relationship between LA and the risk of increasing glucocorticoids [[152](https://pubmed.ncbi.nlm.nih.gov/26848399/)]. ![][image71] -[image71]: /blog/image71.png +[image71]: /blog/seedoils/image71.png This is particularly odd since LA was associated with systemic inflammation in the previous study. Like I said in the beginning, the data is a mess. Nothing seems congruent, because most of it is either cross-sectional or completely uncontrolled or unadjusted. However, there are a few prospective studies investigating SLE and vegetable oil intake. First up is a study by Shin et al. (2017) involving 82 subjects which aimed to explore the differences in plasma fatty acids between those with SLE and those without [[153](https://pubmed.ncbi.nlm.nih.gov/30830319/)]. Ultimately, they discovered that plasma SFAs are more likely to be elevated in those with SLE, whereas plasma PUFA— particularly LA— was more likely to be reduced. ![][image72] -[image72]: /blog/image72.png +[image72]: /blog/seedoils/image72.png At first glance, this may seem like a win for PUFA, or LA more specifically, but there are some interpretive challenges here. For example, PUFA concentrations in tissue could plausibly reduce in the presence of lipid peroxidation cascades, and there is evidence from Shah et al. (2014) that lipid peroxidation metabolites are higher in subjects with SLE [[154](https://pubmed.ncbi.nlm.nih.gov/24636579/)]. -However, the authors remarked that antioxidant status plays an important role in the severity of lipid peroxidation when it does occur. It has been shown that antioxidant supplementation significantly reduces markers of lipid peroxidation in subjects with SLE [[155](https://pubmed.ncbi.nlm.nih.gov/17143589/)-[156](https://pubmed.ncbi.nlm.nih.gov/17143589/)]. It has also been shown by Bae et al. (2002) that antioxidant status can be impaired in subjects with SLE [[157](https://pubmed.ncbi.nlm.nih.gov/12426662/)]. +However, the authors remarked that antioxidant status plays an important role in the severity of lipid peroxidation when it does occur. It has been shown that antioxidant supplementation significantly reduces markers of lipid peroxidation in subjects with SLE [[155](https://pubmed.ncbi.nlm.nih.gov/17143589/)][[156](https://pubmed.ncbi.nlm.nih.gov/17143589/)]. It has also been shown by Bae et al. (2002) that antioxidant status can be impaired in subjects with SLE [[157](https://pubmed.ncbi.nlm.nih.gov/12426662/)]. The second prospective study, analyzed by Minami et al. (2003), is quite a bit larger than the previous studies, with a decent follow-up time [[158](https://pubmed.ncbi.nlm.nih.gov/12672194/)]. Basically, the relationship between dietary intakes and active SLE incidence were investigated over four years in 279 female participants with diagnosed SLE. Overall, there was no association between SLE activity and vegetable fat intake. -However, echoing the sentiments toward antioxidants that have been discussed in some of the wider SLE literature, there was a statistically significant protective effect of vitamin C in reducing SLE activity. There were also non-significant risk reductions with fibre and vitamin A (but not retinol). To hammer this point home, Western dietary patterns are generally considered to be high in LA, but neither Western dietary patterns nor healthier dietary patterns associate either positively or negatively with SLE [[159](https://pubmed.ncbi.nlm.nih.gov/32936999/)-[160](https://pubmed.ncbi.nlm.nih.gov/31718449/)]. +However, echoing the sentiments toward antioxidants that have been discussed in some of the wider SLE literature, there was a statistically significant protective effect of vitamin C in reducing SLE activity. There were also non-significant risk reductions with fibre and vitamin A (but not retinol). To hammer this point home, Western dietary patterns are generally considered to be high in LA, but neither Western dietary patterns nor healthier dietary patterns associate either positively or negatively with SLE [[159](https://pubmed.ncbi.nlm.nih.gov/32936999/)][[160](https://pubmed.ncbi.nlm.nih.gov/31718449/)]. Much to my surprise, the relationship between both SLE and RA have been investigated using MR. In this MR study by Zhao and Schooling (2019), three different statistical tests across two gene variant subgroups were performed [[161](https://pubmed.ncbi.nlm.nih.gov/30409829/)]. ![][image73] -[image73]: /blog/image73.png +[image73]: /blog/seedoils/image73.png Generally speaking, statistically significant inverse associations between genetically elevated plasma LA and both RA and SLE were consistently found. The only inconsistency was when the Egger MR or the MR PRESSO methods were applied. The application of the Egger MR method seemed to nullify the effect in all cases, and the application of the MR PRESSO method only seemed to nullify the effect for RA in the second subgroup analysis. @@ -790,12 +790,12 @@ So, as I do, I decided to gather all the data I could and compile a meta-analysi **Results:** -Altogether, 10 prospective cohort studies were included in the analysis. With respect to the exposures specified in the inclusion criteria, Delcourt et al. (2007) reported only on PUFA [[164](https://pubmed.ncbi.nlm.nih.gov/17299457/)]. Whereas Seddon et al. (2003) investigated both PUFA and vegetable fat [[165](https://pubmed.ncbi.nlm.nih.gov/14662593/)]. Chong et al. (2009), Chua et al. (2006), Cho et al. (2000), and Tan et al. (2009) all explored LA, PUFA, and TFA in their analyses [[166](https://pubmed.ncbi.nlm.nih.gov/19433719/)-[169](https://pubmed.ncbi.nlm.nih.gov/19433717/)]. Parekh et al. (2009) additionally included vegetable fat in their analysis, but did not investigate TFA [[170](https://pubmed.ncbi.nlm.nih.gov/19901214/)]. Similarly, Sasaki et al. (2020) reported on LA and PUFA, but did not report on TFA or vegetable fat [[171](https://pubmed.ncbi.nlm.nih.gov/32181798/)]. Both Christen et al. (2011) and Mares-Perlman et al. (1995) studied associations pertaining to both LA and PUFA [[172](https://pubmed.ncbi.nlm.nih.gov/21402976/)-[173](https://pubmed.ncbi.nlm.nih.gov/7786215/)]. There was significant heterogeneity across all investigated exposures, and no single exposure reached statistical significance. +Altogether, 10 prospective cohort studies were included in the analysis. With respect to the exposures specified in the inclusion criteria, Delcourt et al. (2007) reported only on PUFA [[164](https://pubmed.ncbi.nlm.nih.gov/17299457/)]. Whereas Seddon et al. (2003) investigated both PUFA and vegetable fat [[165](https://pubmed.ncbi.nlm.nih.gov/14662593/)]. Chong et al. (2009), Chua et al. (2006), Cho et al. (2000), and Tan et al. (2009) all explored LA, PUFA, and TFA in their analyses [[166](https://pubmed.ncbi.nlm.nih.gov/19433719/)][[167](https://pubmed.ncbi.nlm.nih.gov/16832021/)][[168](https://pubmed.ncbi.nlm.nih.gov/11157315/)][[169](https://pubmed.ncbi.nlm.nih.gov/19433717/)]. Parekh et al. (2009) additionally included vegetable fat in their analysis, but did not investigate TFA [[170](https://pubmed.ncbi.nlm.nih.gov/19901214/)]. Similarly, Sasaki et al. (2020) reported on LA and PUFA, but did not report on TFA or vegetable fat [[171](https://pubmed.ncbi.nlm.nih.gov/32181798/)]. Both Christen et al. (2011) and Mares-Perlman et al. (1995) studied associations pertaining to both LA and PUFA [[172](https://pubmed.ncbi.nlm.nih.gov/21402976/)][[173](https://pubmed.ncbi.nlm.nih.gov/7786215/)]. There was significant heterogeneity across all investigated exposures, and no single exposure reached statistical significance. ![][image74] -[image74]: /blog/image74.png +[image74]: /blog/seedoils/image74.png -Among the studies with the longest follow-up time, largest cohort size, best adjustment models, and the widest exposure contrasts, the results tended to be null. For example, Chong et al. (2009) adjusted for lutein, zeaxanthin, and sources of omega-3, which are inversely associated with late AMD [[174](https://pubmed.ncbi.nlm.nih.gov/21899805/)-[175](https://pubmed.ncbi.nlm.nih.gov/18541848/)]. Their results were null for every exposure. +Among the studies with the longest follow-up time, largest cohort size, best adjustment models, and the widest exposure contrasts, the results tended to be null. For example, Chong et al. (2009) adjusted for lutein, zeaxanthin, and sources of omega-3, which are inversely associated with late AMD [[174](https://pubmed.ncbi.nlm.nih.gov/21899805/)][[175](https://pubmed.ncbi.nlm.nih.gov/18541848/)]. Their results were null for every exposure. The strongest study of all was Christen et al. (2011). Their analysis included three different adjustment models that help us better ascertain the relationship between AMD and vegetable oils. For example, their analysis showed that LA was associated with AMD only before adjustment for AMD risk factors, and that the association was likely a function of insufficient omega-3. @@ -831,12 +831,12 @@ I'm not sure what sort of mechanistic speculation buttresses the narrative that **Results:** -Altogether 43 studies were obtained from a PubMed and Google Scholar literature search. All but 15 prospective cohort studies were excluded due to either having irrelevant endpoints or insufficient specificity with regards to vegetable oil related exposures. No RCTs were found. Of the 15 studies, four were included in an analysis on Alzheimer's disease [[177](https://pubmed.ncbi.nlm.nih.gov/16710090/)-[180](https://pubmed.ncbi.nlm.nih.gov/22713770/)]. Whereas the remainder were included in an analysis of general dementia, which included global cognitive decline. The majority of the included studies reported on both dietary LA and dietary PUFA [[181](https://pubmed.ncbi.nlm.nih.gov/17413112/)-[185](https://pubmed.ncbi.nlm.nih.gov/33386799/)]. However, both Heude et al. (2003) and Samieri et al. (2008) used biomarker LA and PUFA in their analysis, rather than dietary intake [[186](https://pubmed.ncbi.nlm.nih.gov/12663275/)-[187](https://pubmed.ncbi.nlm.nih.gov/18779288/)]. Dietary PUFA, rather than dietary LA or vegetable fat, was investigated by Okereke et al. (2012), Roberts et al. (2012), and Solfrizzi et al. (2006) [[188](https://pubmed.ncbi.nlm.nih.gov/22605573/)-[190](https://pubmed.ncbi.nlm.nih.gov/22810099/)]. Lastly, only Laitinen et al. (2006) explored the association between vegetable fat and cognitive decline [[191](https://pubmed.ncbi.nlm.nih.gov/16710090/)]. +Altogether 43 studies were obtained from a PubMed and Google Scholar literature search. All but 15 prospective cohort studies were excluded due to either having irrelevant endpoints or insufficient specificity with regards to vegetable oil related exposures. No RCTs were found. Of the 15 studies, four were included in an analysis on Alzheimer's disease [[177](https://pubmed.ncbi.nlm.nih.gov/16710090/)[[178](https://pubmed.ncbi.nlm.nih.gov/12580703/)][[179](https://pubmed.ncbi.nlm.nih.gov/12164721/)][180](https://pubmed.ncbi.nlm.nih.gov/22713770/)]. Whereas the remainder were included in an analysis of general dementia, which included global cognitive decline. The majority of the included studies reported on both dietary LA and dietary PUFA [[181](https://pubmed.ncbi.nlm.nih.gov/17413112/)[[182](https://pubmed.ncbi.nlm.nih.gov/20001761/)][[183](https://pubmed.ncbi.nlm.nih.gov/8982020/)][[184](https://pubmed.ncbi.nlm.nih.gov/34392373/)][[185](https://pubmed.ncbi.nlm.nih.gov/33386799/)]. However, both Heude et al. (2003) and Samieri et al. (2008) used biomarker LA and PUFA in their analysis, rather than dietary intake [[186](https://pubmed.ncbi.nlm.nih.gov/12663275/)][[187](https://pubmed.ncbi.nlm.nih.gov/18779288/)]. Dietary PUFA, rather than dietary LA or vegetable fat, was investigated by Okereke et al. (2012), Roberts et al. (2012), and Solfrizzi et al. (2006) [[188](https://pubmed.ncbi.nlm.nih.gov/22605573/)][[189](https://pubmed.ncbi.nlm.nih.gov/16697546/)][[190](https://pubmed.ncbi.nlm.nih.gov/22810099/)]. Lastly, only Laitinen et al. (2006) explored the association between vegetable fat and cognitive decline [[191](https://pubmed.ncbi.nlm.nih.gov/16710090/)]. **Alzheimer's Disease:** ![][image75] -[image75]: /blog/image75.png +[image75]: /blog/seedoils/image75.png For Alzheimer's disease, results across all exposures were null. However, there were not many studies per subgroup. When the subgrouping is removed the results still don't reach statistical significance (RR 0.74 [0.43-1.26], P=0.26). There is also decently high heterogeneity between the included studies. For example, Rönnemaa et al. (2012), saw a non-significant increase in Alzheimer's risk with increasing LA intake, but Morris saw a statistically significant decrease in Alzheimer's risk with increasing vegetable oil intake. @@ -849,7 +849,7 @@ Given that the two datasets that were investigated in these two studies were pri **Dementia:** ![][image76] -[image76]: /blog/image76.png +[image76]: /blog/seedoils/image76.png Again, we see null findings across all of the investigated exposures. The only statistically significant study, Beydoun et al. (2007), found a 23% reduction in the risk of cognitive decline (RR 0.77 [0.65-0.91], P=0.002). What sets this study apart from most of the others was its robust multivariate adjustment model. In fact, the adjustment model was so comprehensive, it was given its own section in the paper. @@ -860,11 +860,11 @@ However, the cohort study had half as much follow-up time and used different met **Total Dementia:** ![][image77] -[image77]: /blog/image77.png +[image77]: /blog/seedoils/image77.png Results are slightly different when Alzheimer's disease, cognitive decline, and general dementia are all considered together, however. It is noteworthy to point out that when all of the studies are aggregated, vegetable fat associates with a statistically significant 58% reduction in total dementia (RR 0.42 [0.21-0.84], P=0.01). Though, to be clear, more than two thirds of the weight are derived from a single study, so interpret with caution. -In conclusion, it does not appear as though LA, PUFA, or vegetable fat are associated with an increased risk of Alzheimer's disease, cognitive decline, or dementia in humans. These results are consistent with previous meta-analyses by Cao et al. (2019) and Ruan et al. (2018) investigating these particular relationships [[193](https://pubmed.ncbi.nlm.nih.gov/31062836/)-[194](https://pubmed.ncbi.nlm.nih.gov/29701155/)]. However, when all endpoints are considered together, vegetable fat seems to be associated with a reduced risk of total dementia. +In conclusion, it does not appear as though LA, PUFA, or vegetable fat are associated with an increased risk of Alzheimer's disease, cognitive decline, or dementia in humans. These results are consistent with previous meta-analyses by Cao et al. (2019) and Ruan et al. (2018) investigating these particular relationships [[193](https://pubmed.ncbi.nlm.nih.gov/31062836/)][[194](https://pubmed.ncbi.nlm.nih.gov/29701155/)]. However, when all endpoints are considered together, vegetable fat seems to be associated with a reduced risk of total dementia. # **MECHANISTIC AUTOFELLATIO** @@ -890,30 +890,30 @@ I scoured the literature for as many LA substitution trials as I could find. Alt 2. Low-LA diet must not have >10g/day of LA. -Four studies met the inclusion criteria and were included in the analysis [[195](https://pubmed.ncbi.nlm.nih.gov/11246548/)-[198](https://pubmed.ncbi.nlm.nih.gov/25319187/)]. The LA intakes in the high-LA diets ranged from 22.2g/day with Vafeiadou et al. (2015) to 50.8g/day with Junker et al. (2001), with an average of 33.5g/day, across all included studies. The LA intakes in the low-LA diets ranged from 4.8g/day with Iggman et al. (2014) to 7.8g/day with Junker et al. (2001), with an average of 6.4g/day, across all included studies. The average contrast in LA intake was 27g/day across all included studies. +Four studies met the inclusion criteria and were included in the analysis [[195](https://pubmed.ncbi.nlm.nih.gov/11246548/)][[196](https://pubmed.ncbi.nlm.nih.gov/15168040/)][[197](https://pubmed.ncbi.nlm.nih.gov/26016869/)][[198](https://pubmed.ncbi.nlm.nih.gov/25319187/)]. The LA intakes in the high-LA diets ranged from 22.2g/day with Vafeiadou et al. (2015) to 50.8g/day with Junker et al. (2001), with an average of 33.5g/day, across all included studies. The LA intakes in the low-LA diets ranged from 4.8g/day with Iggman et al. (2014) to 7.8g/day with Junker et al. (2001), with an average of 6.4g/day, across all included studies. The average contrast in LA intake was 27g/day across all included studies. ![][image78] -[image78]: /blog/image78.png +[image78]: /blog/seedoils/image78.png There were 12 studies that were captured by the exclusion criteria and had to be excluded from the analysis. ![][image79] -[image79]: /blog/image79.png +[image79]: /blog/seedoils/image79.png **Results:** ![][image80] -[image80]: /blog/image80.png +[image80]: /blog/seedoils/image80.png Altogether, high-LA diets yielded a non-significant increase in CRP when compared to control (P=0.15). The results are ultimately null. However, it may still be possible that the true effect of LA on CRP is hidden. It's plausible that high-LA diets do increase CRP, but they don't tend to increase CRP much more than control. ![][image81] -[image81]: /blog/image81.png +[image81]: /blog/seedoils/image81.png When the effects of high-LA diets are compared to baseline, the results are almost squarely null (P=0.62). Even Junker, 2001, which saw the widest contrast in LA intake ultimately had a null result. But, we're not out of the woods yet. There are still other possibilities to consider. What if the subjects' usual diets are already high in LA that dosing more in an intervention trial doesn't actually do anything to CRP? Perhaps the comparator diets could still prove to be anti-inflammatory in some way. ![][image82] -[image82]: /blog/image82.png +[image82]: /blog/seedoils/image82.png Comparing the effects of low-LA diets to baseline yielded a non-significant decrease in CRP (P=0.21). Again, the results are ultimately null. So, at present it does not appear as though low-LA diets are terribly protective compared to high-LA diets on measures of CRP. @@ -924,7 +924,7 @@ But there is one last thing to discuss. Junker et al. (2001), saw the widest con As described in the Statistical Analyses section, the Mann-Whitney-Wilcoxon test was used to test for statistical significance when distributions were non-normal. This test is specifically designed for non-normal distributions, and applying this test is also best practice in this case. ![][image83] -[image83]: /blog/image83.png +[image83]: /blog/seedoils/image83.png Here we see that CRP is actually reported as median and range, because the distributions of CRP were non-normal. We can also see that all three groups saw non-significant decreases in median CRP from baseline, falling from 0.9 (0.17-5.9) to 0.75 (0.17-7.7). However, the upper bounds for CRP during the starting week of the trial are unusually high in the OO group. This means that estimating the mean and standard deviation will actually yank the variance and the mean much higher than it rightfully should be. @@ -953,10 +953,10 @@ To test this, I scoured the literature for any randomized controlled trials (RCT 4. Low-PUFA controls must replace PUFA with monounsaturated or saturated fat. -Altogether, five studies were included in the analysis. The vast majority of data was collected from Freese et al. (2008), which included data for 8-oxodG, GR, GPx, and CAT [[200](https://pubmed.ncbi.nlm.nih.gov/17671440/)]. Whereas Jenkinson et al. (1999) additionally investigated SOD and LO2 in their investigation [[201](https://pubmed.ncbi.nlm.nih.gov/10452406/)]. Exploration of MDA was contributed by both de Kok et al. (2003) and Södergren et al. (2001) [[202](https://pubmed.ncbi.nlm.nih.gov/12504167/)-[203](https://pubmed.ncbi.nlm.nih.gov/11641740/)]. Lastly, Parfitt et al. (1994) contributed data for CD [[204](https://pubmed.ncbi.nlm.nih.gov/8181259/)]. +Altogether, five studies were included in the analysis. The vast majority of data was collected from Freese et al. (2008), which included data for 8-oxodG, GR, GPx, and CAT [[200](https://pubmed.ncbi.nlm.nih.gov/17671440/)]. Whereas Jenkinson et al. (1999) additionally investigated SOD and LO2 in their investigation [[201](https://pubmed.ncbi.nlm.nih.gov/10452406/)]. Exploration of MDA was contributed by both de Kok et al. (2003) and Södergren et al. (2001) [[202](https://pubmed.ncbi.nlm.nih.gov/12504167/)][[203](https://pubmed.ncbi.nlm.nih.gov/11641740/)]. Lastly, Parfitt et al. (1994) contributed data for CD [[204](https://pubmed.ncbi.nlm.nih.gov/8181259/)]. ![][image84] -[image84]: /blog/image84.png +[image84]: /blog/seedoils/image84.png **Results:** @@ -965,72 +965,72 @@ Normally when I see a bunch of null results I feel like I may have wasted my tim **8-oxo-7,8-dihydro-20-deoxyguanosine (8-oxodG) vs Control** ![][image85] -[image85]: /blog/image85.png +[image85]: /blog/seedoils/image85.png **8-oxo-7,8-dihydro-20-deoxyguanosine (8-oxodG) vs Baseline** ![][image86] -[image86]: /blog/image86.png +[image86]: /blog/seedoils/image86.png **Glutathione Reductase (GR) vs Control** ![][image87] -[image87]: /blog/image87.png +[image87]: /blog/seedoils/image87.png **Glutathione Reductase (GR) vs Baseline** ![][image88] -[image88]: /blog/image88.png +[image88]: /blog/seedoils/image88.png **Glutathione Peroxidase (GPx) vs Control** ![][image89] -[id]: /blog/image89.png +[id]: /blog/seedoils/image89.png **Glutathione Peroxidase (GPx) vs Baseline** ![][image90] -[image90]: /blog/image90.png +[image90]: /blog/seedoils/image90.png **Superoxide Dismutase (SOD) vs Control** ![][image91] -[image91]: /blog/image91.png +[image91]: /blog/seedoils/image91.png **Superoxide Dismutase (SOD) vs Baseline** ![][image92] -[image92]: /blog/image92.png +[image92]: /blog/seedoils/image92.png **Malondialdehyde (MDA) vs Control** ![][image93] -[image93]: /blog/image93.png +[image93]: /blog/seedoils/image93.png **Malondialdehyde (MDA) vs Baseline** ![][image94] -[image94]: /blog/image94.png +[image94]: /blog/seedoils/image94.png **Catalase (CAT) vs Control** ![][image95] -[image95]: /blog/image95.png +[image95]: /blog/seedoils/image95.png **Catalase (CAT) vs Baseline** ![][image96] -[image96]: /blog/image96.png +[image96]: /blog/seedoils/image96.png **Conjugated Dienes (CD) vs Control** ![][image97] -[image97]: /blog/image97.png +[image97]: /blog/seedoils/image97.png **Conjugated Dienes (CD) vs Baseline** ![][image98] -[image98]: /blog/image98.png +[image98]: /blog/seedoils/image98.png The only statistically significant finding was a reduction in 8-oxodG with high-PUFA diets (P=0.02). Which is interesting, because 8-oxodG is a marker of DNA damage, and as such its implications extend far beyond oxidative stress. I thought PUFA was supposed to destroy your DNA with all of those highly reactive, toxic byproducts they create when they oxidize? Well, apparently, like most mechanistic reasoning, that shit just doesn't pan out in the real world. @@ -1046,5 +1046,1233 @@ This in-depth analysis could find no persuasive evidence of harm with vegetable In conclusion, vegetable oils appear to be a health-promoting addition to the diet, and seem to offer a range of health benefits and little to no apparent health risks to the general population. However, one should exercise caution when navigating the current food environment, as vegetable oils are included in many foods that are not particularly health-promoting. If one chooses to consume vegetable oils, it would probably be wise to integrate them into a healthy eating pattern in ways that do not promote the overconsumption of calories. Some possible healthy ways to include vegetable oils in the diet could be in the form of salad dressings or as cooking oils for sauteed vegetables. -# BIBLIDDILYOODILYOGRAPHY""" +Thank you for reading! If you like what you've read and want help me create more content like this, consider pledging your [Support](https://www.uprootnutrition.com/donate). Every little bit helps! I hope you found the content interesting! + +# BIBLIOGRAPHY""" + , articleReferences = + [ { author = "DiNicolantonio, James J., and James H. O’Keefe" + , year = "2018" + , title = "Omega-6 Vegetable Oils as a Driver of Coronary Heart Disease: The Oxidized Linoleic Acid Hypothesis" + , journal = "Open Heart" + , link = "https://doi.org/10.1136/openhrt-2018-000898" + } + , { author = "Mata, P., et al." + , year = "1996" + , title = "Effect of Dietary Fat Saturation on LDL Oxidation and Monocyte Adhesion to Human Endothelial Cells in Vitro" + , journal = "Arteriosclerosis, Thrombosis, and Vascular Biology" + , link = "https://doi.org/10.1161/01.atv.16.11.1347" + } + , { author = "Kratz, M., et al." + , year = "2002" + , title = "Effects of Dietary Fatty Acids on the Composition and Oxidizability of Low-Density Lipoprotein" + , journal = "European Journal of Clinical Nutrition" + , link = "https://doi.org/10.1038/sj.ejcn.1601288" + } + , { author = "Reaven, P. 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L., et al." + , title = "Dietary Fatty Acids and the 10-Year Incidence of Age-Related Macular Degeneration: The Blue Mountains Eye Study" + , journal = "Archives of Ophthalmology (Chicago, Ill.: 1960)" + , year = "2009" + , link = "https://doi.org/10.1001/archophthalmol.2009.76" + } + , { author = "Parekh, Niyati, et al." + , title = "Association between Dietary Fat Intake and Age-Related Macular Degeneration in the Carotenoids in Age-Related Eye Disease Study (CAREDS): An Ancillary Study of the Women’s Health Initiative" + , journal = "Archives of Ophthalmology (Chicago, Ill.: 1960)" + , year = "2009" + , link = "https://doi.org/10.1001/archophthalmol.2009.130" + } + , { author = "Sasaki, Mariko, et al." + , title = "Dietary Saturated Fatty Acid Intake and Early Age-Related Macular Degeneration in a Japanese Population" + , journal = "Investigative Ophthalmology & Visual Science" + , year = "2020" + , link = "https://doi.org/10.1167/iovs.61.3.23" + } + , { author = "Christen, William G., et al." + , title = "Dietary ω-3 Fatty Acid and Fish Intake and Incident Age-Related Macular Degeneration in Women" + , journal = "Archives of Ophthalmology (Chicago, Ill.: 1960)" + , year = "2011" + , link = "https://doi.org/10.1001/archophthalmol.2011.34" + } + , { author = "Mares-Perlman, J. A., et al." + , title = "Dietary Fat and Age-Related Maculopathy" + , journal = "Archives of Ophthalmology (Chicago, Ill.: 1960)" + , year = "1995" + , link = "https://doi.org/10.1001/archopht.1995.01100060069034" + } + , { author = "Ma, Le, et al." + , title = "Lutein and Zeaxanthin Intake and the Risk of Age-Related Macular Degeneration: A Systematic Review and Meta-Analysis" + , journal = "The British Journal of Nutrition" + , year = "2012" + , link = "https://doi.org/10.1017/S0007114511004260" + } + , { author = "Chong, Elaine W. T., et al." + , title = "Dietary Omega-3 Fatty Acid and Fish Intake in the Primary Prevention of Age-Related Macular Degeneration: A Systematic Review and Meta-Analysis" + , journal = "Archives of Ophthalmology (Chicago, Ill.: 1960)" + , year = "2008" + , link = "https://doi.org/10.1001/archopht.126.6.826" + } + , { author = "Wang, Kai, et al." + , title = "Causal Effects of N-6 Polyunsaturated Fatty Acids on Age-Related Macular Degeneration: A Mendelian Randomization Study" + , journal = "The Journal of Clinical Endocrinology and Metabolism" + , year = "2021" + , link = "https://doi.org/10.1210/clinem/dgab338" + } + , { author = "Laitinen, M. H., et al." + , title = "Fat Intake at Midlife and Risk of Dementia and Alzheimer’s Disease: A Population-Based Study" + , journal = "Dementia and Geriatric Cognitive Disorders" + , year = "2006" + , link = "https://doi.org/10.1159/000093478" + } + , { author = "Morris, Martha Clare, et al." + , title = "Dietary Fats and the Risk of Incident Alzheimer Disease" + , journal = "Archives of Neurology" + , year = "2003" + , link = "https://doi.org/10.1001/archneur.60.2.194" + } + , { author = "Luchsinger, Jose A., et al." + , title = "Caloric Intake and the Risk of Alzheimer Disease" + , journal = "Archives of Neurology" + , year = "2002" + , link = "https://doi.org/10.1001/archneur.59.8.1258" + } + , { author = "Rönnemaa, E., et al." + , title = "Serum Fatty-Acid Composition and the Risk of Alzheimer’s Disease: A Longitudinal Population-Based Study" + , journal = "European Journal of Clinical Nutrition" + , year = "2012" + , link = "https://doi.org/10.1038/ejcn.2012.63" + } + , { author = "Beydoun, May A., et al." + , title = "Plasma N-3 Fatty Acids and the Risk of Cognitive Decline in Older Adults: The Atherosclerosis Risk in Communities Study" + , journal = "The American Journal of Clinical Nutrition" + , year = "2007" + , link = "https://doi.org/10.1093/ajcn/85.4.1103" + } + , { author = "González, Sonia, et al." + , title = "The Relationship between Dietary Lipids and Cognitive Performance in an Elderly Population" + , journal = "International Journal of Food Sciences and Nutrition" + , year = "2010" + , link = "https://doi.org/10.3109/09637480903348098" + } + , { author = "Kalmijn, S., et al." + , title = "Polyunsaturated Fatty Acids, Antioxidants, and Cognitive Function in Very Old Men" + , journal = "American Journal of Epidemiology" + , year = "1997" + , link = "https://doi.org/10.1093/oxfordjournals.aje.a009029" + } + , { author = "Vercambre, Marie-Noël, et al." + , title = "Long-Term Association of Food and Nutrient Intakes with Cognitive and Functional Decline: A 13-Year Follow-up Study of Elderly French Women" + , journal = "The British Journal of Nutrition" + , year = "2009" + , link = "https://doi.org/10.1017/S0007114508201959" + } + , { author = "Nozaki, Shoko, et al." + , title = "Association Between Dietary Fish and PUFA Intake in Midlife and Dementia in Later Life: The JPHC Saku Mental Health Study" + , journal = "Journal of Alzheimer’s Disease: JAD" + , year = "2021" + , link = "https://doi.org/10.3233/JAD-191313" + } + , { author = "Heude, Barbara, et al." + , title = "Cognitive Decline and Fatty Acid Composition of Erythrocyte Membranes--The EVA Study" + , journal = "The American Journal of Clinical Nutrition" + , year = "2003" + , link = "https://doi.org/10.1093/ajcn/77.4.803" + } + , { author = "Samieri, Cécilia, et al." + , title = "Low Plasma Eicosapentaenoic Acid and Depressive Symptomatology Are Independent Predictors of Dementia Risk" + , journal = "The American Journal of Clinical Nutrition" + , year = "2008" + , link = "https://doi.org/10.1093/ajcn/88.3.714" + } + , { author = "Okereke, Olivia I., et al." + , title = "Dietary Fat Types and 4-Year Cognitive Change in Community-Dwelling Older Women" + , journal = "Annals of Neurology" + , year = "2012" + , link = "https://doi.org/10.1002/ana.23593" + } + , { author = "Solfrizzi, Vincenzo, et al." + , title = "Dietary Fatty Acids Intakes and Rate of Mild Cognitive Impairment. The Italian Longitudinal Study on Aging" + , journal = "Experimental Gerontology" + , year = "2006" + , link = "https://doi.org/10.1016/j.exger.2006.03.017" + } + , { author = "Roberts, Rosebud O., et al." + , title = "Relative Intake of Macronutrients Impacts Risk of Mild Cognitive Impairment or Dementia" + , journal = "Journal of Alzheimer’s Disease: JAD" + , year = "2012" + , link = "https://doi.org/10.3233/JAD-2012-120862" + } + , { author = "Laitinen, M. H., et al." + , title = "Fat Intake at Midlife and Risk of Dementia and Alzheimer’s Disease: A Population-Based Study" + , journal = "Dementia and Geriatric Cognitive Disorders" + , year = "2006" + , link = "https://doi.org/10.1159/000093478" + } + , { author = "Zietemann, Vera, et al." + , title = "Validation of the Telephone Interview of Cognitive Status and Telephone Montreal Cognitive Assessment Against Detailed Cognitive Testing and Clinical Diagnosis of Mild Cognitive Impairment After Stroke" + , journal = "Stroke" + , year = "2017" + , link = "https://doi.org/10.1161/STROKEAHA.117.017519" + } + , { author = "Cao, G. Y., et al." + , title = "Dietary Fat Intake and Cognitive Function among Older Populations: A Systematic Review and Meta-Analysis" + , journal = "The Journal of Prevention of Alzheimer’s Disease" + , year = "2019" + , link = "https://doi.org/10.14283/jpad.2019.9" + } + , { author = "Ruan, Yue, et al." + , title = "Dietary Fat Intake and Risk of Alzheimer’s Disease and Dementia: A Meta-Analysis of Cohort Studies" + , journal = "Current Alzheimer Research" + , year = "2018" + , link = "https://doi.org/10.2174/1567205015666180427142350" + } + , { author = "Junker, R., et al." + , title = "Effects of Diets Containing Olive Oil, Sunflower Oil, or Rapeseed Oil on the Hemostatic System" + , journal = "Thrombosis and Haemostasis" + , year = "2001" + , link = "" + } + , { author = "Freese, Riitta, et al." + , title = "No Difference in Platelet Activation or Inflammation Markers after Diets Rich or Poor in Vegetables, Berries and Apple in Healthy Subjects" + , journal = "European Journal of Nutrition" + , year = "2004" + , link = "https://doi.org/10.1007/s00394-004-0456-4" + } + , { author = "Vafeiadou, Katerina, et al." + , title = "Replacement of Saturated with Unsaturated Fats Had No Impact on Vascular Function but Beneficial Effects on Lipid Biomarkers, E-Selectin, and Blood Pressure: Results from the Randomized, Controlled Dietary Intervention and VAScular Function (DIVAS) Study" + , journal = "The American Journal of Clinical Nutrition" + , year = "2015" + , link = "https://doi.org/10.3945/ajcn.114.097089" + } + , { author = "Iggman, David, et al." + , title = "Role of Dietary Fats in Modulating Cardiometabolic Risk during Moderate Weight Gain: A Randomized Double-Blind Overfeeding Trial (LIPOGAIN Study)" + , journal = "Journal of the American Heart Association" + , year = "2014" + , link = "https://doi.org/10.1161/JAHA.114.001095" + } + , { author = "Hozo, Stela Pudar, et al." + , title = "Estimating the Mean and Variance from the Median, Range, and the Size of a Sample" + , journal = "BMC Medical Research Methodology" + , year = "2005" + , link = "https://doi.org/10.1186/1471-2288-5-13" + } + , { author = "Freese, R., et al." + , title = "No Effect on Oxidative Stress Biomarkers by Modified Intakes of Polyunsaturated Fatty Acids or Vegetables and Fruit" + , journal = "European Journal of Clinical Nutrition" + , year = "2008" + , link = "https://doi.org/10.1038/sj.ejcn.1602865" + } + , { author = "Jenkinson, A., et al." + , title = "Dietary Intakes of Polyunsaturated Fatty Acids and Indices of Oxidative Stress in Human Volunteers" + , journal = "European Journal of Clinical Nutrition" + , year = "1999" + , link = "https://doi.org/10.1038/sj.ejcn.1600783" + } + , { author = "de Kok, T. M. C. M., et al." + , title = "Analysis of Oxidative DNA Damage after Human Dietary Supplementation with Linoleic Acid" + , journal = "Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research Association" + , year = "2003" + , link = "https://doi.org/10.1016/s0278-6915(02)00237-5" + } + , { author = "Södergren, E., et al." + , title = "A Diet Containing Rapeseed Oil-Based Fats Does Not Increase Lipid Peroxidation in Humans When Compared to a Diet Rich in Saturated Fatty Acids" + , journal = "European Journal of Clinical Nutrition" + , year = "2001" + , link = "https://doi.org/10.1038/sj.ejcn.1601246" + } + , { author = "Parfitt, V. J., et al." + , title = "Effects of High Monounsaturated and Polyunsaturated Fat Diets on Plasma Lipoproteins and Lipid Peroxidation in Type 2 Diabetes Mellitus" + , journal = "Diabetic Medicine: A Journal of the British Diabetic Association" + , year = "1994" + , link = "https://doi.org/10.1111/j.1464-5491.1994.tb00235.x" + } + ] } diff --git a/frontend/src/Config/Pages/Blog/Types.elm b/frontend/src/Config/Pages/Blog/Types.elm index e1bd4b2..8568433 100755 --- a/frontend/src/Config/Pages/Blog/Types.elm +++ b/frontend/src/Config/Pages/Blog/Types.elm @@ -1,5 +1,7 @@ module Config.Pages.Blog.Types exposing (..) +import Config.Helpers.References exposing (..) + type alias BlogArticle = { articleName : String @@ -10,4 +12,5 @@ type alias BlogArticle = , isNewTabLink : Bool , articlePublished : String , articleDescription : String + , articleReferences : List References } diff --git a/frontend/src/Config/Pages/Products/Types.elm b/frontend/src/Config/Pages/Products/Types.elm index 2b073dd..4e612d5 100755 --- a/frontend/src/Config/Pages/Products/Types.elm +++ b/frontend/src/Config/Pages/Products/Types.elm @@ -1,5 +1,7 @@ module Config.Pages.Products.Types exposing (..) +import Config.Helpers.References exposing (..) + type alias NutriDex = { nutriDexTitle : String @@ -12,12 +14,3 @@ type alias Features = { feature : String , featureTitle : String } - - -type alias References = - { author : String - , title : String - , link : String - , year : String - , journal : String - } diff --git a/frontend/src/Pages/Blog.elm b/frontend/src/Pages/Blog.elm index 6be4c07..cefecfb 100755 --- a/frontend/src/Pages/Blog.elm +++ b/frontend/src/Pages/Blog.elm @@ -34,6 +34,9 @@ import Config.Helpers.Response , topLevelContainer ) import Config.Helpers.Viewport exposing (resetViewport) +import Config.Pages.Blog.Records.HunterGatherers exposing (articleHunterGatherers) +import Config.Pages.Blog.Records.NagraGoodrich exposing (articleNagraGoodrich) +import Config.Pages.Blog.Records.SapienDiet exposing (articleSapienDiet) import Config.Pages.Blog.Records.SeedOils exposing (articleSeedOils) import Config.Pages.Blog.Types exposing (..) import Config.Style.Colour as T exposing (..) @@ -149,7 +152,11 @@ blogList device = _ -> List.map desktopBlogMaker ) - [ articleSeedOils ] + [ articleNagraGoodrich + , articleSapienDiet + , articleSeedOils + , articleHunterGatherers + ] ] @@ -175,7 +182,7 @@ desktopBlogMaker article = [ cardContentSpacing [ column fieldSpacer - [ seedOilMaker article ] + [ articleMaker article ] ] ] ] @@ -197,7 +204,7 @@ mobileBlogMaker article = [ mobileCardMaker mobileImageBoxSize mobileImageSize (articleImage article) article.articleLink , column [ width fill ] - [ seedOilMaker article ] + [ articleMaker article ] ] ] ] @@ -213,19 +220,19 @@ articleImage : , description : String } articleImage article = - { src = "blog/" ++ article.articleImage ++ ".png" + { src = "blog/" ++ article.articleImage ++ "thumb.png" , description = article.articleName } -seedOilMaker : BlogArticle -> Element msg -seedOilMaker article = +articleMaker : BlogArticle -> Element msg +articleMaker article = column [ E.width fill , centerX ] [ column [ width fill ] - (seedOilRows article + (articleRows article ++ [ row [] [ paragraph [ F.color colourTheme.textLightGrey @@ -273,9 +280,10 @@ infoRow label value = ] -seedOilRows : BlogArticle -> List (Element msg) -seedOilRows article = +articleRows : BlogArticle -> List (Element msg) +articleRows article = [ infoRow "Author:" article.articleAuthor , infoRow "Published:" article.articlePublished + , infoRow "Duration:" (String.fromInt (wordCount article.articleBody // 225) ++ " minutes") , infoRow "Word Count:" (String.fromInt (wordCount article.articleBody)) ] diff --git a/frontend/src/Pages/Blog/Huntergatherers.elm b/frontend/src/Pages/Blog/Huntergatherers.elm new file mode 100755 index 0000000..5d9cfe4 --- /dev/null +++ b/frontend/src/Pages/Blog/Huntergatherers.elm @@ -0,0 +1,195 @@ +module Pages.Blog.Huntergatherers exposing (Model, Msg, page) + +import Config.Data.Identity exposing (pageNames) +import Config.Helpers.CardFormat + exposing + ( cardContentSpacing + , cardFormatter + , cardMaker + , cardSubTitleMaker + , cardTitleMaker + , desktopCardMaker + , desktopImageBoxSize + , desktopImageSize + , fieldSpacer + , mobileCardMaker + , mobileImageBoxSize + , mobileImageSize + , topLevelBox + ) +import Config.Helpers.Format exposing (..) +import Config.Helpers.Header + exposing + ( Header + , headerMaker + ) +import Config.Helpers.Markdown exposing (..) +import Config.Helpers.References exposing (makeReference) +import Config.Helpers.Response + exposing + ( pageList + , topLevelContainer + ) +import Config.Helpers.StrengthBar + exposing + ( barMaker + , barPadding + ) +import Config.Helpers.ToolTip exposing (..) +import Config.Helpers.Viewport exposing (resetViewport) +import Config.Pages.Blog.Records.HunterGatherers exposing (articleHunterGatherers) +import Config.Pages.Blog.Types exposing (BlogArticle) +import Config.Pages.Contact.Types exposing (..) +import Config.Pages.Interviews.Types exposing (..) +import Config.Pages.Products.Types exposing (..) +import Config.Style.Colour exposing (colourTheme) +import Config.Style.Transitions + exposing + ( hoverFontDarkOrange + , transitionStyleFast + , transitionStyleSlow + ) +import Effect exposing (Effect) +import Element as E exposing (..) +import Element.Background as B +import Element.Border as D +import Element.Font as F +import Html +import Html.Attributes as H exposing (style) +import Layouts +import Page exposing (Page) +import Route exposing (Route) +import Shared exposing (..) +import View exposing (View) + + +page : Shared.Model -> Route () -> Page Model Msg +page shared route = + Page.new + { init = init + , update = update + , subscriptions = subscriptions + , view = view shared + } + |> Page.withLayout toLayout + + +toLayout : Model -> Layouts.Layout Msg +toLayout model = + Layouts.Navbar {} + + + +-- INIT + + +type alias Model = + {} + + +init : () -> ( Model, Effect Msg ) +init () = + ( {} + , Effect.none + ) + + + +-- UPDATE + + +type Msg + = NoOp + + +update : Msg -> Model -> ( Model, Effect Msg ) +update msg model = + case msg of + NoOp -> + ( model + , Effect.none + ) + + + +-- SUBSCRIPTIONS + + +subscriptions : Model -> Sub Msg +subscriptions model = + Sub.none + + + +-- VIEW + + +view : Shared.Model -> Model -> View Msg +view shared model = + { title = pageNames.pageHyperBlog ++ " (hunterGatherers)" + , attributes = [] + , element = articleContainer shared.device + } + + +articleContainer : Device -> Element msg +articleContainer device = + topLevelContainer (articleList device) + + +articleList : Device -> Element msg +articleList device = + column + (case ( device.class, device.orientation ) of + _ -> + pageList + ) + <| + List.concat + [ (case ( device.class, device.orientation ) of + _ -> + List.map articleMaker + ) + [ articleHunterGatherers ] + ] + + +articleMaker : BlogArticle -> Element msg +articleMaker article = + column + topLevelBox + [ cardMaker + [ cardTitleMaker (String.toUpper articleHunterGatherers.articleName) + , cardFormatter + [ cardContentSpacing + [ column + fieldSpacer + [ cardSubTitleMaker + [ articleImage articleHunterGatherers.articleImage + , renderDeviceMarkdown articleHunterGatherers.articleBody + , articleReferences article + ] + ] + ] + ] + ] + ] + + +articleReferences : BlogArticle -> Element msg +articleReferences article = + column + [ width fill + , height fill + , paddingEach + { top = 10 + , right = 0 + , bottom = 0 + , left = 0 + } + ] + [ column [ width fill, F.size 15, spacing 10 ] <| + List.map2 (\x y -> makeReference x y) + article.articleReferences + (List.range 1 (List.length article.articleReferences)) + ] diff --git a/frontend/src/Pages/Blog/Nagragoodrich.elm b/frontend/src/Pages/Blog/Nagragoodrich.elm new file mode 100644 index 0000000..8a54a62 --- /dev/null +++ b/frontend/src/Pages/Blog/Nagragoodrich.elm @@ -0,0 +1,194 @@ +module Pages.Blog.Nagragoodrich exposing (Model, Msg, page) + +import Config.Data.Identity exposing (pageNames) +import Config.Helpers.CardFormat + exposing + ( cardContentSpacing + , cardFormatter + , cardMaker + , cardSubTitleMaker + , cardTitleMaker + , desktopCardMaker + , desktopImageBoxSize + , desktopImageSize + , fieldSpacer + , mobileCardMaker + , mobileImageBoxSize + , mobileImageSize + , topLevelBox + ) +import Config.Helpers.Format exposing (..) +import Config.Helpers.Header + exposing + ( Header + , headerMaker + ) +import Config.Helpers.Markdown exposing (..) +import Config.Helpers.References exposing (makeReference) +import Config.Helpers.Response + exposing + ( pageList + , topLevelContainer + ) +import Config.Helpers.StrengthBar + exposing + ( barMaker + , barPadding + ) +import Config.Helpers.ToolTip exposing (..) +import Config.Helpers.Viewport exposing (resetViewport) +import Config.Pages.Blog.Records.NagraGoodrich exposing (articleNagraGoodrich) +import Config.Pages.Blog.Types exposing (BlogArticle) +import Config.Pages.Contact.Types exposing (..) +import Config.Pages.Interviews.Types exposing (..) +import Config.Pages.Products.Types exposing (..) +import Config.Style.Colour exposing (colourTheme) +import Config.Style.Transitions + exposing + ( hoverFontDarkOrange + , transitionStyleFast + , transitionStyleSlow + ) +import Effect exposing (Effect) +import Element as E exposing (..) +import Element.Background as B +import Element.Border as D +import Element.Font as F +import Html +import Html.Attributes as H exposing (style) +import Layouts +import Page exposing (Page) +import Route exposing (Route) +import Shared exposing (..) +import View exposing (View) + + +page : Shared.Model -> Route () -> Page Model Msg +page shared route = + Page.new + { init = init + , update = update + , subscriptions = subscriptions + , view = view shared + } + |> Page.withLayout toLayout + + +toLayout : Model -> Layouts.Layout Msg +toLayout model = + Layouts.Navbar {} + + + +-- INIT + + +type alias Model = + {} + + +init : () -> ( Model, Effect Msg ) +init () = + ( {} + , Effect.none + ) + + + +-- UPDATE + + +type Msg + = NoOp + + +update : Msg -> Model -> ( Model, Effect Msg ) +update msg model = + case msg of + NoOp -> + ( model + , Effect.none + ) + + + +-- SUBSCRIPTIONS + + +subscriptions : Model -> Sub Msg +subscriptions model = + Sub.none + + + +-- VIEW + + +view : Shared.Model -> Model -> View Msg +view shared model = + { title = pageNames.pageHyperBlog ++ " (NagraGoodrich)" + , attributes = [] + , element = articleContainer shared.device + } + + +articleContainer : Device -> Element msg +articleContainer device = + topLevelContainer (articleList device) + + +articleList : Device -> Element msg +articleList device = + column + (case ( device.class, device.orientation ) of + _ -> + pageList + ) + <| + List.concat + [ (case ( device.class, device.orientation ) of + _ -> + List.map articleMaker + ) + [ articleNagraGoodrich ] + ] + + +articleMaker : BlogArticle -> Element msg +articleMaker article = + column + topLevelBox + [ cardMaker + [ cardTitleMaker (String.toUpper articleNagraGoodrich.articleName) + , cardFormatter + [ cardContentSpacing + [ column + fieldSpacer + [ cardSubTitleMaker + [ articleImage articleNagraGoodrich.articleImage + , renderDeviceMarkdown articleNagraGoodrich.articleBody + ] + ] + ] + ] + ] + ] + + +articleReferences : BlogArticle -> Element msg +articleReferences article = + column + [ width fill + , height fill + , paddingEach + { top = 10 + , right = 0 + , bottom = 0 + , left = 0 + } + ] + [ column [ width fill, F.size 15, spacing 10 ] <| + List.map2 (\x y -> makeReference x y) + article.articleReferences + (List.range 1 (List.length article.articleReferences)) + ] diff --git a/frontend/src/Pages/Blog/Sapiendiet.elm b/frontend/src/Pages/Blog/Sapiendiet.elm new file mode 100755 index 0000000..c75594d --- /dev/null +++ b/frontend/src/Pages/Blog/Sapiendiet.elm @@ -0,0 +1,195 @@ +module Pages.Blog.Sapiendiet exposing (Model, Msg, page) + +import Config.Data.Identity exposing (pageNames) +import Config.Helpers.CardFormat + exposing + ( cardContentSpacing + , cardFormatter + , cardMaker + , cardSubTitleMaker + , cardTitleMaker + , desktopCardMaker + , desktopImageBoxSize + , desktopImageSize + , fieldSpacer + , mobileCardMaker + , mobileImageBoxSize + , mobileImageSize + , topLevelBox + ) +import Config.Helpers.Format exposing (..) +import Config.Helpers.Header + exposing + ( Header + , headerMaker + ) +import Config.Helpers.Markdown exposing (..) +import Config.Helpers.References exposing (makeReference) +import Config.Helpers.Response + exposing + ( pageList + , topLevelContainer + ) +import Config.Helpers.StrengthBar + exposing + ( barMaker + , barPadding + ) +import Config.Helpers.ToolTip exposing (..) +import Config.Helpers.Viewport exposing (resetViewport) +import Config.Pages.Blog.Records.SapienDiet exposing (articleSapienDiet) +import Config.Pages.Blog.Types exposing (BlogArticle) +import Config.Pages.Contact.Types exposing (..) +import Config.Pages.Interviews.Types exposing (..) +import Config.Pages.Products.Types exposing (..) +import Config.Style.Colour exposing (colourTheme) +import Config.Style.Transitions + exposing + ( hoverFontDarkOrange + , transitionStyleFast + , transitionStyleSlow + ) +import Effect exposing (Effect) +import Element as E exposing (..) +import Element.Background as B +import Element.Border as D +import Element.Font as F +import Html +import Html.Attributes as H exposing (style) +import Layouts +import Page exposing (Page) +import Route exposing (Route) +import Shared exposing (..) +import View exposing (View) + + +page : Shared.Model -> Route () -> Page Model Msg +page shared route = + Page.new + { init = init + , update = update + , subscriptions = subscriptions + , view = view shared + } + |> Page.withLayout toLayout + + +toLayout : Model -> Layouts.Layout Msg +toLayout model = + Layouts.Navbar {} + + + +-- INIT + + +type alias Model = + {} + + +init : () -> ( Model, Effect Msg ) +init () = + ( {} + , Effect.none + ) + + + +-- UPDATE + + +type Msg + = NoOp + + +update : Msg -> Model -> ( Model, Effect Msg ) +update msg model = + case msg of + NoOp -> + ( model + , Effect.none + ) + + + +-- SUBSCRIPTIONS + + +subscriptions : Model -> Sub Msg +subscriptions model = + Sub.none + + + +-- VIEW + + +view : Shared.Model -> Model -> View Msg +view shared model = + { title = pageNames.pageHyperBlog ++ " (sapienDiet)" + , attributes = [] + , element = articleContainer shared.device + } + + +articleContainer : Device -> Element msg +articleContainer device = + topLevelContainer (articleList device) + + +articleList : Device -> Element msg +articleList device = + column + (case ( device.class, device.orientation ) of + _ -> + pageList + ) + <| + List.concat + [ (case ( device.class, device.orientation ) of + _ -> + List.map articleMaker + ) + [ articleSapienDiet ] + ] + + +articleMaker : BlogArticle -> Element msg +articleMaker article = + column + topLevelBox + [ cardMaker + [ cardTitleMaker (String.toUpper articleSapienDiet.articleName) + , cardFormatter + [ cardContentSpacing + [ column + fieldSpacer + [ cardSubTitleMaker + [ articleImage articleSapienDiet.articleImage + , renderDeviceMarkdown articleSapienDiet.articleBody + , articleReferences article + ] + ] + ] + ] + ] + ] + + +articleReferences : BlogArticle -> Element msg +articleReferences article = + column + [ width fill + , height fill + , paddingEach + { top = 10 + , right = 0 + , bottom = 0 + , left = 0 + } + ] + [ column [ width fill, F.size 15, spacing 10 ] <| + List.map2 (\x y -> makeReference x y) + article.articleReferences + (List.range 1 (List.length article.articleReferences)) + ] diff --git a/frontend/src/Pages/Blog/Seedoils.elm b/frontend/src/Pages/Blog/Seedoils.elm old mode 100644 new mode 100755 index caec4d6..3832ad1 --- a/frontend/src/Pages/Blog/Seedoils.elm +++ b/frontend/src/Pages/Blog/Seedoils.elm @@ -24,6 +24,7 @@ import Config.Helpers.Header , headerMaker ) import Config.Helpers.Markdown exposing (..) +import Config.Helpers.References exposing (makeReference) import Config.Helpers.Response exposing ( pageList @@ -37,6 +38,7 @@ import Config.Helpers.StrengthBar import Config.Helpers.ToolTip exposing (..) import Config.Helpers.Viewport exposing (resetViewport) import Config.Pages.Blog.Records.SeedOils exposing (articleSeedOils) +import Config.Pages.Blog.Types exposing (BlogArticle) import Config.Pages.Contact.Types exposing (..) import Config.Pages.Interviews.Types exposing (..) import Config.Pages.Products.Types exposing (..) @@ -124,7 +126,7 @@ subscriptions model = view : Shared.Model -> Model -> View Msg view shared model = - { title = pageNames.pageHyperBlog ++ "(seedOils)" + { title = pageNames.pageHyperBlog ++ " (seedOils)" , attributes = [] , element = articleContainer shared.device } @@ -137,16 +139,23 @@ articleContainer device = articleList : Device -> Element msg articleList device = - column pageList <| + column + (case ( device.class, device.orientation ) of + _ -> + pageList + ) + <| List.concat - (case ( device.class, device.orientation ) of + [ (case ( device.class, device.orientation ) of _ -> - [ [ articleMaker ] ] - ) + List.map articleMaker + ) + [ articleSeedOils ] + ] -articleMaker : Element msg -articleMaker = +articleMaker : BlogArticle -> Element msg +articleMaker article = column topLevelBox [ cardMaker @@ -158,9 +167,29 @@ articleMaker = [ cardSubTitleMaker [ articleImage articleSeedOils.articleImage , renderDeviceMarkdown articleSeedOils.articleBody + , articleReferences article ] ] ] ] ] ] + + +articleReferences : BlogArticle -> Element msg +articleReferences article = + column + [ width fill + , height fill + , paddingEach + { top = 10 + , right = 0 + , bottom = 0 + , left = 0 + } + ] + [ column [ width fill, F.size 15, spacing 10 ] <| + List.map2 (\x y -> makeReference x y) + article.articleReferences + (List.range 1 (List.length article.articleReferences)) + ] diff --git a/frontend/src/Pages/Home_.elm b/frontend/src/Pages/Home_.elm index c60e595..ae7bc47 100755 --- a/frontend/src/Pages/Home_.elm +++ b/frontend/src/Pages/Home_.elm @@ -6,17 +6,17 @@ import Config.Helpers.Format ( paragraphFontSize , paragraphSpacing ) +import Config.Helpers.Header + exposing + ( Header + , headerMaker + ) import Config.Helpers.Response exposing ( pageListCenter , topLevelContainer ) import Config.Helpers.Viewport exposing (resetViewport) -import Config.Helpers.Header - exposing - ( Header - , headerMaker - ) import Config.Style.Colour exposing (colourTheme) import Config.Style.Glow exposing (glowDeepDarkGrey) import Config.Style.Icons.Icons diff --git a/frontend/src/Pages/Nutridex.elm b/frontend/src/Pages/Nutridex.elm index a3b88cf..b5f2fee 100755 --- a/frontend/src/Pages/Nutridex.elm +++ b/frontend/src/Pages/Nutridex.elm @@ -22,6 +22,8 @@ import Config.Helpers.Format ( paragraphFontSize , paragraphSpacing ) +import Config.Helpers.Header exposing (..) +import Config.Helpers.References exposing (..) import Config.Helpers.Response exposing ( pageList @@ -34,12 +36,6 @@ import Config.Helpers.StrengthBar ) import Config.Helpers.ToolTip exposing (tooltip) import Config.Helpers.Viewport exposing (resetViewport) -import Config.Helpers.Header exposing (..) -import Config.Helpers.Header - exposing - ( Header - , headerMaker - ) import Config.Pages.Products.Records.NutriDex exposing (productNutriDex) import Config.Pages.Products.Types exposing (..) import Config.Style.Colour exposing (colourTheme) @@ -434,7 +430,7 @@ nutriDexTitleMaker title = [ width fill , centerX , D.widthEach { bottom = 1, top = 0, left = 0, right = 0 } - , D.color (rgb255 200 200 200) + , D.color colourTheme.textLightOrange , paddingEach { top = 40, bottom = 0, left = 0, right = 0 } ] [] @@ -1119,7 +1115,7 @@ nutriDexReferenceTitleMaker = [ 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