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@@ -46,7 +46,7 @@ Also, if insufficiency of K2 and the other fat soluble vitamins are to blame for
 First of all, the claim of 84% of vegans quitting is just blatantly incorrect according to his own citation, which found a 70% dropout rate for vegans. Second of all, this is a ridiculous question. People stop doing health promoting things for all sorts of reasons, and it probably would have been a good idea for him to read the goddamn reference instead of resorting to conspiracy theories. The study includes an inventory of explanations for participant recidivism, and [the craving of animal products only occurred in the minority of recidivists](https://faunalytics.org/wp-content/uploads/2016/02/Faunalytics-Study-of-Current-and-Former-Vegetarians-and-Vegans-%E2%80%93-Secondary-Findings-.pdf).
 
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 Furthermore the study includes a table of motivations for pursuing veganism. Only a measly 1-3% of participants had motivations that were purely ethical in nature. While most motivations were health related. So, it seems like people are generally going on plant-based diets for health related reasons, and abandoning the diets without generally suffering health related costs. This isn't the only reason the question is stupid. Plenty of health promoting behaviours have high recidivism rates, such as exercise.
 
@@ -59,7 +59,7 @@ Of those 11, 6 were vague like "sick", "lightheaded", "not healthy", and "health
 It's not clear why we should accept the implication that a diet is healthy if and only if it can be generally adhered to. There are many examples of diets with poor adherence rates that I don't think Joseph would sign off on being unhealthy, and there are plenty of examples of diets with high adherence rates that Joseph wouldn't consider healthy at all.
 
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 **Claim #3 (**[**04:59**](https://youtu.be/MpxgZGnEF7E?t=299)**):**
 
@@ -72,19 +72,19 @@ Firstly, this is an ecological fallacy. Essentially, Joseph is looking at two te
 Instead, this research is just looking at the average height of each entire country and the average intake of said foods. Such studies are susceptible to something called the [ecological fallacy](https://en.wikipedia.org/wiki/Ecological_fallacy), meaning what applies on a country average level may not apply on an individual level.
 
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 In this graph on average as X increases, so does Y. But if you look at each cluster separately, as X increases Y decreases. A real life example of this is the relationship between smoking and longevity.
 
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 If you plot each country's smoking rate and lifespan you'll see that [the more people smoke the longer they live](https://www.thefunctionalart.com/2018/07/visualizing-amalgamation-paradoxes-and.html). This correlation, of course, breaks at an individual level.
 
 I very much doubt that Joseph would approve of this ecological study. [[6](https://pubmed.ncbi.nlm.nih.gov/1140864/)]
 
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 The study makes no attempt to adjust for socioeconomic or genetic differences in the countries involved. Richer countries tend to have access to more expensive sources of calories, but also have fewer infections and cleaner water, among many other things conducive to better health. They also tend to eat meat. This doesn't tell us what's happening within each of those populations across the spectrum of meat consumption.
 
@@ -97,19 +97,19 @@ Also it's likely that the reason animal protein correlates strongly with height
 Yovana Mendoza was a so-called "raw" vegan. As you can see from the picture he flashed, she was on a meme starvation diet of only raw food averaging an abysmal ~1000 calories a day.
 
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 Raw food diets are associated with many stupid beliefs revolving around self-purification, including extensive fasting periods (49% of study participants), not supplementing B12 (7% took any supplement at all), and enemas (16% of them). [[7](https://pubmed.ncbi.nlm.nih.gov/10436305/)]
 
 Some believe once you are "purified" you lose your period which is a sign you're clean, for example. As you approach 100% raw food, pretty much half of them complain of amenorrhea, probably due to insufficient calories.
 
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 As you can see, raw diets associate with considerably low BMI scores.
 
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 Rawvana also [made a video](https://youtu.be/hMO4m0rZAB8?t=27) telling us how since she's gotten healthier on her raw vegan diet her "eyes have become greener", so I don't know how much stock we should put in her health advice, Joseph.
 
@@ -126,7 +126,7 @@ Both studies showed that vegans had statistically significantly lower retinol st
 Now, let's get to the mechanistic fuckery. Joseph claims that there are genetic differences in carotenoid to retinol conversion capacity that could lead to deficiency in some who are relying on carotenoids over retinol. Right off the bat, Joseph's own reference contradicts his claim, as the entire variance in the population sample had fasting plasma retinol within the reference range.
 
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 > _...the lowest plasma concentration was 963.8 nM, indicating that all volunteers had adequate serum vitamin A concentrations._
 
@@ -171,14 +171,14 @@ Here's a quick intro for vitamin K2. There are many different vitamin K isomers
 First, we'll look at bioavailability of MK4. He mentions animal livers (especially goose liver), egg-yolks, hard cheese and full-fat dairy. I couldn’t find any study on bioavailability of MK4 from foods rather than supplements. But, we can look at studies with doses one could plausibly obtain from diet alone. In probably the best study on this subject, researchers assessed **420 μg of MK-4 compared to 420 μg of MK-7**. [[35](https://pubmed.ncbi.nlm.nih.gov/23140417/)] As you can see from this chart, the only reasonable way to obtain this is with goose liver. [[36](https://pubmed.ncbi.nlm.nih.gov/11356998/)]
 
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 The other things he recommended simply don’t have enough. To get this amount it would take **8.9 kilograms of hard cheese, 52.5 liters of whole milk, or 52.4 average eggs.** The amount of goose liver it would take to get this dose of MK-4 is roughly **115g of liver,** however this has **over 10,000μg of retinol, the upper limit is 3000μg** and hypervitaminosis A is no joke.
 
 But regardless, let’s say someone managed to eat this amount of MK-4 regularly. Is it actually absorbed? It wouldn't appear so.
 
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 At no time point after the oral administration of 420μg of MK4 is it actually detectable in the blood.
 
@@ -193,10 +193,10 @@ What Joseph didn't mention was that 29% of the vegan children did not consume vi
 I mention this because it's clear that a large chunk of the cohort was not actually supplementing vitamin B12 and vitamin D. Both of which are nutrients that are strongly associated with normal growth. There was also little to no consideration for other dietary variables, and the analysis itself is cross-sectional with extremely small sample-sizes.
 
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 Perhaps also worth noting are the similar lean mass, lower fat mass, and preferable LDL-C and hs-CRP values of the vegans. But he didn't mention that.
 
@@ -207,7 +207,7 @@ Perhaps also worth noting are the similar lean mass, lower fat mass, and prefera
 Let's start with the British study. These results are trivially explainable by the lower caloric intakes for vegans in his reference.
 
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 Also, while the vegans tended to fall below the 50th percentile for weight, the vast majority experienced normal growth, and the lower weight (and in some cases height) may be attributable to the lower caloric intake. The authors actually take note of this, but Joseph didn't mention it.
 
@@ -226,17 +226,17 @@ In the Farm Study was a 1989 study involving children ages four months to ten ye
 Across vegan children, growth was skirting the 50th percentile on average. This is exactly where these growth trajectories should be.
 
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 Same for weight.
 
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 We also have the VeChi Diet Study. [[40](https://pubmed.ncbi.nlm.nih.gov/31013738/)] Vegan and omnivorous children had similar caloric intakes. Omnivores had the highest protein, fat, and added sugar intake, while vegans had the highest total carb and fibre intake. In fact, the vegans were still able to consume a median of 2.25g of protein per kg bodyweight. While there were a few outliers in each group, growth was generally very similar overall.
 
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 There are explanations for the children who may have been stunted or wasted, and they're nothing that is necessarily inherent to vegan diets themselves. These reasons include: short parents, inadequate caloric intake, exclusively breastfeeding longer than recommended (probably due to hippie vegan parents doing dumb hippie things).
 
@@ -261,12 +261,12 @@ Joseph then concludes (from two studies were the majority did not supplement B12
 If Joseph wanted to know if B12 supplements work differently than animal foods, he could turn his attention to this interventional study that found that fortified cereal was more effective at raising B12 than pork. [[46](https://pubmed.ncbi.nlm.nih.gov/31519167/)]
 
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 Also, various doses of cheapo, vanilla-ass cyanocobalamin rescue vitamin B12 deficiency in clinically deficient vegans. [[47](https://pubmed.ncbi.nlm.nih.gov/29499976/)] This is confirmed by clinically meaningful reductions in both methylmalonic acid and total homocysteine. If Joseph knows of any better biological correlates for B12 absorption and utilization, as well as evidence that they're uniquely affected by animal foods, I'd love to hear from him about it.
 
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 **Claim #14 (**[**11:38**](https://youtu.be/MpxgZGnEF7E?t=698)**):**
 
@@ -325,7 +325,7 @@ Firstly, despite whole wheat flour being higher in phytic acid than white wheat
 Secondly, other compounds that are common in plant foods but are absent (or virtually absent) from animal foods may have pleiotropic effects that mitigate or even overcome the effect of phytates on iron absorption, with vitamin C probably being the most prominent example. In regards of counteracting phytic acid, 50mg (less than an orange worth) does more than 50g of meat. [[62](https://pubmed.ncbi.nlm.nih.gov/2911999/)]
 
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 It also doesn't follow that one needs to consume animal products to meet iron needs, which Joseph heavily implies. Increased intake through diet and/or supplementation are clearly possible.
 
@@ -372,7 +372,7 @@ Vegans, especially those who menstruate, might want to err on the side of cautio
 Previously having less edible material is trivially true of animal foods produced from modern animal agriculture.
 
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 **Claim #21 (**[**14:58**](https://youtu.be/MpxgZGnEF7E?t=898)**):**
 
@@ -381,7 +381,7 @@ Previously having less edible material is trivially true of animal foods produce
 What point is Joseph trying to make here? We could try to formalize it, perhaps.
 
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 **Claim #22 (**[**15:34**](https://youtu.be/MpxgZGnEF7E?t=934)**):**
 
@@ -400,12 +400,12 @@ Lastly, one of the two "high quality" studies in the review that Joseph cited ev
 Here is the prevalence of depression forest plot from that meta-analysis.
 
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 And mean depression scores.
 
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 Also, just for flavour, I'll point out that Joseph's reference was funded by the beef industry.
 
@@ -486,7 +486,7 @@ On average, vegans do in fact tend to have a lower bone mineral density and high
 BMI has been shown to causally increase bone mineral density, which in turn has been shown to causally decrease risk of fracture. This effect mediation has been found independently in observational studies, and the differences in bone mineral density seem to align with what we would expect based on the differences in BMI. [[89](https://pubmed.ncbi.nlm.nih.gov/33784428/)][[90](https://pubmed.ncbi.nlm.nih.gov/36260985/)][[91](https://pubmed.ncbi.nlm.nih.gov/24862213/)][[92](https://pubmed.ncbi.nlm.nih.gov/15817133/)]
 
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 So the question that is interesting here, from a causal perspective, is whether vegans have weaker bones and higher risk of fracture independently of BMI and other important confounders such as calcium and vitamin D. Vitamin D has not been taken into account at all in the EPIC-Oxford study. BMI and dietary calcium were adjusted for, but only via categorisation, which is known to bias results when examining continuous variables with non-linear responses. [[93](https://pubmed.ncbi.nlm.nih.gov/17938055/)]
 
@@ -529,7 +529,7 @@ These data don't represent any official guidelines. And I'm not sure how shitty
 In fact, some animal foods rank higher than some plant foods, and in the aggregate there is non-inferiority between some animal foods and some plant foods. For example, seafood ranks particularly high, and is non-inferior to both fruits and vegetables. Both meat and dairy are also non-inferior to grains. If Joseph wants to make some kind of claim about a vegan conspiracy to suppress the health value of animal foods, he'll have to explain why seafood gets such a remarkable score here.
 
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 # EVEN MOAR NUTRIENTS THO
 
@@ -576,7 +576,7 @@ Regarding creatine, all studies he cited were on supplemental creatine with dose
 I'm sorry, Joseph. But tracer studies disagree. [[113](https://pubmed.ncbi.nlm.nih.gov/33693735/)] In fact, tofu appears to be on par with pork, and better than eggs, in terms of its contribution to total positive protein balance in the human body.
 
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 If you're going to try to make this point to shit on tofu, would you please be consistent and also shit on pork and eggs?
 
@@ -639,7 +639,7 @@ Bruh, this is a meta-analysis of rodent studies with a blurb about how the resul
 In isolation, leghemoglobin actually had better bioavailability than iron(II)-sulfate, and when part of a food matrix, here as fortification for corn tortillas, had similar (ie non stat sig different) bioavailability compared to bovine heme iron. [[124](https://pubmed.ncbi.nlm.nih.gov/16478282/)]
 
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 As an added fun fact that may blow up the brains of Joseph's audience, leghemoglobin is actually evolutionarily just as old as hemoglobin. See the following figure from Biochemistry 6th edition by Berg, Tymoczko and Styer.
 
@@ -688,10 +688,10 @@ Show me the study that actually divulges that any of these sorts of foods have a
 Well, as long as we're appealing to authorities, we should point out that both the French and German governments recommend limiting meat intake to no more than 500g per week and 600g per week, respectively.
 
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 # VEGAN MIDGET BABIES THO
 
@@ -722,7 +722,7 @@ Finally, two cautionary narrative review articles by Miedziaszczyk et al. and Pa
 This just seems like pure speculation. Maybe optimal is not achievable without a supplement on any natural diet. I mean, think about it. What's the argument for omnivorous diets necessarily providing optimal amounts of all nutrients? If there's no argument for that, then it's possible that even the diet that he's recommending is horribly insufficient in some way.
 
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 How has Joseph determined that the optimal range for nutrient intakes aren't above what could be obtained from omnivorous diets? Seems like his argument here is begging the question. If it's the case that optimal levels of nutrients are only practical to obtain from supplements, then we'd all benefit— not just vegans.
 

frontend/src/Config/Pages/Blog/Records/SweetDeception.elm

@@ -34,12 +34,12 @@ The IMCL hypothesis attempts to highlight the potential impact of IMCL accumulat
 The mechanistic case for the IMCL hypothesis was first outlined in the late 1990s with two small studies by Jacob, et al. and Perseghin, et al., which discovered relationships between IMCL and insulin resistance in T2DM-free subjects who were born of parents with T2DM [[1](https://pubmed.ncbi.nlm.nih.gov/10331418/)][[2](https://pubmed.ncbi.nlm.nih.gov/10426379/)]. In these experiments, the offspring of those with T2DM were subjected to the gold-standard measure of whole-body insulin sensitivity, the hyperinsulinemic-euglycemic clamp test (HEC). It was discovered that there was an inverse association between IMCL and insulin sensitivity, which led researchers to suspect that perhaps this biomarker was relevant to the pathophysiology of T2DM.
 
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 Fast forward to 2004, and another small study from van Loon, et al. would introduce the hypothesis' first paradox [[3](https://pubmed.ncbi.nlm.nih.gov/15165998/)]. In this experiment, muscle biopsies and less precise (but still adequate) measures of insulin sensitivity were deployed in an investigation of subjects who were either sedentary, afflicted with T2DM, or who were trained athletes. The study found that the IMCL concentrations of IMCL were actually statistically significantly higher in athletic subjects compared to either sedentary or T2DM-afflicted subjects. Yet, the athletic subjects did not suffer from impaired insulin sensitivity or the hyperglycemia that is characteristic of T2DM.
 
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 Researchers Coen and Goodpaster attempted to reconcile the findings in 2012 [[4](https://pubmed.ncbi.nlm.nih.gov/22721584/)]. They hypothesized that IMCL behaves differently in the context of T2DM, and that while IMCL serves as a fuel source in athletic subjects, in sedentary subjects with T2DM the IMCL seems to produce more disruptive mediators like ceramides and diacylglycerols. However, the authors tend to play fast and loose with their causal inferences, often citing animal research to buttress clear implications about what holds true in human beings. In fact, the majority of their supporting evidence is derived from mice, despite mice generally being poor facsimiles for human subjects [[5](https://pubmed.ncbi.nlm.nih.gov/31307492/)].
 
@@ -64,19 +64,19 @@ The mechanisms, epidemiological, and experimental evidence for this hypothesis w
 The author first refers to literature they themselves conducted, including three primary human trials demonstrating disturbances to energy expenditure, markers of liver function, as well as measures of IHL accumulation [[10](https://pubmed.ncbi.nlm.nih.gov/26376619/)][[11](https://pubmed.ncbi.nlm.nih.gov/21952692/)][[12](https://pubmed.ncbi.nlm.nih.gov/22828276/)]. The first trial discovered that isocaloric feeding of fructose compared to glucose over a ten-week period significantly increased hepatic fat.
 
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 However, it's unclear what the clinical significance of this finding is, considering that the fructose-based intervention resulted in significant overfeeding and only increased fasting glucose by 5% compared to the glucose-based control. Seems like the authors tried pretty damn hard to induce a T2DM phenotype feeding fructose to subjects, and were ultimately unable to achieve that. In fact, they weren't really able to get close. Even the oral glucose tolerance test results, though far from ideal, showed an altogether normal blood glucose curve for the fructose group.
 
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 The second trial was unremarkable, and suggested that fructose consumption may decrease energy expenditure over time when isocalorically compared to glucose. Again, it's interesting, but it's far from demonstrating a cause and effect relationship between T2DM and sugar. The third trial is a bit more complicated to unpack. Basically, subjects were split into two groups, 25% of calories as either fructose or glucose as parts of eucaloric diets over 10 weeks, with the primary endpoints beings measures of liver function. Overall, the results of the trial suggest a significantly detrimental effect of fructose compared to glucose on a number of markers related to liver function. However, it's slightly more complicated than that.
 
 While it's true that the treatment effect showed a benefit of glucose over fructose, it's also true that the marker of liver function that was negatively perturbed was gamma-glutamyl transferase (GTT). The change in GGT was also barely statistically significant compared to baseline, while markers such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT) showed a non-significant decrease. Glucose showed greater reductions that were barely statistically significantly different from that of fructose.
 
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 Other than that, fructose did seem to increase uric acid levels to a statistically significant degree, making fructose a potential aggravating factor for conditions such as gout. But again, this is a far cry from causally linking fructose consumption to the development of T2DM, especially since fructose seemed to do nothing particularly interesting to markers of liver function. It is true that sugar intake is severely negatively associated with health outcomes [[13](https://pubmed.ncbi.nlm.nih.gov/34444794/)]. However, while this is a consistent finding, clinical trials on sugar consistently fail to demonstrate a connection between sugar intake and the development of T2DM.
 
@@ -89,7 +89,7 @@ Suffice it to say, there would be little, if any, room for sugar while on such a
 Despite these improvements, recidivism continued to climb. As of two years, the CCI group had crept back into the diabetic range on average [[15](https://pubmed.ncbi.nlm.nih.gov/31231311/)]. By, 3.5 years, the CCI group was once again firmly within the diabetic range on average, having regained a significant amount of weight [[16](https://www.hsrd.research.va.gov/publications/esp/virtual-diet-brief.pdf)][[17](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7208790/)].
 
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 To be clear, there was a clear distinction between remission and reversal, as defined by the authors. Remission was a much more robust measure of traction against T2DM than reversal, even though it sounds like the latter is stronger than the former. Remission was defined in two parts; partial remission and complete remission. Partial remission was defined as "sub-diabetic hyperglycemia of at least 1 year duration, HbA1c level between 5.7-6.5%, without any medications (two HbA1c measurements)" and complete remission was defined as "Normoglycemia of at least 1 year duration, HbA1c below 5.7%, without any medications (two HbA1c measurements)". Reversal was defined more loosely, as "sub-diabetic hyperglycemia and normoglycemia (HbA1c below 6.5%), without medications except metformin" (Athinarayanan, et al., (2019), Supplement Table 2).
 
@@ -106,12 +106,12 @@ The underlying premise is that PUFAs, particularly omega-6 fatty acids found in
 Since I've already covered how the human outcome data flies in the face of this hypothesis in a previous article [[18](https://www.the-nutrivore.com/post/a-comprehensive-rebuttal-to-seed-oil-sophistry)], I won't rehash all of it here. But, essentially there is no human outcome data supporting this effect across multiple cohort studies and multiple RCTs. In the epidemiology, tight markers of seed oil consumption show a consistent inverse association with T2DM [[19](https://pubmed.ncbi.nlm.nih.gov/29032079/)].
 
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 Additionally, there have been several interventions feeding large amounts of PUFA to subjects, to the exclusion of SFA, and measuring long term effects on insulin sensitivity [[20](https://www.sciencedirect.com/science/article/abs/pii/0163782781900709)][[21](https://pubmed.ncbi.nlm.nih.gov/1347091/)]. In both Houtsmuller, et al. (1979) and Watts, et al. (1992), long term feeding of PUFA was associated with improvements in insulin sensitivity. In the case of the former trial, the insulin sensitivity measure, an oral glucose tolerance test (OGTT), showed improvement to glucose tolerance among diabetics over time. These results were aggregated by Hooper, et al. back in 2020 in an exploratory analysis [[22](https://pubmed.ncbi.nlm.nih.gov/32428300/)].
 
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 Additionally, we can also see that Ley, et al. (2004) showed an improvement in OGTT results, but with the substitution of CHO for SFA, rather than PUFA for SFA (which is kinda funny) [[23](https://pubmed.ncbi.nlm.nih.gov/14739050/)].
 
@@ -132,22 +132,22 @@ Now that we have a clear understanding of the model, let's discuss the overwhelm
 For the first study by Ravikumar, et al., a single-arm trial of 10 subjects, the drug pioglitazone was investigated for its effects on markers of T2DM, particularly postprandial endogenous glucose production (EGP) using isotope labeled glucose, as well as IHL. After 16 weeks of treatment, the pioglitazone group experienced an increase in total body weight equal to +6.2kg on average. Yet, the pioglitazone group also experienced a decrease in IHL.
 
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 However, to be fair, the pioglitazone group also experienced a significant decrease in IMCL as well, however there was no significant correlation between decreases in IMCL and EGP. There was however, a direct association between IHL and EGP. Although this trial was not controlled, it certainly doesn't produce results expected on the IMCL hypothesis, and it lends further credence to the TCH. Additionally, many markers of T2DM subsequently improved, such as plasma glucose, hemoglobin A1c (HbA1c), and even TGs, with the changes being -2.3mmol/L, -1.9%, and 0.4mmol/L, respectively.
 
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 It can also be inferred that there was a meaningful increase in insulin sensitivity, given the fact that plasma glucose dropped despite the same amount of insulin being produced by subject. Essentially, glucose disposal per unit insulin went up, implying that insulin signalling had improved.
 
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 In the second study by Petersen, et al., eight subjects with T2DM were compared to 10 healthy volunteers in a non-randomized weight loss trial over an average of seven weeks. Essentially, subjects were followed up until normoglycemia was achieved, so not every subject was subjected to the same amount of weight loss for the same time period. In this time, body weight dropped by an average of 8kg in the T2DM group. This was marked with commensurate drops in plasma glucose, plasma insulin, and TG, at -2.4mmol/L, -108pmol/L, and -0.3mmol/L, respectively.
 
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 The most interesting and surprising finding was that there was no significant change in IMCL despite weight loss. But, subjects did end up achieving normoglycemia and near normal insulin sensitivity as determined by a HEC. However, much like the previous study, insulin sensitivity was directly associated with IHL reduction. Once again, this flies in the face of the IMCL hypothesis, and offers further support for the TCH as the T2DM approached nearly normal levels of IHL. Although neither of these papers directly test for evidence of the sugar or oxidation hypotheses, it should be noted that both of these trials involve the consumption of both sugar and most likely animal products.
 
@@ -156,12 +156,12 @@ In light of this evidence, Steven and Taylor conducted another preliminary human
 In terms of other T2DM markers, such as plasma glucose, the response to the diet was heterogeneous among participants with long-term T2DM. Some showed similar responses to those in the short-term group and some responded slowly. By the end of the study, 87% of the short-term group and 50% of the long-term group achieved non-T2DM fasting plasma glucose levels. HbA1c levels also decreased in both groups, with a more significant reduction observed in the short-term group. However, there was an unforeseen result— about half of subjects did not respond to the treatment at all, which was not expected given nearly all previous research.
 
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 Given these results and Dr. Taylor's previous characterization of the PFT concept, the most likely hypothesis seemed clear— these people just needed to lose more weight, which we'll get to later. For now, there was enough evidence of the effectiveness of weight loss for T2DM treatment that Dr. Taylor and his colleagues decided it was time to test the efficacy of the treatment in a real-world outpatient scenario. A cluster-randomized experiment was designed and undertaken, and would come to be known as the Diabetes Remission Clinical Trial (DiRECT) [[31](https://pubmed.ncbi.nlm.nih.gov/29221645/)].
 
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 The DiRECT trial involved 298 subjects across 49 primary care practices (or clusters) randomized two groups, a control group receiving the standard of care for T2DM management, and the treatment group receiving a three stage program: stage one, total diet replacement; stage two, food reintroduction; phase three, weight maintenance. For the first stage, the treatment group received a liquid diet consisting of four packets of meal replacement formula, which totaled around 825-853 kcal/day for three to five months (depending on patient-specific goals). For the second stage, after subjects completed the first weight loss phase of the trial, food was gradually reintroduced over a period of two weeks to two months. During the last stage, patients were followed up over the course of around a year. The results were encouraging.