Comprehensive Debunk of an Anti-Vegan Nutrition Copypasta
https://www.reddit.com/r/AntiVegan/comments/e3c2om/i_made_an_evidencebased_antivegan_copypasta_is/
1. NUTRITION
1.1. Nutrition authorities
1.2. Vegan studies are low quality and hide their conflicts of interest
1.3. Veganism is unsustainable
1.4. Putting anti-meat studies into context
1.5. Sneaky vegan propaganda examples
1.6. Vegan diets aren’t “proven to reverse heart disease”
1.7. Factually deficient diet
1.8. Supplements
1.9. Mental disorders
1.10. Eating disorder
1.11. Patrik Baboumian
1.12. Other athletes
1.13. The vegan diet is not species-appropriate
1.14. Other anti-vegan copypastas on nutrition
1. NUTRITION
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1.1. Nutrition authorities
Vegans lie to claim that health organizations agree on their diet:
1) There are many health authorities that explicitly advise against vegan diets, especially for children. [1]
Swiss Federal Commission for Nutrition
- The positive effects of a vegan diet on health determinants cannot be proven, but there are relevant risks regarding nutritional deficiencies. Children and pregnant women are advised against adopting a vegan diet due to the risks described above.
The study in this report on the micronutrient status and intake in omnivores, vegetarians and vegans in Switzerland concludes that “Despite substantial differences in intake and deficiency between groups, our results indicate that by consuming a well-balanced diet including supplements or fortified products, all three types of diet can potentially fulfill requirements for vitamin and mineral consumption.”
It was shown that the vegan diet can fulfill macronutrient needs, that vegans have higher intakes of several micronutrients, and that the vegan diet can provide health benefits, “A balanced vegan diet can cover macronutrient needs…”, “…vegans have a higher intake resp. status for several nutrients: magnesium, vitamins C, B1, B6, folic acid, as recorded and measured in the Swiss study by Schüpbach et al. It can be expected that a vegan diet also provides a wide array of phytochemicals (e.g. carotenoids, phenolics), with potential health benefits”. It is also stated that “Schüpbach et al. show that all diet groups show low intakes / status for some micronutrients.”
“…the FCN’s report concludes that a vegan diet can only cover all of an adult’s nutritional needs if it is well planned and prepared and appropriately supplemented with vitamins and micronutrients.” This report has essentially the same position as the position of the Academy of Nutrition and Dietetics which is later criticized in this copypasta: “appropriately planned vegetarian, including vegan, diets are healthful, nutritionally adequate, and may provide health benefits for the prevention and treatment of certain diseases.”
Under the heading of Pregnancy and Breastfeeding, the report says “Piccoli et al. found in their narrative review that only iron and vitamin B12 could be critical in some vegan or vegetarian diets, particularly when the increased needs for iron and vitamin B12 supplementation are not taken into account.” Key words: “some”, and “could”.
Then the report also goes on to say that taking a vitamin D is recommended for all pregnant women; that all of the diet groups had their zinc levels below recommended levels; that all pregnant women should be checked for an iron deficiency and supplemented when necessary, and that vegans only need to additionally monitor B12 levels. So as long as pregnant vegan women track the amount of B12 fortified foods they eat, and take a B12 supplement when necessary, in addition to the other nutrients pregnant women in all diet groups are recommended to keep track of, their diet will be nutritionally adequate. “Independently of the diet form, vitamin D supplementation (600 IU/day) is recommended for all pregnant women.”, “Most studies showed that the zinc status was lower in the vegetarian groups than in the non-vegetarian (omnivore) groups; both were however below the recommended levels.”, “Pregnancy is linked with increased nutrient needs, with iron, iodine, zinc and vitamin D being critical, as well as selenium. Iron deficiency should be monitored and accordingly supplemented. Vegans should in addition monitor their vitamin B12 status and in any case use supplements for this vitamin.” So it’s clearly not just vegan pregnant women who should take supplements.
Lastly, there’s a systematic narrative review on vegan–vegetarian diets in pregnancy [1]. It found that vegan diets can be safe during pregnancy if the nutrient intake is well looked-after. “The duration of pregnancy was available in six studies and was similar between vegan–vegetarians and omnivores. The nine heterogeneous studies on microelements and vitamins suggest vegan–vegetarian women may be at risk of vitamin B12 and iron deficiencies.”, “Within these limits, vegan–vegetarian diets may be considered safe in pregnancy, provided that attention is paid to vitamin and trace element requirements.”
- There is still a lack of data whether the basic nutritional requirements are met and whether the development of children and adolescents fed on a vegan diet is secured on a long-term perspective. These data should be collected and analyzed more systematically. There is in our view up to now no evidence that a vegan diet can be recommended for these age groups
This is a very strange thing to be claimed by this report, because when you actually read what it says under the heading of Infants / Children, it goes over key nutrients, and explains that “Clinical signs of [zinc] deficiency are rare among vegetarian and vegan children”, “Children with decreased dietary intake, lack of sun exposure or with a dark skin are at risk of a hypovitaminosis D and are encouraged to supplement with 600 IU of vitamin D3”, “The FCN recommends a supplementation with 400 IU/day [of calcium] for every infant up to 1 year, regardless the type of nutrition and with 600 IU/D for toddlers up to 18 years. If this recommendation is followed, the risk of rickets or hypocalcemia is very low”, “To prevent a deficiency the FCN-publication … recommends partially replacing self-prepared food with iodine supplemented food or adding iodine supplementation of 50 µg per day”, from the study this is cited from, “weaning infants [in general]… may be at risk of inadequate iodine intakes”, so it doesn’t only apply to those on a vegan diet. The only point they do have is that “an unsupplemented vegan diet is lacking in vitamin B12”, for which a study is cited, but in the same study it’s also stated that “Deficiency prevalence of 0% was reported among vegans who consumed vitamin B12-fortified foods.” Therefore, if one were to supplement with vitamin B12 or eat B12 fortified foods in adequate quantity on a vegan diet, then they wouldn’t have anything else to worry about more so than people in other diet groups.
Perhaps the people who wrote this report weren’t aware, but there is actually data that the nutritional requirements of children on a vegan diet are met. It was a study on the growth and development of British vegan children [2], which found that “The majority of children grew and developed normally but they did tend to be smaller in stature and lighter in weight than standards for the general population.” Although the weight and height was found to be lower in males, both were in the healthy range, and it wasn’t shown to be statistically significant. “It is concluded that provided sufficient care is taken, a vegan diet can support normal growth and development.”
Additionally, there was research conducted in Germany on the vegan children [3], which concluded that “VG [vegetarian] and VN [vegan] diet in early childhood provides comparable amounts of energy and a macronutrient pattern in accordance with recommendations and can ensure normal growth, as there were no significant differences in proxy-reported anthropometrics compared to OM [omnivore] children of the same age.”
- Based on these data, there is no evidence for the position stated in the previous report, that vegan diets are healthy diets.
This is taken from the conclusion, where, before that, it’s stated that a well-planned vegan diet is nutritionally adequate. “Data from Switzerland and other countries show that a vegan diet, when carefully planned to cover energy and macronutrient needs and mandatorily combined with supplements/ fortified food, can be comparable, from a purely nutrient perspective, to other dietary forms, at least for healthy adults.”, and admits that “All these studies are based on small numbers of participants (with a possible selection bias), with different inclusion criteria of diets, different duration and adherence to a specific diet.”
A study on the nutritional adequacy of vegetarian dietary intakes [4], which wasn’t taken into account in the FCN report, found that “Nutritional inadequacies can arise from consuming omnivore, vegetarian and vegan diets. Over time such inadequacies may result in nutrient deficiencies thus it is important to consume a variety of nutrient rich foods to ensure nutrition requirements are being met.” This both supports the point that a vegan diet isn’t necessarily nutritionally deficient, and that the vegan diet group isn’t the only diet group which can be prone to deficiencies. If all diet groups can be nutritionally inadequate then it doesn’t make sense to single out the vegan diets and say that there’s no evidence that they’re healthy.
- The scientific evidence available to date is not sufficient to claim that vegan and vegetarian diets are associated with a significant reduction of total mortality
I don’t know how they’re defining sufficient here, but there is certainly evidence that “higher adherence to a healthy plant‐based diet index is associated with a 19% and 11% lower risk of cardiovascular disease mortality and all‐cause mortality, respectively…” in a general population of middle‐aged adults [5].
In a prospective cohort study on the animal vs plant protein intake [6], it was found that “High animal protein intake was positively associated with cardiovascular mortality and high plant protein intake was inversely associated with all-cause and cardiovascular mortality, especially among individuals with at least 1 lifestyle risk factor. Substitution of plant protein for animal protein, especially that from processed red meat, was associated with lower mortality, suggesting the importance of protein source.”
- The reduction in IHD and all-cause mortality with vegetarian diet stems mainly from the Adventist studies, and there is much less convincing evidence from studies conducted in other populations.
A reason isn’t provided for why the Adventist studies don’t accurately represent the effect of a vegan diet on IHD and all-cause mortality, or why we should dismiss them. A meta-analysis and systematic review [7], which evaluated over 124,000 people, found that “All-cause mortality in vegetarians was 9% lower than in nonvegetarians. The mortality from ischemic heart disease was significantly lower in vegetarians than in nonvegetarians.” Another systematic review with meta-analysis of observational studies on the vegan diet and multiple health outcomes [8] reported “a significant protective effect of a vegetarian diet versus the incidence and/or mortality from ischemic heart disease (-25%) and incidence from total cancer (-8%). Vegan diet conferred a significant reduced risk (-15%) of incidence from total cancer.”
European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN)
https://www.ncbi.nlm.nih.gov/m/pubmed/28027215/
- Vegan diets should only be used under appropriate medical or dietetic supervision to ensure that the infant receives a sufficient supply of vitamin B12, vitamin D, iron, zinc, folate, n-3 LCPUFA, protein, and calcium, and that the diet is sufficiently nutrient and energy dense. Parents should understand the serious consequences of failing to follow advice regarding supplementation of the diet.
- Although theoretically a vegan diet can meet nutrient requirements when mother and infant follow medical and dietary advice regarding supplementation, the risks of failing to follow advice are severe, including irreversible cognitive damage from vitamin B12 deficiency, and death.
There are only two sources cited in this report for these statements. One is a study published in 2003, which actually shows something very different, that vegetarians “appear to have no greater incidence of iron deficiency anemia”, and that with “current methods, it is not possible to effectively evaluate the influence of vegetarian diets on zinc nutrition”, so this study doesn’t prove their point at all. The other study on vegetarian infant and child nutrition, published in 2011, makes nearly the same statements as some of the evidence in the previous report; that a vegan diet “has at least to be supplemented with vitamin B12, with special attention to adequate intakes of calcium and zinc and energy-dense foods containing enough high-quality protein for young children”. Clearly this isn’t good evidence that vegan diets should be advised against for children, especially when we have a greater amount of evidence showing that vegan children develop normally. Deficiencies can lead to health detriment and death, this part is true, but what is yet to be shown is that vegans have a higher prevalence of health detriment than other diet groups. This same study also states the following: “A vegetarian diet has been shown to be associated with lower mortality of ischemic heart disease and lower prevalence of obesity”.
German Nutrition Society (DGE)
- Any diet that does not lead to the intake of adequate levels of essential nutrients and energy is unfavourable. The DGE recommends a diet that includes all groups of foods in the nutrition circle — including animal products.
- Special care is needed for groups with special requirements for nutrient supply, e.g. pregnant women, lactating women, infants and toddlers.
- On a vegan diet, it is difficult or impossible to ensure adequate supply of some nutrients. The most critical nutrient is vitamin B12. Other potentially critical nutrients on a vegan diet include protein resp. indispensable amino acids and long-chain n-3 fatty acids (EPA and DHA), other vitamins (riboflavin, vitamin D) and minerals (calcium, iron, iodine, zinc and selenium).
- With some nutrients, a vegan diet without fortified foods or dietary supplements leads to inadequate intake, which may have considerable unfavourable consequences for health.
- The risk of nutrient under-supply or a nutritional deficiency is greater in persons in sensitive phases of life, such as pregnancy, lactation and in infants, children and adolescents taking or being given a vegan diet, than in healthy adults on a vegan diet.
- Since rejecting any animal foods increases the risk of nutrient deficiencies and thus of health disorders, a vegan diet is not recommended by the DGE during pregnancy or lactation, or for children or adolescents of any age.
In this report, there’s a list of the statements and recommendations of other associations and societies, the majority of which agree that a well-planned vegan diet, with supplementation when necessary, is nutritionally adequate, this includes National Health and Medical Research Council in the nutrition recommendations for Australia, the Portuguese National Programme for the Promotion of a Healthy Diet and — for adults — the British Nutrition Foundation, and The Canadian Paediatric Society. In this same list, it is stated that the German Nutrition Society rejects a vegan diet for healthy infants, unless dietary supplements are taken. Hence, as long as you take supplements for the nutrients you’re deficient in, or if enough fortified foods are eaten, such that your nutrient intake is adequate, it is healthy even for infants.
The studies cited for the claim that there are potentially critical nutrients in a vegan diet all actually found that “In terms of nutrition, vegan and vegetarian diets can be nutritionally adequate, provided they are carefully planned”. Moreover, it was found in this study that “there is a moderate reduction in mortality from CHD among vegetarians compared to meat-eaters”. “At the macronutrient level, the diet of Danish vegans is in better accordance with the NNR [Nordic Nutrition Recommendations] than the diet of the general Danish population.”, though intake of some micronutrients was lower in vegans. In the same study, it was also found that the general population had lower intake of other nutrients than that of vegans. In the last study, it’s stated that “eliminating all animal products from the diet increases the risk of certain nutritional deficiencies”. This doesn’t necessarily mean that a given vegan will be deficient, but rather that it should be recommended to vegans or those considering the vegan diet to keep track of the key nutrients which are found to be low in vegans, adjust their diets to include more plant-based foods with the key nutrients, and supplement when that cannot be done. There were also found to be positive effects of the vegan diet for health, like lowering blood cholesterol concentrations, lowering the incidence of stroke, and lowering mortality from stroke and ischemic heart disease. In addition, vegans were found to consume more foods with cardioprotective effects.
French Pediatric Hepatology/Gastroenterology/Nutrition Group
https://www.ncbi.nlm.nih.gov/pubmed/31615715
- The current craze for vegan diets has an effect on the pediatric population. This type of diet, which does not provide all the micronutrient requirements, exposes children to nutritional deficiencies. These can have serious consequences, especially when this diet is introduced at an early age, a period of significant growth and neurological development.
- Even if deficiencies have less impact on older children and adolescents, they are not uncommon and consequently should also be prevented. Regular dietary monitoring is essential, vitamin B12 and vitamin D supplementation is always necessary, while iron, calcium, docosahexaenoic acid, and zinc should be supplemented on a case-by-case basis.
In the full document [9] it is stated that vegan infants and children get adequate amounts of protein, “Studies have shown that the milk from vegetarian mothers is nutritionally adequate and allows for normal growth in the first 6 months of life”, “Protein intake is generally reached in a vegan diet with the consumption of a variety of plants.”, “In the vegan children over 4 years of age, growth is also similar to that of omnivore children”, “The growth of vegan adolescents is also identical to that of omnivore adolescents, with a lower protein intake, but which also meets the French recommended nutritional intake (RNI).”
The evidence that’s used to prove that vegan children are likely to suffer from a B12 deficiency is as follows. One is a case study of 2 vegan children with a severe B12 deficiency, which is weak evidence at best. Of course, precautions should be taken to avoid B12 deficiency, either by supplementing or consuming B12 fortified foods in adequate amounts. The next one is a study conducted on 19 participants, 13 strict vegetarian and 6 omnivorous lactating women, which found that “Milk vitamin B-12 was inversely related to length of time on a vegetarian diet and positively correlated with maternal serum vitamin B-12”. The last source is a meta-analysis, which only included one study on pregnant women, conducted in Ethiopia. These pregnant women consumed either maize or fermented enset as their major energy source, so it’s not even about pregnant vegan women. There would have to be a control group for such a study too, to compare the percentage of B12 deficiencies for pregnant women on a vegan diet and for pregnant women with some other diet, like the standard diet of some country. It’s concluded in all of these sources that it should be recommended to those with a low dietary intake of B12 to supplement. This is barely an argument against a vegan diet, as those who do take B12 supplements and those who consume enough B12 through fortified foods won’t become deficient, and “…it appears in the two longitudinal studies of vegan children that supplementation is provided in the majority of cases.”
In this exact report it is clearly stated that children breastfed on a vegan diet aren’t any more likely to develop a calcium deficiency, and those who aren’t breastfed can gain adequate amounts of calcium with rice or soy based infant formula. It is stated that “Study results are sometimes contradictory”, as some studies show that vegan children have the same calcium intake, and some show that the calcium intake in vegan children is lower. “Prepubertal children on a vegetarian diet had significantly lower total and lumbar spine BMD z-scores, but absolute values of bone mineral density did not differ.” While the total BMD was lower in vegetarian children, what’s yet to be proven is that this leads to an increased risk of negative health outcomes due to it, while they have the same absolute values of BMD. Even if it was the case that there were negative health outcomes from some vegan children not consuming adequate amounts of calcium, this doesn’t mean that the vegan diet is unhealthy or harmful, as it could easily be recommended to vegans to keep track of their dietary nutrition.
While it is said that a greater level of supplementation of vitamin D compared to the general population is necessary, this doesn’t mean that vegans are the only group prone to vitamin D deficiencies, as there are many other groups which require supplementation as well, like people who don’t get enough sun exposure either by not going outside during sunny weather, or by having high skin pigmentation, or even people who wear clothes which cover most of your body while outside.
It’s stated that all pregnant women are prone to iron deficiencies, and that the levels of iron in vegan women is identical to those of omnivorous women. Additionally, in some cases, vegetarian children have higher levels of iron than omnivores. The statement made for adolescents is contradictory to the research cited, as the research is stated to be inconsistent, “Vegetarian and vegan adolescents are exposed to iron deficiency. A Swedish study showed that iron ingested by vegan teenagers was identical to or even greater than their omnivore counterparts. The results from a few investigations that studied the frequency of iron deficiency anemia are also sometimes inconsistent. The Swedish study mentioned above showed that among adolescent vegan girls, even though 20% had low ferritin (versus 13% among omnivores), only 6.6% had anemia due to iron deficiency, compared to 20% among omnivores.”
The zinc concentrations in breast milk were found to be the same regardless of maternal diet. The zinc levels weren’t found to be significantly different between dietary groups. It’s stated that “Low zinc levels were found in Guatemalan vegetarian and vegan children compared to omnivore children”, however, when I found the full version of this study [10], there was no mention of the diet groups of these children, so it can’t possibly be used to prove the claim made. The other study cited on zinc status in children found no difference between vegetarian and omnivore children. In vegetarian adolescents, there was found to be “no difference in plasma zinc levels, infections, impaired growth, and pubertal development… compared to omnivore adolescents.”
“The breast milk of vegetarian women contains lower levels of DHA than that of omnivore women, but the birth parameters of newborns born to vegetarian mothers are no different.” For children over 4 years of age, a claim is made that one study found that the omega-6/omega-3 ratio was very high, however they link to a study which found that it didn’t cause any negative health effects. While the study does suggest that vegans had lower levels of DHA, no negative health consequences were found to stem from this. The last study on adolescents also found that vegans had higher levels of ALA, and lower levels of EPA and DHA, but once again, there is no evidence provided that their lower levels of omega-3s had negative health consequences.
In conclusion, if you want to inform the general population about the effect of a vegan diet on health, it doesn’t make sense to say that “vitamin B12 and vitamin D supplementation is always necessary, while iron, calcium, docosahexaenoic acid, and zinc should be supplemented on a case-by-case basis”. Though it is true that vegans generally have lower intake of B12, but B12 fortified foods can be consumed in a lot of cases, instead of using supplements, though they should be used when necessary. Vitamin D supplementation isn’t always necessary for vegans, for the same reason, as vitamin D fortified foods exist, and because vitamin D should be supplemented by all people who don’t synthesize enough vitamin D from exposure to the sun and don’t get enough from their diets. This is very common among Americans [11] and Europeans [12]. As for the other nutrients, the lower levels in vegans either haven’t been shown to produce negative health outcomes, or omnivores also had below recommended levels of the nutrient. In fact, as the vegan diet is often associated with better health outcomes, like having lower all-cause mortality [5], clearly the vegan diet has a net-positive impact on health.
Sundhedsstyrelsen (Danish Health Authority)
https://www.sst.dk/da/udgivelser/2018/~/media/2986643F11A44FA18595511799032F85.ashx
- Exclusively vegan nutrition for infants and young children (under 2 years of age) is not recommended as it may be very difficult to meet the child’s nutritional needs during the first years of life with this diet.
This report is in Danish, and so I can’t do a full review of it, but I found the studies cited which were about vegans and vegetarians, and I found their position on the vegan diet in children on an official website. They state that children can develop normally on a vegan diet “if given the right dietary supplements and the energy intake is adequate”. The first study they cite is the same study as was cited by the German Nutrition Society in their position on the vegan diet, which stated that “At the macronutrient level, the diet of Danish vegans is in better accordance with the NNR [Nordic Nutrition Recommendations] than the diet of the general Danish population.” Some of the micronutrients were found to be lower in vegans, but nearly the same amount of other micronutrients, such as B6, were found to be higher in vegans. The next is a case study of 2 vegan children with a severe B12 deficiency, the same as used in the French position. The vegan diet wasn’t necessarily what caused the B12 deficiency, but rather, the carelessness of the children’s parents and their failure to adequately look after their own and their children’s nutrition did. The next piece of evidence used is an article by professional staff, including a dietitian and 2 general practitioners, stating “Deficiency of B12 is seen after several years on a vegan diet where no B12 fortified foods or supplements have been added”. This is extremely self-evident, clearly if you don’t consume anything containing B12, whether food or supplements, then you’re going to be B12 deficient. This expert also states that all vegetarians, assumedly including vegans, should take calcium and vitamin D supplements. They say this is because it’d be hard to get enough calcium without consuming dairy, and it’d be hard to get enough vitamin D without consuming animal products, especially fish and meat. However, plant milks are often fortified with calcium, as well as vitamin D so the replacement of cow’s milk with plant milks should be enough to ensure adequate calcium and vitamin D levels in vegans. In this article it is also stated that almost every fifth Dane has a vitamin D deficiency, so it’s recommended for them to also take supplements. To conclude, this article isn’t great evidence against veganism, more so a recommendation of what you should be eating as a vegan. The last source cited is Position of the American Dietetic Association and Dietitians of Canada, which states that “Well-planned vegan and other types of vegetarian diets are appropriate for all stages of the life cycle, including during pregnancy, lactation, infancy, childhood, and adolescence.”
Académie Royale de Médecine de Belgique (Royal Academy of Medicine of Belgium)
https://updlf-asbl.be/assets/uploads/ARMB_-_Veganisme_AVIS_COMPLET.pdf
- The committee considers that the vegan diet is inappropriate and therefore not recommended for unborn children, children and adolescents, as well as pregnant and lactating women.
- Compulsory supplementation, metabolic imbalances and the obligation of medical follow-up, including blood sampling, are therefore not eligible.
The link they provide doesn’t work, and there are no other sources of the report that could be found, only articles written about it. The points made can be discredited in virtue of the evidence found in reports from other European countries, as all of them state that while they don’t recommend a vegan diet, that a well-planned vegan diet with supplementation is nutritionally adequate.
Spanish Paediatric Association
https://www.ncbi.nlm.nih.gov/pubmed/31866234
- A vegetarian or a vegan diet, as in any other kind of diet, needs to be carefully designed. After reviewing current evidence, even though following a vegetarian diet at any age does not necessarily mean it is unsafe, it is advisable for infant and young children to follow an omnivorous diet or, at least, an ovo-lacto-vegetarian diet.
I think it’s important to include the sentence which comes after that, that “Children who follow balanced vegetarian diets, and who are growing and developing normally, require the same health checks as any other healthy child.” If vegetarian, including vegan diets, aren’t necessarily unsafe and the parents or guardians of the child pay attention at the nutrition of the child, then it doesn’t make sense advise against a vegan diet. To go back to the original claim which this evidence is supposed to provide, how are vegans lying that health organizations agree on the vegan diet? Most of the time what vegans cite is the position of the Academy of Nutrition and Dietetics, which states that a well-planned vegan diet is nutritionally adequate, and are appropriate for all stages of life. The authorities cited in this copypasta make very similar statements. Evidently, you can be healthy on a vegan diet, even as an infant or a child if your nutrition is well-planned, so you consume a variety of plant-based foods with key nutrients, and if you supplement when that is indeed necessary.
Argentinian Hospital Nacional de Pediatría SAMIC
https://www.ncbi.nlm.nih.gov/pubmed/31339288
- Vitamin B12 deficiency is one of the most serious complications of vegetarianism and its variants. Infants born to vegan mothers are at greater risk of serious deficiency, being more vulnerable to their effects. B12 deficiency is not usually suspected by the pediatrician in healthy infants with neurological symptoms
Like in the Spanish Paediatric Association position, an important to include sentence was missed out in this quote, and that is “Our purpose is to alert about the importance of supplying vegan mothers with B12 before conception until the end of breastfeeding.” One can see from this that as long as vegan mothers take a vitamin B12 supplement while breastfeeding, there will be no risk of deficiency, and their child will be healthy.
The Dutch national nutritional institute, Stichting Voedingscentrum Nederland
- A vegan diet can be adequate but increases the risk for various deficiencies. The report then describes the various risks of deficiencies and how they can be circumvented.
- A vegan diet for children can be adequate but is associated with an increased risk of: being smaller and lighter than their peers, worse psycho-motor development and reduced bone density. Help from a professional is advisable.
- The literature on the effects of a vegan diet on pregnant women is limited, but the available research indicates that a healthy pregnancy in combination with a vegan diet is possible, under the precondition that the women pay special attention to maintaining a balanced diet.
This is getting very desperate. These are barely points against veganism. As long as children, and vegans of any age, in general, take care to plan their diets and consume a variety of plant-based foods, including fortified foods and supplements, as is advised by this Dutch report, they will be healthy. Vegetarian diets, including vegan diets, also reduce the risk of certain diseases, according to this report. “A carefully planned vegetarian diet according to the Wheel of Five can have a positive effect on health because it can reduce the risk of certain diseases shrink. A vegetarian diet, possibly combined with supplements, that is well composed contains enough nutrients.”
2) The Academy of Nutrition and Dietetics was founded by Seventh-day Adventists[2], an evangelistic vegan religion[3] that owns meat replacement companies. Every author of their position paper[4] is a career vegan, one of them is selling diet books that are cited in the paper. One author and one reviewer are Adventists who work for universities that publicly state[5] to have a religious agenda. Another author went vegan for ethical reasons[6]. They explicitly report “no potential conflict of interest”. Their claims about infants and athletes are based on complete speculation (they cite no study following vegan infants from birth to childhood) and they don’t even mention potentially problematic nutrients like Vitamin K[7] or Carnitine[8].
The first link cited doesn’t work, however it is true that the founders were Seventh-day Adventists, however it is not a vegan religion as they claim. It is a Christian religion which advocates healthy eating in the form of vegetarian diets. I don’t know what they mean by “career vegan” but they do seem to be involved in research on vegetarian diets, which makes sense. Let’s assume that all of the claims about the Academy of Nutrition and Dietetics, and the authors of their papers, are true. The only problem which can come from this is data manipulation: they could be providing studies or positions which aren’t reflective or representative of the real effects of vegetarian and vegan diets, but for this there must be evidence. Until evidence is provided for some kind of misinformation or misrepresentative data being spread by them, it is unreasonable to believe it to be the case. In addition, their position is almost identical to the vast majority of the positions of other health authorities which were cited in this copypasta, that is to say a well-planned vegan diet with supplementation is nutritionally adequate. The same way the authors of their paper may be biased towards a vegan diet, the studies which were authored by omnivore researchers may be biased against it, what matters is the research itself. If no methodological problem can be found in their research, then there is no problem with the authors having conflict of interest. It must be noted that conflicts of interest should be reported anyway, as to not mislead people.
Their claim that the Academy of Nutrition and Dietetics doesn’t cite a study following vegan infants from birth to childhood is completely untrue, at least in their latest position published in 2016. They cite “Considerations in planning vegan diets: Infants”, which itself cites a study I shared the findings from previously, which found that vegan children develop normally, though they do tend to be smaller, however the size differences were within the healthy range. While they cite no studies on vegan athletes, the nutritional needs of athletes are going to be similar to non-athletes, with some nutrient intakes needing to be higher, like protein. As long as the athletes plan their vegan diets well, there’s no reason to think they’ll have adverse effects. Just to be thorough, here’s a study vegan athletes [13], which concluded that “Based on an abundant body of scientific evidence about vegetarian and vegan diets in relation to health, it has been proven that the tremendous health benefits delivered by vegan diets are compatible with health and form a prerequisite for sports performance… Moreover, on this solid basis, vegan diets applied to sports-related dietary tactics are compatible with high performance and competitive sports, too.”
The proof in this copypasta that vitamin K is a problematic nutrient is a case study of literally one child who was breastfed by their vegan mother, so obviously there’s no comparison to be made. For all we know, vegans could overall have higher levels of vitamin K. This is like if I cited a case study of an omnivorous child having a vitamin C deficiency, and claimed that omnivorous diets are unhealthy because omnivorous children are more likely to have a vitamin C deficiency. Like a 2 year old boy who had severe developmental delay and symptoms of scurvy [14]. It’s noted that “The patient had a history of poor oral dietary intake he existed on a diet of milk products” Now we have definitive proof that omnivorous diets are unhealthy, right? Their claim that carnitine is a problem nutrient is also based on a case study of just one child, this isn’t good evidence that vegans have increased prevalence of carnitine deficiency. Carnitine isn’t an essential nutrient anyway, as it can be synthesized by your own body. This child was unable to synthesize it for some reason, but “responded promptly to treatment with L-carnitine”. A person for whom it is impossible to synthesize L-carnitine in adequate quantities, which is very rare, supplements can be recommended to be taken to prevent deficiency.
3) Many, if not all, of the institutions that agree with the AND either just echo their position, don’t cite any sources at all, or have heavy conflicts of interest. E.g. the Dietitians of Canada wrote their statement with the AND[9], the USDA has the Adventist reviewer in their guidelines committee[10], the British Dietetic Association works with the Vegan Society[11], the Australian Guidelines cite the AND paper as their source[12] and Kaiser Permanente has an author that works for an Adventist university[13].
Well this is a very strange claim to make when your first claim was that many health authorities advise against the vegan diet when the vast majority of them agree that a well-planned vegan diet with supplementation is nutritionally adequate, and may actually have health benefits. Do all of them also have conflict of interest? If the position papers put out by these nutrition authorities are representative of the majority of other health authorities, then what’s the problem with them having conflict of interest? Though the Dietitians of Canada did cite the Adventist studies as evidence, the source which is supposed to prove that they wrote their statement with AND mentions nothing about AND, not in the short pubmed version, nor in the full version. USDA does indeed have an Adventist reviewer in their guidelines committee, Joan Sabaté, 1 out of 20 people. He didn’t even contribute to writing the position, so the relevance of this fact is very questionable. Funnily enough, they cited an article on the Nutrition Coalition website, which claims to not be supported by industries, however it turns out that several of the members have received industry funding [15].
The position of USDA, formerly known as the American Dietetic Association, and the Dietitians of Canada has over 250 citations, clearly they provided citations. Maybe they meant some other authority. The British Dietetic Association cites their food fact sheet, which itself has 20 citations. While not as many as the USDA and Dietitians of Canada did, it’s still not 0 as is claimed. Is there a problem with the British Dietetic Association working with the Vegan Society? They’re not getting funded by the Vegan Society, they just link to their websites which have information about how to get certain nutrients on a vegan diet. Unless it can be shown that working together with the Vegan Society influences the British Dietetic Association into making untrue or misinformative statements, this can be discarded outright.
The claim that the Australian Guidelines cite the AND paper is false as well. Firstly, the Australian guidelines quote and cite the AND once in the whole paper. There were 1128 citations in total, so it’s pathetic to say that there’s somehow conflict of interest here.
Kaiser Permanente, does indeed have an author who works at an Adventist University, by the name of Mohamed Ismail. How is this at all relevant to conflict of interest? Just working at an Adventist university doesn’t make you more prone to bias towards the vegan diet. Their paper on plant-based diets has 46 citations [16]. Once again, it’s quite clear that citations are provided, as they were for all of the positions. So that claim is completely untrue. The author of this copypasta hasn’t shown a shred of evidence that these “conflicts of interest” have led to the researchers or the papers misrepresenting data.
4) In the EU, all nutritional supplements, including B12, are by law[14] required to state that they should not be used as a substitute for a balanced and varied diet.
Obviously supplements shouldn’t be used as a substitute for a balanced diet, this doesn’t mean, however, that taking supplements is bad, or that you shouldn’t do it when it’s necessary. A person can have a varied diet and still require supplementation, like is the case with pregnant women, and even people who don’t spend much time out on the sun. As was stated previously, “Deficiency prevalence of 0% was reported among vegans who consumed vitamin B12-fortified foods.”
5) In Belgium, parents can get imprisoned[15] for imposing a vegan diet on children.
This is no argument against the vegan diet, it’s an appeal to legality. Just because something is illegal doesn’t mean that it is bad in some way, as many things in the past have been illegal, while not being harmful. An argument has to be provided for why the vegan diet is bad, one that’s better than “it can lead to health problems for growing children”, as an omnivorous diet can lead to health problems for growing children. It’s been shown that atherosclerosis begins in adolescence and young adulthood, elevated levels of LDL cholesterol is what is used to determine the progression [17], “The associations of CAD risk factors with fatty streaks and raised lesions in young adults are consistent with the cellular and molecular mechanisms derived from emerging knowledge of oxidized LDL, macrophages, and scavenger receptors. An elevated LDL concentration is the most common determinant of progression”. The optimal concentration of LDL cholesterol is 50–70 mg/dl, as this is the point at which “atherosclerosis progression and coronary heart disease events are minimized” [18]. Vegans have been shown to have lower LDL cholesterol levels than the controls, which were consuming an omnivorous diet [19].
[1] https://pastebin.com/g72uMQr9
[2] https://vndpg.org/resources/academy-co-founder-lenna-frances-cooper/
[3] https://www.mdpi.com/2077-1444/9/9/251/htm
[5] https://i.imgur.com/wabV8au.jpg
[6] https://en.wikipedia.org/wiki/Vesanto_Melina#Career
[7] https://www.ncbi.nlm.nih.gov/pubmed/19748244
[8] https://www.ncbi.nlm.nih.gov/pubmed/6703771
[9] https://www.ncbi.nlm.nih.gov/pubmed/12778049
[10] https://www.nutritioncoalition.us/news/2020-dietary-guidelines-committee
[13] http://www.llu.edu/pages/faculty/directory/faculty.html?eid=1a39e02
[14] https://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX:32002L0046
[15] https://qz.com/1622642/making-your-kids-go-vegan-can-mean-jail-time-in-belgium/
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1.2. Vegan studies are low quality and hide their conflicts of interest
The supposed science around veganism is highly exaggerated. Nutrition science is in its infancy[1] and the “best” studies on vegans rely on indisputably and fatally flawed[2] food questionnaires that ask them what they eat once and then just assume they do it for several years:
Just because nutrition science is young doesn’t mean that there haven’t been significant findings or that they’re somehow wrong. It’d have to be shown that they are wrong to be able to argue this. The claim that vegans rely on indisputably and fatally flawed food questionnaires is just factually incorrect. Many of the studies I’ve cited aren’t based on just food-questionnaires. On top of that, food questionnaires are actually fairly accurate, as found by a study on reliability and validity of food frequency questionnaire and nutrient biomarkers [20], “Twenty-six nutrients were examined and reliability was very good or better for 77% of the plasma nutrient biomarkers and for 88% of the FFQ [food frequency questionnaire] estimates.”
1) Vegans aren’t even vegan. They frequently cheat[3] on their diet and lie[4] about it
This is straight up blatant misinformation. Vegans don’t frequently cheat on their diet; all that those articles prove is that some non-vegetarians or non-vegans lie about being vegetarian or vegan. The way they phrase is incorrect; it wouldn’t make sense to call someone who eats meat a vegan, so it’s not vegans lying about being vegan or cheating on their diet, as clearly they aren’t vegan. It could also be possible that some people who consider themselves vegan have some private definition of vegan which includes in it the consumption of animal products. This would make “vegans lie about being vegan” an equivocation, as you’d be using the private definition of vegan in the first half, and the commonly-used definition in the second, as it’s not talking about the same thing.
2) Self-imposed dieting is linked to binge eating disorder[5], which makes people forget and misreport about eating the food they crave.
Dieting is different to having a balanced diet. Dieting is often done in order to lose weight over a short period of time. Having a vegan diet means you’re planning on it being long-term, so therefore you should plan your diet to make sure you get enough nutrients. What’s yet to be proved is that vegans have significantly more cases of binge-eating disorders than people in other diet groups, like omnivores, pescetarians, etc.
3) The vast majority of studies favoring vegan diets were conducted on people who reported to consume animal products[6] and by scientists trained at Seventh-day Adventist universities{7]. They have contrasting results when compared to other studies[8]. The publications of researchers like Joan Sabate[9] and Winston Craig[10] (reviewers and authors of the AND position paper, btw) show that they have a bias towards confirming their religious beliefs[11]. They brag about their global influence on diet, yet generally don’t disclose this conflict of interest. They have pursued[12] people for promoting low-carbohydrate diets.
This is a gross misrepresentation of the facts. They don’t provide any evidence for the claim that the vast majority of studies were conducted on people who reported to consume animal products, instead what they provide is a screenshot. A screenshot which comes from one study, Adventist Health Study 2, where vegans were identified by the scientists as people who ate less than 1 serving of animal products per month. This is just how they were identified; it doesn’t represent how many animal products these people actually consumed. Even if the vegans consumed no animal products at all, they’d still be classed under the less than 1 serving of animal products per month. The second source is just a graph which makes claims about funding, supposedly, but no citations are provided.
The claim that the Adventist health studies have contrasting results when compared to other studies has 1 citation, and that’s the FCN report. In this report, it is stated that “the authors found that 3 SDA studies showed a significant mean reduction of IHD mortality. The non-SDA studies confirm this risk reduction, but to a lesser extent”. The non-Adventist studies which are cited as evidence on cerebrovascular disease mortality , commonly known as strokes, are all based on vegetarians, or vegans grouped in with vegetarians, or had a small number of participants. One cannot say from this that the difference found between the Adventist studies and non-Adventist studies is due to religious bias or funding, as the non-Adventist studies were fundamentally different from the Adventist studies. They are comparing different groups, so it’s not surprising that they get different results. In the epic-oxford study, for example, the data was over-adjusted so the omnivore group had similar blood pressure to the vegetarians, which skewed the findings. To quote Dr Malcolm Finlay [21], a consultant cardiologist, “Unfortunately, the claim that vegetarians have a higher risk of strokes isn’t really supported by the data, and on my reading, this is putting too much weight on a complex statistical method to try and correct for the fact that the vegetarians were very much healthier than meat eaters. This is almost certainly because their conclusions are based on adjusted hazard ratios: where the researchers basically put the question “what if the meat eaters didn’t have higher blood pressure” … But there is a clear and well-known effect on diet and blood pressure and diabetes, so correcting for these things and assuming they aren’t caused by diet might be inappropriate.” To add to this, since one of the largest risk factors for stroke is age, and since the vegetarians were less likely to die from cardiovascular disease, it’s likely that the increased rate of strokes in the vegetarians can be explained by the vegetarians living to the age when the stroke risk increases.
In the German study, the sample size was very small. Only 60 of the subjects were vegan, compared to the 1165 vegetarians and 679 nonvegetarians. Significant results cannot be found about vegans since there was such a minute group of them in this study.
Joan Sabate and Winston Craig may have bias towards confirming their religious beliefs, but all scientists may have biases towards or against something they’re working on based on their beliefs. The researchers who supposedly find that vegan diets are unhealthy could be said to have a bias against vegan diets because of the expectation in society that vegans are weak and frail, or because they don’t want to prove something they’ve been advised against by many people in their life. Bias within itself isn’t a good reason to dismiss research, as people can be biased and still get the right result. Some researchers, who are against smoking, research the effects of smoking on cancer and find that smoking does indeed increase lung cancer risk. Should we dismiss their research because they were against smoking before conducting their study?
The evidence used to prove the claim that “They have pursued people for promoting low-carbohydrate diets” is one article which uses the same kind of points as this copypasta, except with more conspiracy theory mixed in. The genetic fallacy [22] is used to discredit the research Joan Sabate and Winston Craig conducted and worker on. Just because the vegan diet may have started from religious beliefs and just because some vegan researchers are religious doesn’t prove that their research itself is flawed. The article also poisons the well by constantly calling back to the religious beliefs of some pro-vegan researchers. The article states things like “The New Nutrition Science implicates meat eating as not just harming people, but harming the planet, too!” After presenting nutrition science to be ran by religion in an attempt to make it seem like the position that animal products are detrimental to health and environment is a ridiculous position to hold, once again no argument is provided against this. The diet recommendations given by Adventists is criticized, ones which promote the consumption of fruits, vegetables, cereals, legumes, and nuts, and advise against the consumption of animal products. It’s framed as a conspiracy ran by the Adventist church. What they seem to have missed is that dietary guidelines are nearly the same in every country [23], so it’d have to be a world-wide conspiracy of scientists and researchers recommending higher plant-based food consumption, and lower animal product consumption. They vehemently condemn industry funding by plant-based product producing companies, yet completely leave out the fact that the animal agriculture industry spends millions on lobbying and making sure that their products are held to be healthy staple foods [24]. In the article, it’s stated that the person who was supposedly attacked by Adventists or researchers who support a plant-based diet, Gary Fettke, is an advocate for a low carbohydrate diet. The only evidence provided for this is that there was an investigation done on him due to his promoting of a low-carbohydrate diet.
4) 80–100% of observational studies are proven wrong[13] in controlled trials.
100% of observational studies couldn’t have been proven to be wrong in controlled trials, as we have examples where it isn’t the case, like with data on smoking increasing the risk of lung cancer, saturated fats increasing the risk of CVD, and aspirin decreasing the risk of CVD. The review which is linked to back up their claim examined 12 RCTs and claimed that the results were different to the results from the observational data. However, this observational data just isn’t provided. The researchers don’t explain how those 12 studies were chosen or why they are representative of all randomized controlled trials compared to their observational study counterparts, if they were supposed to be. Obviously observational studies are a lower quality of evidence than RCTs, and hence, are lower on the hierarchy of evidence [25], but they can’t be dismissed outright. They still provide useful results if they are well controlled.
[1] https://sandpit.bmj.com/site_images/2018/food_timeline_v13_web.png
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4527547/
[3] https://www.psychologytoday.com/us/blog/animals-and-us/201109/why-are-there-so-few-vegetarians
[4] https://www.mirror.co.uk/news/uk-news/millions-brits-lying-being-vegan-21554332
[5] https://en.wikipedia.org/wiki/Binge_eating_disorder#Causes
[6] https://i.imgur.com/x2sfW96.jpg
[7] https://i.imgur.com/6s35X68.jpg
[9] https://www.researchgate.net/profile/Joan_Sabate
[10] https://www.researchgate.net/profile/Winston_Craig
[11] https://m.egwwritings.org/en/book/705.19
[12] https://isupportgary.com/articles/seventh-day-adventist-plant-based-nutrition
[13] https://rss.onlinelibrary.wiley.com/doi/full/10.1111/j.1740-9713.2011.00506.x
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1.3. Veganism is unsustainable
A vegan diet is not sustainable for the average person. Ex-vegans vastly outnumber current vegans, of which the majority[1] have only been vegan for a short time. Common reasons[2] for quitting are: concerns about health (23%), cravings (37%), social problems (63%), not seeing veganism as part of their identity (58%). 29% had health problems[3] such as nutrient deficiencies, depression or thyroid issues, of which 82% improved after reintroducing meat. There are likely more people that quit veganism with health problems than there are vegans. Note that this is a major limitation of cohort studies on vegans as they only analyze the people who did not quit. (survivorship bias)
The first sentence is just a baseless claim. Even if it is the case that ex-vegans vastly outnumber vegans, this doesn’t dictate how sustainable veganism is or whether it should be followed. The main age group of the survey cited was 18–34 years, as the survey was done online, and that’s the same as the main age group which uses social media. It’s possible, therefore, that a lot of the older vegans weren’t even able to participate in the survey as they don’t use social media or use it way less. The rest of these claims are just as bad. Even if it is the case that the majority of vegans have only been vegan for a few years, or that some vegans quit because they thought they had health problems, this says nothing about whether you can be vegan without causing yourself health problems. About the health problems, the claim that is supposedly backed up is misleading at best. What the results of the survey actually state is that “71% of former vegetarians/vegans experienced none of the above. It is quite noteworthy that such a small proportion of individuals experienced ill health.” And to put the cherry on the cake, these former vegetarians or vegans weren’t even medically tested to see if they actually had any of these health problems when they were vegetarian or vegan. The survey only asked if they ever experienced those health problems, so it could be the case that they thought they had health problems when they didn’t. This is almost as bad as the study conducted by Andrew Wakefield on the effects of MMR vaccine on autism in children [26], which has been used by the anti-vax movement to prove that vaccines are bad, when what the study reported on in reality is if the parents of the children perceived their children to show signs of autism some time after they were administered the vaccine. What this copypasta does is very similar, as they leave out the fact that their source is a survey, and that the participants weren’t actually compared in terms of health by medical professionals. They criticize vegan studies for supposedly being based on surveys, yet they use literal surveys when they think it can be used to prove their point.
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1.4. Putting anti-meat studies into context
Vegans use appeals to authority or observational (non-causal) studies with tiny risk factors to vilify animal products. Respectable epidemiologists outside of nutrition typically reject these[1] because they don’t even reach the minimum threshold to justify a hypothesis and might compromise public health[2]. The study findings are usually accompanied by countless paradoxes such as meat being associated with positive health outcomes in Asian cohorts[3]:
Appeals to authority, when stated by themselves are obviously bad, as while a given authority can know a lot about a topic, it doesn’t indicate that everything they say about the topic is true or that the authority is to be trusted over the evidence. From what I’ve seen, however, when most vegans claim some authority supports them, they are citing a consensus statement made by large institution which is based on studies.
Though observational studies usually can’t prove causality, they can at least point very strongly towards it, especially when a lot of the relevant factors are controlled for. It’s somewhat interesting that this point is brought up, because the vast majority of the data on the health effects of a vegan diet which is cited in this copypasta is also based on observational studies, like the position papers of nutritional authorities; Almost all, if not all of the studies aren’t interventions assigned to some of the participants [27]. You can’t on one hand dismiss observational studies and deny their usefulness and on the other use observational data to prove your point without looking at least a little bit like a hypocrite.
There’s almost certainly a mistake made here, surely what they mean is relative risk, as in the comparison of the risk for a disease in the control group and the vegan group. But again, they don’t go into detail and name these relative risks. Clearly, having a 15% decrease of incidence from total cancer [8] isn’t a tiny relative risk. The lifetime risk of developing all cancers is 40% [28]. Thus, a relative risk of 1.15 would bring the total risk in the general population up by about 6%. It’s interesting that they criticize vegans for appealing to authority, yet do this themselves when they state that “respectable epidemiologists” reject the relative risks, though in reality they cite just one paper by one person, Samuel Shapiro. He doesn’t even reference any studies on nutrition in his paper, he just argues that epidemiology with small relative risks should be ignored. Relative disease risk needs to be interpreted in the context of how prevalent that disease is. The more prevalent the disease, the lower the maximum relative risk. This is because the relative risk is worked out by dividing the prevalence of a disease in the exposed group, which in this case is the omnivorous diet group, by the prevalence of the disease in the non-exposed group, which in this case is the vegan diet group. The maximum possible relative risk for heart disease, for example, can only be 4. To give an example, in the case of vegan men in the SDA Health Study 2 [29], the relative risk for ischemic heart disease for omnivores compared to vegans is 2.2 since the prevalence of ischemic heart disease in vegans was 0.45. Here’s a video which goes into more detail about relative risk, for those interested [30]. Back to Shapiro — in his paper, he holds that a relative risk of at least 2 must be reached for it to be considered significant, however, this is quite arbitrary. There are other epidemiologists who don’t share his view. Some, for example, like Gunther F Craun and associates argue, in their paper [31], that a moderate to strong association for decreased risk is reached at values of relative risk lesser than 0.9.
The part about reaching the minimum threshold to justify a hypothesis isn’t backed up by anything except for the Shapiro paper, with which other predominant epidemiologists don’t agree. The claim that it might compromise public health is completely unfounded, they just link to a Wikipedia page which explains that healthcare personnel should consider the negative effects of an intervention, which is true, but it doesn’t prove their point. In fact, it’s a way greater danger to expose the general population to a greater risk of non-communicable diseases like cancer when a vegan diet has been shown to decrease that risk. It’d have to be shown that recommending a well-planned vegan diet will do more harm than good.
Apparently all of the “countless paradoxes” they could find is a single pooled analysis of Asian prospective cohort studies. In these Asian studies, the meat intake was abysmally low already, “Red meat consumption was substantially lower in the Asian countries than in the United States.” And the difference between intakes was extremely small too, so it’s only to be expected that the findings were different to the studies with way larger ranges of intakes of meat. Moreover, the Asian cohorts didn’t separate the dietary groups, and therefore didn’t compare a vegan diet to the standard Asian diets. It cannot be inferred from this that a vegan diet would have worse health outcomes than one of the standard Asian diets.
1) Vegans like to say that meat causes cancer by citing the WHO’s IARC[4]. But the report actually says there’s no evaluation on poultry/fish and that red meat has not been established as a cause of cancer. More importantly, Gordon Guyatt (founder of evidence-based medicine, pescetarian) criticized them[5] for misleading the public and drawing conclusions from cherry-picked epidemiology[6] (they chose only 56 studies out of the supposed 800+). A third of the committee voting against meat were vegetarians[7]. Before the report was released, 23 cancer experts from eight countries looked at the same data[8] and concluded that the evidence is inconsistent and unclear.
I haven’t personally seen many vegans citing WHO’s IARC to prove that meat causes cancer, and this copypasta doesn’t give any examples of it happening. The IARC report [32] actually states at the very beginning that “The term ‘carcinogenic risk’ in the IARC Monographs series is taken to mean that an agent is capable of causing cancer.” And concluded in their evaluation that red meat is a group 2A carcinogen, which means it’s probably carcinogenic, and processed meat is a group 1 carcinogen, which means it is carcinogenic. This means both red meat and poultry are carcinogenic if they are processed. There is also other good research on the topic, like the study I cited previously. It wasn’t on the effect of meat by itself on cancer risk but the effect of a vegan diet, which excludes all animal products, showing that vegans do indeed have lower incidence of cancer [8], to a significant extent. There’s also research on meat intake by itself, like this study on the effect of heme iron in meat on cancer of the stomach and the esophagus [33], which is the tube connecting the throat and the stomach. It found that the higher your intake of iron from meat sources, the higher your risk of stomach and esophageal cancers, “Esophageal cancer was positively associated with higher intakes of heme iron and total iron from meat sources. Risk of stomach cancer was elevated among those with higher intakes of heme iron and total iron from meat.” There’s also a meta-analysis of 60 eligible studies on red and processed meat consumption and colorectal cancer risk [34], which found that higher meat consumption is associated with higher colorectal cancer risk “we found consumption of red and processed meat was associated with the risk of overall CRC but not RC.” It is noted that “colorectal cancer (CRC) is the second most frequently diagnosed cancer in females and the third most frequent in males, with an estimated 693,900 deaths worldwide each year.” It is true that poultry and fish weren’t evaluated in the IARC report on cancer. There is little research done on the effect on cancer risk from consuming poultry alone compared to no consumption of animal products, but there is evidence that consuming poultry is still detrimental to health for other reasons. In a study on meat consumption and risk of 25 common conditions [35], poultry intake was associated with several diseases, with the only positive effect being a lower risk of iron-deficiency anemia, “Poultry meat intake was associated with a higher risk of gastro-oesophageal reflux disease, gastritis and duodenitis, diverticular disease, gallbladder disease, and diabetes, and a lower risk of IDA.” There’s also a randomized controlled trial study on effects of red meat, white meat, and nonmeat protein sources [36]. It was found that, “…compared with nonmeat as the major protein source, diets containing high amounts of either red or white meat, and without differences in other macronutrients, result in higher concentrations of LDL cholesterol and apoB, and that these effects are primarily attributable to increases in large, cholesterol-rich LDL particles.” It is concluded that “The findings are in keeping with recommendations promoting diets with a high proportion of plant-based food but, based on lipid and lipoprotein effects, do not provide evidence for choosing white over red meat for reducing CVD risk.” As for fish, there is currently no good evidence that fish increases the risk of cancer.
Gordon Guyatt is stated to have founded evidence-based medicine, but this is false, he just coined the term, which is very different [37], “Although this term was introduced in 1991, the foundation for this new strategy was accomplished through years of work by many others. In fact, EBM encompasses a broad range of topics, from clinical epidemiology to biomedical informatics to evidence-based guidelines.” In his critique, Gordon uses the same kind of reasoning as some encountered in this copypasta, that epidemiology is rarely able to establish causation, even though it was able to do so with the effects on lung cancer from smoking. He says this is because in the case of smoking, the relative risk was very large, but as I’ve explained previously, the maximum relative risk is inversely proportional to the prevalence of the disease. Gordon states “To keep things in perspective: for colon cancer, which was the focus of the WHO report, the absolute risk of contracting this cancer in one’s lifetime is less than 4.5%. An increased relative risk of 1.17 raises the absolute risk to no more than 5.3%.” An absolute risk increase of even such a small amount would result in millions of deaths worldwide, and is comparable to smoking, since the risk of lung cancer death is so low in non-smokers [38]. Later, he rants about advice on anti-oxidants which doctors used to give but no longer do due to new evidence, which is completely irrelevant to the topic at hand. One of his points is that weak associations are untrustworthy due to bias associated with other lifestyle factors, like lifestyle, or socioeconomic factors. Good thing that epidemiological studies are usually controlled for lifestyle factors then, so that the bias is reduced significantly. He cites two studies which he claims to be “far more trustworthy evidence”, which are randomized controlled trials. However, these studies do not prove his claims. The first, the Polyp Prevention Trial [39], was a study on two groups, the first group was the control and continued to eat what they used to eat before, about 90 grams of red meat a day, and the second group decreased their meat consumption by only 20%, which means they still ate 70 grams of red meat per day. The study itself lists several reasons for why the incidence of polyps didn’t decrease in the group which ate less red meat like: the disease may take 30–40 years to develop so the trial length of just 4 years is inadequate, and that the intervention was inadequate because “The 20% reduction in the consumption of red and processed meat among subjects in the PPT intervention group may have been too small to affect the risk of recurrence of adenomas.” When explaining the second study [40], Gordon says that the women on the low fat diet reduced their red meat intake by 20%, but the only thing mentioned about 20% in the study is that the fat intake of those women was reduced to 20% of their total energy. The study wasn’t even on the reduction of red meat consumption on cancer rates; it was on reduction of fat intake and increase of vegetable, fruit, and grain intake. The difference in meat intake was very small, the women in the intervention group only reduced their meat intake by 1.4 servings per week, that’s 0.2 less servings of meat per day. If a serving size is 65 grams, then the decrease of meat intake in the intervention group was only 13 grams. Needless to say, this is a minuscule change. Additionally, it was actually found that the women in the intervention group had a significantly lower risk of breast cancer, contrary to Gordon’s claim, “With additional long-term follow-up of the WHI DM trial participants, deaths after breast cancer continued to be reduced in the dietary intervention group throughout 17.7 years of cumulative follow-up.” Gordon’s critique falls straight on its face, he fails at: criticizing WHO, showing that they misled the public, and showing that they used cherry-picked data.
IARC actually evaluated way over 800 studies, it’s actually over 4000 different full-text articles [41]. Nearly 2900 of them didn’t meet the inclusion criteria. Of 1212 publications left, 1170 of them reported on exposures to things other than red meat or processed meat. It’s clearly not as simple as this copypasta presents. They give good reasons for not including all of the studies, “those with a sample size of fewer than 100 cases were excluded”, “studies based on mortality data were excluded or given less weight”, and explain other reasons for excluding studies, to avoid bias. Neither does this copypasta, nor the source they cite explain why excluding biased data is bad in this context, or if the IARC was indeed doing something dishonest by excluding a lot of the studies they found to be uninformative. The source cited to explain why the studies were cherry-picked states that WHO ignored the studies which showed no effect or protective effect. Yet, once again, it isn’t shown which studies are meant by this, and no examples are given. The IARC report didn’t exclude studies for no reason, so an argument has to be made why the reasons were faulty. Until then it is unreasonable to believe that the report cherry-picked data.
Their own source says that “He [Dr. David Klurfeld] estimates ¼ to ⅓ of the committee making the decision against red meat were vegetarians”, as opposed to the 1/3 stated by this copypasta, though perhaps this wasn’t considered to be a great difference. Did Dr. Klurfeld include his working out or show evidence for that proportion of the committee being comprised of vegetarians? If you guessed no, you’d be right. Here’s the direct quote: “I’m not going to tell you exactly what number of people on this committee were vegetarians but my informal assessment is at least a quarter to a third”. Even if this was the case, it’d mean the vegetarians were outnumbered. Is there a good reason to believe that the minority of the committee is able to make the decisions without the non-vegetarians participating and overriding their decisions if they didn’t agree? This is what is implied here, but no argument is made for it. Due to these reasons this point can be dismissed outright.
Although the perspective article written by the experts didn’t come to exactly the same conclusions as the IARC report, they didn’t just conclude that the evidence is inconsistent and unclear, “Meat consumption may be associated with an increased risk of CRC in ‘Western’ food cultures. This may be due to a real cause-and-effect relationship but it should be kept in mind that associations may suffer from confounding effects.” Though now there is better evidence for the effect of meat consumption on risk of other types of cancer, which couldn’t have been evaluated by these experts at the time of writing the perspective.
2) The idea that dietary raised cholesterol causes heart disease has never been proven[9].
“LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature.”
This review starts by talking about the effect of total cholesterol on atherosclerosis, which is not the same as the claim made by most vegans, nor is it the focus of the original EAS (European Atherosclerosis Society) consensus statement. To put it simply, total cholesterol is made up of LDL cholesterol and HDL cholesterol, and while the reduction of LDL cholesterol has been associated with lower incidence of atherosclerosis, total cholesterol doesn’t have the same predictive capability. The first contention of Ravnskov, who is the main writer of this review, is that the claim that LDL causes CVD is based on “selected patient groups”. He states that “people with high LDL-C should have more atherosclerosis than those with low LDL-C”. Besides not explaining what low or high levels of LDL-C look like, this is a gross oversimplification of the argument as it ignores the fact that atherosclerosis is a multifactorial disease.
The first four references are case reports and case studies with laughable amounts of subjects, and they all only reported on total cholesterol, so they can’t be used to prove that LDL-C doesn’t cause atherosclerosis. The first reference in this review is a bare-bones case report of 123 people who died in car crashes, so the results are based on random dead bodies which don’t represent any particular group of people. There are no specific details given about the serum cholesterol of these corpses, nor about the prevalence of atherosclerosis in them, so any conclusions made from it are, at best, questionable.
The rest 3 studies had a little over 300 subjects in total. All of them reported on TC instead of LDL, and concluded that there was no correlation between total cholesterol and atherosclerosis, except they also showed that either when certain groups were excluded or when the subjects were put into groups according to their atherosclerosis, there was found to be a correlation. In the second study “When all the cases were divided into arbitrary groups according to the amount of atherosclerosis, a rise in the levels of mean serum total cholesterol was seen in the first six successive groups of aortic atherosclerosis.” In the third study, it was noted that there was a trend present between higher values of total cholesterol and atherosclerosis when those with values of TC over 300 mg/dL were excluded. In the forth study, “It was confirmed that the average level of cholesterol in individuals suffering from atherosclerosis is higher than that in those without atherosclerotic symptoms.” But either way, these studies are simply not good evidence compared to the cohorts and meta-analyses of cohorts there are which prove that LDL-C is causally associated with atherosclerosis.
Ravnskov then refers to a study on 304 asymptomatic women which he claims demonstrates no association between LDL-C and coronary artery calcification. It’s clearly shown in this study that those under 55 years old with calcified plaque had significantly higher LDL-C, but not those over 55, “The total cholesterol and LDLC were significantly higher in the EBT+ group compared with the EBT− group.” Since calcified plaques are highly correlated with age, unless there were massive discrepancies in LDL among the older patients it would be expected that major differences wouldn’t be observed. Reflected in their third table on women over 55, the mean LDL-C values between the two groups, those with calcified plaque and those without, were hardly different at all, with both being higher than ideal. The lipid values in this study were short duration measurements, and therefore fail to appropriately consider the importance of long-time exposure to LDL.
Ravnskov mentions results from “one exception”, a study on a subcohort of individuals in the Progression of Early Subclinical Atherosclerosis cohort, which was of significantly higher quality than the other case-studies he cited. Their results showed as LDL increases, so does presence of atherosclerosis. His response to these findings is “However, association does not prove causation.” He used poorly detailed case studies which don’t specifically consider LDL-C and the multifactorial nature of CVD to prove causation (or the absence of it) while dismissing results from a larger, comprehensive prospective cohort that considers time, dose, and other risk factors. He states that stress can raise cholesterol by 10–50% within a half hour, then somehow concludes it may cause atherosclerosis via a mechanism other than LDL-C, such as hypertension. The relationship between LDL-C and atherosclerosis is temporal, so cumulative exposure to LDL is what matters, not short-term fluctuations like is the case with stress. He provides no evidence for the “mechanisms other than an increase in LDL-c” that supposedly cause atherosclerosis.
Ravnskov reasons that if LDL-C causes CVD, values in untreated patients with the condition should be higher than normal. This is false because it completely ignores the patients’ LDL levels in the past, and the presence of additional risk factors which can change CVD risk, as well as the possibility that they may have adopted lifestyle changes to reduce their risk. He mentions an American study of about 140,000 patients with acute myocardial infarction, commonly known as heart attacks, who had, according to Ravnskov, “lower than normal” LDL at admission, in addition to another study with the same finding. In the first study, the mean LDL value was 105 mg/dL, which might be lower than the average in the general population, but it’s actually not low enough. As seen in the PESA cohort [42], this easily allows for the progression of ASCVD even in complete absence of other risk factors like smoking, hypertension, diabetes, and so on; which were present in the sample population of this study [43]. Over 21% of the participants used lipid lowering medication, which obviously pulled the mean downward. Lastly, it is actually well-acknowledged by researchers that LDL decreases after 24 [44] and up to 48 [45] hours following an acute MI. Such a phenomenon makes post-MI LDL values likely unreliable. This point is highly important with respect to the second study Ravnskov references, in which lower LDL (<105 mg/dL) following myocardial infarction was associated with much higher mortality after 3 years. On top of the observation that worse health status, most notably diabetes, predicts greater decreases in LDL post-MI, “Diabetes is a strong independent predictor of LDL-C decrease”, the authors of this paper note that previous research has demonstrated the severity of the event does the same, “It has been suggested that LDL-cholesterol levels acutely decrease more with larger myocardial infarction within a few days of hospitalization.” It’s possible that reverse causality is at play, other conditions such as cancer and infections could be responsible for a decrease in LDL, and which in turn cause the increased mortality. Ravnskov says it’s more likely that CVD is caused by infections since LDL inactivates “almost all types of microorganisms and their toxic products”. He uses claims uses four of his own publications full of mechanistic speculations and selective citations to prove that individuals with low LDL have a significantly increased risk of infectious disease and cancer. These RCTs had incredibly low incidences of cancer/infections, some showing single digit case differences which made the results significant because of how low the number was. More comprehensive meta-analyses of RCTs, some of which are even mentioned in his editorials, have shown statin treatment does not increase the risk of cancer [46][47][48] or infection incidence/mortality [49], “statins, despite producing marked reductions in LDL-C, are not associated with an increased risk of cancer.”, “In 27 randomised trials, a median of five years of statin therapy had no effect on the incidence of, or mortality from, any type of cancer.”, “Especially, the use of statin was significantly associated with a reduction of cancer-specific mortality of colorectal cancer supported by a convincing level of evidence, which can be interpreted that it has a noteworthy association.”, “Meta-analysis showed no effect of statins on the risk of infections or on infection related deaths”. Mendelian randomization [50], a tool far better suited to determine causal relationships, demonstrates that not just acute, but lifelong genetically determined lower LDL does not increase the risk of cancer, “Low plasma LDL cholesterol levels were robustly associated with an increased risk of cancer, but genetically decreased LDL cholesterol was not”. “This finding indicates that low LDL cholesterol levels are secondary to a preclinical cancer or that a confounding factor causes both low plasma LDL cholesterol and an increased risk of cancer.”
Ravnskov tries his best to explain why Mendelian randomization studies are unreliable, but provides a source which goes against what he tries to claim. The study he cites actually just acknowledged some of the problems with Mendelian randomization studies, and states exactly how these problems have been addressed, and how this type of study has improved in methodology, allowing causal relationships to be drawn from them, “Power, linkage disequilibrium, pleiotropy, canalization and population stratification have all been recognized as potential flaws in the Mendelian randomization approach as methods have been developed.”, “The next decade will see a deeper understanding of the properties of genetic variants which will be crucial to the appropriate implementation and interpretation of Mendelian randomization analyses. Over the past decade, Mendelian randomization has provided a novel and flexible paradigm to understand the causal nature of associations between modifiable risk factors and common diseases.” To add to this, there is remarkable consistency in the results from Mendelian randomization studies on the effect of LDL on coronary artery disease [51], “Since single-variable MR cannot address statistical bias due to covariation among multiple risk variables, we performed MVMR on dataset A to adjust for co-variables and found that both LDL-c and TG were positively associated with risk for CAD” ,so it cannot be waved away with a simple “Other genes in the same individual may have opposite effects”, which he’s yet to provide evidence for.
This is just a few chapters being addressed in this review, but as is clearly seen, the evidence provided by it is weak and cherry-picked. Bigger studies and meta-analyses show that decreased LDL does not cause increased mortality from cancer or infection, and in fact, it causes better health outcomes such as low to no incidence of atherosclerosis [52], “Considered together, the strong and consistent evidence from the genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized intervention trials discussed here, supported by mechanistic evidence to be presented in the second Consensus Statement on LDL causality, establishes that LDL is not merely a biomarker of increased risk but a causal factor in the pathophysiology of ASCVD.” Going over the whole paper by Ravnskov would take too long, so check out Matt Madore’s full debunk of it [53], where he goes over all of the relevant sections.
“The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression.”
The first study in the section about “inconvenient questions”, in this paper [54], wasn’t on LDL cholesterol, it was on total cholesterol, which is a weak predictor of atherosclerosis as opposed to LDL, and so the question connected to it can be dismissed. The second study reported that the LDL levels of the subjects who had calcified plaque were significantly higher, “Mean age, TC, LDL-C, and TC/HDL-C were significantly higher and HDL-C lower in the EBT+ compared with EBT− group.” However, the authors of this study decided to concentrate on the fact that a lot of the patients with calcified plaque wouldn’t be diagnosed of being at risk for atherosclerosis by a certain guideline, which is a problem. This fact can be agreed upon, and the guidelines changed, but this doesn’t mean that LDL-C isn’t a causal factor of atherosclerotic plaque, as quite the opposite is shown by the results. It has to be mentioned that this study didn’t look at non-calcified plaque even though non-calcified plaque also exists and is an important factor in CVD. The third study in this paper has been addressed in the analysis of Ravnskov’s review: in women under 55 who had calcified plaque also had significantly higher LDL levels. This study also only looked at calcified plaque in women, but not the non-calcified plaque. The fourth study only found no correlation between the total cholesterol levels of the patients and plaque because there was no comparison done on LDL levels and the progression of plaque, however the authors concluded by stating that both calcified and non-calcified plaque should be assessed in patients in order to recommend to them statin treatment, “Our study confirms the observations of others who used calcium scoring and extends the conclusion to include all plaque, calcified and uncalcified, detected at coronary CTA. Coronary CTA may provide incremental information beyond risk factors and may significantly influence therapeutic decisions regarding prophylactic therapy for CAD”, which is agreeable. The fifth study only looks at calcified plaque so it’s not surprising that the researchers didn’t find a significant correlation between plaque and levels of LDL, as they didn’t assess all plaque. There was also no comparison between significantly low (below 70 mg/dl) LDL cholesterol levels, and higher levels. All this makes this study entirely unuseful for determining whether LDL has a causal association with atherosclerotic plaque. What the authors of this paper did with the sixth study [55] is incredibly dishonest: they only mentioned that there was no association found between LDL cholesterol levels and calcified plaque, “Why did Arad et al. in the St. Francis Heart Study find no correlation between LDL levels and coronary calcium scores in 4903 asymptomatic individuals?”, but didn’t mention that it’s clearly stated, in the same study, that LDL cholesterol is significantly associated with CAD events, “In multiple logistic regression, only age, male gender, LDL cholesterol, HDL cholesterol, and two-year change in calcium score were significantly associated with subsequent CAD events.”, which are a more important outcome than just calcified plaque. The seventh study [56] both only looked at total cholesterol instead of LDL cholesterol, and only calcified plaque instead of calcified and non-calcified plaque. In the eighth study, although the effect of LDL seen on the risk of calcium in the coronary artery was smaller than that of HDL, there was still an effect present, “LDL cholesterol and HDL cholesterol were not associated with the progression of existing CAC, even in unadjusted models, but both were associated (HDL negatively) with the risk of incident CAC.”, and once again this study wasn’t looking at non-calcified plaque, on which LDL could have a greater impact. The ninth study [57] only looked at calcified plaque in the coronary artery, however it was noted that the participants, who were all Korean, had much lower coronary calcium scores than American participants in another study, likely because of having a lower prevalence of risk factors such as hyperlipidemia (which includes having lower cholesterol levels among the Korean population compared to the American population), “The coronary calcium scores of this Korean asymptomatic population was much lower than those of an American population evaluated in an earlier study; these differences are likely because of the different risk factor profiles such as hyperlipidemia.” If anything, this study is evidence that having lower cholesterol protects against calcified plaque. In the tenth study, the subjects with calcified plaque in the coronary arteries clearly had (20%) higher levels of LDL cholesterol than the subjects without calcified plaque, even though the authors decided to concentrate on oxidized LDL instead of all LDL, for which there was no association. Both groups, however, had levels of LDL above the ideal levels (50–70 mg/dl). The eleventh study [58] only looked at calcium scores again, but the patients with calcified plaque had a significantly higher BMI than the patients who didn’t have any calcified plaque [59], “The American men with coronary calcium score 0 had significantly higher levels of fasting glucose, BMI, and waist circumference than those with coronary calcium score = 0.” The BMI difference alone is enough to explain why one group had calcified plaque and the other didn’t as having a higher BMI is associated with much higher calcium scores [60], “Obese patients had higher median calcium score compared to non-obese subjects (14.7 vs. 1.4, respectively, p = 0.019).” This doesn’t mean that LDL isn’t a factor for calcified plaque as the study wasn’t comparing the calcium scores in people with higher LDL with the calcium scores in people with low LDL. The next few studies, the ones which conducted EBT tests on the patients were only evaluating the calcified plaque in the patients, and the majority of them only measured the progression of the calcium score. It’s been shown that while higher LDL isn’t associated with the progression of existing plaque calcification, it is associated with the risk of incident calcification [61], “LDL cholesterol and HDL cholesterol were not associated with the progression of existing CAC, even in unadjusted models, but both were associated (HDL negatively) with the risk of incident CAC.” This means that higher LDL likely doesn’t progress the calcification of plaque, but it does allow for the calcified plaque to exist in the first place (if you have low LDL your entire life, it’s unlikely that you’ll develop plaque, and hence it cannot become calcified).
“Dietary cholesterol reduces circulating levels of small, dense LDL particles, a well-defined risk factor for CHD.”
The egg studies in the first paper [62] had at least 1 problem: In the first study it was found that those children who were classed as hyperresponders increased their LDL significantly by consuming eggs, “hyperresponders experienced significant increases both in LDL and HDL cholesterol as a result of the dietary cholesterol challenge”, the claim about the results showing that the LDL:HDL ratio stayed the same during the intervention can be dismissed due to a meta-analysis of randomized trials [63] showing that the consumption of dietary cholesterol increases the ratio, “In conclusion, the consumption of cholesterol increases the ratio of total to HDL-cholesterol concentrations, which would predict increased risk of coronary heart disease.”; The second study [64] did almost the same thing, “Although the addition of 640 mg of cholesterol to the diet did result in an increase in plasma cholesterol in hyperresponders, the LDL/HDL ratio was maintained.”, “As expected, a very significant increase in dietary cholesterol was observed for hyper- and hypo-responders during the egg period.”, and to add to this the saturated fat intake was high even during the placebo intervention; The third study used an egg substitute with 0 cholesterol, but the saturated fat in the substitute wasn’t even mentioned, and, in fact, saturated fat wasn’t mentioned anywhere in the study, even though this is obviously an important factor; In the fourth study[65], the saturated fat intake as a percentage of total energy intake of the egg group and no egg group were over 10.5% and 12.5% respectively, which are both high, and the cholesterol intake in both groups only differed by 150 mg, meaning the baseline consumption was 300 mg (high enough to only make a small difference when 150 mg are added); In the fifth study [66], the participants also consumed a diet high in saturated fat, which influenced their serum cholesterol levels; In the sixth study [67], the baseline cholesterol intake wasn’t recorded, and neither were saturated fat intakes taken into account even though the authors noted that greater saturated fat intake is associated with greater risk of CHD, hence supporting the lipid hypothesis, “Many studies have shown that saturated fats and trans-fats have a greater impact than did dietary cholesterol in raising blood cholesterol levels. Diets high in saturated fatty acids raised serum LDL-c levels. Reduction in intakes of saturated fatty acids lowered LDL-c levels and reduces risk for CHD”; In the last study, the participants were losing weight at the same time as going through the intervention, which muddled the results as weight loss is known to cause a decrease in serum LDL [68], making the results unuseful for people who plan on maintaining their weight.
“Cholesterol does not cause coronary heart disease in contrast to stress.”
This paper is much more like a newspaper article than an actual scientific paper [69], as it goes over the history of the research on the topic of cholesterol rather than looking at up-to-date studies and trials. The main claim, that stress is a risk factor for CHD can be entirely granted, “For what it’s worth, stress elevates cholesterol far more than dietary fat intake and also contributes to smoking and hypertension.” But, what has not been shown in this is that the randomized controlled trials on the effect of the replacement of saturated fat with polyunsaturated fat [70], and on decreasing dietary cholesterol [63] are wrong in their results which unequivocally show that both saturated fat and dietary cholesterol increase serum LDL, and thereby increase the risk of CHD.
“The fallacies of the lipid hypothesis.”
This is another paper by Uffe Ravnskov, like the first one from the paste bin in LDL, though this study was released a decade before the other one. A lot of the points and arguments made are similar if not the same, and fail to stand up to scrutiny as shown by Matt Madore’s analysis [53]. Ravnskov only mentions epidemiological studies on saturated fat’s effect on cholesterol, and on the effect of LDL cholesterol on atherosclerosis. Perhaps there weren’t many RCTs on both of these topics at the time, but there most definitely are now [70][52], which are of higher quality than epidemiological studies. This paper is therefore outdated and doesn’t address the latest arguments and data.
Low cholesterol is a risk factor for in-hospital mortality
http://www.ncbi.nlm.nih.gov/pubmed/12967690
http://www.ncbi.nlm.nih.gov/pubmed/19033015
The problems with these studies is they don’t take into consideration the fact that the LDL levels of the patients with low LDL could’ve been high throughout their lives, and have only changed recently, whether it be because of a post-scare intervention or because of a disease which both lowers their cholesterol and increases their risk of mortality. They cannot rule out reverse-causation. This is why RCTs are needed, and RCTs show that lowering LDL cholesterol using interventions, such as the use of statins [71], lower all-cause mortality, “Statins represent a major advance in the fight against cardiovascular diseases. They are able to lower total cholesterol and LDL cholesterol effectively and safely”, “In conclusion, through meta-analysis of the clinical trials on statins, we are able to show that statins reduce coronary events and all-cause mortality, with no increase in non-coronary mortality.”
Amyotrophic lateral sclerosis patients with elevated LDL/HDL ratio survive by more than 12 months longer.
Firstly, this has the same problems as the previous few studies on in-hospital mortality. Secondly, LDL has been proven to be a causal risk factor for ALS [72], “Among the four lipids, we found that only LDL is causally associated with ALS and that higher LDL level increases the risk of ALS in both the European and East Asian populations.” And lastly, patients with ALS aren’t representative of the general population, and hence the fact that higher LDL is associated with longer survival time isn’t indicative of the effect of higher LDL in people without ALS.
Replacing saturated fat with carbohydrates increases small, dense LDL particles, shifts to an overall atherogenic lipid profile, and increases incidence of diabetes and obesity. Replacing saturated fat with omega 6 polyunsaturated fats increases risk of cancer, increases risk of coronary heart disease, cardiovascular events, and death to heart disease and overall mortality, increases oxidized LDL-C, reduces HDL-C.
First, this editorial talks about a study on low-carbohydrate dieters compared to low-fat dieters [73], where the low-carbohydrate group seemingly had better outcomes in terms of inflammation, body-mass, and even lipids. However, this study had several flaws: it didn’t differentiate between refined and unrefined carbohydrates that the participants were consuming, even though refined carbohydrates are associated with worse health outcomes, while unrefined ones aren’t [74]; the low-carbohydrate dieters actually dropped their calorie consumption to a greater degree (by more than 200 calories more) than the low-fat dieters, which would explain the greater weight loss and greater decrease in inflammation [75], “In conclusion, long-term moderate CR without malnutrition induces a significant and persistent inhibition of inflammation without impairing key in vivo indicators of cell-mediated immunity.”; and the serum LDL of the low-carbohydrate dieters actually increased during the intervention, while the serum LDL of the low-fat dieters decreased by a small amount. Then this editorial attempts to make the argument that saturated fat increases large LDL particles which supposedly aren’t as atherogenic. A meta-analysis [76] on this topic found that it is not possible to judge which type of LDL is more harmful, as is discussed in the later section about eggs.
Several other papers are cited to prove that a low-carbohydrate diet leads to greater weight loss and lipid improvement than a low-fat diet, however all of them have substantial flaws. The first study [77] didn’t report on the macronutrient intakes of the two diet groups, meaning we can’t even know how much saturated fat or carbohydrates, and polyunsaturated fat they were consuming. In the second study [78], the low-carbohydrate group decreased their calorie intake by more than 400 calories more than the conventional diet group, making the comparison entirely unfair, and would of course lead to greater weight loss and other health outcomes among the low-carbohydrate group. The third study didn’t differentiate between refined and unrefined carbohydrates consumed by the participants, and neither did it report on polyunsaturated fat intake, which has been shown to be an important factor in health outcomes when replacing saturated fat. Additionally, all groups couldn’t keep to their respective diets, with their macronutrient intake fluctuating, with the greatest adherence to the diets being at 2 months. Thus, the conclusions made from the results in the study are highly suspect, as Barry Sears put it in his letter to the editor [79]. The fourth study [80] didn’t report on macronutrient intake, so we can’t know whether both groups consumed the same amount of calories, and therefore whether the health risk factor change is attributable to the particular diets or the change in energy intake, or to which degree the dieters followed their respective diets. The fifth study conducted an unfair comparison between the low-carbohydrate group and the other diet groups, especially the low-fat diet group since neither the total fat nor the saturated fat as a percentage of total energy intake changed in the low-fat group. Additionally, there was a high drop-out rate among the low-carbohydrate group as opposed to the drop-out rate of the low-fat group, as detailed by Dr Arne Astrup’s letter to the editor [81], “Moreover, the dropout rate was 15% in the Mediterranean group, 22% in the low-carbohydrate group, and only 10% in the low-fat group.” Neither of these criticisms are addressed by the reply to this letter by the authors.
To prove that replacing saturated fat with polyunsaturated fat, this paper cites reviews on studies which will be addressed in the section about the review of 17 systematic reviews and the review of 19 meta-analyses, all of which either have major flaws or the findings are misrepresented and skewed. Another study [82] is cited to prove that the replacement of saturated fat with polyunsaturated fat leads to a greater amount of deaths, but this is highly misleading as the control group in that study started off with significantly less risk factors than the intervention group, which would easily explain the few more deaths in the intervention group compared to the control group as the causes of deaths were diseases which take a long time to develop. It must be noted that over time, the risk factors in the intervention group decreased nearly 4-fold while that of the control group stayed the same, with the intervention group having more than 1.6 times the % of people with no risk factors compared to the control group. The other study cited for this point isn’t available anywhere on the internet. There’s no evidence of its existence except as a citation in this editorial, which is strange to say the least. The first study cited as evidence that a higher polyunsaturated fat intake is harmful is mainly based on animal studies, and are therefore mechanistic in nature, and cannot tell us about the effects it actually has on humans. The next study is a mice study, so it has the same problem as previously. The third and fourth studies were on the omega-3 to omega-6 ratio, with the results showing that a higher omega-6 to omega-3 ratio increases prostate cancer risk. This, in no way, is a problem, as it can be recommended to people with prostates to consume a low omega-6 to omega-3 ratio. The same can be said about the next study on breast cancer, it can be recommended to people with breasts to consume a lower omega-6 to omega-3 ratio. The last study [83] cited on this claim is stated to have found “a greater than threefold increased risk of death due to carcinoma” in the intervention group where saturated fat was replaced by polyunsaturated fat, but this is very misleading, as the intervention group also had a greater amount of people with chronic obstructive pulmonary disease, which was the primary or the contributory cause of death, “Chronic obstructive pulmonary disease was present in clinically significant degree in many of these subjects and probably contributed to many of the deaths”. The total amount of people who died due to carcinomas was also very small, 2 in the control group, and 7 in the intervention group, meaning this result is statistically underpowered to give an accurate representation of the risk of death from carcinomas caused by replacing saturated fat with polyunsaturated fat.
Low cholesterol is associated with mortality from cardiovascular disease.
It’s stated within this study itself that the higher death rate among individuals with lower total cholesterol can be explained by chance, confounding factors like smoking, competing factors, as well as other things. It is also mentioned that “reverse epidemiology” is, or could be at play, as certain health conditions cause people to have low total cholesterol and increase their risk of dying, meaning the low cholesterol isn’t the cause of death, the disease is, “Associations compatible with the concept of “reverse epidemiology” have been described in several other chronic conditions such as end-stage renal disease, malignancies, chronic obstructive lung disease, AIDS as well as in the elderly.” It is also noted that another study found that lower levels of cholesterol in people during their midlife, which is the period of people’s lives when they’re less likely to have certain health conditions which lower their total cholesterol, is not only associated with better survival but better quality of life as well, “Strandberg et al. suggested that low serum cholesterol level in midlife predicted not only better survival but also better physical function and quality of life (QOL) in old age.” Lastly, total cholesterol is a worse predictor of heart disease than LDL cholesterol, which has been known for a long time, which means this study isn’t even only addressing the strawman version of the lipid hypothesis.
Egg consumption improves lipid profile, blood pressure, and reduces risk for cardiovascular mortality and diabetes.
http://www.ncbi.nlm.nih.gov/pubmed/20683785
http://www.ncbi.nlm.nih.gov/pubmed/11023005
http://www.ncbi.nlm.nih.gov/pubmed/18991244
http://www.ncbi.nlm.nih.gov/pubmed/21776466
http://www.ncbi.nlm.nih.gov/pubmed/19369056
http://www.ncbi.nlm.nih.gov/pubmed/21134328
http://www.ncbi.nlm.nih.gov/pubmed/15164336
http://www.ncbi.nlm.nih.gov/pubmed/18203890
Some of these studies fail to take into account the baseline dietary cholesterol of the participants. The reason this is a major flaw is because we know that even at moderate intakes of dietary cholesterol, there’s little change in blood cholesterol levels if more dietary cholesterol is added [84], “At moderate dietary cholesterol intakes, little additional change in serum cholesterol would be expected.” The higher your cholesterol intake, the smaller the change in your blood cholesterol levels if you add more cholesterol to your diet. Meaning if you add one or two eggs to your diet when your intake of animal products full of cholesterol is already high, the change in your serum cholesterol will be negligible. This has been known for years, and yet studies like these come out and completely ignore that fact. The first paper was addressed in a previous section.
The second paper [85] mentions a prospective study on the consumption of eggs, which, according to the paper, found that “the relative risk of CHD was the same whether the participants consumed fewer than one egg a week or more than one egg a day”. In reality, the authors of that cohort [86] even noted that the null relationship they found may have been because the Western diet is so high in cholesterol already, and that a RCT found that adding 1 egg to the diet of vegetarians increased their LDL cholesterol levels by a significant amount, “One potential alternative explanation for the null finding is that background dietary cholesterol may be so high in the usual Western diet that adding somewhat more has little further effect on blood cholesterol. In a randomized trial, Sacks et al found that adding 1 egg per day to the usual diet of 17 lactovegetarians whose habitual cholesterol intake was very low (97 mg/d) significantly increased LDL cholesterol level by 12%.” The results of this RCT are concordant with the results of the previously mentioned meta-analysis of RCTs [63], “We showed that consuming one additional egg daily will increase the ratio of total to HDL-cholesterol concentrations by 0.040 units, which would imply an increase in the risk of myocardial infarction of 2.1%. The calculated increase in risk may be small in an individual patient, but in view of the widespread consumption of diets high in cholesterol it may be substantial at the population level.” The only RCT mentioned in this paper was on subjects with very high levels of LDL cholesterol, “Subjects had LDL-C between 3.36 and 4.91 mmol/L (130 and 190 mg/dL)”, which adequately explains why they found only a small increase in LDL when the subjects consumed more eggs, due to the hyperbolic relationship between baseline dietary cholesterol intake and additional dietary cholesterol [84]. This paper is invalidated by the fact that the quality of evidence provided is low in comparison to the quality of evidence supporting the hypothesis that increasing egg intake will increase serum LDL-C levels, and thereby increase the risk of CVD.
The next study provided was comparing normal egg consumption to consumption of eggs high in omega-3s, making it unuseful for disproving the lipid hypothesis. There was also a major flaw with this study, so even if the results they got could somehow be used to put a dent in the lipid hypothesis, it would still be an unreliable source of information in the first place. The participants were split into two groups, one group started eating an extra standard egg per day, while the other group started eating an extra omega-3 egg per day, and then the groups switched diets after one month. The major flaw with this study is that the researchers didn’t record what the participants ate before the study and during the study, meaning they could’ve been decreasing or increasing their consumption of other products, or even decreasing their consumption of eggs overall. This makes the results entirely unuseful except as a pilot study.
The next review [87] was based on the studies which were already addressed. The only randomized controlled trial [88] mentioned doesn’t even oppose the lipid hypothesis, it just states that people with insulin resistance and obesity should concentrate more on restricting calories than fat, which could be done at the same time as decreasing saturated fat intake and cholesterol intake, “The results suggest that dietary management of insulin resistance and obesity can focus more on restricting calories and less on restricting dietary fat.” Most importantly, the subjects had high levels of cholesterol, meaning it’d be expected for their cholesterol to not significantly increase when they added eggs to their diet.
The next study found that the egg group had higher levels of large LDL-C, but what the authors tried to do was justify the increase in LDL-C with the increase in HDL and the fact that the LDL particles were larger than in the egg substitute group, “Although an increase of the larger LDL subclass was observed for all subjects, the EGG group had a greater increase (P<.05). The EGG group also presented a higher number of large HDL particles (P<.01) compared to the SUB group.” They fail to provide evidence that HDL mitigated the negative health effects of the LDL-C increase, or that large LDL causes less damage. In fact, although in the past it’s been found that higher HDL levels are correlated with lower risk of ASCVD, the results from Mendelian randomization studies on individuals with genetically higher HDL and clinical trials on HDL increased by medications show that higher HDL isn’t causally associated with lower risk of ASCVD, and high levels of HDL in epidemiological studies haven’t shown to reliably decrease the risk either [89], “Mendelian randomization does not support a link of causality and to date, attempts to raise HDL-C pharmacologically have not yielded the expected outcomes.” Large LDL has been found to be responsible for the development of atherosclerosis, and hence it can’t be said to be less harmful than small LDL [76], “Finally, large cholesterol-rich LDL is the predominant type of LDL in familial hypercholesterolemia, and it is firmly established that this LDL is responsible for their premature atherosclerosis. Thus, large and small LDL are atherogenic, and it is not possible to judge which if any is more harmful, overall.”
The next study was comparing eggs consumption to lean meat consumption, so both of the groups were consuming dietary cholesterol. The lean meat group consumed an average of 227.5 mg of cholesterol per day, whereas the egg group consumed an average of 589.5. It was found that during the study, the serum cholesterol levels of the egg group increased, and the serum cholesterol levels of the lean meat group decreased, though these results weren’t found to be statistically significant. The reason this result wasn’t found to be statistically significant is explained in the study: the participants were obese and had type 2 diabetes, which made them less responsive to dietary cholesterol, “As insulin-resistant subjects are less responsive to dietary cholesterol than normal subjects, it is not surprising that we observed a similar effect in overweight individuals with type 2 diabetes.”
The next study [90] found an increase in large LDL in hyperresponders who consumed eggs, and somehow concluded that the consumption of cholesterol doesn’t negatively influence the atherogenicity of the cholesterol, “Because LDL peak diameter was not decreased and the larger LDL-1 subclass was greater in hyperresponders following egg intake, these data indicate that the consumption of a high-cholesterol diet does not negatively influence the atherogenicity of the LDL particle.” As addressed before, large LDL may be just as harmful as small LDL, “The burden of proof for any newly proposed risk factor is that it must add significantly to risk assessment by existing measurements, or that it is equivalent but more economical. LDL subtyping does not meet either of these expectations. Metabolic studies demonstrate that large and small LDL subtypes are atherogenic.” To add to all of this, the researchers didn’t record the baseline diets of the two groups, meaning the participants could have decreased their dietary cholesterol and saturated fat, which would have obviously influenced the results of the study.
In the eighth study, there was no mention of saturated fat, so the fact that the researchers found little difference in the serum cholesterol increase between the group consuming eggs and the group consuming an egg substitute isn’t surprising. The egg substitute group could’ve added more saturated fat to their diets than the egg group during the intervention, which would increase their LDL-C levels to a greater degree. Both groups also had high levels of LDL-C, which could indicate that both groups had a high intake of saturated fat, though perhaps more so for the egg group.
The ninth study was on mice, which seems at this point like a desperate attempt to find any evidence to prove their claims. Studies on mice can be discarded completely when there are studies on humans, as humans are more like humans than mice, making the results on human subjects that much more reliable for determining the effects of the intervention being studied on humans.
The last paper tried to make a similar argument to the ones that have already been addressed, like the fact that eggs promote the formation of large LDL, and the claim that there isn’t a connection between egg consumption and heart disease. The most comprehensive meta-analysis [91] of RCTs to-date on the effects of eggs found that the consumption of eggs significantly increases LDL-C, “Meta-analysis of 66 RCTs with 3,185 participants revealed that egg consumption can significantly increase TC, LDL-C, HDL-C, TC/HDL-C, apoA1/and B100, but there was no significant effect on other serum lipids.” Though it has to be mentioned that the authors of this meta-analysis appear to be motivated. They try to say that consuming one egg per day can be safe, even though dietary cholesterol consumption has the biggest effect when someone consumes little to no dietary cholesterol. Adding one egg per day to your diet, when you’re consuming no other sources of dietary cholesterol, will increase your serum cholesterol even more, per egg consumed, than if you add another egg on top of that, due to the hyperbolic nature of the relationship between dietary cholesterol and serum cholesterol levels.
“A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”
http://www.ncbi.nlm.nih.gov/pubmed/20071648
http://ajcn.nutrition.org/content/early/2010/01/13/ajcn.2009.27725.abstract
There are serious methodological flaws with this (Siri-Tarino) meta-analysis, as detailed by a letter to the editor [92]. It turns out that the authors of this meta-analysis assumed that the effect of saturated fat can be measured without taking into account what that saturated fat is being replaced by, “First, the notion that there exists such a thing as ‘‘the effect of saturated fat’’ is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.” It also used a faulty method for determining the effects of replacing saturated fat by polyunsaturated fat, without actually using studies where such a replacement happened, “To estimate the effect of replacing saturated by polyunsaturated fat, Siri-Tarino et al selected 5 studies that reported relative risks adjusted for intake of carbohydrate, protein, and fats but not of polyunsaturated fat. They then combined these 5 numbers and presented the outcome as the effect of replacing saturated by polyunsaturated fat. It requires a leap of faith to assume that the outcome of such a calculation truly represents what happens when saturated fat is replaced by polyunsaturated fat.” Lastly, a large portion of the studies used relied on a dietary assessment method deemed to provide a poor estimation of the dietary intakes of subjects, “A major weakness of the meta-analysis is the imprecision of dietary assessment methods used in the underlying studies. About half of the studies used 1-d dietary assessments or some other unvalidated method. Food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual.” Clearly, all of these factors make the meta-analysis unreliable. It also must be mentioned that there’s a meta-analysis of RCTs [70] which found a relationship between the replacement of saturated fat with polyunsaturated fat and a lower risk of CHD, “increasing PUFA consumption as a replacement for SFA reduced the occurrence of CHD events by 19%; each 5%E greater PUFA consumption reduced CHD risk by 10%.”
Recommendations of the American Heart Association from 1982 are based on misinterpretation, obsolete science, and arbitrary choices without explanation.
The both of the editorials bring up the same points, though the one published in 1984 is behind a paywall, so the free one will have to be addressed instead. Firstly, it’s addressing the AHA recommendations from 1982, even though there has been a lot more research done since then, and AHA has released newer recommendations backed up by better research. So even if the level of evidence previously was poor, what’s left to be addressed is the evidence provided now. There’s no reason to bring up a recommendation which is coming up on its 40th year and try to debunk it when there’s a new recommendation out. To address the first point in the article cited, that “No documentation is offered as evidence that a reduction in fat intake has health benefits.” — the new recommendations by AHA are based on trials which found that replacing saturated fat with polyunsaturated fat reduces the risk of CHD, “A few clinical outcome trials have documented that replacement of saturated fat with polyunsaturated fats reduces the risk of developing CHD… A range of 25% to 35% for total fat is an appropriate level of intake in a healthy dietary pattern.” The second point, that there isn’t evidence for saturated fats increasing LDL, in the new recommendations this is backed up with several studies, “Trans fatty acids tend to increase LDL cholesterol levels slightly less than saturated fatty acids, whereas saturated fatty acids increase HDL cholesterol concentrations but trans fatty acids do not.”, “Saturated and trans fatty acid intakes are directly related to LDL cholesterol levels.” The third point, that there isn’t evidence that replacing saturated fats with polyunsaturated fats will improve health has been addressed. The last point, that there isn’t good evidence for dietary cholesterol raising blood cholesterol levels is also addressed in the new recommendations, as it was found that dietary cholesterol does indeed increase LDL levels, though to a lesser extent than saturated fat and trans fat, “dietary cholesterol and excess body weight are positively related to levels of LDL cholesterol.”, “Increased dietary cholesterol intake also raises LDL cholesterol concentrations.” Additionally, there’s other evidence that increasing dietary cholesterol will also increase your blood cholesterol levels [84], though there is nuance in that dietary cholesterol doesn’t increase much when your blood cholesterol levels are already high, “Serum cholesterol concentration is clearly increased by added dietary cholesterol but the magnitude of predicted change is modulated by baseline dietary cholesterol. The greatest response is expected when baseline dietary cholesterol is near zero, while little, if any, measurable change would be expected once baseline dietary cholesterol was > 400–500 mg/d.” This effect, which has been well-known for years isn’t even mentioned by the article, either because of the lack of knowledge or other incompetence.
“Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.”
This paper [93] actually supports the lipid hypothesis, as it is noted that “Based on the best evidence from human studies, replacing SFA with PUFA (e.g., vegetables, vegetable oils) lowers CHD risk, whereas replacing SFA with CHO [carbohydrates] has no benefits.” And it is also explained that replacing SFA with unrefined carbohydrates could have benefits, “replacing SFA with less processed, higher fiber, lower glycemic index CHO could provide benefit, whereas replacing SFA with more processed, lower fiber, higher glycemic index CHO might have no effects or even be harmful.” These results can be confirmed by a different. previously-mentioned meta-analysis [70], “reducing dietary saturated fat reduced the risk of combined cardiovascular events by 21%”.
“We conclude that major weight loss was associated with a late rise in serum cholesterol, possibly from mobilization of adipose cholesterol stores, which resolved when weight loss ceased.”
This point is completely irrelevant to the lipid hypothesis, but it’s also based on a very limited amount of research. The study cited was conducted on 6 obese women: they lost weight over the course of 5–7 months. A different study on 14 obese patients who lost weight on a low calorie diet over 9 months [94] found a decrease in LDL cholesterol in the first three months, after which the patients’ cholesterol levels stayed the same, “Changes in total, LDL and HDL cholesterol were biphasic during the hypocaloric diet, showing a decrease during the first 3 months, and subsequently approaching or reaching baseline values.”
“The results show that dietary and plasma saturated fat are not related, and that increasing dietary carbohydrate across a range of intakes promotes incremental increases in plasma palmitoleic acid, a biomarker consistently associated with adverse health outcomes.”
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0113605
Conclusion: The lipid hypothesis is foolish.
Not only was there a very low amount of participants in this study (16 people in total), but they were also eating a high amount of saturated fat (13.6% of total energy intake) before the study, as their baseline, and during the study they were given even more saturated fat to eat as their starting point. The diet of these participants changed over 18 weeks, and the changes happened every 3 weeks, going from high saturated fat intake to a lower saturated fat intake. During the first phase, 29% of the participants’ total energy intake consisted of saturated fat, which is an insanely high proportion, and the lowest percentage the participants got to was 11%. The reason this is a massive problem is because it’s been shown in a meta-analysis of RCTs [70], with around 59,000 participants, which is 3,500 times bigger than this study, that no decrease in CVD events and mortality is seen when saturated fat intake makes up more than 9–10% of your total energy intake, however a massive drop in CVD events and mortality is seen below 9% and especially at 8%. It was noted that there was a decrease in LDL levels of the participants with the lowest intake of saturated fat compared to higher intakes, “There was a reduction in LDL in participants with reduced SFA compared to higher SFA”. The point about higher carbohydrate intake causing adverse health outcomes is unrelated to decreasing saturated fat intake, as one can decrease their saturated fat intake while keeping their carbohydrate intake the same, but instead, increasing their intake of polyunsaturated fats. It also must be mentioned that the adverse health outcomes from carbohydrates only come from the refined carbohydrates [95], “replacement of saturated fat with carbohydrates, particularly refined carbohydrates and added sugars as has occurred over the past few decades, has been associated with dyslipidemia and either no improvement in CVD risk or even increased CVD risk”, unrefined carbohydrates like whole grains have been shown to decrease the risk of CHD when they replace saturated fat [74], “Professionals Follow-up Study (1986–2010) suggested that lowering energy from SFA by 5% and proportionally increasing PUFA, monounsaturated fatty acids (MUFAs) or carbohydrates from whole grains was associated with a 25%, 15% and 9% lower risk of CHD, respectively.”
3) Here’s a compilation[10] of large, government-funded clinical trials to oppose the claims made to blame meat and saturated fat for diabetes, cancer or CVD. Note that these have been ignored WHO and guidelines.
The theory that red meat is bad for human health and causes obesity, diabetes, heart disease, cancer and even premature death is not substantiated by rigorous science.
The newly released EAT-Lancet report, as many reports before it, have managed to cast red meat as the nutritional boogeyman by relying on a weak kind of science: epidemiology.
A prominent example of this was the World Health Organization’s 2015 designation of red meat as a carcinogen (for colorectal cancer). But this decision depended entirely upon epidemiological data which showed that the “relative risk” of getting this cancer for red meat eaters, compared to non-meat eaters, was only 1.17 to 1.18. Relative risks below 2 are generally considered in the field of epidemiology to be too small to establish a reliable correlation.
https://www.gwern.net/docs/statistics/causality/2004-shapiro.pdf
Except we know from rigorous science that most animal products, not just red meat, increase all cause mortality [96], while plant foods like whole grains, vegetables, and fruit decrease it, “With increasing intake (for each daily serving) of whole grains, vegetables, fruits, nuts, and fish, the risk of all-cause mortality decreased; higher intake of red meat and processed meat was associated with an increased risk of all-cause mortality in a linear dose-response meta-analysis. Optimal consumption of risk-decreasing foods results in a 56% reduction of all-cause mortality, whereas consumption of risk-increasing foods is associated with a 2-fold increased risk of all-cause mortality.” For red meat in particular, it has been found that increasing consumption of it will increase risk of total mortality, cardiovascular disease, colorectal cancer, and type 2 diabetes [97], “the long-term consumption of increasing amounts of red meat and particularly of processed meat is associated with an increased risk of total mortality, cardiovascular disease, colorectal cancer and type 2 diabetes, in both men and women.”, “The large cohort studies (HPFS, NHS I and II, NIH-AARP, EPIC, E3N) … took into account all known risk factors such as BMI, smoking status, blood pressure, general nutritional habits, alcohol consumption, ethnicity, diabetes etc. Even after including these risk factors in a multivariate analysis, the relationship was preserved, which supports the suspicion of causality.”
There’s no argument here for why epidemiology is a weak science, especially when the relevant confounding factors are controlled for. Of course, randomized controlled trials are of a higher quality, all else held equal, but this doesn’t mean that epidemiology is in any sense weak. Dismissing epidemiological data means that most of the studies and authorities which are used as evidence in this copypasta should be dismissed too. Especially when their evidence is of a lower quality; has less participants, less controls, is shorter in time, and is lower on the evidence hierarchy.
The “relative risk too low” argument has been addressed in the first section of 1.4.
The fact is, there is no evidence to back up claims that red meat is bad for health. Randomized controlled trials on humans, considered the gold standard of scientific research, do not support the idea that red meat causes any kind of disease.
The meta-analysis of RCTs [98] which comes up when you search for “RCT red meat” on Google concluded that “Substituting red meat with high-quality plant protein sources, but not with fish or low-quality carbohydrates, leads to more favorable changes in blood lipids and lipoproteins.” And as seen previously, more favorable changes in LDL cholesterol, which is what is meant by blood lipids, decreases the risk of atherosclerosis.
ON THE SATURATED FATS IN MEAT
The two largest-ever NIH-funded, multi-center clinical trials (the Women’s Health Initiative and the Minnesota Coronary Survey) where saturated fats were either reduced or replaced by unsaturated fats, on nearly 54,000 men and women, concluded that saturated fats had no effect on cardiovascular mortality or total mortality. A 2016 (27 years later) analysis of buried data from the Minnesota Coronary Survey found a 22% higher risk of death for each 30 mg/dL reduction in serum cholesterol.
https://www.ncbi.nlm.nih.gov/pubmed/16467234
I’m convinced at this point that they aren’t reading their own sources, or deliberately obfuscating what is found in them. In the Women’s Health Initiative Randomized Controlled Dietary Modification Trial, the decrease in saturated fat intake was only 2.9%, so of course no big change in cardiovascular mortality would be present. Additionally, it’s clearly stated in the last sentence of the results that, “Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.”
The results of the Minnesota Coronary Survey don’t prove that saturated fats don’t have an effect on cardiovascular disease, as LDL cholesterol wasn’t reported on, while being a major risk factor for cardiovascular disease. In this study, those who were younger (35–39 years old) than the main group being tested (those over 65 years old) had beneficial outcomes. The major flaw with this study is that after the initial 512 participants who were assigned based on 8 controlled risk factors, the rest 8500+ of them only had their age and sex controlled for, “The original population was initially stratified into 512 cells on the basis of eight variables. These were: age, sex, length of stay in the hospital, weight, blood pressure, diabetes, cigarette smoking, and evidence by electrocardiogram of a previous myocardial infarction. When new subjects were admitted later, they were divided among four cells, based on only age and sex.”
In the 2016 analysis of the Minnesota Coronary Survey, more than 75% of the participant results were excluded, as the complete dataset wasn’t recovered, which puts into doubt the conclusions made from the data. Smoking status, detailed dietary intake data, weight loss, and coronary disease status all weren’t part of the metrics of this re-evaluation, all of which could have an effect on the incidence of cardiovascular disease. The other shortcomings of the original study still apply.
A review of 17 systematic reviews concludes that diets that replace saturated fat with polyunsaturated fat do not convincingly reduce cardiovascular events or mortality. Another review of 19 meta-analyses concluded that the effects of saturated fat on heart disease were inconsistent but tended to show a lack of association.
The first meta-analysis in the “fat or fiction” review showed positive effects on coronary mortality and coronary event when replacing saturated fats with polyunsaturated fats. The second meta-analysis wasn’t even reviewing data testing the idea that replacing SFA with PUFA will reduce cardiovascular events or mortality, the studies were testing high compared to low consumption of SFA, PUFA and other types of fats. It’s mentioned in the Post-Script of that meta-analysis that another meta-analysis of 11 cohort studies found that there is a “significant decrease in CHD death and CHD events when PUFA replaces SFA.” Also, the “low” intakes of SFA were between 7–11% of energy intake, which is at or above where the steepest change in risk is seen [70], meaning it’s unlikely the risk decrease would’ve been detected. The third meta-analysis found a decrease in CHD death and MI when replacing SFA with PUFA, though the mortality benefit wasn’t reported on. As stated previously, there was a reply [92] made to the fourth meta-analysis (Siri-Tarino 2010) describing the massive problems with it, which makes it an entirely unreliable source of information. In the fifth meta-analysis, there was a use of trans-fat based margarine in the intervention group, which muddled the results. Even though the researchers state they adjusted the results for it, what they really did was adjust for MUFA which they call an “imperfect surrogate for trans fatty acids”, so they acknowledge that MUFA and TFA aren’t the same but ignore this, supposedly because they had no data on TFA. They could not rule out that nutrients other than PUFA and SFA contributed to the results, “the SDHS dataset does not contain sufficient information to rule out the possibility that changes in nutrients other than n-6 LA and SFAs could have contributed to, or reduced, the observed unfavorable effects of the LA intervention.” The most damning fact of all is that the intervention group’s intake of saturated fat only decreased to 9.3% of total energy intake, which is higher than at the point at which the risk drops significantly. The intervention group might have as well not decreased their SFA intake at all, and just increased their PUFA intake. The next 3 “meta-analyses” are taken from 3 different sections of 1 meta-analysis, Chowdhury et al, so they’re counting 1 meta-analysis as 3 separate ones. There was a correction [99] made to this meta-analysis, which corrected for multiple numerical errors, but still ended with a misleading statement. After the correction, the RR for increased PUFA intake became 0.87 as opposed to the 0.93 before the correction. This would have changed the conclusion of the meta-analysis, as the result became statistically significant after the correction. The authors disagree, providing no actual reason for why the conclusion wouldn’t change, “These corrections, however, do not affect the main conclusions reported in the original article.” There was also a scientific response [100], which tore into this meta-analysis for using unreliable data, “with exclusion of the outlying SDHS (Sydney Diet Heart Study), the included randomized, controlled trials (RCTs) show benefit of replacing saturated fatty acids (SFAs) with PUFAs.” The 9th meta-analysis found that replacing SFA by PUFA decreases CHD mortality and CHD incidence, “A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events and a 13% lower risk of CHD deaths.” In the 10th meta-analysis, where apparently no statistically significant mortality benefit or cardiovascular event benefit was noticed, fails in the same way as the 6th meta-analysis. They decided to include the SDHS even though they knew that in that study, saturated fat was replaced by some polyunsaturated fat and some trans fat, which has negative effects on CHD, making it unreliable, “Moreover, the meta-analysis of RTCs by Mozaffarian et al reported a significant reduction in CHD events (by 19%) following the replacement of SFA by PUFA. However, adapting (for secondary prevention) and updating (including new data from the Sydney Diet Heart Study) the meta-analysis by Mozaffarian et al, as was carried out in a sensitivity analysis investigating the replacement of SFA by PUFA in the present study, resulted in neither beneficial nor detrimental effects on all outcome parameters.” If this study is excluded, a statistically significant positive effect is seen. To add to that, the group with low values of saturated fat intake is ranged from 7.2% to 14%, most of which is above the level at which there is the greatest risk decrease, making the conclusion of this meta-analysis unuseful. In the 11th meta-analysis (Harcombe et al) 8 studies out of 10 included had either incredibly poor quality or had completely different results to what was reported in the meta-analysis: in the MRC (Soy Oil) study [101], there was no adjustment for smoking, the control group actually ate less overall, including less fat, and lost more weight than the intervention group, which are all confounding factors, even in the test diet, nearly a half of the calories came from fat, and the percentage of total energy intake of saturated fat wasn’t recorded, and LDL cholesterol wasn’t measured; The Minnesota Coronary Survey had massive flaws which I described in the previous section; The DART study [102] actually found that men who ate a higher ratio of PUFA to SFA had a decreased risk of mortality, though there were many flaws with the study, it didn’t report on trans fat intake, nor on the LDL-C concentrations, nor on the percentage of total energy SFA took up, plus it only adjusted for energy intake, smoking, and age, not blood pressure, or weight; The issues with the WHI study was described previously, but using the link the meta-analysis provided there was more information found on just how wrong the meta-analysis was to include this study, because the group which had the lowest levels of saturated fat had a reduced CHD risk, “Compared with those in the entire comparison group, a trend was observed toward reduction of CHD risk among those in the intervention group who reached the lowest levels of saturated fat”; In the Corn Oil study, the intervention group replaced some saturated fats with 80g of oil, which doesn’t at all represent what people would actually eat instead of foods with high saturated fat, so the study wasn’t investigating the effects of replacing SFA with PUFA in an average diet, the people in the test group commonly complained about having diarrhea because of this overload of oil, though the average amount of oil consumed didn’t even reach 80g a day, “But many found the treatment burdensome: distaste, nausea, and diarrhoea were the commonest complaints.”, and the weight loss in the corn oil group could have been caused by the diarrhea, making the results of this study more unreliable, and additionally the levels of saturated and LDL-C weren’t recorded so we can’t even know if the test group actually consumed less saturated fat or had lower levels of LDL-C than the control group; To go back to the meta-analysis, it states that, “Woodhill et al reported that survival was significantly better in the control than the diet group.”, but this extremely misleading, as the study actually says that “none of the dietary factors were significantly related to survival.”, also, the group which was supposed to consume less saturated fat only dropped their intake to 9.8% of total energy, which is well above the level at which a risk drop is seen, and “It [was] concluded that because of multiple changes in lifestyle men who have had myocardial infarction are not a good choice for testing the lipid hypothesis.”, which completely goes against what the meta-analysis tried to use this study for; In the next study [103], both the control group and the intervention group decreased their total cholesterol levels throughout the study, but at the end their levels are still considered borderline high, and as the biggest changes in risk are seen when cholesterol is at levels considered low or very low, the study couldn’t have picked up on this effect, which makes it a highly unreliable source of information to disprove the lipid-hypothesis; The meta-analysis states that the last study, the Veterans Trial [104] “noted the absence of any benefit for longevity and expressed concern about toxicity of the intervention.” But this is, once again, very misleading, as what they also found was that the intervention group which consumed less saturated fat and more unsaturated fat had a lower incidence of myocardial infarctions, coronary heart disease, cerebral infarction, etc., “For all primary and secondary end points combined, eight year incidence rates were 47.7% and 31.3% for the control and experimental groups, respectively”, and as for the toxicity of the intervention, it was specifically stated that no toxic effect was found, including findings from other studies, “The Finnish trial also yielded no evidence of a toxic effect during six years of unsaturated fat feeding.” Clearly, this meta-analysis is full of misrepresentations, false or selective information. The 12th meta-analysis, by Christopher Ramsden included 5 of the studies which I already went over, the Minnesota Coronary Experiment, the Sydney Diet Heart Study, the Veterans Trial, the (Rose) Corn Oil Trial, and the Soy Oil Trial, all of which have major methodological flaws or actually show the opposite effect to what the meta-analysis claims. The 13th meta-analysis found that there was a decrease in cardiovascular disease risk when replacing saturated fats with polyunsaturated fats, “Replacing the energy from saturated fat with polyunsaturated fat appears to be a useful strategy”. The 14th, 15th and 16th meta-analyses weren’t on the replacement of saturated fat by unsaturated fat, instead they were reviewing studies on high vs low consumption of omega-6s, high vs low consumption of polyunsaturated fats, and high vs low consumption of omega-3s. These meta-analyses certainly cannot be used to prove that replacing saturated fats with polyunsaturated fats has no positive outcome as that’s not what was being tested. The last meta-analysis, the American Heart Association meta-analysis, which didn’t report on mortality but did report on CHD events, found a decrease in events when SFA was replaced by PUFA. It should be obvious now that there is overwhelming evidence that when saturated fat is replaced by polyunsaturated fat, there is a decrease in risk of CHD events and death, and that the evidence used by the opposition of this fact is either misleading or of very poor quality.
The second review uses some of the meta-analyses as in the first, which I have already addressed, like Siri-Tarino et al, Chowdhury et al, Harcombe et al. The first observational meta-analysis used, Jakobsen et al, found that replacing saturated fats with polyunsaturated fats decreased CHD events and mortality. The second observational meta-analysis failed to evaluate the replacement of saturated fats with polyunsaturated fats, only high vs low intakes of saturated fat, though they didn’t report what the low or high levels were. The first study (Hu FB, Stampfer MJ, Manson JE, et al. 1999) in this meta-analysis which was on saturated fat found that a higher ratio of polyunsaturated fat to saturated fat is strongly associated with decreased CHD risk, “The ratio of polyunsaturated to saturated fat was strongly and inversely associated with CHD risk”. The second study is the WHI study, which has been addressed. In the third study (Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer M, Willett WC.), it was found that there is a significant positive association between higher saturated fat intake and the risk for coronary disease, “For men in the top versus the lowest fifth of saturated fat intake (median = 14.8% v 5.7% of energy) the multivariate relative risk for myocardial infarction was 1.22 and for fatal coronary heart disease was 2.21.” The fourth study (Pietinen P, Ascherio A, Korhonen P, et al.) on Finnish men compared low to high intakes of saturated fat, except the lowest group consumed 34.7g of saturated fat per day, which is a very high amount. If we assume that these men consumed 2500 calories per day, even though it’s likely to be lower, the percentage of their energy which would have come from saturated fat would’ve been at least 12%, which is way above the level at which there is a drop in risk of CHD. The last study (Hu FB, Stampfer MJ, Manson JE, et al. 1999) found that replacing saturated fats with polyunsaturated fats decreased CHD risk, “We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent”. The review states that the next meta-analysis (Skeaff et al (2009)) concluded that the evidence concerning dietary fat effect on CHD is unreliable, which technically isn’t a lie but it’s as close to one as you get. The authors of the meta-analysis state in the post-script section that there is another meta-analysis with significantly high quality on the topic, in which main finding was that replacing SFA with PUFA significantly decreases risk of CHD, “The Pooling Project combined the results from 11 cohort studies — each meeting criteria for quality of dietary assessment, years of follow-up, and ascertainment of events — to examine the effect on CHD death and CHD events of replacing SFA with MUFA, PUFA or carbohydrate. The main finding was a significantly decreased risk of CHD death and CHD events when PUFA replaces SFA.” Farvid et al (2014), the next meta-analysis which I haven’t gone over previously, found that “A 5% of energy increment in LA [polyunsaturated fat] intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events and a 13% lower risk of CHD deaths”. The review states that the next meta-analysis (de Souza et al (2015)) found that “SFAs are not associated with all-cause mortality or CHD.”, but once again, this is, at best, misleading. In the “Replacement of saturated fats by unsaturated fats” section, this meta-analysis clearly states that replacing saturated fats with polyunsaturated fats decreased CVD risk and CHD risk, “In cohort studies that have directly modeled substitution effects, replacement of saturated fat by polyunsaturated fat conferred the greatest reduction in risk of CVD”, “At these levels (P:S ratio of >1 to 2.5) significant CHD benefits were seen, consistent with the finding that favorable effects of diets with reduced saturated fat on cardiovascular risk might depend on a significant reciprocal increase in polyunsaturated fat or high quality carbohydrate from whole fruits, vegetables, pulses, and grains, which tend to have a lower glycaemic index.” The last observational meta-analysis (Zhu Y, Bo Y, Liu Y.) has massive flaws which make it entirely unreliable. It included studies which adjusted the results for LDL-C, like The Framingham study, Atkinson C et al, Chiuve SE WHS, so they were basically comparing people with the same levels of cholesterol, regardless of how much saturated fat they ate. The reason this is a problem is because LDL-C is increased by dietary saturated fat, and LDL-C causes increased risk of coronary and cardiovascular heart diseases. Additionally, this meta-analysis included stroke studies independent of CHD, which skewed the risk because they didn’t adjust for competing risk, which is a problem because if more people die from CVD, it means there’ll be less people who’ll reach the age at which the risk of strokes increases. All of this drives down the effect of saturated fat on CHD in well-controlled studies, as an average is taken of all of the studies included. As one can easily see, the majority of the observational meta-analyses support the fact that replacing saturated fat with polyunsaturated fat decreases CHD risk, and the ones which don’t have major flaws. The authors of this review either intentionally misrepresented the findings of the meta-analyses, cherry picked the conclusions from them, or simply didn’t read them. Now onto the list of meta-analyses of RCTs. The first meta-analysis found that replacing SFA with PUFA reduces CHD events. The second meta-analysis (Ramsden et al 2010) included most of the studies which have been addressed, like the MRC Soy study, the LA Veterans study, the DART, the Rose Corn Study, the SDHS, and the Minnesota CS which either have poor methodology or show the exact opposite of what this meta-analysis claims. The Oslo Diet Heart Study found that a diet low in saturated fats and high in polyunsaturated fats reduced CHD relapses significantly, “the incidence of fatal and nonfatal myocardial reinfarction was found to be significantly reduced.”, “Major coronary heart disease (CHD) relapses, including fatal and nonfatal events (MI), were significantly reduced.” The same goes for the next study, the Finnish Mental Hospital Study (FMHS), “One of the hospitals received the SCL diet, i.e. a diet low in saturated fats and cholesterol and relatively high in polyunsaturated fats, while the other served as the control with a normal hospital diet.”, “It is concluded that the use of the serum-cholesterol-lowering diet exerted a substantial preventive effect on CHD.” The next meta-analysis, Hooper et al 2010, found that reducing saturated fat intake reduces the risk of cardiovascular events. Ramsden et al 2013, Schwingshackl and Hoffman 2014, Hooper et al 2015, Ramsden et al 2016, and Harcombe et al 2016 have been addressed already. Hamley et al made the same mistakes as the Ramsden et al. 2010, by including studies which contradict their conclusions. The last RCT meta-analysis also found that reducing SFA intake and replacing it with PUFA reduces CHD risk. In conclusion, this review of meta-analyses, like the previous one, only managed to misrepresent findings of meta-analyses and include meta-analyses based on studies with inferior methodology. For more information on why these meta-analyses are unusable, read Matthew Madore’s analysis of them and many of the studies previously seen [105].
ON RED MEAT AND CANCER
Two large NIH-funded, multi-center clinical trials on altogether more than 50,000 men and women who significantly cut back on red-meat consumption (while increasing fruits, vegetables and grains) did not see any risk reduction for polyp re-occurrence or any kind of cancer.
https://www.ncbi.nlm.nih.gov/pubmed/10770979
https://www.ncbi.nlm.nih.gov/pubmed/16467232
In the first study they cite, the Polyp Prevention Trial Study Group, the participants in the intervention group only reduced their red meat intake by 20g a day, so they were still consuming 74g of red meat a day on average, compared to the 90g a day for the control group. Needless to say, this is a minuscule change in consumption; it’s likely that no significant results were seen because of this. Additionally, that study was only looking at colorectal cancer, and it only lasted for 4 years. Because cancer takes a long time to develop, it’s unlikely that the study would’ve picked up on any changes, especially since they were only testing for 1 type of cancer. I’ve already addressed the second study, the WHI, but just to reiterate: the meat consumption of the intervention group only decreased by 1.4 servings per week, a small change again. It’s also mentioned in the conclusion of this study that even though the study had 8.1 years of follow-up, a longer study may yield more definitive results “However, nonsignificant trends were observed suggesting a reduced risk with a low-fat dietary pattern and incidence rate differences between groups are in agreement with design assumptions on acknowledging the dietary differences achieved. Because the health implications of a low-fat dietary pattern may take years to be fully realized, longer, planned, nonintervention follow-up may yield a more definitive comparison.” This study was also only on breast cancer, not “any kind of cancer” like the copypasta claims. Even with these flaws the study found a 9% reduction of breast cancer incidence in the intervention group, though this could be due to chance because of the statistical non-significance, “breast cancer incidence was 9% lower for women in the dietary intervention group”. The third link provided goes to a more detailed analysis of the WHI study, which went over ovarian cancer risk and total cancer risk. It was found that a low-fat diet with lower consumption of red meat and higher consumption of vegetables, fruits, and grains may reduce ovarian cancer risk, and there is also a possible reduction in total invasive cancer risk, “In summary, the DM trial indicates that a low-fat eating pattern may reduce ovarian cancer risk, although this finding needs to be interpreted in the context of comparisons for five cancer sites. The DM trial also suggests a possible reduction in total invasive cancer.” The last link is also on the WHI study, where it is mentioned that the study had flaws which could have prevented it from seeing the change in risk of colorectal cancer between the control and the intervention group. The intervention didn’t achieve the reduction in fat which the study was supposed to observe, and if this was accounted for, the hazard ratio of the intervention group would have been 0.86, “Using food frequency data, the WHI intervention on average achieved only about 70% of the designed reduction in fat. If design assumptions are revised to take into account this departure from goal, the predicted HR would have been 0.86, an effect size excluded by these results. The power to detect this effect size under the observed comparison group incidence rate and the achieved adherence is approximately 40%.” There was no systematic testing for signs cancerous growths, which would mean that the incidence rates of colorectal cancer were underestimated, “Furthermore, there was no study-specified colonoscopy, nor was there systematic screening for adenomatous polyps; hence, the incidence of both colorectal cancer and polyps or adenomas would be underestimated.”
ON RED MEAT AND HEART DISEASE
Two meta-analyses of randomized controlled trials (in the Journal of Clinical Lipidology and the American Journal of Clinical Nutrition) both found that red meat had either neutral or positive effects on most cardiovascular outcomes (blood pressure, cholesterol and other lipids).
The first meta-analysis [106] is pathetic. Firstly, the studies weren’t even on all red meat, they were just on beef consumption, so it can’t be used to prove that red meat has neutral or positive effects. Secondly the studies it evaluated didn’t decrease total meat consumption, the intervention group just ate lean poultry or lean fish, compared to the control which ate lean red beef, so the participants were still consuming high or extremely high amounts of meat a day (with 2 exceptions). Only one of the studies reached a duration of 18 weeks, which is about 4.5 months, the rest lasted 12 weeks or less, which is a short amount of time, even for RCTs. To add to all of this, the cholesterol levels of the participants in all of the studies except for 1 were either borderline high or high, which makes the results of this meta-analysis very unreliable. This is because we know that cholesterol levels follow a hyperbolic curve, meaning the less dietary cholesterol you consume, the higher the increase will be if you eat something containing dietary cholesterol [84]. There’s hardly any difference in the cholesterol contained in lean beef and lean chicken, which is exactly why no difference is seen. At some point, when you consume a very large amount of dietary cholesterol, consuming a bit less or a bit more won’t change the cholesterol levels in your blood significantly, if at all, “The greatest response is expected when baseline dietary cholesterol is near zero, while little, if any, measurable change would be expected once baseline dietary cholesterol was > 400–500 mg/d.” Additionally, there’s a much bigger and better meta-analysis [98] on the same topic, on the replacement of meat with a variety of foods, which found that “Substituting red meat with high-quality plant protein sources, but not with fish or low-quality carbohydrates, leads to more favorable changes in blood lipids and lipoproteins.”, “In comparison with chicken or poultry diets, red meat showed no significant differential effects on lipid variables.” So, clearly, just replacing red meat with some other type of meat won’t decrease your cholesterol levels, but your cholesterol levels will decrease if you replace the red meat in your diet with high quality plant protein sources, which includes unrefined carbohydrates like soy.
In the second meta-analysis, the foods which the control group ate in place of red meat were very different, so most of the RCTs were conducting research on different comparisons, which makes this meta-analysis prone to having its results swayed. Another problem with it is the same as with the previous meta-analysis: the cholesterol levels of both of the groups were high, 3.18 mmol/L for the intervention and 3.13 mmol/L for the control (equivalent to about 120+ mg/dl), which makes it unlikely for the meta-analysis to have seen much of a difference in LDL-C levels, even if one group consumed slightly less or slightly more saturated fat and cholesterol. This is because of the effect described previously, the more dietary cholesterol you consume to start off with, the lower the change in your blood cholesterol levels when you consume more. Additionally, saturated fat wasn’t reported on, meaning the intervention groups in the studies could have been consuming a lower amount of saturated fat than the control group, which would further skew the results. As explained previously, there is a meta-analysis with far better methodology which found that the replacement of meat with high-quality plant protein sources decreases LDL-C, while replacing red meat with things other than high-quality plant protein intake, there was no significant difference in LDL-C.
ON RED MEAT AND TYPE 2 DIABETES
Red meat cannot possibly cause diabetes, because glucose (sugar) is the principal driver of type 2 diabetes, and meat contains no glucose. Moreover, red meat availability has dropped dramatically as diabetes has skyrocketed, making any proposed connection between red meat and diabetes self-evidently unreasonable:
https://www.ers.usda.gov/webdocs/publications/82220/eib-166.pdf?v=42762
https://www.cdc.gov/diabetes/statistics/slides/long_term_trends.pdf
This is a laughable point because they didn’t even provide a study on the effect of red meat on type 2 diabetes, so they threw together 2 sources, the first one of which found that red meat consumption has decreased over time, and the second shows that cases of obesity have increased. The reason this is an incredibly bad inference to make is because there are other things which have changed over time and are risk factors of T2D, such as obesity [107], which obviously weren’t controlled for in this extremely informal assessment by the copypasta. If you look at actual meta-analyses on the effect of red meat on incidence of diabetes, you’ll see that higher consumption of red meat is associated with increased risk of type 2 diabetes [108][109], “An increase of 42 g or more per day compared to no increase, compounded the risk of diabetes in the course of 4 years by 48 %.”, “Each additional daily 100 g of red meat was positively associated with T2D risk.”
Epidemiology has given us some spectacular health failures over recent decades: hormone replacement therapy, anti-oxidant vitamins and caps on dietary cholesterol, to name a few.
Just because there are certain downfalls of epidemiology doesn’t mean that they are unreliable. Each individual topic needs to be addressed. Painting epidemiology in such a light is misleading, as epidemiology is also the reason we know that smoking causes cancer, that aspirin decreases the risk of heart disease, etc. Also, the point about dietary cholesterol caps is false. Firstly, it’s the thing which this copypasta desperately tried to prove in the first place, or at least the very relevant point that dietary cholesterol isn’t bad, so including it in the list is deceptive. Secondly, they completely failed to show that dietary cholesterol doesn’t impact serum cholesterol or that it doesn’t cause heart disease, so they’re straight up wrong. To summarize, this copypasta doesn’t have any evidence showing that red meat doesn’t cause negative health effects, so it has to point to unrelated topics, which were studied through epidemiology, and the conclusions of which were later falsified.
HERE ARE THE FACTS ABOUT EPIDEMIOLOGY
At best, epidemiological studies can show only association and cannot establish causation, which means that the data can be used to suggest hypotheses but not to prove them. Observational studies that link nutrition with disease generally find tiny differences in risk (relative risks of 1–2) which are not enough to generate confidence that an association is real.
Epidemiological studies rely on self-reported food surveys which can often be imprecise. Researchers from the Mayo Clinic tested “memory-based dietary assessment methods” and found that the nutritional data collected was “fundamentally and fatally flawed.”
The first point has been addressed previously: causation can be proved by well-controlled epidemiological studies, low relative risks can map out into being large absolute risks, which has the potential to save millions of lives since some diseases have a high prevalence in the general population.
The type of food surveys criticized in the paper cited, Archer et al, aren’t the only method of collecting data on the nutritional intake of the participants of studies, “often imprecise” is an over exaggeration. The researchers who use the food surveys described are aware of the limitations, which are far from being “fundamentally and fatally flawed”. Using these questionnaires in combination with other methods leads to having reliable results. Furthermore, there was an editorial paper [110] published, not long after the release of Archer et al, picking apart the arguments made in the paper. It goes into far more detail than I have, and explains how these food surveys are made to be reliable. In this editorial, it was concluded that the authors of Archer et al use data collected using the same methods to come to conclusions about other aspects of health, making them hypocrites at best, “To argue that these data represent a waste of resources, while concurrently citing scientific findings that those same data collection methods were used to document the importance of diet and activity in health, is scientific doublespeak — and an impediment to scientific progress in obesity and nutrition research.”
Only a small number of nutritional related epidemiological studies are ultimately confirmed by more rigorous scientific studies. In 2005, Stanford’s John Ioannidis analyzed several dozen highly cited studies and concluded that subsequent clinical trials could only reproduce around 20% of observational findings. A 2011 paper published by Significance analyzed 52 claims made in nutritional studies, and none — 0% — withstood the scrutiny of subsequent clinical trials.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/
https://rss.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1740-9713.2011.00506.x
The first paper is based on incredibly bad reasoning and argumentation; Ioannidis inappropriately calculated relative risk [111], and according to his poor calculation, since heavy smoking has a relative risk of about 2.5, it will result in a life expectancy of 35 years, assuming an 80 year life expectancy for non-smokers, which is straight up false. There was an analysis done of Ioannidis’ paper, showing exactly where he faltered and explaining the misleading mistakes made, making his paper’s findings unfounded, “Unfortunately, while we agree that there are more false claims than many would suspect — based both on poor study design, misinterpretation of p-values, and perhaps analytic manipulation — the mathematical argument in the PLoS Medicine paper underlying the “proof” of the title’s claim has a degree of circularity.”, “the claims that the model employed in this paper constitutes a “proof” that most published medical research claims are false, and that research in “hot” areas is most likely to be false, are unfounded.”
The second paper is also a pile of misinformation. The “52 claims made in nutritional studies” actually came from 12 studies, not 52 separate studies. Additionally, a large proportion of the studies were on the same or very similar topics, like the effects of vitamin E, vitamin C, and beta-carotene on health; The paper barely analyzed a small proportion of the research done on nutrition, and the claims made based on the epidemiology but then claimed that “100% of the observational claims failed to replicate”. This is technically true, with the caveat being that it was 100% out of the studies they specifically picked and which are far from being representative of all epidemiology. In 2013, a better analysis [112], which evaluated more topics and way more studies, was released on the Concordance Between the Findings of Epidemiological Studies and Randomized Trials in Nutrition, which found that (out of the topics evaluated) 2/3 of the summaries in RCTs and epidemiology agree with each other, “In 23 out of 34 associations the summary findings from meta-analyses of epidemiological studies and of RCTs were in the same direction.” It must also be mentioned that there’s another meta-analysis [168] on the same topic which found that the reason some epidemiological studies don’t get the same results as randomized trials is because the intake of nutrients is different between them, and when the intake is identical, the results are similar, as one would expect, “When the type of intake or exposure between both BoE was identical, the estimates were similar (and the analysis showed low statistical heterogeneity). For pooled estimate of continuous outcomes, no differences were observed between randomised controlled trials and cohort studies, except for smaller systolic and diastolic blood pressure estimates in the BoE of trials.”
4) Much of the anti-meat push is coming from biased institutions like Adventist universities or Harvard School of Public Health who typically don’t disclose their conflicts of interest. The latter conducted bribed studies for the sugar industry[11] and was chaired by a highly influential supporter of vegetarianism[12] for 26 years. He published hundreds of epidemiological anti-meat papers (e.g. the Nurses’ Health Studies), tried to censor[13] publications that oppose his views and wants to deemphasize the importance of experimental science. He has financial ties to seed oil, nut, fruit, vegetable and pharmaceutical industries and is part many plant-based movements like Blue Zones, True Health Initiative (Frank Hu, David Katz, Dean Ornish), EAT-Lancet and Lifestyle Medicine (Adventists, Michael Greger).
This copypasta is repeating itself at this point. Firstly, every institution is going to be biased in some way, so to single out a couple is misleading. There will always be members inside those institutions who have some incentive to not change their mind, which makes any research they do prone to bias. Clearly, this isn’t a good argument. Every piece of research needs to be examined on its own to find if there are flaws with it, and just saying that the authors are biased because their study was funded by some industry doesn’t indicate whether or not the study is bad. Secondly, disclosing conflict of interest is a good thing, and it should be disclosed when appropriate. The source about Dr Walter Willet, the chair of Harvard School of Public Health, doesn’t even come close to proving that the papers he published are misleading or have bad methodology, it only states that he supported vegetarianism. His financial ties to industries and plant-based movements also don’t come anywhere near to proving that the evidence he uses or publications he authors are deceptive; Bias doesn’t indicate whether or not a given paper is good research. On top of that, Dr Willet has made public statements, multiple times, condemning products which contain large amounts of sugar, and the research funded by the industry [166], “There is abundant evidence that the huge increase in soda consumption in the past 40 years is the most important single factor behind America’s obesity epidemic. These steps will greatly assist in creating a new social norm, in which healthier beverages are the preferred choice,” and condemning industry funding [167], “The dangers of industry funding are much clearer now,” Willett said. “Industry can basically distort the body of literature.” One of the implicated researchers from the 1960s was chair of Harvard’s Nutrition Department, according to the Times.” The only arguments made against what Dr Willet supports are ones I’ve addressed previously. On top of that, there isn’t any evidence provided for the claims made in the arguments, which is highly suspicious. Although I know where the 0–20% figure comes from (a misleading paper, as formerly addressed), the rest of the claims are left baseless. The third source provided is mostly lacking in evidence, instead concentrating on badmouthing True Health Initiative and its council, namely Walter Willet, Frank Hu and David Katz. THI wasn’t trying to censor publications which opposed their views, as the copypasta claimed of Walter Willet to do, they instead wrote a letter to Dr Laine, the leading researcher behind a laughably bad paper on red meat’s effect on health (NutriRecs) [113], asking him to retract it. The letter [114] clearly detailed the problems with this paper and why it needed to be retracted, as it could spread misinformation, “The “guidelines” slated for publication are thus at odds not only with the vast weight of prior evidence, much of it omitted from these “systematic” reviews- but at odds with the very data on which they claim to be based. That the authors contend “very low certainty” in their own findings is in no way a logical or even rational basis to recommend…the opposite.” Evidently, this is far from being some kind of censoring. Just to give a bit more understanding of the paper asked to be retracted: it concluded that adults don’t need to change their meat consumption, which was based on a distorted version of the GRADE criteria (The Grading of Recommendations Assessment, Development and Evaluation). The authors of the paper used these criteria to label all of the studies they looked at as being evidence of low quality, when this is far from being true. The reason this study is laughable is because if you look at all of the 4 systematic reviews done for it on the effects of red meat on health, you’ll find that the majority of the studies included in these reviews found a decrease in risk of diseases as red meat intake was reduced. The paper assumed that there would be a greater effect of red meat on negative health outcomes in the studies specifically on dose-response effects in comparison to the studies on dietary patterns, even though this assumption is unwarranted and straight up backwards, because the greatest change in meat intake was in the latter studies. They used this to downgrade the evidence from studies on dose-response, even though there was shown to be a clear positive effect on health outcomes from reducing meat intake by 3 servings per week. This finding would’ve upgraded the quality of evidence of these studies from low to at least moderate [115], and it was dishonest of the authors to not do so.
[1] https://www.gwern.net/docs/statistics/causality/2004-shapiro.pdf
[2] https://en.wikipedia.org/wiki/Primum_non_nocere
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778858/
[4] https://www.iarc.fr/wp-content/uploads/2018/07/Monographs-QA_Vol114.pdf
[6] https://www.diagnosisdiet.com/full-article/meat-and-cancer
[8] https://www.sciencedirect.com/science/article/pii/S0309174014000564?via%3Dihub
[9] https://pastebin.com/Pujbztr7
[10] https://pastebin.com/cqAJ0gvF
[11] https://www.ncbi.nlm.nih.gov/pubmed/27617709
[13] https://www.tamus.edu/wp-content/uploads/2020/01/JAMA-Article-1.15.20.pdf
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1.5. Sneaky vegan propaganda examples
Popular sources that promote “plant-based diets” are actually just vegan propaganda in disguise:
1) Blue zones are bullshit[1]. The longest living populations paradoxically consume the highest amount of meat[2]. Buettner cherry-picks and ignores areas that have both high consumption of animal products and high life expectancies (Hong Kong, Switzerland, Spain, France, … ). He praises Adventists for their health, but doesn’t do the same for Mormons. Among others, he misrepresents the Okinawa diet by using data from a post WWII famine[3]. The number of centenarians in blue zones is likely based on birth certificate fraud[4]. The franchise also belongs to the SDA church now[5].
The article cited on blue zones is full of misinformation. Let’s start off with the first piece of evidence provided for one of the claims, that the Roseto effect, a phenomenon by which a close-knit community supposedly experiences a reduced rate of heart disease, is a factor which contributed to people in blue zones experiencing less heart disease. To start off, there isn’t any evidence given that the communities in blue zones are “close-knit” or even an explanation for how that’s measured. Secondly, there is very little evidence for the Roseto effect, the only one I was able to find is a study called “The Roseto Effect: A 50-Year Comparison of Mortality Rates” [116], which tried to establish causality while being bare-bones, “The social changes that occurred in Roseto in the 1960s are reflected in sharply increased rates of heart attack among men under the age of 65.” The authors claimed that the increase of heart attacks in men of Roseto were because of the social changes like the communities of Roseto becoming less close-knit over time, even though one of the social changes was that the education levels increased. Additionally, “Marriages, which had traditionally been to Italians were becoming ethnically mixed”. Why didn’t the authors blame the increase in heart attacks on people becoming more educated or marrying people of other ethnicities instead? That would be as ridiculous as what they tried to do by blaming the communities becoming less tightly-knit for the increase in heart attacks. To put the nail in the coffin, the study [117] used in the conclusion didn’t control for factors which very much influence the risk of heart attacks. The authors blew right over the fact that people of Roseto were getting less exercise over time even though this would obviously impact the incidence of heart attacks. The consumption of trans fat wasn’t controlled for, and the authors didn’t measure LDL cholesterol and HDL cholesterol separately, which could explain why they noticed no difference in total cholesterol levels (LDL could’ve increased while HDL decreased, ending up with the total staying the same while a risk factor for heart attacks increased).
To address the claim of this copypasta directly, the idea that there are “areas that have both high consumption of animal products and high life expectancies” is misleading, as the studies which compare low consumption of animal products to high consumption in those very areas find that the low consumption groups have better health outcomes. Let’s take Hong Kong, a study on meat consumption in Hong Kong [118] found that the men consumed significantly more meat and red meat than the women, and subsequently had a significantly higher rates of diseases, “Whereas meat, and especially red meat intakes among males are significantly higher than those in females across all adult age groups, so are burden of diseases.” The same is true for the Swiss population, according to another study, which found that vegans had the greatest benefit in terms of health, “Processed meat consumption by the average man was associated with an increased risk of 24 μDALY/p/d which can be interpreted as approximately 13 min of healthy life lost each day; increased risks were then followed by low whole grains, low nuts and seeds, and high alcohol… and the largest benefit is seen for vegans having only 0.024 μDALY/kcal consumed.” A study done on the Spanish population [119] also found that a higher intake of animal protein (which necessitates a higher intake of animal products in an average diet) is associated with a significant increase in risk of CVD incidence and CVD and cancer deaths, “the higher consumption of animal protein was associated with a significantly increased risk of cardiovascular disease and cardiovascular and cancer death but not the consumption of vegetable protein.” There’s also a study which explains why the incidence of disease is lower in France even though their animal product intake is higher [120], as it was found that people in France consumed more vegetables and vegetable oils, “Given a high intake of cholesterol and saturated fat, the country in which people also consume more plant foods, including small amounts of liquid vegetable oils, and more vegetables (more antioxidants) had lower rates of CHD mortality.”. Additionally, among the French population, those who consumed a high amount of butter had a high incidence of CVD, and those who consumed olive oil as their chief fat had a lower incidence of CVD, “Butter consumption was high in the northern regions such as Moselle, where the incidence of cardiovascular disease was high. Olive oil was the chief fat consumed in southern France (along with some peanut oil), and the cardiovascular disease incidence was low in the South of France, department of Var.” This same study goes over 39 other countries, and when put on a graph of cholesterol and saturated fat intake or milk intake, there is a significant association between the higher consumption of these and an increased risk of death. It is clear that Buettner hasn’t just cherry-picked a few countries which confirm his view. It’s amazing how this copypasta accuses others of cherry-picking when it includes an overwhelmingly high amount of cherry-picking, like the second source which is just a screenshot of a graph of meat consumption and life expectancy, which shows a correlation between higher meat consumption and higher life expectancy. From this, you would think that eating meat is good, but I decided to dig a little further to find where this graph came from. It turns out to be from a study which didn’t even separate the high-income countries from the low-income countries to look at the correlation between meat intake and health without the possibility of confounding factors getting in the way. This is a major flaw with the study which makes it unreliable as evidence for the argument that higher meat intake is associated with better health. However, there is a study which did this [121], and evaluated 164 countries just like the previous study, and it actually concluded that “Red meat and alcohol consumption appeared to have a negative impact on LE in high-income countries (HIC) and upper-middle-income countries (UMIC), although it had no significant association with LE in low-income countries (LIC) or lower-middle-income countries (LMIC).” The reason meat intake wasn’t associated with life expectancy in low-income countries is also explained; Countries with low incomes also have higher rates of undernutrition, which drives down the life expectancies, “Most of the African countries lie in low income and middle-income countries and in those countries such countries did not consume red meat even at the beneficiaries level, and life expectancy counted low due to high undernutrition.” You also have to consider that people in low-income countries receive worse healthcare as well, which would impact their death rates.
Next, the fact that Buettner doesn’t praise Mormons for their health doesn’t prove anything; they may not be on his radar. The third source is once again a screenshot, presumably because the author of this copypasta was afraid of giving the full source. The argument made here is very poor, if the lower food intake, including lower animal products intake, is caused by the post famine then it should’ve effected the rest of Japan too, but it’s obvious that Okinawans still had a lower intake of animal products, as well as lower overall calorie intake, both of which contributed to them having a lower risk of diseases [122]. The point about centenarians can be outright ignored; it’s completely unimportant, as those people who consume less animal products have better health outcomes. Nor does it matter that the blue zones franchise belongs to SDA church, as this in no way invalidates the findings from the countries in blue zones, as well as studies from non-blue zones which unequivocally show that higher animal product consumption, and as a result of that, higher saturated fat and cholesterol intake, is associated with higher risks of diseases.
2) The website “nutritionfacts.org” is run by a vegan doctor who is known to misinterpret and cherry-pick[6] his data. He and many other plant-based advocates like Klaper, Kahn and Davis all happen to be ethical vegans[7].
The first part of this is true. Dr Michael Greger, who runs nutritionfacts cherry-picks some of the research he includes in his videos. This of course doesn’t mean that every video he makes on nutrition will be full of misinformation or cherry-picking, but there are better resources like veganhealth.org [123] and theveganrd.com [124] which vegans should stick to instead. The second point is irrelevant at best; Doctors having moral standards is by no means a bad thing or something that stops them from giving good advice.
3) EAT-Lancet is pushing a nutrient deficient “planetary health diet” because it’s essentially a global convention of vegans[8]. Their founder and president is the Norwegian billionaire, hypocrite[9] and animal rights activist Gunhild Stordalen. In 2017, they co-launched FReSH — a partnership[10] of fertilizer, pesticide, processed food and flavouring companies.
As shown previously, a well-planned plant-based diet doesn’t only meet nutritional requirements, as confirmed by the vast majority of national nutrition authorities, but also has protective effects against non-communicable diseases. The source they cite to prove that EAT-Lancet is “essentially a global convention of vegans” is an article which claims 31 out of the 37 authors “have, through their work, been promoting vegetarian, anti-meat views since before joining the EAT-Lancet Commission”, which doesn’t exactly make them “a convention of vegans”. In fact that claim is left unsubstantiated. To give an example: the first author, Ashkan Afshin, contributed to an analysis of impact of dietary habits on cardiovascular and diabetes mortality, which took the optimal intake for processed meat to be zero. This was because they defined optimal level as the level with the lowest amount of harm, “For metabolic risk factors and dietary factors with harmful effects, optimal level was defined as the exposure levels associated with the lowest level of harm.” This is a logical definition to make, as what else could constitute an optimal level except for the level at which the least amount of harm is caused? This is a far cry from being pro-vegetarian and in no way proves that someone is vegan. Clearly, this is lousy evidence at best. The rest of the evidence that the majority of the authors are pro-vegetarian continues in a similar manner, citing papers and studies which the authors partook in making, and which either found that meat is bad for health or environment, or promote a higher intake of fruit and vegetables. No arguments are made for why these papers, studies or reports are misleading, or showing that they have faulty methodology, so it can only be assumed that whoever wrote this article didn’t actually have any arguments. It seems more and more like this article is just anti-science, as whenever somebody has something to do with studies which plainly show how bad animal products are, they are framed as biased, seemingly for no reason. Let’s imagine this in a different situation: there’s a group of authors 90% of whom have something to do with research on cigarettes, and they keep on finding that smoking is bad for health and the environment. Are they “essentially a convention of anti-smokers”, and therefore shouldn’t be trusted? Obviously not. Just because there is a consensus between authors that something is bad, let’s say inhaling car exhaust, this doesn’t mean that people shouldn’t listen to them. To conclude on this point: some of the authors may be vegan, but this hasn’t been proven in any reasonable way by the source cited, so the claim is left unsubstantiated. The second point is completely irrelevant, as it is a genetic fallacy [22]. The founder of some group being a billionaire and a hypocrite doesn’t indicate the truthhood of the statements made by the group, and therefore cannot discredit them. The last point is also utterly ridiculous. The reason EAT-Lancet co-launched fresh is specifically so that they can work with these companies to create more healthy and less environmentally damaging products and food [125], “FReSH turns the conventional “farm to fork” approach on its head by working from “fork to farm” to develop, implement and scale transformative solutions that are aligned with science-based targets. This means starting with people and focusing on their consumption habits. Then working back through the food system — from retail, packaging and distribution to how and what is grown — to determine what levers business can pull to contribute to food system reform in order to create healthy and enjoyable food for all, produced responsibly, within planetary boundaries by 2030.” Is the attempt to make companies cause less harm to the health of consumers and the environment supposed to be a bad thing?
4) The China Study, aka the Vegan Bible, has been debunked[11] by hundreds of people including Campbell himself[12] in his actual peer-reviewed publications on the study.
The China study isn’t cited very commonly now-a-days. The vegans I’ve seen talk about nutrition use more recent and better data. This is also far from being “sneaky vegan propaganda” as the authors of the China Study thought it was good research at the time of making it, and some time afterwards, until they were able to find the flaws with it.
5) The Guardian, a pro-vegan newspaper that frequently depicts meat as bad for health and the environment, has received two grants[13] totaling $1.78m from an investor of Impossible Foods.
There’s no argument here against the claims made by The Guardian. The fact that they may have some kind of bias doesn’t indicate that the articles they publish are misleading. One can receive grants while publishing truthful information, they are by no means mutually exclusive. If they want to show that The Guardian does indeed publish misinformation, they’d have to show evidence just for that, not the evidence that they get funding.
[1] https://benjamindavidsteele.wordpress.com/2019/05/28/blue-zones-dietary-myth/
[2] https://i.imgur.com/koHTXmH.png
[3] https://i.imgur.com/ZrDUNi4.png
[4] https://www.biorxiv.org/content/10.1101/704080v2
[5] https://www.adventisthealth.org/blog/2020/april/adventist-health-acquires-blue-zones-as-part-of-/
[6] https://twitter.com/KevinH_PhD/status/1169630461087248390
[7] https://pastebin.com/6yanQrcS
[8] https://ninateicholz.com/majority-of-eat-authors-vegan-vegetarian/
[10] https://i.imgur.com/stv6Rj0.png
[11] https://deniseminger.com/the-china-study/
[12] https://pastebin.com/D7D9FYhZ
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1.6. Vegan diets aren’t “proven to reverse heart disease”
A widespread lie is that the vegan diet is “clinically proven to reverse heart disease”. The studies by Ornish[1] and Esselstyn[2] are made to sell their diet, but rely on confounding factors like exercise, medication or previous surgeries (Esselstyn had nearly all of them exercise while pretending it was optional). All of them have tiny sample size, extremely poor design and have never been replicated[3] in much larger clinical trials, which made Ornish suggest[4] that we should discard the scientific method. Both diets included dairy.
[1] https://www.medpagetoday.com/blogs/skeptical-cardiologist/80783
It’s true that a vegan, or plant-based diet hasn’t been proven to reverse heart disease. There are very specific criteria for reversal in the medical field, which the studies by Ornish and Esselstyn aren’t able to reach. However, this doesn’t mean that a plant-based diet hasn’t been proven to alleviate some of the symptoms of heart disease and decrease the risk of them happening, which is a massive achievement within itself. For example: the “large clinical trial” cited, which happens to be the WHI study again. It was actually found that those women who had the lowest intake of saturated fat, trans fat, and the highest intake of vegetables and fruit had a reduction in the incidence of CHD. Ornish didn’t suggest that we should discard the scientific method, he came nowhere near to that. He simply wrote an article detailing some of the flaws with RCTs, and suggested that scientists need to come up with “more creative experimental designs”.
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1.7. Factually deficient diet
Vegan diets are devoid of many nutrients and generally require more supplements than just B12. Some of them (Vitamin K2, EPA/DHA, Vitamin A) can only be obtained because they are converted from other sources, which is inefficient, limited[1] or poor[2] for a large part of the population. EPA+DHA from animal products have an anti-inflammatory effect[3], but converting it from ALA (plant sourced) does not seem to work the same[4]. Taurine is essential[5] for many people with special needs, while Creatine supplementation improves memory[6] only in those who don’t eat meat.
[1] https://www.ncbi.nlm.nih.gov/pubmed/9637947
[2] https://www.sciencedaily.com/releases/2009/11/091118072051.htm
[3] https://www.ncbi.nlm.nih.gov/pubmed/28900017
[4] https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201801157
The first source cited is used to prove that the conversion of ALA into EPA+DHA is inefficient, but it wasn’t actually comparing the levels of those fatty acids in vegans and non-vegans. A study [126] which compared these two found that vegans have similar levels of EPA and DHA as omnivores who don’t take omega-3 supplements, “vegans have low baseline omega-3 levels, but not lower than omnivores who also consume very little docosahexaenoic and eicosapentaenoic acids.” To add to that, the reason EPA and DHA intake matters is because it’s been shown to reduce CHD risk, but only in omnivorous diets. The risk of CHD in vegans is already significantly lower than in omnivores, and so there’s no evidence that having higher levels of EPA/DHA would benefit vegans, “Omega-3 treatment reduces risk for CHD death but these data are from omnivorous populations, and whether vegans would derive similar benefit is unclear. It is well-known that cardiovascular risk in vegans/vegetarians is significantly reduced compared to omnivore controls, and thus at present, there is no direct evidence that raising the omega-3 index would confer additional health benefits over and above their already-protective vegan diet.” Neither of the two of the other studies cited on omega-3s showed that vegans had more inflammation than omnivores because of this. The second of the two sources was conducted on people with high levels of cholesterol, which clearly isn’t a problem for the majority of vegans [127][128], “Vegetarians, and most especially vegans, have a much lower risk of hypercholesterolemia (for both total cholesterol and LDL) and a less atherogenic profile.” And therefore, the results of this study cannot be applied to vegans. The study cited to prove that vitamin A conversion is inefficient was conducted on women from the UK, who weren’t specified to be vegan. In fact, veganism isn’t even mentioned. A different study [129] which actually compared the levels of vitamin A (retinol) in the blood of vegans (VN) and of omnivores (OV) found that even though serum retinol was lower in vegans, the levels were still within normal range, “plasma retinol concentrations in our subjects were mainly in the normal range with <10 % showing deficiencies, even in the VN subjects. Thus, β-carotene intake seems to be sufficient in this setting.” Next, there’s vitamin K, which once again hasn’t been proven to be so low in vegans as to cause a deficiency. In fact, vegans have a higher intake of vitamin K, as found in a study [130], “… individuals adhering to vegan diets consumed significantly more magnesium, folate, and vitamin K as compared to their omnivorous counterparts”. For taurine, no evidence is provided that vegans have a higher rate of deficiency. Although vegans have slightly lower levels of taurine than omnivores [131], this hasn’t been associated with any negative impacts on health, and neither is there an agreed-upon level of taurine which is considered to be a deficiency, so this point can be dismissed entirely. The last nutrient mentioned, creatine, is supported by extraordinarily bad evidence. The study cited tested the memory of vegetarians and meat-eaters using 2 tests, one before taking a creatine supplement or a placebo, and one after. During the first test, both vegetarians and meat-eaters got similar scores, but in the second test, after the vegetarians and non-vegetarians took a creatine supplement, vegetarians got better scores than meat-eaters, while meat-eaters got significantly worse scores both in the creatine and the placebo group. If anything, this makes an argument for being vegan while taking a creatine supplement, as the lowest decrease in memory was only observed in the vegetarian group which supplemented.
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1.8. Supplements
The US supplement industry is poorly regulated[1] and has a history of spiking their products with drugs. Vitamin B complexes were tainted with anabolic steroids[2] in the past, while algae supplements have been found to contain aldehydes[3]. Supplements and fortified foods can cause poisoning[4], while natural products generally don’t. Even vegan doctors caution and can’t agree[5] on what to supplement.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330859/
[2] https://www.nbcnews.com/healthmain/fda-warns-steroids-vitamin-b-supplement-6C10765769
[3] https://www.ncbi.nlm.nih.gov/pubmed/30529885
The first paper provided didn’t actually look at all supplements, especially the ones vegans are recommended to take. B12 isn’t mentioned at all, however, there are studies which looked at the effects of B12 supplementation [132], and found that “No adverse effects have been associated with excess B12 intake from food or supplements in healthy individuals.” The point made in this paper about vitamin D is misleading, they state that pill potency was found to range between 9% and 140%, but it was also found that the average dose between 5 pills were within 89% to 105% range, meaning that if you take a vitamin D supplement every day or every other day, your average amount of vitamin D intake will be quite accurate to what is stated on the supplement bottle, and it would be enough to stop any potential deficiencies, “The potency of pills from different lots ranged from 9% to 140% of the stated dose; mean potencies over 5 lots ranged from 89% to 105%.” It has to be noted that not all vegans need to take a vitamin D supplement, only those who are at risk of developing a deficiency, and who have had their blood levels of vitamin D checked. The fact that some supplements were tainted in the past doesn’t reflect the safety of them today. Some types of paint used to contain lead which caused serious health problems; does this mean we shouldn’t use paint? To add to that, vegans don’t need to take vitamin B complexes, they just need B12 in particular, which is what’s most often recommended. There’s also no evidence that taking omega 3 supplements as a vegan will improve your health, so it is unnecessary. The evidence they cite for supplements and fortified foods causing poisoning was just a Wikipedia page which didn’t even go over the percentage of people who get hypervitaminosis out of the ones who take supplements or eat fortified foods, so for all we know it could be a minuscule amount. As stated previously, B12 toxicity isn’t known of. Even high intakes of B12 supplements aren’t associated with any adverse effects. It’s also mentioned that hypervitaminosis, or vitamin toxicity, is only caused by high amounts of supplement intake or large intake of highly fortified food, and it can easily be avoided by not taking more than the recommended amount, “Generally, toxic levels of vitamins stem from high supplement intake and not always from natural sources but rather the mix of natural, derived vitamins and enhancers (vitamin boosters).”, “vitamin overdose can be avoided by not taking more than the normal or recommended amount of multi-vitamin supplement shown on the bottle and not ingesting multiple vitamin-containing supplements concurrently.” To address the last point, that vegan doctors can’t agree on what to supplement: not all doctors need to agree on the same topic, though most of the doctors cited agree upon taking a B12 supplement, and the fact that vegans need to take this supplement is supported by data. Most of them also agree upon taking a vitamin D supplement when necessary, which isn’t the case for all vegans. Doctors aren’t the be-all and end-all of information, they are human and they can get things wrong sometimes, which is why it’s important to see if they provide any sources for their claims, like studies. Studies and meta-analyses is what people should rely upon for reliable information, as well as experts, professionals, and other sources which accurately portray and assess studies and meta-analyses.
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1.9. Mental disorders
Restrictive dieting has psychological consequences[1] including aggressive behavior, negative emotionality, loss of libido, concentration difficulties, higher anxiety measures and reduced self-esteem. There is an extremely strong link[2] between meat abstention and mental disorders. While it’s unknown what causes what, the vegan diet is low in or devoid of[3] several important brain nutrients.
[1] https://www.ncbi.nlm.nih.gov/pubmed/8655907
[2] https://www.tandfonline.com/doi/full/10.1080/10408398.2020.1741505
[3] https://www.bbc.com/future/article/20200127-how-a-vegan-diet-could-affect-your-intelligence
The first study provided doesn’t even mention veganism, so it can’t be used as evidence against a vegan diet. The “extremely strong link” is supported by studies with poor methodology, and a part of them specifically mention that they could not prove causality or the possibility of inverse-causality. It’s also a very obvious case of hypocrisy, as this copypasta criticizes vegans for using observation studies to prove causation, when they use the same but ones of worse quality which don’t take into account the time component of disease and lifestyle choices. All except for 1 of the studies are cross-sectional, meaning they cannot prove causation, as worse mental health could be causing the participants to try vegetarianism. Baines et al: “this is a cross-sectional analysis, so that no inferences about causation can be made.” The number of vegetarians in Bas et al [133] was very low, with only 31 vegetarian participants, and only 2 of them were vegan, which makes it likely that the results this study got aren’t representative of most vegans, “We assume that this is the first study related with vegetarianism and eating disorders in Turkey, therefore, our study was limited by the self-reporting of vegetarianism and eating disorder behaviors, and the cross-sectional design of the study.” Beezhold et al (2015): “Considering our previous research, we have found that increasing restriction of animal foods (e.g. going from vegetarian to vegan) is associated with improved mood.” Beezhold et al (2010): “Vegetarians reported significantly less negative emotion than omnivores”. Beezhold and Johnston, which is the only RCT included, which means it’s quality is significantly higher than that of other studies included, found that vegetarians reported significantly better mood than omnivores and fish eaters, “Restricting meat, fish, and poultry improved some domains of short-term mood state in modern omnivores.” Though there were flaws with this study too, like the fact that it only lasted 2 weeks, and therefore the results can’t be extrapolated people who abstain from animal to products for a longer period of time. Boldt et al: “The results revealed that endurance runners had a high QOL regardless of the race distance or diet choice. These findings support the notion that adhering to a vegetarian or vegan diet can be an appropriate and equal alternative to an omnivorous diet.” Forestell and Nezlek: “Michalak and colleagues have shown that psychological disorders typically precede the adoption of vegetarianism. Thus, it is possible that depressed individuals try to improve their well-being by adopting vegetarian dietary habits.”, “The cross-sectional nature of our data did not provide a basis for drawing inferences about causal relationships between dietary habits and personality.” Hibbeln et al [134]: “This study does not resolve the question of whether adoption of a vegetarian diet will increase, or decrease the risk of depressive symptoms or affect mental well-being or what specific nutrients, if any, may influence those risks, but does suggest that a randomized controlled trial of selected nutrients or foods may be warranted.” The meta-analysis cherry-picked the results Lavallee et al, stating that it found that “Vegetarian diet related to higher levels of depression and anxiety among Chinese students.”, even though the study wasn’t only on Chinese students, and in fact, it found that in students from the US, Russia, and Germany there was no association between vegetarianism and worse mental health, “Vegetarianism is not associated with mental health in the US, Russia, or Germany, but is associated with anxiety and depression in China in this study.” Lindeman [135]: “The present studies do not answer the question about the causal relations between low psychological well-being and negative views of the world on the one hand, and adopting a vegetarian diet on the other.” Matta et al: “the fact that any food item exclusion was associated with increased risk of depression suggests that the association between vegetarian diets and depression could be only a particular instance of a broader association between depressive symptoms and food exclusion, regardless of food types. This may not apply to very specific food restriction patterns such as vegan diet but further studies including a larger sample of participants with a vegan diet are needed.” Michalak et al: “there was no evidence for a causal role of vegetarian diet in the etiology of mental disorders.” I couldn’t find the full version of Neumark-Sztainer et al, but it was of cross-sectional design like the rest, and the participants were vegetarian, not vegan. Perry et al [136]: “the restricted vegetarians (e.g. vegans, lacto- and lacto-ovo vegetarians) appear to be more ”stable“ and healthy adolescent vegetarians, with over half having been vegetarian for over 2 years, and with less involvement in unhealthy weight control behaviors.”, “It may also be that semi-vegetarianism, for some, is the first step toward a more stable, restricted vegetarianism, and that once the transition is made or the vegetarianism is maintained for over 2 years, there might be fewer health-compromising weight control behaviors exhibited.”, “Additionally, our study points to semi-vegetarians as less stable and more at risk for involvement in weight control practices than the restricted vegetarians.” Pfeiler and Egloff [137]: “Regarding personality variables, vegetarians were more open, and gave higher scores in trust and optimism about the future than meat eaters… Additionally, vegetarians reported a better current health status and a higher satisfaction with their health compared to meat eaters.” Stokes et al only had 17 vegetarian participants, and no vegan participants. Timko et al [138]: “Based on findings presented here it seems that the appearance of disordered eating (and hence the potential of vegetarianism as a risk factor for eating disorders) may have been an artifact of the high number of semi-vegetarians included in prior research.”, “Overall, there were no differences between groups in terms of depression, anxiety, or stress…” Wirnitzer et al: “There was no significant association between diet group and stress perception”, “vegan endurance runners had the highest scores for mental health. These findings were in line with previous studies, which showed that both endurance running and adhering to a vegan dietary pattern caused good mood states.” Only 7 out of the 18 studies actually included vegans, and 4 out of those found no association between the vegan diet and mental health and 1 found better mental health in vegans.
The article cited as proof that vegan diets lack important brain nutrients presents a study on Kenyan schoolchildren, who were fed one type of soup out of 3, one containing meat, another containing milk, the third containing vegetable oil, and some children didn’t eat soup at all. The researchers then measured how these children did in a few different tests to compare their intelligence over time. It found that the group of children which consumed soup with meat did better on one of the tests, which is what’s used as evidence by the article that the vegan diet is detrimental to brain health. However, there are several glaring flaws with this RCT, like the fact that these schoolchildren were all nutritionally deficient in several nutrients which means the results are unlikely to carry over to people who get adequate nutrition, “In addition, these data suggest that meat, milk and energy are not equivalent dietary supplements for children facing mild to moderate undernutrition and multiple micronutrient deficiencies.” Secondly, the soup eaten by the children is not at all a good representation of a meal on a vegan diet, vegans wouldn’t just add some plant oil to their soup as a replacement for meat or milk, we would add other good sources of protein like legumes, meat replacements like tofu, whole nuts and seeds, therefore the results aren’t indicative of the effects of a vegan diet on the brain. Unlike what this article claims, there is at least 1 RCT on the effects of a vegan diet on the brain [139], aside from the misrepresentative junk they cited. This study was conducted on office workers, with about half of them assigned to the intervention group which was instructed to eat a low-fat vegan diet, and half assigned to the control group which made no dietary changes. It was found that the intervention group significantly improved their indicators for depression, anxiety, and work productivity, meaning the vegan diet is actually good for your brain, “In summary, this study demonstrates that a dietary intervention using a low-fat vegan diet in the workplace improves indicators for depression, anxiety, and work productivity in a large, multicenter, corporate setting.” As for the nutrients claimed to be lacking on a vegan diet, the majority of them (creatine, taurine, EPA and DHA, B12, D3) have been addressed in the previous sections. The next nutrient to address is carnosine; carnosine levels have been found to be unaffected by the vegetarian diet [140] which excludes the highest animal sources of carnosine, meat, “Carnitine and carnosine homeostasis was unaffected by a 3- or 6-month vegetarian diet, respectively.” The last nutrient of concern mentioned is B6. The article claims that potatoes are the best source of B6 on a vegan diet, and that you’d have to eat 750g of potatoes to get your daily recommended intake of B6, however this is far from being true. Potatoes aren’t the best source of B6. Let’s take bananas, for example: 1 banana is enough to fulfill 30% of your daily B6 requirements. Alternatively, just half a tablespoon of nutritional yeast, which you can add to your food as a seasoning will give you more B6 than is necessary for the day.
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1.10. Eating disorder
A vegan diet alone fulfills the diagnostic criteria of an eating disorder[1].
[1] https://en.wikipedia.org/wiki/Avoidant/restrictive_food_intake_disorder#Criteria
Another great example of the author(s) of this copypasta not checking their sources properly. A Wikipedia page is cited, which only mentions that the criteria for a restrictive food disorder are: substantial weight loss, nutritional deficiency, dependence on a feeding tube or dietary supplements, significant psychosocial interference. However, what’s left out is what this eating disorder is caused by [141][142]: “Low appetite and lack of interest in eating or food. Extreme food avoidance based on sensory characteristics of foods e.g. texture, appearance, color, smell. Anxiety or concern about consequences of eating, such as fear of choking, nausea, vomiting, constipation, an allergic reaction, etc. The disorder may develop in response to a significant negative event such as an episode of choking or food poisoning followed by the avoidance of an increasing variety of foods.” None of which apply to people who go vegan for ethical reasons. It’s also very clearly stated in the criteria that this eating disorder doesn’t apply to things like cultural practices such as religious fasting, making this point entirely moot, “The disturbance is not better explained by lack of available food or by an associated culturally sanctioned practice.”
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1.11. Patrik Baboumian
Patrik Baboumian, the strongest vegan on earth, lied about holding a world record that actually belongs to Brian Shaw[1]. Patrik has never even been invited to World’s Strongest Man. He dropped the weight[2] during his “world record”, which was done at a vegetarian food festival where he was the only competitor. His unofficial deadlift PR is 360kg[3], but the 2016 world record was 500kg. We can compare his height-relative strength with the Wilks Score and see that he is being completely dwarfed by Eddie Hall (208 vs 273). Patrik also lives on supplements. He pops about 25 pills a day[4] to fix common vegan nutrient deficiencies and gets over 60% of his protein intake from drinking shakes[5].
[1] https://youtu.be/iJcvZIAsTfs
[2] https://youtu.be/ZTaGZ6KLDwI?t=82
[3] https://www.greatveganathletes.com/patrik-baboumian-vegan-strongman/
[4] https://youtu.be/aPJWOWePRGs?t=158
[5] https://barbend.com/vegan-strongman-patrik-baboumian-diet/
This is tangential to vegan nutrition but let’s address it anyway. Patrik Baboumian has a world record of carrying a 555kg yoke for over 10 meters, whereas Brian Shaw carried a 710kg yoke for 4 meters, so the lifts they did aren’t even the same. You can’t get a world record in something you didn’t do. Dropping the weight during the yoke walk isn’t against the rules, and it still counts as a world record. It’s completely irrelevant that nobody else tried this world record or to beat it during the same festival, what matters is that there isn’t anyone else at any other time who succeeded in carrying a heavier weight for the same distance. Patrik didn’t claim to have a world record in the deadlift, so it doesn’t matter that the max amount of weight he can deadlift is lower than that of some other strongman. The fact that he’s dwarfed by Eddie Hall also doesn’t prove anything, as they are both way stronger than the average person, or even the average weightlifter. Plenty of strongmen take supplements, like Eddie Hall [143] and Hafthor Bjornsson [144], so Patrik isn’t the only strongman doing this. Other strongmen also tend to get a large amount of protein from protein shakes [145]. A study on the prevalence of supplements among young athletes [146] found that 82% of athletes take supplements, and 54% take protein supplements, “The prevalence rate of the intake of sports supplements was 82.2%, with the protein supplements being predominant (54.5%).” Patrik preferred getting most of his protein by drinking at the time of making the video of what he eats in a day, as it’s easier for him. He also mentions that his diet changes over time, so it’s likely that he doesn’t get the same amount of protein from shakes all the time. This clearly says nothing about veganism or the vegan diet, as most vegans don’t do this.
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1.12. Other athletes
Here’s a summary[1] on almost every pro athlete that either stopped being vegan, got injured, has only been vegan a couple of years, retired or was falsely promoted as vegan.
https://docs.google.com/spreadsheets/d/1UKOY15ZEHjbl-j2JFkyDsx8JIsiiJLJUJmpEIXM-SxU/htmlview#
It doesn’t matter that some athletes stop being vegan, or that some get injured while being vegan, as there are plenty of non-vegan athletes who also injure themselves. Here we should be looking at the proportion of athletes who get injured on a vegan diet compared to the proportion of athletes who get injured on a non-vegan diet. Of course this data isn’t provided. However, there are multiple papers and studies on the effects of a vegan diet on athletes. A narrative review of studies on this topic found that vegans have an advantage in healing sports injuries [147], “Advantages in prevention of illnesses and diseases, and therapy of sports injuries”, “Shorter or even no periods of sick leave or rehabilitation from sports accidents or injuries, thus least absence from training with no further stagnation or regression in performance level”. A meta-analysis of RCTs [148] on the effect of vegetarian, including vegan, diets on athletes found that a vegetarian diet didn’t hinder performance, “the vegetarian-based diet did not improve performance, nor did it hinder it. There appeared to be no differences at least acutely between a vegetarian based diet and an omnivorous diet in muscular power, muscular strength, anaerobic or aerobic performance.” Although there were some limitations with this meta-analysis of RCTs, it’s the only meta-analysis of RCTs there is on this topic in summer 2021. As a final point, it’s also been found in another review of studies [149] that a well-planned vegan diet is appropriate and nutritionally adequate for athletes, “With proper planning, athletes can achieve all their nutritional needs via a vegetarian or vegan diet.”
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1.13. The vegan diet is not species-appropriate
Historically, humans have always needed animal products and are highly adapted to meat consumption. There has never been a recorded civilization of humans that was able to survive without animal foods. Isotopic evidence shows that the first modern humans ate lots of meat[1] and were the only natural predator of adult mammoths. Most of their historic technology and cave paintings revolved around hunting animals. Our abilities to throw[2] and sweat[3] likely developed for this reason. Our stomach’s acidity is in the same range as obligate carnivores[4] and its shape has changed so much[5] that we can’t even digest cellulose anymore. The vegan diet is born out of ideology, species-inappropriate and could negatively affect future generations[6].
The cooked starch hypothesis that vegans use is inconsistent[7] with many observations.
[1] https://www.ncbi.nlm.nih.gov/pubmed/30872714
[2] https://phys.org/news/2013-06-chimps-humans-baseball-pitcher.html
[3] https://en.wikipedia.org/wiki/Endurance_running_hypothesis#Endurance_running_and_persistence_hunting
[4] https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0134116
[5] https://nature.berkeley.edu/miltonlab/pdfs/kmilton_foodevolution.pdf
There is no indication of how viable and good for health a certain diet is from whether or not there were civilizations of humans following that diet. Even if humans are highly adapted to meat consumption, that still doesn’t tell us that it’s healthy. The goal behind eating meat in the early humans wasn’t to be healthy, it was to survive. People would rather eat something which will damage them in the long run but allow them to survive at least til their reproductive age than starve to death, but clearly this doesn’t mean that that food is good for you when you have other options. If humans were indeed “highly adapted” to meat consumption, or animal product consumption in general, then you’d expect there to be good evidence that people consuming these kinds of foods have better health outcomes than people who don’t, but as shown previously, this clearly isn’t the case; Vegans are by far the healthiest group, though they’re not eating their “species-appropriate” diet. Even when comparing vegans to another healthy diet group [150] which includes animal products, the group on a vegan diet still has better health biomarkers, “A low-fat vegan diet improved body weight, lipid concentrations, and insulin sensitivity, both from baseline and compared with a Mediterranean diet.” If the vegan diet produces better health outcomes than other diets, which it has been shown to do over and over again, it is species appropriate. There is no evidence that it could negatively affect future generations, not even anything close. The evidence provided for this point is based on a single cat study; humans aren’t cats, so any results found in the study are irrelevant to the effects of diet on humans.
The source cited to prove that the cooked starch hypothesis is inconsistent with many observations doesn’t itself provide any evidence. It’s just a list of claims which don’t mention any specific studies, so these claims can be dismissed, but just for the sake of being thorough, they’ll be addressed. The first claim, that humans only started cooking their food about 1 million years ago, while brain size started increasing over 2 million years ago, is incorrect. There is evidence that humans started cooking their food around 1.9 million years ago [151], “Together, our results indicate that the behaviorally driven adaptations of food processing (reduced feeding time and molar size) originated after the evolution of Homo but before or concurrent with the evolution of H. erectus, which was around 1.9 Mya.”, which is relatively close to the time period when brain size started significantly increasing. The second claim, that grain consumption is much more recent, is irrelevant, as grains didn’t have to be around for humans to be able to find sources of starch, like roots and tubers, which are mainly made of starch [152], “Starch constitutes up to 80% of the dry weight of edible roots and tubers and, if left undisturbed in the ground, they remain stable and can be harvested as needed over a period of months.” The third claim, that human brain development is dependent on nutrients found in animal products is misleading, not only because it doesn’t address the fact that human size started increasing because early humans started cooking starches, but also because those nutrients can be gotten on a vegan diet in the present, meaning there is no argument here that vegans will have any detrimental effect on their brains due to their diet. It’s possible that early humans had to eat animal products to survive, because they had no other options, but the starch hypothesis still stands, and the claim made doesn’t contradict it. There is, of course, no evidence provided for the next claim, that ketogenic diets provide beneficial effects on cognitive health, however I was able to find some. The only studies I was able to find on the effects of a keto diet on cognitive health [153] were either conducted on mice, and therefore the results aren’t generalizable to humans, or they were conducted mainly on patients with Alzheimer’s disease, with some conducted on patients with mild cognitive impairment, which constitute a minority of people. Therefore the results of these studies also can’t be extrapolated to healthy individuals without Alzheimer’s or cognitive impairment. Additionally, a ketogenic diet can also be vegan, so even if there are greater positive effects on cognitive health on a ketogenic diet, it can be achieved at the same time as decreasing your risk of heart disease, by eating plant-based foods [154], “A self-selected low-carbohydrate vegan diet, containing increased protein and fat from gluten and soy products, nuts and vegetable oils, had lipid lowering advantages over a high-carbohydrate, low-fat weight loss diet, thus improving heart disease risk factors.”
The next claim, that Neanderthals ate mostly meat and had the largest brains can be dismissed, as Neanderthals also went extinct, while humans didn’t. To add to this, total brain volume only accounts for 2% change in intelligence [155], “Yet TBV accounts for a relatively small share in overall variation in cognitive performance (ΔR2 ≈ 2%).”, meaning it’s not a particularly important metric to worry about, as there are much greater contributing factors to human intelligence than brain size. The claim that human brain size is declining is very misleading, as humans are becoming more intelligent despite the decrease in brain size. There’s also no correlation between people eating a vegan diet, or a diet void of meat and a decreased intelligence. The claim that latitude is correlated with brain size and higher meat consumption, doesn’t account for all other differences between the people living in different climates and latitudes. It’s actually been found that the change in brain size is also accompanied by larger eye size, and that these changes are accounted for by the need for humans to adapt to having less light the further from the equator they are [156], “We have shown that human orbital volume significantly increases with absolute latitude independently of phylogeny, brain size and body mass, suggesting that there has been selection for larger eyeballs under progressively lower light conditions.”, “Finally, owing to tight scaling between visual system components, larger eyeballs will necessitate proportionately enlarged visual cortices, and hence, a parallel positive latitudinal trend in these brain regions.”
The claim that people from Inuit tribes consume raw meat and their brains develop fine is demonstrably false. In a study on Inuit children, it was found that the children who had higher concentrations of heavy metals and PCBs in their spinal column had lower IQ, higher prevalence of attention deficit hyperactivity disorder, and significantly worse fine motor functions due to PCBs [157], “higher cord mercury (Hg; used as an index of MeHg exposure because seafood diet is the predominant exposure source in this population) and cord Pb concentrations were associated with reduced IQ scores (Jacobson et al. 2015), and cord Hg and child Pb levels with higher prevalence of behaviors consistent with attention deficit hyperactivity disorder.”, “Cord blood Hg, current blood Hg, and current plasma PCB153 concentrations were associated with poorer performance on the Santa Ana Form Board after statistical control for covariates. However, after adjustment for other contaminants, only the effect of current PCB153 remained statistically significant,” Lastly, on this point, eating raw meat is extremely detrimental to health as raw meat contains often debilitating or lethal bacteria [158], “Like any raw meat products we encounter at home or in restaurants, raw meat diets actually have the potential to carry pathogenic bacteria or dangerous microorganism.” Inuit infants have a very high mortality from infectious diseases and a high prevalence of infectious diseases in children [159], “Bacterial and viral infections account for much of the excess morbidity and mortality in Inuit infants compared to other Canadian infants, despite significant advances in living standards and health care delivery”, “Studies in Canadian Inuit infants and children reported a prevalence of OM of between 7 and 31%, compared to less than 1% in the United States, the United Kingdom, Denmark and Finland.”
The claim that there isn’t evidence that cooking increases the bioavailability of energy is also incredibly demonstrably false. Cooking foods, especially plant foods increases its energy bioavailability [160], “Here we have reviewed evidence pertinent to the hypothesis that an important and consistent effect of cooking food is a rise in its net energy value. We find strong support for positive impacts of cooking on plant foods.” The claim that there are many animals which have the same brain size as humans and none of them cook can be completely granted. Those animals haven’t created vaccines or know how to use electricity to make their lives easier, or made rockets which go to space. It’s irrelevant what other animals eat because it doesn’t indicate the best food for humans. The claim that some other animals have to operate on fatty acids or ketones and that humans had to do it in the past also doesn’t indicate that operating on them is best for us. Vegans can get more than enough fatty acids when necessary, as there are plenty of plants containing fats, like the copious amount of different varieties of nuts and seeds, some of which would’ve been available even to early humans [161], “Nut and fruit availability is greater in summer and autumn in the contemporary Upper Jordan Valley. When the data of all of the archaeological layers at GBY are combined, the highest productivity and availability of food plant species are in spring (32 species) and summer (32 species)”.
The claim that human brains mostly don’t require insulin to receive energy from carbohydrates is pretty close to the truth but still irrelevant. There are significant parts of the brain which rely upon insulin [162], “there is a significant element of brain glucose uptake that is insulin sensitive, with a dose-response curve that is shifted well to the left of dose-response curves for other insulin-sensitive tissues, such as muscle or liver.” The human brain is an organ that must be prioritized, as when it doesn’t receive enough energy it can either cause severe problems or death, meaning that when there isn’t much food around, it has to be easy for the brain to get enough energy. The animals that didn’t evolve this trait likely would’ve had a harder time surviving when food was scarce, so it became evolutionarily beneficial for some parts of the brain to be able to get energy without insulin. The claim that human brains have limited glycogen stores is also irrelevant, as clearly having larger stores wasn’t beneficial. People in the past and in the present are able to get food often enough to stay alive and well, making large glycogen stores mostly useless. The next claim is straight up false, the hypothesis doesn’t rely upon the “myth” that a human brain requires 130 grams of carbs a day. Firstly, it isn’t a myth, as it’s meant to be a recommendation for people following a diet with either a moderate to high amount of carbohydrates. The fact that people on a keto diet are able to function with less carbohydrate consumption doesn’t in any way disprove the hypothesis, it just means that human brains are able to function even when carbohydrate intake is low and fat intake is high. The claim that keto diets are protective against hypoglycemia is especially irrelevant as it is rare for someone to get hypoglycaemia if they’re not diabetic [163], “an estimate of 189 hypoglycemic episodes is predicted in a non diabetic population of 37 898, giving a cumulative incidence of 50 per 10 000 admissions.” Additionally, a vegan diet has been shown to be effective at preventing and treating type 2 diabetes [164], “There is a general consensus that the elements of a whole-foods plant-based diet — legumes, whole grains, fruits, vegetables, and nuts, with limited or no intake of refined foods and animal products — are highly beneficial for preventing and treating type 2 diabetes.” Lastly, the origins of the starch hypothesis aren’t indicative of their truthhood. A hypothesis can be made by a biased person, and still be one of the best if not the best hypotheses.
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1.14. Other anti-vegan copypastas on nutrition
Compilations of nutrition studies:
1) Veganism slaughter house[1] (80+ papers).
2) 70+ papers[2] comparing vegans to non-vegans.
3) Scrolls and tomes against the Indoctrinated.[3]
4) Zotero folder[4] of 120+ papers.
[1] https://pastebin.com/rc6QmXeQ
[2] https://pastebin.com/mfrhgayb
[3] https://www.reddit.com/r/keto/comments/328bpa/scrolls_and_tomes_against_the_indoctrinated/
[4] https://www.zotero.org/groups/2466685/ketosciencedatabase/collections/LZHCC8J3
I won’t be going over these other copypastas but they generally have a lot of the same points as were addressed in this one.
6. LIST OF LACKING NUTRIENTS
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List of known nutrients that vegan diets either can’t get at all or are typically low in, especially when uninformed and for people with special needs. Vegans will always say that “you can get X nutrient from Y specific source”, but a full meal plan with sufficient quantities will essentially highlight how absurd a “well-planned” vegan diet is.
1) Vitamin B12
2) Vitamin B6 (Pyridoxal, Pyridoxamine)
3) Choline
4) Niacin (bio availability)
5) Vitamin B2
6) Vitamin A (Retinol, variable Carotene conversion)
7) Vitamin D3 (winter, northern latitudes, synthesis requires cholesterol)
8) Vitamin K2 MK-4 (variable K1 conversion)
9) Omega-3 (EPA/DHA; conversion from ALA is inefficient, limited, variable, inhibited by LA and insufficient for pregnancy)
10) Iron (bio availability)
11) Zinc (bio availability)
12) Calcium
13) Selenium
14) Iodine
15) Protein (per calorie, digestibility[1], Lysine, Leucine, elderly people[2], athletes)
16) Creatine (conditionally essential)
17) Carnitine (conditionally essential)
18) Carnosine
19) Taurine (conditionally essential)
20) CoQ10
21) Conjugated linoleic acid
22) Cholesterol
23) Arachidonic Acid (conditionally essential)
24) Glycine (conditionally essential)
If a vegan diet is deficient in all of these nutrients, you’d expect them to have way worse health outcomes, and it just isn’t the case, as proven previously. Of course it’s important to plan your diet well as a vegan, and even as a non-vegan, to make sure you’re getting all essential nutrients, and to supplement when it’s necessary. Some of these nutrients are hardly essential, especially cholesterol, which were addressed in earlier points. There are many nutritionally adequate vegan meal plans on the internet [165].
Special thanks to Matt Madore for helping with most of the claims on cholesterol, and for proofreading my debunk, Frogpole for helping with the section on epidemiology compared to clinical trials, TheDreadPirateLilly for helping with information on Adventists, and Study Archives (the discord server) for providing ease of access to studies and explanations of data.
Matt Madore’s twitter: https://twitter.com/MattMadore576/
And the site he writes for: https://www.mynutritionscience.com
Study Archives: https://discord.gg/DkHtx7N
- Vegan–vegetarian diets in pregnancy: https://obgyn.onlinelibrary.wiley.com/doi/full/10.1111/1471-0528.13280
- Growth and development of British vegan children: https://academic.oup.com/ajcn/article-abstract/48/3/822/4716540
- Macronutrient Intake, and Anthropometrics of Vegetarian, Vegan, and Omnivorous Children (1–3 Years): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6521189/
- Nutritional Adequacy of Vegetarian and Omnivore Dietary Intakes: https://www.researchgate.net/publication/266024027_Nutritional_Adequacy_of_Vegetarian_and_Omnivore_Dietary_Intakes
- Plant‐Based Diets Are Associated With a Lower Risk of Incident Cardiovascular Disease, Cardiovascular Disease Mortality, and All‐Cause Mortality in a General Population of Middle‐Aged Adults: https://www.ahajournals.org/doi/10.1161/JAHA.119.012865
- Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2540540
- Cardiovascular disease mortality and cancer incidence in vegetarians: a meta-analysis and systematic review: https://pubmed.ncbi.nlm.nih.gov/22677895/
- Vegetarian, vegan diets and multiple health outcomes: A systematic review with meta-analysis of observational studies: https://pubmed.ncbi.nlm.nih.gov/26853923/
- https://www.sfpediatrie.com/sites/www.sfpediatrie.com/files/medias/documents/vegan_diet_archives_oct_2019.pdf (full text)
- Growth and body composition of periurban Guatemalan children in relation to zinc status: a cross-sectional study (no mention of diets): https://www.researchgate.net/publication/14760077_Growth_and_body_composition_of_periurban_Guatemalan_children_in_relation_to_zinc_status_A_cross-sectional_study
- Prevalence of Vitamin D Deficiency and Associated Risk Factors in the US Population (2011–2012): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6075634/
- Vitamin D deficiency in Europe: pandemic?: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5527850/
- Vegan Diet in Sports and Exercise — Health Benefits and Advantages to Athletes and Physically Active People: A Narrative Review: https://clinmedjournals.org/articles/ijsem/international-journal-of-sports-and-exercise-medicine-ijsem-6-165.php
- Infantile Scurvy: Two Case Reports: https://www.hindawi.com/journals/ijpedi/2010/717518/
- Coalition is full of baloney on nutrition guidelines: https://thehill.com/blogs/congress-blog/healthcare/257353-coalition-is-full-of-baloney-on-nutrition-guidelines
- Nutritional Update for Physicians: Plant-Based Diets: https://www.researchgate.net/publication/236909487_Nutritional_Update_for_Physicians_Plant-Based_Diets
- Origin of atherosclerosis in childhood and adolescence: https://academic.oup.com/ajcn/article/72/5/1307s/4730131
- Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal: https://www.sciencedirect.com/science/article/pii/S0735109704007168
- Cardiometabolic risk factors in vegans; A meta-analysis of observational studies: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6301673/
- Reliability and Validity of Food Frequency Questionnaire and Nutrient Biomarkers in Elders With and Without Mild Cognitive Impairment: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042482/
- Expert reaction to study on meat-eating, fish-eating and vegetarian diets and risk of heart disease and stroke: https://www.sciencemediacentre.org/expert-reaction-to-study-on-meat-eating-fish-eating-and-vegetarian-diets-and-risk-of-heart-disease-and-stroke/
- https://www.logicallyfallacious.com/logicalfallacies/Genetic-Fallacy
- The dietary guidelines are virtually identical in every country in the world: https://thedietwars.com/the-dietary-guidelines-are-virtually-identical-in-every-country-in-the-world-while-obesity-ranges-from-1-6-south-korea-to-41-4-qatar-a-30-fold-difference-therefore-the-dietary-guidelines-canno/
- Which industries are spending more money to influence policymakers: https://thedietwars.com/lobbying-big-meat-or-big-sugar/
- Hierarchy of evidence pyramid: https://www.researchgate.net/figure/Hierarchy-of-evidence-pyramid-The-pyramidal-shape-qualitatively-integrates-the-amount-of_fig1_311504831
- Andrew Wakefield MMR Lancet paper: https://briandeer.com/mmr/lancet-paper.htm
- Observational Studies: Cohort and Case-Control Studies: https://www.researchgate.net/publication/45583746_Observational_Studies_Cohort_and_Case-Control_Studies
- Lifetime Risk of Developing or Dying From Cancer: https://www.cancer.org/cancer/cancer-basics/lifetime-probability-of-developing-or-dying-from-cancer.html
- Vegetarian Dietary Patterns and Mortality in Adventist Health Study 2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191896/
- Carnivores Try Statistics: Relative Risk Too Low Tho: https://www.youtube.com/watch?v=3ePYPWs-oBY
- HOW TO INTERPRET EPIDEMIOLOGICAL ASSOCIATIONS: https://www.who.int/water_sanitation_health/dwq/nutrientschap9.pdf
- Carcinogenicity of consumption of red and processed meat: https://www.researchgate.net/publication/283443910_Carcinogenicity_of_consumption_of_red_and_processed_meat
- Heme iron from meat and risk of adenocarcinoma of the esophagus and stomach: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261306/
- Red and processed meat consumption and colorectal cancer risk: a systematic review and meta-analysis: https://www.oncotarget.com/article/20667/text/
- Meat consumption and risk of 25 common conditions: outcome-wide analyses in 475,000 men and women in the UK Biobank study: https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-021-01922-9
- Effects of red meat, white meat, and nonmeat protein sources on atherogenic lipoprotein measures in the context of low compared with high saturated fat intake: a randomized controlled trial: https://academic.oup.com/ajcn/article/110/1/24/5494812
- History of evidence-based medicine: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263217/
- Disease Consequences of Cigar Smoking: https://www.researchgate.net/publication/265537122_Disease_Consequences_of_Cigar_Smoking
- The Polyp Prevention Trial: https://cebp.aacrjournals.org/content/cebp/16/9/1745.full.pdf
- Low-Fat Dietary Pattern and Cancer Mortality in the Women’s Health Initiative (WHI) Randomized Controlled Trial: https://academic.oup.com/jncics/article/2/4/pky065/5278702
- Red and Processed Meat and Colorectal Cancer Incidence: Meta-Analysis of Prospective Studies: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0020456
- Normal LDL-Cholesterol Levels Are Associated With Subclinical Atherosclerosis in the Absence of Risk Factors: https://www.sciencedirect.com/science/article/pii/S0735109717412320
- Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines [PDF]: http://scholar.google.com/scholar_lookup?hl=en&volume=157&publication_year=2009&pages=111-117&author=A+Sachdeva&author=CP+Cannon&author=PC+Deedwania&title=Lipid+levels+in+patients+hospitalized+with+coronary+artery+disease%3A+an+analysis+of+136%2C905+hospitalizations+in+get+with+the+guidelines
- Cholesterol Levels Decrease soon after Acute Myocardial Infarction: https://pubmed.ncbi.nlm.nih.gov/26233997/
- Lipid Profile of Patients with Acute Myocardial Infarction (AMI): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6519978/
- Statins, Low-Density Lipoprotein Cholesterol, and Risk of Cancer: https://www.sciencedirect.com/science/article/pii/S0735109708023966
- Lack of effect of lowering LDL cholesterol on cancer: meta-analysis of individual data from 175,000 people in 27 randomised trials of statin therapy: https://pubmed.ncbi.nlm.nih.gov/22276132/
- Statin and Cancer Mortality and Survival: An Umbrella Systematic Review and Meta-Analysis: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074262/
- Statins and prevention of infections: systematic review and meta-analysis of data from large randomised placebo controlled trials: https://www.bmj.com/content/343/bmj.d7281
- Low-Density Lipoprotein Cholesterol and the Risk of Cancer: A Mendelian Randomization Study: https://academic.oup.com/jnci/article/103/6/508/2568717
- In-depth Mendelian randomization analysis of causal factors for coronary artery disease: https://www.nature.com/articles/s41598-020-66027-4
- Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel: https://academic.oup.com/eurheartj/article/38/32/2459/3745109
- LDL Denialists: The Ramblings of Uffe Ravnskov: https://www.mynutritionscience.com/ldldenialists/
- The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.841.9606&rep=rep1&type=pdf
- Coronary Calcification, Coronary Disease Risk Factors, C-Reactive Protein, and Atherosclerotic Cardiovascular Disease Events: https://core.ac.uk/download/pdf/82432606.pdf
- Association of coronary heart disease with age-adjusted aortocoronary calcification in patients with familial hypercholesterolaemia: https://onlinelibrary.wiley.com/doi/epdf/10.1046/j.1365-2796.2000.00630.x
- Comparison of the coronary calcium score with the estimated coronary risk: https://ur.booksc.eu/book/59249641/5dd4d8
- World Health Organization–Defined Metabolic Syndrome Is a Better Predictor of Coronary Calcium Than the Adult Treatment Panel III Criteria in American Men Aged 40 –49 Years: https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.832.5827&rep=rep1&type=pdf
- Much lower prevalence of coronary calcium detected by electron-beam computed tomography among men aged 40–49 in Japan than in the US, despite a less favorable profile of major risk factors: https://www.semanticscholar.org/paper/Much-lower-prevalence-of-coronary-calcium-detected-Sekikawa-Ueshima/e1549b7df908ba88370b04ee55669ce74a4317f3
- Relationship between Obesity and Coronary Artery Disease Defined by Coronary Computed Tomography Angiography: https://www.scielo.br/j/ijcs/a/vzmnZ4Yv8Qt4JJbvXBkcyJj/?format=pdf&lang=en
- Risk Factors for the Progression of Coronary Artery Calcification in Asymptomatic Subjects: https://www.ahajournals.org/doi/10.1161/circulationaha.106.674143
- Revisiting Dietary Cholesterol Recommendations: Does the Evidence Support a Limit of 300 mg/d?: https://www.researchgate.net/publication/45495122_Revisiting_Dietary_Cholesterol_Recommendations_Does_the_Evidence_Support_a_Limit_of_300_mgd
- Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis: https://academic.oup.com/ajcn/article/73/5/885/4739583
- Pre-Menopausal Women, Classified as Hypo- or HyperResponders, do not Alter their LDL/HDL Ratio Following a High Dietary Cholesterol Challenge: https://www.internationalegg.com/app/uploads/2005/11/Eggconsumptionforpre-menopaulwomen.pdf
- Consumption of One Egg Per Day Increases Serum Lutein and Zeaxanthin Concentrations in Older Adults without Altering Serum Lipid and Lipoprotein Cholesterol Concentrations: https://academic.oup.com/jn/article/136/10/2519/4746690
- Maintenance of the LDL Cholesterol:HDL Cholesterol Ratio in an Elderly Population Given a Dietary Cholesterol Challenge: https://www.researchgate.net/publication/7452148_Maintenance_of_the_LDL_CholesterolHDL_Cholesterol_Ratio_in_an_Elderly_Population_Given_a_Dietary_Cholesterol_Challenge
- High-density lipoprotein cholesterol changes after continuous egg consumption in healthy adults: https://www.researchgate.net/publication/5279608_High-density_lipoprotein_cholesterol_changes_after_continuous_egg_consumption_in_healthy_adults
- Lipoprotein responses to weight loss and weight maintenance in high-risk obese subjects: https://www.nature.com/articles/1601375
- Cholesterol does not cause coronary heart disease in contrast to stress: https://moscow.sci-hub.se/3078/fdf6054f7084fff36fb9ebab8a501433/rosch2008.pdf
- Reduction in saturated fat intake for cardiovascular disease: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011737.pub2/full
- Meta-analysis of large randomized controlled trials to evaluate the impact of statins on cardiovascular outcomes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884492/
- Causal effects of blood lipids on amyotrophic lateral sclerosis: a Mendelian randomization study: https://academic.oup.com/hmg/article/28/4/688/5185599#130197708
- Comparison of Low Fat and Low Carbohydrate Diets on Circulating Fatty Acid Composition and Markers of Inflammation: https://www.researchgate.net/publication/5800547_Comparison_of_Low_Fat_and_Low_Carbohydrate_Diets_on_Circulating_Fatty_Acid_Composition_and_Markers_of_Inflammation
- Convincing evidence supports reducing saturated fat to decrease cardiovascular disease risk: https://nutrition.bmj.com/content/bmjnph/1/1/23.full.pdf
- Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans: https://www.aging-us.com/article/100994/text
- Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal: https://academic.oup.com/jcem/article/88/10/4525/2845681
- A Randomized Trial of a Low-Carbohydrate Diet for Obesity: https://www.researchgate.net/publication/10748749_A_Randomized_Trial_of_a_Low-Carbohydrate_Diet_for_Obesity
- The Effects of Low-Carbohydrate versus Conventional Weight Loss Diets in Severely Obese Adults: One-Year Follow-up of a Randomized Trial: https://www.acpjournals.org/doi/full/10.7326/0003-4819-140-10-200405180-00007
- Letters From the Global Literature: Unresolved Issues and Responses: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100132/
- A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: https://www.semanticscholar.org/paper/A-Low-Carbohydrate%2C-Ketogenic-Diet-versus-a-Low-Fat-Yancy-Olsen/73ca6c1890e8400c2d7591cdaa53404cd99fd149
- Weight Loss With a Low-Carbohydrate, Mediterranean, or Low-Fat Diet: https://www.researchgate.net/publication/51409896_Weight_Loss_With_a_Low-Carbohydrate_Mediterranean_or_Low-Fat_Diet
- Effect of the Anti-Coronary Club program on coronary heart disease. Risk-factor status: https://thescienceofnutrition.files.wordpress.com/2014/03/effect-of-the-anti-coronary.pdf
- A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis: https://thescienceofnutrition.files.wordpress.com/2014/03/a-controlled-clinical-trial-of-a-diet-high-in-unsaturated-fat-in-preventing-complications-of-atherosclerosis.pdf
- Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.549.6029&rep=rep1&type=pdf
- The Impact of Egg Limitations on Coronary Heart Disease Risk: Do the Numbers Add Up?: https://scholar.google.com/scholar_lookup?title=The+impact+of+egg+limitations+on+coronary+heart+disease+risk%3A+do+the+numbers+add+up%3F&author=McNamara+DJ&publication+year=2000&journal=J+Am+Coll+Nutr&volume=19&doi=10.1080%2F07315724.2000.10718978&pages=540S-548S
- A Prospective Study of Egg Consumption and Risk of Cardiovascular Disease in Men and Women: https://www.researchgate.net/publication/13081447_A_Prospective_Study_of_Egg_Consumption_and_Risk_of_Cardiovascular_Disease_in_Men_and_Women
- Effects of eggs on plasma lipoproteins in healthy populations: https://www.ovosbrasil.com.br//wp-content/uploads/2016/09/2010-Fernandez-M_Effects-of-eggs-on-plasma-lipoproteins-in-healthy-populations_Conecticut.pdf
- Effects of Insulin Resistance and Obesity on Lipoproteins and Sensitivity to Egg Feeding: https://www.ahajournals.org/doi/pdf/10.1161/01.ATV.0000082461.77557.C7
- HDL cholesterol and ASCVD risk stratification: A debate: https://doi.org/10.1016/j.atherosclerosis.2019.01.001
- High Intake of Cholesterol Results in Less Atherogenic Low-Density Lipoprotein Particles in Men and Women Independent of Response Classification: https://www.ovosbrasil.com.br//wp-content/uploads/2016/09/2004-Herron_High-Intake-of-Cholesterol-Results-in-Less-Atherogenic-Low-Density-Lipoprotein-Particles-in-Men-and-Women-Independent-of-Response-Classification_EUA.pdf
- The responses of different dosages of egg consumption on blood lipid profile: An updated systematic review and meta‐analysis of randomized clinical trials: https://www.researchgate.net/publication/342100187_The_responses_of_different_dosages_of_egg_consumption_on_blood_lipid_profile_An_updated_systematic_review_and_meta-analysis_of_randomized_clinical_trials
- Saturated fat and heart disease: https://academic.oup.com/ajcn/article/92/2/459/4597396
- Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence: https://www.researchgate.net/publication/42768984_Saturated_Fat_and_Cardiometabolic_Risk_Factors_Coronary_Heart_Disease_Stroke_and_Diabetes_a_Fresh_Look_at_the_Evidence
- The short- and long-term effects of a low-fat, cholesterol-free, hypocaloric diet on serum triglyceride and cholesterol distribution in severely obese humans: https://pubmed.ncbi.nlm.nih.gov/3570636/
- Saturated Fatty Acids and Risk of Coronary Heart Disease: Modulation by Replacement Nutrients: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943062/
- Food groups and risk of all-cause mortality: a systematic review and meta-analysis of prospective studies: https://academic.oup.com/ajcn/article/105/6/1462/4569801
- Health Risks Associated with Meat Consumption: A Review of Epidemiological Studies: https://econtent.hogrefe.com/doi/10.1024/0300-9831/a000224
- Meta-Analysis of Randomized Controlled Trials of Red Meat Consumption in Comparison With Various Comparison Diets on Cardiovascular Risk Factors: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.035225
- Correction: Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: https://www.acpjournals.org/doi/10.7326/L14-5009-9
- https://cdn.discordapp.com/attachments/495731928608145415/495778169597460500/Chowdhurry_editor_debates.pdf
- https://cdn.discordapp.com/attachments/846223699056394241/858526345654042624/CONTROLLED_TRIAL_OF_SOYA-BEAN_OIL_IN_MYOCARDIAL_INFARCTION.pdf
- https://www.google.com/url?client=internal-element-cse&cx=partner-pub-4875515510538773:2201650450&q=https://academic.oup.com/eurheartjsupp/article-pdf/3/suppl_D/D75/9795901/D75.pdf&sa=U&ved=2ahUKEwi52OvDgbfxAhUeAhAIHUNaCUwQFjACegQICRAB&usg=AOvVaw2KrYQXKJd3NptftVMaiKKX
- LOW-FAT DIET IN MYOCARDIAL INFARCTION: https://thescienceofnutrition.files.wordpress.com/2014/03/low-fat-diet-in-myocardial-infarction-a-controlled-trial.pdf
- A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis: https://thescienceofnutrition.files.wordpress.com/2014/03/a-controlled-clinical-trial-of-a-diet-high-in-unsaturated-fat-in-preventing-complications-of-atherosclerosis.pdf
- Review Sows Confusion About Saturated Fats: https://matt576.medium.com/study-sows-confusion-about-saturated-fats-d494ad8c9310
- A meta-analysis of randomized controlled trials that compare the lipid effects of beef versus poultry and/or fish consumption: https://beeflovingtexans.com/wp-content/uploads/2018/07/Maki.pdf
- Adult Obesity Facts: https://www.cdc.gov/obesity/data/adult.html
- Health Risks Associated with Meat Consumption: A Review of Epidemiological Studies: https://econtent.hogrefe.com/doi/pdf/10.1024/0300-9831/a000224
- Food groups and risk of type 2 diabetes mellitus: a systematic review and meta-analysis of prospective studies: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506108/
- Editorial: The Validity of Self-reported Dietary Intake Data: Focus on the “What We Eat In America” Component of the National Health and Nutrition Examination Survey Research Initiative: https://www.mayoclinicproceedings.org/article/S0025-6196(15)00394-8/fulltext
- https://twitter.com/dylanarmbruste3/status/1387442008558477316
- Concordance Between the Findings of Epidemiological Studies and Randomized Trials in Nutrition: An Empirical Evaluation and Citation Analysis: https://www.ncbi.nlm.nih.gov/books/NBK138246/
- Unprocessed Red Meat and Processed Meat Consumption: Dietary Guideline Recommendations From the Nutritional Recommendations (NutriRECS) Consortium: https://www.acpjournals.org/doi/10.7326/M19-1621
- https://www.truehealthinitiative.org/wp-content/uploads/2019/09/Annals-letter-9-30-19.pdf
- Patterns of Red and Processed Meat Consumption and Risk for Cardiometabolic and Cancer Outcomes: https://www.acpjournals.org/doi/full/10.7326/M19-1583
- The Roseto Effect: A 50-Year Comparison of Mortality Rates: https://ajph.aphapublications.org/doi/pdf/10.2105/AJPH.82.8.1089
- Roseto, Pennsylvania 25 years later — highlights of a medical and sociological survey: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376462/
- Health and Greenhouse Gas Emission Implications of Reducing Meat Intakes in Hong Kong: https://publications.waset.org/10006219/health-and-greenhouse-gas-emission-implications-of-reducing-meat-intakes-in-hong-kong
- ASSOCIATION OF HIGH DIETARY PROTEIN INTAKE WITH THE RISK OF WEIGHT GAIN AND TOTAL DEATH IN SUBJECTS AT HIGH RISK OF CARDIOVASCULAR DISEASE: https://www.researchgate.net/publication/279977231_ASSOCIATION_OF_HIGH_DIETARY_PROTEIN_INTAKE_WITH_THE_RISK_OF_WEIGHT_GAIN_AND_TOTAL_DEATH_IN_SUBJECTS_AT_HIGH_RISK_OF_CARDIOVASCULAR_DISEASE
- Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. A paradox: https://www.ahajournals.org/doi/10.1161/01.CIR.88.6.2771
- Influence of Alcohol and Red Meat Consumption on Life Expectancy: Results of 164 Countries from 1992 to 2013: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071474/
- Caloric Restriction, the Traditional Okinawan Diet, and Healthy Aging: The Diet of the World’s Longest-Lived People and Its Potential Impact on Morbidity and Life Span: https://www.researchgate.net/publication/5859391_Caloric_Restriction_the_Traditional_Okinawan_Diet_and_Healthy_Aging_The_Diet_of_the_World%27s_Longest-Lived_People_and_Its_Potential_Impact_on_Morbidity_and_Life_Span
- https://veganhealth.org
- https://www.theveganrd.com
- https://eatforum.org/initiatives/fresh/
- Blood docosahexaenoic acid and eicosapentaenoic acid in vegans: Associations with age and gender and effects of an algal-derived omega-3 fatty acid supplement: https://www.clinicalnutritionjournal.com/article/S0261-5614(14)00076-4/fulltext
- Association between plant-based diets and plasma lipids: a systematic review and meta-analysis: www.ncbi.nlm.nih.gov/pmc/articles/PMC5914369/
- A Comprehensive Review of the Prevention and Treatment of Heart Disease with a Plant-Based Diet: https://juniperpublishers.com/jocct/pdf/JOCCT.MS.ID.555847.pdf
- Micronutrient status and intake in omnivores, vegetarians and vegans in Switzerland: https://www.researchgate.net/publication/283260354_Micronutrient_status_and_intake_in_omnivores_vegetarians_and_vegans_in_Switzerland
- Comparison of Correlates of Bone Mineral Density in Individuals Adhering to Lacto-Ovo, Vegan, or Omnivore Diets: A Cross-Sectional Investigation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4446759/
- Plasma and urine taurine levels in vegans: https://academic.oup.com/ajcn/article-abstract/47/4/660/4694739?redirectedFrom=fulltext
- Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline: https://www.ncbi.nlm.nih.gov/books/NBK114302/
- Vegetarianism and eating disorders: association between eating attitudes and other psychological factors among Turkish adolescents: http://yunus.hacettepe.edu.tr/~tonta/courses/fall2007/sb5002/vegetarianism.pdf
- Vegetarian diets and depressive symptoms among men: https://www.researchgate.net/publication/318747842_Vegetarian_diets_and_depressive_symptoms_among_men
- The state of mind of vegetarians: Psychological well-being or distress?: https://www.researchgate.net/publication/235630786_The_state_of_mind_of_vegetarians_Psychological_well-being_or_distress
- Characteristics of Vegetarian Adolescents in a Multiethnic Urban Population: https://www.humanesociety.org/sites/default/files/archive/assets/pdfs/farm/veg_adolescents_perry2001.pdf
- Examining the “Veggie” Personality: Results from a Representative German Sample: https://www.diw.de/documents/publikationen/73/diw_01.c.571626.de/diw_sp0941.pdf
- Will the real vegetarian please stand up? An investigation of dietary restraint and eating disorder symptoms in vegetarians versus non-vegetarians: https://foodethics.univie.ac.at/fileadmin/user_upload/p_foodethik/Timko__C.__2012._Will_the_real_vegetarian_please_stand_up.pdf
- A Multicenter Randomized Controlled Trial of a Nutrition Intervention Program in a Multiethnic Adult Population in the Corporate Setting Reduces Depression and Anxiety and Improves Quality of Life: The GEICO Study: https://www.researchgate.net/publication/260193549_A_Multicenter_Randomized_Controlled_Trial_of_a_Nutrition_Intervention_Program_in_a_Multiethnic_Adult_Population_in_the_Corporate_Setting_Reduces_Depression_and_Anxiety_and_Improves_Quality_of_Life_The
- Changing to a vegetarian diet reduces the body creatine pool in omnivorous women, but appears not to affect carnitine and carnosine homeostasis: A randomised trial: https://www.researchgate.net/publication/323968303_Changing_to_a_vegetarian_diet_reduces_the_body_creatine_pool_in_omnivorous_women_but_appears_not_to_affect_carnitine_and_carnosine_homeostasis_A_randomised_trial
- What Are Eating Disorders?: https://www.psychiatry.org/patients-families/eating-disorders/what-are-eating-disorders
- DSM-5 Changes: Implications for Child Serious Emotional Disturbance [Internet]: https://www.ncbi.nlm.nih.gov/books/NBK519712/table/ch3.t18/
- https://youtu.be/LXh0Pzw3LVc?t=554
- https://youtu.be/ZuXAk4i-UrQ?t=306
- https://youtu.be/LXh0Pzw3LVc?t=1411
- Prevalence, knowledge and attitudes towards using sports supplements among young athletes: https://jissn.biomedcentral.com/articles/10.1186/s12970-019-0294-7
- Vegan Diet in Sports and Exercise — Health Benefits and Advantages to Athletes and Physically Active People: A Narrative Review: https://clinmedjournals.org/articles/ijsem/international-journal-of-sports-and-exercise-medicine-ijsem-6-165.pdf
- Vegetarian and Omnivorous Nutrition — Comparing Physical Performance: https://www.researchgate.net/publication/283495301_Vegetarian_and_Omnivorous_Nutrition_-_Comparing_Physical_Performance
- Update on vegetarian and vegan athletes: a review: https://www.researchgate.net/publication/348441698_Update_on_vegetarian_and_vegan_athletes_a_review
- A Mediterranean Diet and Low-Fat Vegan Diet to Improve Body Weight and Cardiometabolic Risk Factors: A Randomized, Cross-over Trial: https://www.tandfonline.com/doi/full/10.1080/07315724.2020.1869625
- Phylogenetic rate shifts in feeding time during the evolution of Homo: www.ncbi.nlm.nih.gov/pmc/articles/PMC3167533/
- The Importance of Dietary Carbohydrate in Human Evolution: https://www.researchgate.net/publication/280735260_The_Importance_of_Dietary_Carbohydrate_in_Human_Evolution
- Influence of the Mediterranean and Ketogenic Diets on Cognitive Status and Decline: A Narrative Review: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231139/
- Effect of a 6-month vegan low-carbohydrate (‘Eco-Atkins’) diet on cardiovascular risk factors and body weight in hyperlipidaemic adults: a randomised controlled trial: https://bmjopen.bmj.com/content/4/2/e003505
- Are Bigger Brains Smarter? Evidence From a Large-Scale Preregistered Study: https://journals.sagepub.com/doi/10.1177/0956797618808470
- Latitudinal variation in light levels drives human visual system size: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259958/
- Altered Fine Motor Function at School Age in Inuit Children Exposed to PCBs, Methylmercury, and Lead: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5035542/
- Raw Food Consumption And Its Effects On Human Health: An Analysis Of Halalan Toyyiban Concept: https://www.researchgate.net/publication/328804579_Raw_Food_Consumption_And_Its_Effects_On_Human_Health_An_Analysis_Of_Halalan_Toyyiban_Concept
- An overview of factors influencing the health of Canadian Inuit infants: https://www.tandfonline.com/doi/pdf/10.3402/ijch.v62i1.17526
- The energetic significance of cooking: https://www.semanticscholar.org/paper/The-energetic-significance-of-cooking.-Carmody-Wrangham/9fdf0152f8fd809c8277a95390f64de68954dfaa
- The plant component of an Acheulian diet at Gesher Benot Ya‘aqov, Israel: https://www.pnas.org/content/113/51/14674
- The Role of Insulin in Human Brain Glucose Metabolism: https://diabetes.diabetesjournals.org/content/51/12/3384
- Hypoglycemia in Non-Diabetic In-Patients: Clinical or Criminal?: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388042/
- A plant-based diet for the prevention and treatment of type 2 diabetes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5466941/
- https://www.youtube.com/watch?v=M8GhWgy5g_8
- HSPH’s Walter Willett endorses sugary drinks ban on Boston city property: https://www.hsph.harvard.edu/news/hsph-in-the-news/sugary-beverages-boston-ban/
- Holes in Harvard Sugar Study Expose Dangers of Industry Funding: https://www.thecrimson.com/article/2016/9/14/sugar-study-exposes-dangers/
- Evaluating agreement between bodies of evidence from randomised controlled trials and cohort studies in nutrition research: meta-epidemiological study: https://www.bmj.com/content/374/bmj.n1864
