The Winter of Their Discontent

I realize it’s currently summer. But someone forwarded to me the post of yet another ex-vegan food blogger who divulged to the world this past winter that she was giving up the vegan diet. This time it was Kristen of KristenRaw.com in her post of March 17, 2013, My Vegan Diet Caused Health Problems. Would Primal, Paleo, Or “Real Food” Be Better?

A few paragraphs in, Kristen lists a couple of common threads that she has noticed among the meat-curious vegans:

“We were vegan, some quite smugly, thinking it was the human ideal of a smart-n-healthy diet, but then, only after several years, started to experience health problems, and then switched back to omnivore, and the health problems disappeared….What we also have in common — made somewhat easy no doubt due to having adapted to a strict (vegan) diet for many years — are the strict kinds of omnivore foods we eat now vs what we were eating pre-vegan….Even more so for former raw fooders, whose restrictions (such as avoiding grains) make some vegans’ diets look like junk food.”

Kristen’s story is the typical one – she became vegan for animal rights reasons and at first she did great on the vegan diet and got into raw foodism, etc. After a few years she started to not feel so well, she tried everything to make it better, she went back to eating animal products and within hours she started to have a miraculous turn around in her health.

She originally tried to counter her health problems with, “superfoods, fancy juicers, superherbs, tonic herbs, prepping foods various ways to optimize nutrients, following rules for combining or not combining certain foods like having vitamin c with iron rich plants – just to name a few….”

Although there isn’t much to indicate that Kristen was suffering from iron deficiency, I’m impressed with her attempt to add vitamin C to meals with iron rich plants which is scientifically based. In terms of the rest of her attempts to reclaim her health, if only she knew about all the vegans who are not failing, who she might describe as “junk food vegans.”

At one point, Kristen’s cholesterol was measured at 95 mg/dl. Her animal food cravings started out with “dreams of eggs.” Craving eggs seems to be a common theme, and I take the egg cravings as a possible sign of nutrient deficiency for a few reasons. One, eggs are fairly disgusting, especially if you haven’t eaten them in a long time and don’t happen to be craving them. If someone said they were craving Häagen-Dazs, I’d be skeptical of a nutritional basis. KFC? Might be the 11 herbs and spices. But eggs? Something must going on here.

To sum up the situation, we have someone with very low cholesterol at 95 mg/dl craving one of the main sources of cholesterol, eggs. And after eating animal products, she quickly started to feel better. Following Occam’s razor, it seems to me a safe bet that she was craving eggs because her body needed cholesterol and she improved so quickly because she got an immediate boost from it.

Admittedly, I don’t know for certain if this is what is going on. Eggs are also high in choline and sulfur. And perhaps people just cannot crave what they need and these cravings are the brain misfiring. But, in my humble opinion, the evidence is mounting to implicate low cholesterol in many of these cases of failed raw foods/whole foods vegans.

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89 Responses to “The Winter of Their Discontent”

  1. Richard Says:

    “That’s interesting. Kristen’s cholesterol was 95 mg/dl, quite a bit lower than 110 to 150. I say it’s interesting because about 110 mg/dl is about the cutoff where people who write me with problems that I cannot pin on anything else”.

    Jack,

    a low cholesterol level may be a marker for poor nutrition, wasting disease, cancer, hyperthyroidism, and liver disease. There’s actually people who are with insanely low cholesterol levels (hypobetalipoprotenemia) and MOST of them do well, and in fact tend to live 9-12 years longer than their peers.

  2. Jack Norris RD Says:

    Richard,

    > people who are with insanely low cholesterol levels (hypobetalipoprotenemia) and MOST of them do well, and in fact tend to live 9-12 years longer than their peers

    I’ve looked for information on this and haven’t found any. Do you have citations for studies showing these people live longer? I’d be interested to know. But even if this is the case, it doesn’t mean that Kristen’s low cholesterol level wasn’t a problem for how she felt and her disrupted menstrual cycle and that eating cholesterol and saturated fat didn’t do a great deal to ameliorate her problems.

  3. Richard Says:

    Jack,

    Only those with the most severe forms homozygot hypobetalipoprotenemia face problems, but most of the cases are bening and leaves their carries with improved longevity and good health.

    See Daniel Steinberg’s article for sources:

    “Third, in some kindreds with hypobetalipoproteinemia, LDL cholesterol levels can be <15 mg/dL throughout life, yet the affected members show perfectly normal growth and development and actually have increased longevity.40,41"

    http://circ.ahajournals.org/content/118/6/672.full

    In addition see,

    Familial Hypobetalipoproteinemia: Absence of Atherosclerosis in a Postmortem Study
    http://jama.jamanetwork.com/article.aspx?articleid=360289

    Glueck C.J, Kelley W, Gupta A, Fontaine R.N, Wang P, Gartside P.S; Prospective 10-year evaluation of hypobetalipoproteinemia in a cohort of 772 firefighters and cross-sectional evaluation of hypocholesterolemia in 1,479 men in the National Health and Nutrition Examination Survey I. Metabolism. 46 1997:625-633.

    People at SW medical center have identified people with homozygot PCSKY-9 knock-out mutation; these people have their life-time LDLs around 7-14mg/dl, all so far identified individuals have been in excellent health.

    Rare Mutation Ignites Race for Cholesterol Drug
    http://www.nytimes.com/2013/07/10/health/rare-mutation-prompts-race-for-cholesterol-drug.html?pagewanted=1&smid=tw-share&_r=0

  4. Jack Norris RD Says:

    Thanks, Richard. I’ll check it out.

  5. Dan Says:

    People with a PCSK9 genetic mutation have lifelong lower LDL cholesterol levels and their rate of cardiovascular events is approximately 50% lower than the rest of the population (http://www.ncbi.nlm.nih.gov/pubmed/16554528). See also http://www.ncbi.nlm.nih.gov/pubmed/23083789

    Periods of rapid weight loss can actually cause transient hypercholesterolemia as shrinking adipose cells liberate stored cholesterol (http://www.ncbi.nlm.nih.gov/pubmed/2035468). Clearly that was not the case here.

    I have seen many individuals with ultra-low LDL cholesterols on statins and other lipid meds who are thriving. They do not seem to complain about craving eggs or other cholesterol-rich sources, although I suppose it’s possible.

    The only way to properly test the hypothesis that diet-induced hypocholesterolemia caused craving in this case is to give a cholesterol supplement and see if the craving is attenuated. However, the 40% of people who strongly respond to placebos would mean you would have to do a placebo-controlled blinded n-of-1 trial to see.

    As mentioned previously, some people tolerate ultra-low fat diets (Ornish, Esselstyn, etc) but there could be key genetic differences between tolerators and non-tolerators and it’s certainly possible that this individual was genetically predestined to be a non-tolerator. Speaking only from my own case, I seem to require a certain amount of fat to induce satiety. There are genetic polymorphisms involved in weight loss response to specific diets so I do not see why other (or the same) genes could underpin craving, if it is truly based on biochemistry and not just culture and psychology.

  6. Tyler Says:

    I found this amusing, someone asking about a tofu craving on “paleo hacks”:

    http://paleohacks.com/questions/207582/craving-tofu-why

  7. Tyler Says:

    Dan:

    “As mentioned previously, some people tolerate ultra-low fat diets (Ornish, Esselstyn, etc) but there could be key genetic differences between tolerators and non-tolerators and it’s certainly possible that this individual was genetically predestined to be a non-tolerator.”

    What reason is there to believe, excluding potential diseases/genetic disorders, that there are such non-tolerators? Are there studies that demonstrate this? Given the large number of diverse societies that have subsisted on a low-fat diet, its hard to believe that non-tolerators would exist beyond rare genetic disorders/those with diseases.

  8. Dan Says:

    Tyler, are you familiar with the concept of genetic diversity between individuals and populations? It is the underpinning of evolutionary biology. I am trying to posit reasons for why this individual, or any individual for that matter, might not be able to tolerate a very low fat diet. Could it be that fat is satiating to some individuals? Is this genetic, biochemical, psychological or cultural? There are more genetic differences than “meet the eye” (see for example http://www.ncbi.nlm.nih.gov/pubmed/23446828). Many people have complained that they just can’t hack a low fat, or very low fat, diet.

  9. Tyler Says:

    Dan:

    Yes, there is genetic diversity between individuals and ethnic groups…..but you’re putting the cart before the horse. As I asked, what reason is there to believe that there is a class of healthy people that can’t tolerate low-fat diets? Before we try to give an explanation, shouldn’t one confirm the existence of this class of people? Personal anecdotes aren’t evidence, when people change their diets there are tons of confounding variables and there are plenty of ways one could craft a unhealthy low-fat diet. If we were to take such personal anecdotes seriously, one should also make similar conclusions about vegetarian and vegan diets. Perhaps there is a class of people that can’t thrive on a vegan diet? Plenty of personal anecdotes of people suggesting that this is the case….so perhaps the group is pretty big.

    Absence serious evidence that such a class of people exist, I think the hypothesis is implausible. Low-fat diets are extremely common in human populations, any genes that prevented one from thriving on such diets would quickly be eliminated. This is especially true of “civilized” populations, for example, until somewhat recently the vast majority of Europeans were consuming a semi-vegetarian diet rich in whole grains and legumes where fat intake would have been between 10~20%.

  10. Dan Says:

    >>As I asked, what reason is there to believe that there is a class of healthy people that can’t tolerate low-fat diets?

    ….from dropout rates in trials comparing different macronutrient compositions. There are fairly equal dropout rates on low fat vs low carb diets – so I take this to mean that some people do best on a certain type of diet (whether for cultural, psychological or physiological reasons who knows?).

    >>Perhaps there is a class of people that can’t thrive on a vegan diet?

    From all the reports on the internet, it seems to be a pretty big group. Likely they have not balanced their diet properly and therefore are missing key micro or macronutrients.

    >>until somewhat recently the vast majority of Europeans were consuming a semi-vegetarian diet rich in whole grains and legumes where fat intake would have been between 10~20%.

    I don’t find these cross-cultural comparisons to be very enlightening any more. People adapt to whatever the local climate and cuisine would support. Humans, like canids, are scavengers. Just because one group of people eat a certain macronutrient composition does not mean this should be extrapolated to all people (I believe the paleo dieters make the same mistake). Anyway, the evidence is that macronutrient distributions (fat:protein:carb) vary dramatically in pre-westernized cultures. Look at the local fauna and flora, and what instruments are available and whether the society is agricultural, nomadic, hunger-gatherer, etc – that will determine what people eat. And I don’t think that people who are genetically intolerant of low fat diets would have died off – they could simply have moved to areas with abundant game – we know humans are incredibly nomadic.

  11. Jack Norris RD Says:

    Commenter Richard above said this:

    2) Optimal low density lipoprotein is 50 to 70 mg/dl; lower is better and physiologically normal
    http://content.onlinejacc.org/article.aspx?articleid=1135650

    That paper is just a review paper and they say:

    “Evidence from hunter-gatherer populations while they were still following their indigenous lifestyles showed no evidence for atherosclerosis, even in individuals living into the seventh and eighth decades of life (15,16). These populations had total cholesterol levels of 100 to 150 mg/dl…”

    So is citation 15 a study that measured the cholesterol levels of such people? Of course not. It’s a citation for another review:

    Cordain L, Eaton SB, Brand Miller J, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: meat based, yet non- atherogenic. Eur J Clin Nutr 2002;56 Suppl 1:S42–52.

    And Cordain et al’s review says:

    “Over the past 64y, anthropological research has consis- tently demonstrated relatively low serum cholesterol and triacylglycerol levels among indigenous populations that derive the majority of their diet from animal products (Bang & Dyerberg, 1980; Biss et al, 1971; Corcoran & Rabinowitch, 1937; Day et al, 1976; Eaton et al, 1988a; Leonard et al, 1994; Scott et al, 1958; Shaper et al, 1961; Wilber & Levine, 1950).”

    The full Bang & Dyerberg citation is:

    Bang HO & Dyerberg J (1980): Lipid metabolism and ischemic heart
    disease in Greenland Eskimos. Adv. Nutr. Res. 3, 1 – 22.

    I can only find this paper cited, I cannot find an actual abstract for this paper. Anyone else want to try?

    Interestingly, Cordain also says:

    “For the majority (53%, n = 122) of the world’s foraging cultures the dietary fat intake would lie between 36 and 43% of total energy (Cordain et al, 2000a),..”

    Not exactly an argument for very low-fat diets.

    I’m now tracking down the second citation for Cordain. If that doesn’t bear fruit, I’m probably going to quit this (excuse the non-vegan phrase) wild goose chase.

  12. Dan Says:

    Jack are you familiar with this paper? http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0006590

    Tsimane are an amazonian tribe of hunter-foragers. mean+/-SD
    total cholesterol, 138+/-29 mg/dL and LDL, 75+/-22 mg/dL. These are very low values. They don’t get arterial disease. The mean total LDL in those who are 70+ years old is only 120 mg/dL. Compare that with US figures.

    “Whereas no Tsimane show high risk levels of total cholesterol and LDL, 20% of U.S. adults have elevated levels of each blood lipid, even though many Americans use lipid-lowering medications. The prevalence of high triglycerides for most age groups in the U.S. is double that of the Tsimane. There is little indication of age increases in these measures among Tsimane. Values are similar across ages after 40 and do not show increased CVD risk at older ages in any parameter”

    What is the actual question you are trying to answer? What lipid levels are like in indigenous vegans or near-vegans?

  13. Jack Norris RD Says:

    > What is the actual question you are trying to answer?

    At what level does low cholesterol become a problem. I’ve narrowed it down to somewhere between 160 and 0 mg/dl.

    And what I’m currently doing is weeding through many of the links people provided me with in this thread and checking them out.

  14. Dan Says:

    According to this follow-up paper from the same group (http://www.ncbi.nlm.nih.gov/pubmed/20721985), total cholesterol in 415 Tsimane people was mean 138.0, with a range of 69 to 258.

    In a follow-up paper, they demonstrate that these people lack the ‘normal’ increase in BP seen with aging – http://www.ncbi.nlm.nih.gov/pubmed/22700319

    Prevalence of hypertension is far below that seen in the West too (in Canada about 20% of the population has hypertension).

    On the other hand, they carry a lot of parasites and get a lot of infectious diseases, but don’t appear to develop cardiovascular disease.

  15. Jack Norris RD Says:

    > According to this follow-up paper from the same group (http://www.ncbi.nlm.nih.gov/pubmed/20721985), total cholesterol in 415 Tsimane people was mean 138.0, with a range of 69 to 258. On the other hand, they carry a lot of parasites and get a lot of infectious diseases, but don’t appear to develop cardiovascular disease.

    Good, then we can strive for a cholesterol level between 69 and 258 mg/dl.

  16. Tyler Says:

    “For the majority (53%, n = 122) of the world’s foraging cultures the dietary fat intake would lie between 36 and 43% of total energy (Cordain et al, 2000a),..”

    Not exactly an argument for very low-fat diets”

    But what is it an argument for exactly? Not much. Nearly everything about his study is problematic, but even if we assume its accurate it doesn’t tell us anything. Hunter and gather societies represent a very small fraction of the human population over the last ~10,000 years and we really have no idea whether modern hunter gathers are representative of how people lived 10,000+ years ago. The vast majority of people were horticulturists and agriculturists and these populations tend to eat lower fat diets since most food staples were starchy low-fat crops. In this context, its very unlikely that genes that prohibited one from subsisting on low-fat diets would be common.

    Of course all this is conjecture, what you need are studies that show that there is a class of healthy people that can’t tolerate low-fat diets. Do you know of such a study?

  17. Tyler Says:

    Dan:

    ….from dropout rates in trials comparing different macronutrient compositions. There are fairly equal dropout rates on low fat vs low carb diets – so I take this to mean that some people do best on a certain type of diet.

    There is another explanation, namely, people have trouble alternating their long-term habits and/or have trouble adopting a lifestyle that runs counter to mass society. We know that both of these psychological factors exist while no studies have shown that there are some people that “need more fat’ and others that “need less fat”.

    “Likely they have not balanced their diet properly and therefore are missing key micro or macronutrients.”

    Right..and my point of mentioning this is to point out that you guys aren’t being consist. When personal anecdotes conflict with something you want to believe then they are explained away by “missing some micro-nutrient, etc” but when personal anecdotes corroborate what you wish to believe they are supporting evidence. Its the confirmation bias at work….

    But in this case, its a bit strange because the person being discussed didn’t even have a low-fat diet…yet its being blamed.

    “I don’t find these cross-cultural comparisons to be very enlightening any more. People adapt to whatever the local climate and cuisine would support. Humans, like canids, are scavengers. Just because one group of people eat a certain macronutrient composition does not mean this should be extrapolated to all people (I believe the paleo dieters make the same mistake). Anyway, the evidence is that macronutrient distributions (fat:protein:carb) vary dramatically in pre-westernized cultures. Look at the local fauna and flora, and what instruments are available and whether the society is agricultural, nomadic, hunger-gatherer, etc ”

    I wasn’t making a cross-cultural comparison, nor was I suggesting one should use this information to extrapolate a diet…instead I was making an evolutionary argument. For the last ~10,000 years or so the vast majority of people subsisted on lower fat diets and there would have been intense selection pressure against genes that made it difficult for one to thrive on lower fat diets.

    Macro-nutrient ratios likely varied a lot before agriculture, but not so much after and the last 10,000 years would have changed our underlying biology.

  18. Dan Says:

    J Am Coll Cardiol. 2011 Apr 19;57(16):1666-75. doi: 10.1016/j.jacc.2010.09.082.
    Cardiovascular event reduction and adverse events among subjects attaining low-density lipoprotein cholesterol <50 mg/dl with rosuvastatin. The JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin).
    Hsia J, MacFadyen JG, Monyak J, Ridker PM.
    Source
    AstraZeneca LP, 1800 Concord Pike, Wilmington, DE 19850-5437, USA. judith.hsia@astrazeneca.com
    Abstract
    OBJECTIVES:
    The purpose of this study was to assess the impact on cardiovascular and adverse events of attaining low-density lipoprotein cholesterol (LDL-C) levels <50 mg/dl with rosuvastatin in apparently healthy adults in the JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) trial.
    BACKGROUND:
    The safety and magnitude of cardiovascular risk reduction conferred by treatment to LDL-C levels below current recommended targets remain uncertain.
    METHODS:
    A cohort of 17,802 apparently healthy men and women with high-sensitivity C-reactive protein ≥2 mg/l and LDL-C <130 mg/dl were randomly allocated to rosuvastatin 20 mg daily or placebo, and followed up for all-cause mortality, major cardiovascular events, and adverse events. In a post-hoc analysis, participants allocated to rosuvastatin were categorized as to whether or not they had a follow-up LDL-C level <50 mg/dl.
    RESULTS:
    During a median follow-up of 2 years (range up to 5 years), rates of the primary trial endpoint were 1.18, 0.86, and 0.44 per 100 person-years in the placebo group (n = 8,150) and rosuvastatin groups without LDL-C <50 mg/dl (n = 4,000) or with LDL-C <50 mg/dl (n = 4,154), respectively (fully-adjusted hazard ratio: 0.76; 95% confidence interval: 0.57 to 1.00 for subjects with no LDL-C <50 mg/dl vs. placebo and 0.35, 95% confidence interval: 0.25 to 0.49 for subjects attaining LDL-C <50 mg/dl; p for trend <0.0001). For all-cause mortality, corresponding event rates were 0.67, 0.65, and 0.39 (p for trend = 0.004). Rates of myalgia, muscle weakness, neuropsychiatric conditions, cancer, and diabetes mellitus were not significantly different among rosuvastatin-allocated participants with and without LDL-C <50 mg/dl.
    CONCLUSIONS:
    Among adults with LDL-C <130 mg/dl and high-sensitivity C-reactive protein ≥2 mg/l, rosuvastatin-allocated participants attaining LDL-C <50 mg/dl had a lower risk of cardiovascular events without a systematic increase in reported adverse events.

    Jack, you have a great sense of humor, which I suppose you need with this website! You've got a lot of cranks posting – like me! 🙂

    PS, two last questions re: DHA. If it is critical for neurosynaptic function, as the basic science suggests, why would lifelong vegans who are DHA-deprived for decades only be developing cognitive dysfunction after age 60? I have seen dementia in people under the age of 60 – it is not uncommon – and presumably those vegans who develop DHA-induced cognitive dysfunction or dementia must have genetic vulnerabilities predisposing them to the effects of ultra-low DHA levels in their diet. I have one lady with florid frontotemporal dementia in her early 50's (not a vegan!).

    Second question – why recommend DHA every 2-3 days? Is it because vegan DHA is expensive? But if DHA is critical for some individuals, and dementia takes years to develop, why wait until age 60 to start it every day? (and miss 60 years of neural existence)

  19. Jack Norris RD Says:

    Dan,

    I don’t consider you a crank. You seem genuinely interested in finding out what’s true rather than defending a particular point of view.

    > PS, two last questions re: DHA. If it is critical for neurosynaptic function, as the basic science suggests, why would lifelong vegans who are DHA-deprived for decades only be developing cognitive dysfunction after age 60? I have seen dementia in people under the age of 60 – it is not uncommon – and presumably those vegans who develop DHA-induced cognitive dysfunction or dementia must have genetic vulnerabilities predisposing them to the effects of ultra-low DHA levels in their diet. I have one lady with florid frontotemporal dementia in her early 50’s (not a vegan!).

    Good point. Vegan children also seem to develop fine (as long as they have a source of B12 and aren’t on an extreme diet). But I have been concerned that people who have lived off fish for DHA their entire lives might not be able to get the DHA-producing mechanisms going in later life. There’s also been a suggestion that older people have a more difficult time converting ALA to DHA, which is why it becomes more important later in life. It is possible, I suppose, that DHA isn’t necessary at all, and maybe DPA suffices.

    > Second question – why recommend DHA every 2-3 days? Is it because vegan DHA is expensive? But if DHA is critical for some individuals, and dementia takes years to develop, why wait until age 60 to start it every day? (and miss 60 years of neural existence)

    I’m trying to minimize supplementation while still being prudent.

  20. Dan Says:

    Tyler,

    I don’t want to belabor this argument but as a health practitioner, I have seen numerous individuals fail on a true low fat diet. Just to give you one example. The other day I saw a man whose atherosclerotic plaque burden has doubled in the past two years despite excellent adherence to Esselstyn, as evidenced by his very low LDL level (half what it was before Esselstyn two years ago, at which point in time his plaque was not increasing by much – I’ve been following him for 4 years). Unfortunately, in swapping out fat for carbs, his triglycerides and HDL have dramatically deteriorated and he has developed metabolic syndrome. He does not eat any processed food or sugar. I confirmed with a preventive cardiologist that many diabetics in his practice require more insulin after starting on Esselstyn and Ornish diets – again, swapping out fat for carbs would be the cause. Clearly the person I mentioned did not tolerate a low fat diet – or at least, his bodily system did not tolerate it. He was eating vegetables, whole grains, fruit, legumes and soy but no oil, fish, meat, eggs or nuts whatsoever (since these are prohibited on Caldwell Esselstyn’s diet).

    There have been more than a dozen well-conducted randomized controlled trials showing that low glycemic index diets and low carb high fat diets dramatically remediate metabolic syndrome and type 2 diabetes. Long term endpoints are not known. But to me, it makes perfect sense. Metabolic syndrome, which is often characterized by a rising tide of blood sugars and glycosylated hemoglobin A1c values (for the latter, upwards from 0.056 to 0.063 and beyond) are diseases of glucose and carbohydrate intolerance.

    Jack,

    Thanks for your kind words. Regarding “people who have lived off fish for DHA their entire lives might not be able to get the DHA-producing mechanisms going in later life” …. this could be due to epigenetic mechanisms, since presumably DHA synthesis is largely under genetic control (other than contributions from dietary intake level of the key precursors and competition by omega-6 LA).

    We may know a lot more about fatty acids in the near future, at least at mega-levels. There are two prescription grade EFAs on the market – Lovaza (purified DHA) and Vascepa (purified icosapentyl-EPA). At least for the latter, there is a very large (~8,000) patient trial in the works looking at hard endpoints (http://clinicaltrials.gov/ct2/show/NCT01492361?term=vascepa&rank=10). No doubt Lovaza is also competing in this market for trial patients. However, the doses are far higher than what are being recommended to vegans/vegetarians, and I doubt there will be subgroup analyses on vegans/vegetarians (although there may be analyses by pre-intervention DHA/EPA status). If vegans/vegetarians are 2% of the general population, and typically don’t like taking medication (at least many of them), they will be under-represented in these trials and there will be very few cases of true deficiency. Moreover, I don’t know if cognition will be studied (possibly in substudies – not sure). By the way, I’ve started taking B12 b.i.d. by following your example (TDD 150 mg/day). Thanks very much for that!

  21. Andreas Says:

    Dan,

    Unless those people were placed in cages like rodents, they aren’t going to admit to binging on processed foods. Period. It doesn’t matter wether they eat low fat or high fat.

  22. Tyler Says:

    “I don’t want to belabor this argument but as a health practitioner, I have seen numerous individuals fail on a true low fat diet. Just to give you one example. The other day I saw a man whose atherosclerotic plaque burden has doubled in the past two years despite excellent adherence to Esselstyn…”

    What is this suppose to support exactly? This is an anecdote from a diseased patient…and there isn’t even a way to confirm what the patient was actually consuming. What I suggested is that its implausible that there is a common genetic variant that prevents healthy people from thriving on a low-fat diet. Whether there are some disease states or rare genetic variants that could cause this is a different question.

    “There have been more than a dozen well-conducted randomized controlled trials showing that low glycemic index diets and low carb high fat diets dramatically remediate metabolic syndrome and type 2 diab”

    There are studies showing improvements utilizing a high carbohydrate whole foods based diet.

  23. bananabender Says:

    The “problem” with vegan diets is usually pretty simple – not enough calories. Most vegans seem to think that a plant-based diet is simply a matter of eliminating animal products. They don’t realise that eating 2000+ calories requires a MASSIVE intake of fruits, vegetables’ legumes and grains. [ Irish peasants ate about 4kg/9lbs of potatoes every day.]

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