Why Animal Foods Are Good For You – Part 1 – The Conversion Fallacy

Since writing my article on the morality of eating meat, as was expected, one major point of contention is my claims about the nutritional benefits of eating animal foods. If they are needed for optimal health, many recognize, it is harder to justify veganism by claiming that eating meat is frivolous, unnecessary, or even harmful.

Initially attempting to write a single article, I quickly found there was too much material to give a thorough overview of the evidence. So, instead, this ongoing series of articles will illuminate the science based reasons why humans should eat animal foods to maintain optimal health.

In my podcast ‘What is a healthy diet?‘, I made the blanket claim that all animal products are unhealthy. Since then, the weight of the evidence has convinced me otherwise. Not that all animal products are healthy, but that certain kinds of animal products are healthy. This series will present that evidence.

The first article is about what I’ve come to call ‘the conversion fallacy‘.

There are several nutrients which are said to be found in both animals and plants, but this claim is misleading, because the forms of nutrients have important health-related consequences. Often plant foods contain nutrients (or precursors to nutrients) which we must convert to a useable form before they can do us much good. Some claim (or more often, insinuate) that since the body can synthesize these substances, there is no need to have them in our diets. This is often backed up with cherry picked data and arguments that ignore the vast catalog of research showing specific benefits from consuming these nutrients in their more useable forms.

This article will focus on three major examples: Vitamin A, Vitamin K2, and Omega-3’s.

Image by yangui on flickr. CC BY-NC-ND 2.0

Animal Fat: image by yangui on flickr. CC BY-NC-ND 2.0


Vitamin A

Vitamin A is important. It is a major contributor to visual, immune system, and reproductive health, as well as bone growth and general growth in children.1 It also helps the fats in our cells resist oxidative damage,2 3 and it protects against asthma and allergies,4 5 kidney stones,6 and fatty liver disease.7

It’s useable form (retinol) is mostly found in animal fats and liver tissues. However, beta-carotene, a precursor form of vitamin A, can be found in many plant foods, such as carrots and sweet potatoes. The body can convert beta-carotene to retinol, but conversion rates are highly variable (between 3% and 28%). The highest rates are from supplements dissolved in oil (~28%), or certain foods with added fat to the meal, as beta-carotene needs fat for it’s conversion, while eating raw, unprocessed vegetables yields the worst results (~3-5%).8 9 10 11 12 This suggests that the common wisdom in vegan circles to eat high proportions of raw food and limit fat consumption may increase the chances of developing vitamin A deficiency. Saturated animal fats assist in the conversion to a higher degree than polyunsaturated plant fats.13

Many other factors can also affect the strength of the conversion. Overweight individuals,14 as well as people with thyroid issues,15 and zinc deficiencies (also common in vegetarian diets)16 have trouble converting beta-carotene to retinol, while diabetics may have trouble absorbing beta-carotene.17 Two studies, though both had small sample sizes, showed that 45% of the healthy participants converted little to no beta-carotene at all!18 19

In 2001, the Food and Nutrition Board of the Institute of Medicine revised their estimated efficiency for conversion from 17% to 8%.20 Using this conversion ratio, let’s look at how easy it is to get our RDA (recommended daily allowance) from vegetable sources. Carrots are one of the best plant sources of beta-carotene.  100 grams (about a cup) of raw carrots will yield about 26000IU of beta carotene,21  which converts to about 2100IU of retinol22 (this will be slightly higher if the carrots are cooked). Given that the RDA is 3000IU, this looks pretty good, right? Just eat a cup of carrots every single day, throw in some kale, sweet potatoes, and tomatoes, and you’re good! Well, maybe.

Given what we’ve shown above with the inherent variability of beta-carotene conversion, it may not be wise to rely solely on plant products. If you happen to be a 3% converter, a cup of carrots will only yield 780IU of vitamin A (and suddenly you need four cups to meet the RDA). Also, the more beta-carotene you eat, the less efficient the conversion becomes,11 so there is an inherent self-limiting aspect to using it alone to meet vitamin A requirements.

There are also plenty of good reasons to think that the RDA for vitamin A is actually too low. Like many RDA values, it is set at the minimum required amount to avoid overt deficiency symptoms (plus some buffer), not for optimal health. Research into various extremely healthy tribal cultures has estimated that their vitamin A intake could have been as high as 30,000 to 50,000 IU.23 24 25 Also, each of the healthiest and longest lived cultures on the planet had some amount of animal fats (and hence preformed vitamin A) in their diet, even if that amount was relatively low (though as noted above, it was often quite high). To assume that a diet completely devoid of this nutrient in it’s preformed state is both safe and optimal is a faith-based, rather than an evidence-based, position.

Some research into vegetarian children has shown them to have lower serum levels of vitamin A, with case reports of outright deficiencies.26 27 28 Research in adults is mixed. One study showed that while the omnivores in the study consumed less vitamin A (even after factoring in the beta-carotene conversion) than the vegetarians, they still had a higher serum levels.29 Another group of vegetarians who were studied had higher serum levels than the omnivores they were matched with.30 Vegetarian diets, of course, can still include eggs, butter, and milk – all of which are vitamin A rich foods, and without knowing exactly what all of the participants were eating, it’s hard to conclude much based on these analyses.

A review of the medical literature which looked at over 120,000 participants in 8 countries concluded that beta-carotene on it’s own was insufficient to meet the body’s need for vitamin A.31


Vitamin K2

The story of Vitamin K2 is similar. K2 is almost exclusively found in animal foods. The fermented food natto is a vegan source of vitamin K2, but it’s consumption is not very common outside of Japan. Apparently the taste is difficult for most people to acquire. Vitamin K1 is found in abundance in the plant world, and our bodies are able to convert K1 to K2.32 33 The realization that vitamin K2 is an important factor for health is a recent one, so research into K1 to K2 conversion is more limited than with Vitamin A and beta-carotene, but there is evidence that consuming K2 has health benefits that K1 does not.

The Rotterdam study, which looked at around 5000 subjects for 7-10 years, found that K2 intake, and not K1, was associated with lower all cause mortality and arterial calcification.34  This finding was recently backed up by another large study, looking at 16,000 women, which showed a clear, linear progression – the more K2 in the diet, the less likely the participants were to experience coronary heart disease.35 K1 showed no effect. These studies, however, are both observational, and hence cannot determine causation in the same way lab research can.

Researchers in the Netherlands found that in a laboratory setting, once again, K2, and not K1, protected against arterial calcification in rats.36 The same research group later found that extremely high doses of either vitamin K1 or K2 were able to reverse the process.37 Leon Schurgers, lead researcher on that paper, commented that “The effect of K1 and the conversion rate of K1 to K2 was due to the extremely high dose of K vitamins used in this model. This would be probably less in a normal diet, even with supplemental K1. In contrast, the Rotterdam study showed a significant protective benefit with natural Vitamin K2 at just 45mcg per day, whereas K1 had no correlation at all.”38 It was also found that mice who were genetically bred to lack MGP, a protein that depends on K2 for it’s production, develop calcium deposits in the arteries so serious that they die within a few weeks of birth.39 A similar mutation in the human gene that regulates vitamin K2 production doubles the likelihood of atherosclerotic diseases like coronary disease, stroke, and aortic disease.40

These mice who lacked MGP also developed osteopenia and spontaneous fractures.39 In Japan, it has long been common wisdom that natto (that K2 rich soybean dish) was good for promoting bone health. Research has confirmed that areas in Japan which consume more natto have lower incidences of hip fractures.41 Bone geometry and strength have been shown to be positively impacted by K supplementation, with K2 having a much more pronounced effect than K1.42 43 Some research has shown a potential benefit from K2 on bone quality during osteoporosis treatment,44 but others have concluded that while K2 definitely helps stimulate bone formation, sustains bone density, and can help prevent fractures, it’s usefulness as an osteoporosis treatment itself requires more research.45 One randomized controlled trial found that K2 supplementation reduced bone fractures by 56% in treated osteoporosis patients when compared to control groups,46 while another study found K2 alone to be only slightly less effective as the drug ‘etidronate’ at preventing spinal fractures, while the two combined had a synergistic effect.47

Vitamin K2 has also shown some possible protective benefit from various forms of cancer. A recent observational study (which again, only prove correlation, not causation) involving 12,000 men found that dietary intake of K2, and not K1 (starting to see a pattern here) was strongly protective against prostate cancer,48 as well as less strongly protective for all other cancers.49 Other research has suggested a possible benefit against lung cancer,50 as well as anti-tumor properties.51 52 Some research has also shown a potential benefit of combining K2 with a drug called ACE-I against liver cancer,53 though a meta analysis has failed to show that K2 alone can be effective against preventing liver cancer recurrence.54

fish

By superfem on flickr. CC-BY 2.0


Omega-3’s

You know the story by now. We can get omega-3’s in their short-chain form (ALA) from plants, but in order to get the long-chain omega-3’s (EPA and DHA) that our body makes the most use of, we need to consume fish, or other animal products like grass fed milk or butter (or take vegan supplements made from algae).

Research into omega-3’s is extremely extensive, and benefits have been demonstrated in a wide variety of health indicators and disease outcomes. Inflammation plays a crucial role in many degenerative diseases, including cancer, cardiovascular disease, and autoimmune diseases. Omega-3’s are anti-inflamatory,55 56 57 58 and have demonstrated benefits in inflammation specific diseases like rheumatoid arthritis and inflammatory bowel disease.59 60 A full review of the benefits of omega-3’s would likely make this article three times as long as it already is, so I’ve decided to focus on a single health outcome, which is also related to inflammation: heart disease.

The sheer amount of evidence into this topic is staggering and difficult to wade through, but generally, the evidence seems to indicate protective effects of dietary and supplemental EPA and DHA, with 11 meta-analyses coming to the conclusion that there was a marked protective effect,61 62 63 64 65 66 67 68 69 70 71 one showing an existent, yet small effect,72 while three did not show any effect.73 74 75 Two of the three negative meta-analyses focused only on omega-3 supplementation, rather than dietary omega-3 consumption, which suggests that the positive effects of EPA and DHA may be more pronounced with whole food sources like wild-caught fish, than they are from supplemental sources. There are a number of reasons this could be true, including the benefit of consuming EPA and DHA along with the other nutrients abundant in fish (like selenium), and some research bears this out.76 Another potential reason is that the oils in omega-3 supplements are often oxidized (rancid),77 78 and rancid oils have been shown not to have the same health benefits.79 80 For this reason, if you can’t eat fish directly and will be supplementing, research and choose a high quality supplement, and maybe even ask the manufacturer whether they take steps to prevent their oil from becoming rancid.

Of the meta-analyses that differentiated, a much smaller (or no) effect was reported for ALA consumption.61 67 This makes sense, given that EPA and DHA are the most active forms of omega-3 in our bodies, and most studies put the conversion factor for ALA to EPA and DHA at somewhere around 5% or less,81 82 though it has been shown that women are better converters than men.83

Vegetarians and vegans have much lower circulating DHA (and often EPA) levels than omnivores,84 85 86 87 88 89 90 91 92 though one study, well circulated in vegan circles, suggests that the difference, while present, is not so large.93 Of course, a single observational study could never override years of more tightly controlled research showing the opposite to be true. It has also been shown that only consumption of DHA (and not EPA or ALA) can improve blood DHA status.94 95 However, serum levels are only part of the story. DHA does much of it’s important work in the body in the tissues, forming part of our cell walls. Studies have also shown that vegans and vegetarians have lower tissue levels of EPA and DHA,92 and more generally that dietary intake of EPA and DHA are directly reflected in tissue levels.96 97

Research has also shown that mothers who consume fish or fish oil have more DHA in their breast milk,98 99 100 while DHA levels in the breast milk of vegetarians are low.92 101 Low DHA in breast milk will affect the fetus’ DHA levels and general development,102 103 and has been shown to have negative effects on the child’s cognition.104 105


For Vegans

While it is generally preferable to get dietary nutrients from whole foods, which in these cases means animal products, I urge those who wish to remain vegan for ethical or environmental reasons to supplement with vegan sources of EPA/DHA, consume some natto or take vegan supplemental K2, as well as supplement with extra beta-carotene (as there is not, to my knowledge, a vegan source of preformed vitamin A).


Thanks for reading!

I welcome any and all comments and criticism in the comments section

Stay tuned for part 2 in the series, ‘the missing ingredients’, where I will discuss some nutrients that simply cannot be found in plants at all.

 

Author’s note: I am not an expert, but rather an interested layperson. I do not for a minute think that I am the only human being immune to confirmation bias. If I have misunderstood or misrepresented some of the presented research, or overlooked some crucial piece of conflicting research, I would greatly appreciate being informed of that, either in the comments section here, or via this blog’s contact form.

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  3. Vitamin A inhibits doxorubicin-induced membrane lipid peroxidation in rat tissues in vivo.  (back)
  4. Vitamin A status in children with asthma.  (back)
  5. Serum vitamin A concentrations in asthmatic children in Japan.  (back)
  6. Antilithogenic and litholytic action of vitamin A vis-a-vis experimental calculi in rats  (back)
  7. Altered lipid catabolism in the vitamin A deficient liver.  (back)
  8. The importance of beta-carotene as a source of vitamin A with special regard to pregnant and breastfeeding women.  (back)
  9. Advanced Nutrition and Human Metabolism (5th Edition) pg.376  (back)
  10. Estimation of carotenoid accessibility from carrots determined by an in vitro digestion method.  (back)
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  12. Influence of dietary fat on beta-carotene absorption and bioconversion into vitamin A.  (back)
  13. Intestinal absorption of β-carotene ingested with a meal rich in sunflower oil or beef tallow: postprandial appearance in triacylglycerol-rich lipoproteins in women  (back)
  14. Short-term (intestinal) and long-term (postintestinal) conversion of β-carotene to retinol in adults as assessed by a stable-isotope reference method  (back)
  15. Beta-carotene, vitamin A and carrier proteins in thyroid diseases  (back)
  16. Low zinc intake decreases the lymphatic output of retinol in rats infused intraduodenally with beta-carotene.  (back)
  17. Retinol, alpha-tocopherol and carotenoids in diabetes.  (back)
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  19. Variability of the conversion of beta-carotene to vitamin A in women measured by using a double-tracer study design.  (back)
  20. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001)   (back)
  21. carotene in carrots, raw – 7,990mcg converts to approx. 26,000IU  (back)
  22. Oregon State University Vitamin A resource  (back)
  23. Traditional and modern Greenlandic food – dietary composition, nutrients and contaminants.  (back)
  24. Retinol Content of Wild Foods Consumed by the Sahtú  (back)
  25. WAPF – Vitamin A Saga – Not a direct source, but makes mention of the Vitamin A levels found generally in the diets of the peoples studies by Weston A Price.  (back)
  26. Lipids and vitamin A and E status in vegetarian children  (back)
  27. Vegan Diet and Vitamin A Deficiency  (back)
  28. Joel and Sergine Le Moaligou convicted of causing child’s death  (back)
  29. Nutrient intake and vitamin status of healthy French vegetarians and nonvegetarians.  (back)
  30. Selected Vitamins and Trace Elements in Blood of Vegetarians  (back)
  31. The contribution of β-carotene to vitamin A supply of humans.  (back)
  32. Elucidation of the mechanism producing menaquinone-4 in osteoblastic cells.  (back)
  33. The UBIAD1 prenyltransferase links menaquinone-4 [corrected] synthesis to cholesterol metabolic enzymes.  (back)
  34. Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study.  (back)
  35. A high menaquinone intake reduces the incidence of coronary heart disease.  (back)
  36. Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.  (back)
  37. Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats.  (back)
  38. Vitamin K2 Shown to Reverse Arterial Calcifications – NPI center  (back)
  39. Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein.  (back)
  40. VKORC1 haplotypes are associated with arterial vascular diseases (stroke, coronary heart disease, and aortic dissection).  (back)
  41. Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of vitamin K2: possible implications for hip-fracture risk.  (back)
  42. Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women.  (back)
  43. Vitamin K2 improves bone strength in postmenopausal women  (back)
  44. Menatetrenone (vitamin K2) and bone quality in the treatment of postmenopausal osteoporosis.  (back)
  45. Effects of vitamin K2 on osteoporosis.  (back)
  46. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis.  (back)
  47. Combined treatment with vitamin k2 and bisphosphonate in postmenopausal women with osteoporosis.  (back)
  48. Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg).  (back)
  49. Dietary vitamin K intake in relation to cancer incidence and mortality: results from the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg).  (back)
  50. Apoptosis induction of vitamin K2 in lung carcinoma cell lines: the possibility of vitamin K2 therapy for lung cancer.  (back)
  51. Vitamin K2-induced antitumor effects via cell-cycle arrest and apoptosis in gastric cancer cell lines.  (back)
  52. Vitamin K2-induced cell growth inhibition via autophagy formation in cholangiocellular carcinoma cell lines.  (back)
  53. Combined treatment of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis.  (back)
  54. Role of vitamin K2 in preventing the recurrence of hepatocellular carcinoma after curative treatment: a meta-analysis of randomized controlled trials.  (back)
  55. Omega-3 fatty acids and inflammation  (back)
  56. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids.  (back)
  57. n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases  (back)
  58. Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation.  (back)
  59. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis.  (back)
  60. Omega-3 polyunsaturated fatty acids and immune-mediated diseases: inflammatory bowel disease and rheumatoid arthritis.  (back)
  61. n−3 Fatty acids from fish or fish-oil supplements, but not α-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review  (back)
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  63. Long-term effect of high dose omega-3 fatty acid supplementation for secondary prevention of cardiovascular outcomes: A meta-analysis of randomized, double blind, placebo controlled trials  (back)
  64. Seafood omega-3 intake and risk of coronary heart disease death: an updated meta-analysis with implications for attributable burden  (back)
  65. Prevention of sudden cardiac death with omega-3 fatty acids in patients with coronary heart disease: a meta-analysis of randomized controlled trials.  (back)
  66. Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease  (back)
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  68. Omega-3 fatty acids in high-risk cardiovascular patients: a meta-analysis of randomized controlled trials  (back)
  69. n−3 Fatty acids and cardiovascular disease  (back)
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  72. Omega 3 Fatty acids and cardiovascular outcomes: systematic review and meta-analysis.  (back)
  73. Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis.  (back)
  74. Efficacy of omega-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease: a meta-analysis of randomized, double-blind, placebo-controlled trials.  (back)
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  76. Fish, long-chain omega-3 polyunsaturated fatty acids and prevention of cardiovascular disease–eat fish or take fish oil supplement?  (back)
  77. Quality analysis of commercial fish oil preparations.  (back)
  78. Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements  (back)
  79. Effect of omega-3 dietary supplements with different oxidation levels in the lipidic profile of women: a randomized controlled trial.  (back)
  80. Oxidation of Marine Omega-3 Supplements and Human Health  (back)
  81. Efficiency of conversion of alpha-linolenic acid to long chain n-3 fatty acids in man.  (back)
  82. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)?  (back)
  83. Conversion of alpha-linolenic acid to longer-chain polyunsaturated fatty acids in human adults.  (back)
  84. Polyunsaturated fatty acid status of Dutch vegans and omnivores.  (back)
  85. DHA status of vegetarians.  (back)
  86. Very low n-3 long-chain polyunsaturated fatty acid status in Austrian vegetarians and vegans.  (back)
  87. Fatty acid composition of erythrocyte, platelet, and serum lipids in strict vegans.  (back)
  88. Fatty acid patterns in triglycerides, diglycerides, free fatty acids, cholesteryl esters and phosphatidylcholine in serum from vegetarians and non-vegetarians.  (back)
  89. Long-chain n–3 polyunsaturated fatty acids in plasma in British meat-eating, vegetarian, and vegan men  (back)
  90. Serum fatty acid, lipid profile and dietary intake of Hong Kong Chinese omnivores and vegetarians.  (back)
  91. Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine.  (back)
  92. Studies of vegans: the fatty acid composition of plasma choline phosphoglycerides, erythrocytes, adipose tissue, and breast milk, and some indicators of susceptibility to ischemic heart disease in vegans and omnivore controls.  (back)
  93. Dietary intake and status of n-3 polyunsaturated fatty acids in a population of fish-eating and non-fish-eating meat-eaters, vegetarians, and vegans and the product-precursor ratio [corrected] of α-linolenic acid to long-chain n-3 polyunsaturated fatty acids: results from the EPIC-Norfolk cohort.  (back)
  94. alpha-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans.  (back)
  95. Short-term supplementation of low-dose gamma-linolenic acid (GLA), alpha-linolenic acid (ALA), or GLA plus ALA does not augment LCP omega 3 status of Dutch vegans to an appreciable extent.  (back)
  96. Dietary intake and adipose tissue level of specific fatty acids in a selected group from the Lower Silesia population.  (back)
  97. Fatty acid composition of subcutaneous adipose tissue and diet in postmenopausal US women  (back)
  98. Docosahexaenoic Acid in Breast Milk Reflects Maternal Fish Intake in Iranian Mothers  (back)
  99. The effects of fish oil supplementation in pregnancy on breast milk fatty acid composition over the course of lactation: a randomized controlled trial.  (back)
  100. Seafood consumption, the DHA content of mothers’ milk and prevalence rates of postpartum depression: a cross-national, ecological analysis  (back)
  101. The influence of a vegetarian diet on the fatty acid composition of human milk and the essential fatty acid status of the infant.  (back)
  102. Maternal docosahexaenoic acid supplementation and fetal accretion.  (back)
  103. Essential fatty acid transfer and fetal development.  (back)
  104. Maternal DHA and the development of attention in infancy and toddlerhood.  (back)
  105. Maternal supplementation with very-long-chain n-3 fatty acids during pregnancy and lactation augments children’s IQ at 4 years of age.  (back)

11 thoughts on “Why Animal Foods Are Good For You – Part 1 – The Conversion Fallacy

  1. Matt Berkowitz says

    By Matt Berkowitz:

    This article presents itself as extremely well-researched and cited from the scientific literature, but will unfortunately mislead many who do not have the background in the larger order research that’s necessary to understand these issues.

    First thing to be said is that this article takes a highly reductionist view of nutrition, focusing only on three nutrients without mentioning the context of what an overall healthy diet should be comprised of.

    Regarding Vitamin A, the data is cherry-picked to fit the author’s conclusions that animal meats are necessary. The most up-to-date studies published on vitamin A, regarding beta-carotene conversion to retinol, was published by the USDA here: http://ajcn.nutrition.org/content/87/4/1067.1.full It is very clear that our bodies CAN make the necessary conversion ratios for most people.

    The study used in the author’s article to come up with the lower 3% conversion figure for vitamin A was for “in vitro digestion” (your foot note 10). The other article referenced (foot note 11) shows a conversion factor around 10-12:1 for most vegetables. As for the 45% figure of people who had vitamin A deficiencies, the sample sizes were 11 for both.
    These are such small samples that the studies aren’t even worth mentioning. Because the 3% figure is for “in vitro”, your caveat at the end is moot. And as the author denoted, the IU’s of usable retinol would be more than enough for a cup of carrots (or sweet potatoes, squash, etc.) for the 10-12:1 ratio.

    And your last study (the meta-analysis) about vitamin A deficiency across 8 countries says nothing about why the deficiency exists. It is at least as possible to be deficient in vitamin A from the Standard American Diet compared to a vegetarian / vegan diet when one takes a larger picture.

    Regarding, vitamin K2, the author here has simply chosen, for whatever reason, to highlight the studies that show benefits of K2 supplementation, while only passively mentioning the reality that our bodies can convert K1 to K2, as well as synthesize it itself (not mentioned here).

    Much of the research cited is on rats – this is not applicable to humans necessarily. Some studies that have found benefits from K2 supplementation have been the Japanese ones, where natto was the source, not animal protein. The ones where the focus was on animal protein is ironic, when a litany of literature finds significant links between cholesterol, fat, saturated fat, etc. and all-cause mortality (though the author will likely discount this literature). What, are we supposed to conclude that the ingestion of foods, which have been linked to cause cancer, is also great for preventing cancer? I will state bluntly that it is absolutely irresponsible and neglectful to suggest one eats animal foods to prevent against supposed K2 deficiency symptoms when such foods have been repeatedly linked to cause a whole range of health problems.

    And that brings us to Omega-3. It is true that vegetarians / vegans can be deficient in this essentially fatty acid, with many studies showing non-meat eaters to have higher deficiencies. However, one tablespoon of flax seeds or chia seeds (the best plant sources of Omega-3) constitutes your daily requirement of Omega-3. Yes, this is in the ALA format, not EPA or DHA. But the author referenced one study (foot note 93) which demonstrates the body’s ability to make this conversion. One has to consume enough though, obviously, for the results to be high enough. Perhaps the other studies referenced (many of which were small sample sizes, by the way) were for people who were not being diligent with regard to their ALA intake. It’s worth noting that the RDA’s for Omega-3 are 1.6g and 1.1g for men and women respectively. The author points out that these may be low – fair enough. But with a tablespoon of flax or chia per day, plus the recommended 9 servings of fruits / vegetables per day, one will get well over this amount. Now, this may be lower than omnivores who consume fish (and other animal products), who, by the way, get their Omega-3 from plants, perhaps the omnivores are getting too much. Research has also been done (not mentioned here) to show possible deleterious effects of consuming *too much* Omega-3 (such as: http://www.ncbi.nlm.nih.gov/pubmed/22968891)

    Coming back to the larger picture… We need to take the whole diet into account and not get hung up on individual micronutrients. All-cause mortality for vegetarians / vegans is generally lower than for meat-eaters (See Michael Greger’s excellent presentation, “Uprooting the Leading Causes of Death”: http://www.youtube.com/watch?v=30gEiweaAVQ But we can’t get carried away with the “vegan” and “vegetarian” labels anyway, as that does not say enough about what comprises a healthy diet. So, whatever value can be gained from this article is the reinforcement that we must research what will, holistically be healthy, rather than view it from a hyper-reductionist perspective.

    • aaron says

      ‘ First thing to be said is that this article takes a highly reductionist view of nutrition, focusing only on three nutrients’

      It is the first article in a series which will,  cumulatively, present the larger context for what constitutes a healthy diet. I would give you a pass on this if I wasn’t so abundantly clear about this fact in the article.

      ‘ The most up-to-date studies published on vitamin A, regarding beta-carotene conversion to retinol, was published by the USDA here: http://ajcn.nutrition.org/content/87/4/1067.1.full It is very clear that our bodies CAN make the necessary conversion ratios for most people.’

      i’m confused, because what you link to is not research,  it’s a letter that points out some mathematical errors in the USDA database that actually estimated the conversion of beta-carotene to vitamin A as being too high.  Did you even read what you are referencing here? It backs up my position of beta carotene having a lower conversion rate than many state,  and it’s final supported conversion rate is 12:1 or 8%, which is exactly what I say is the consensus in my article. 

      If you are going to say I cherry picked data,  at least point to research that actually conflicts with my own,  rather than confirms it.

      ‘ The study used in the author’s article to come up with the lower 3% conversion figure for vitamin A was for “in vitro digestion” (your foot note 10).’

      Actually,  three of the studies I referenced there back up the 3% conversion rate (footnotes 8, 10, and 11. 11 references even more research to back up that number,  which is a commonly found conversion rate for raw unprocessed veggies),  and only one was in vitro. 

      ‘ The other article referenced (foot note 11) shows a conversion factor around 10-12:1 for most vegetables.’

      I like how you say ‘the other’ as if there was only two when there is actually four,  which list the rates,  again,  between 3 and 28%, with multiple studies on either end of that spectrum.  Either way,  yes 12:1, or 8% is the current consensus,  as I stated. 

      ‘ And as the author denoted, the IU’s of usable retinol would be more than enough for a cup of carrots’

      A cup of carrots,  given a 12:1 ratio would yield about 2/3 of the RDA,  not ‘more than enough’.

      ‘ And your last study (the meta-analysis) about vitamin A deficiency across 8 countries says nothing about why the deficiency exists. It is at least as possible to be deficient in vitamin A from the Standard American Diet compared to a vegetarian / vegan diet when one takes a larger picture.’

      This is so garbled I’m having trouble understanding the point,  but of course the SAD could be deficient in vitamin A.  The literature review looked at whether beta carotene alone was enough to meet dietary needs and found that it wasn’t. 

      ‘ Regarding, vitamin K2, the author here has simply chosen, for whatever reason, to highlight the studies that show benefits of K2 supplementation, while only passively mentioning the reality that our bodies can convert K1 to K2, as well as synthesize it itself’

      There is no evidence that the body can synthesize K2 without K1,  so I’m not sure what your differentiation there means.  The whole point of the article is about nutrients that can be converted from other nutrients,  so it is made abundantly clear that that is the case. 

      The reason I mention all of the research is because it specifically shows thatK2 consumption has benefits that K1 consumption doesn’t.  So whether the body converts it is moot when we have data that shows K1 consumption does not yield the benefits. 

      ‘ What, are we supposed to conclude that the ingestion of foods, which have been linked to cause cancer, is also great for preventing cancer? I will state bluntly that it is absolutely irresponsible and neglectful to suggest one eats animal foods to prevent against supposed K2 deficiency symptoms when such foods have been repeatedly linked to cause a whole range of health problems.’

      I will refrain from commenting on this too much,  but the evidence against animals foods will be a topic of a later article in which I will give it a thorough review and analyses.  Suffice to say that I believe these foods do not cause cancer or heart disease.

      ‘However, one tablespoon of flax seeds or chia seeds (the best plant sources of Omega-3) constitutes your daily requirement of Omega-3. ‘

      Right,  but I wasn’t talking about meeting requirements, I was talking about optimal intake to get the benefits described in the 11 meta analyses I published,  which rely directly on taking EPA and DHA,  and on getting more than what’s in a tablespoon of seeds.

      ‘ But the author referenced one study (foot note 93) which demonstrates the body’s ability to make this conversion.’

      The author also referenced two studies which showed that supplemental ALA will not raise blood DHA levels,  which you ignored. The general consensus is that ALA consumption will maintain DHA /EPA levels at a low but constant position, but for optimal levels the nutrients should be consumed directly.  If you have actual research that refutes that I’m open but your hand waving is both tedious and annoying. 

      ‘perhaps the omnivores are getting too much. Research has also been done (not mentioned here) to show possible deleterious effects of consuming *too much* Omega-3 (such as: http://www.ncbi.nlm.nih.gov/pubmed/22968891)’

      That study shows that were no harmful effects.  Again,  I have to ask,  did you even read what you are referencing? Twice now you’ve referenced literature that backs my points up and not yours.  So now we have a ton of literature showing the benefits of high DHA/EPA intake, and confirmation that it isn’t dangerous.  Thanks.  🙂

      ‘ Coming back to the larger picture… We need to take the whole diet into account and not get hung up on individual micronutrients. ‘

      People who’ve had micronutrient deficiencies will disagree,  and know that its sometimes important to get in depth on this stuff. 

      But again,  of course I agree the big picture is important.  I just think the smaller pieces should actually be well researched before we fit them in to the big picture,  so we don’t make mistakes about what that big picture is.

  2. Matt Berkowitz says

    “i’m confused, because what you link to is not research, it’s a letter that points out some mathematical errors in the USDA database that actually estimated the conversion of beta-carotene to vitamin A as being too high. Did you even read what you are referencing here? It backs up my position of beta carotene having a lower conversion rate than many state, and it’s final supported conversion rate is 12:1 or 8%, which is exactly what I say is the consensus in my article.

    If you are going to say I cherry picked data, at least point to research that actually conflicts with my own, rather than confirms it.”

    I should have said, “was referenced by the USDA” (not “published by the USDA). My point was to highlight the consensus of the 8-12% conversion ratio, and that the 3% figure is erroneous.

    “Actually, three of the studies I referenced there back up the 3% conversion rate (footnotes 8, 10, and 11. 11 references even more research to back up that number, which is a commonly found conversion rate for raw unprocessed veggies), and only one was in vitro.”
    10 is about in vitro consumption. 11 I commented on – that most of the vegetables in the table of conversion ratios are in the 8-12% ratio. And that harping on the 3% figure is misleading. I think you’re harping on this figure because it fits your conclusion.

    “A cup of carrots, given a 12:1 ratio would yield about 2/3 of the RDA, not ‘more than enough’.”

    This is a much more in-depth article by the National Institutes of Health regarding vitamin A conversion. It is very clear from the research overall presented here that plant sources of vitamin A are sufficient. http://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/

    “I will refrain from commenting on this too much, but the evidence against animals foods will be a topic of a later article in which I will give it a thorough review and analyses. Suffice to say that I believe these foods do not cause cancer.”

    I hope you dig deep – beyond what Taubes presented in his saturated fat section of Good Calories, Bad Calories, which is so pathetically researched and manipulated I wouldn’t even know where to start to refute it. But I’ll wait until you write your article to comment. 🙂

    “Right, but I wasn’t talking about meeting requirements, I was talking about optimal intake to get the benefits described in the 11 meta analyses I published, which rely directly on taking EPA and DHA, and on getting more than what’s in a tablespoon of seeds.”

    Again, there are many contradictory studies that show that ALA conversions are sufficient for “optimal intake” of Omega-3’s (see next point). Not to mention other negative symptoms that occur when consuming animal products with EPA/DHA.

    “The author also referenced two studies which showed that supplemental ALA will not raise blood DHA levels, which you ignored. The general consensus is that ALA consumption will maintain DHA /EPA levels at a low but constant position, but for optimal levels the nutrients should be consumed directly. If you have actual research that refutes that I’m open but your hand waving is both tedious and annoying.”

    And it’s annoying that you highlight only the studies that seem to fit your conclusion, giving them a much higher weight towards your conclusion (or rather, already dominant position). Here’s just one of them: http://www.ncbi.nlm.nih.gov/pubmed/19500961

    Quotes from study:
    “There is no evidence of adverse effects on health or cognitive function with lower DHA intake in vegetarians.”
    “In the absence of convincing evidence for the deleterious effects resulting from the lack of DHA from the diet of vegetarians, it must be concluded that needs for omega-3 fatty acids can be met by dietary ALA.”

    “That study shows that were no harmful effects. Again, I have to ask, did you even read what you are referencing? Twice now you’ve referenced literature that backs my points up and not yours. So now we have a ton of literature showing the benefits of high DHA/EPA intake, and confirmation that it isn’t dangerous. Thanks.”

    The first one didn’t corroborate your view, but highlighted the erroneous 3% figure. But my bad here – you’re right. I meant to link to another article:
    http://www.redorbit.com/news/health/1112987268/omega-3-fatty-acid-excessive-intake-health-hazards-102913/ The authors still support eating fish moderately, but that isn’t the point of contention here. It was simply an aside point that excess Omega-3 intake is possible, and the reality that omnivores having higher serum levels of Omega-3 doesn’t mean this is preferred – especially when you review the literature that supports the “ALA conversion to EPA / DHA is sufficient” position.

    “But again, of course I agree the big picture is important. I just think the smaller pieces should actually be well researched before we fit them in to the big picture, so we don’t make mistakes about what that big picture is.”

    I agree. But then the best way to frame these issues are in the context of these larger order health issues. The way you’ve done it here is very isolated and obscures the bigger picture.

    • aaron says

      ” My point was to highlight the consensus of the 8-12% conversion ratio, and that the 3% figure is erroneous. ”

      It’s not erroneous, it’s just on the outer edges of the bell curve. It’s been demonstrated many times in different research.

      “10 is about in vitro consumption. 11 I commented on – that most of the vegetables in the table of conversion ratios are in the 8-12% ratio. And that harping on the 3% figure is misleading. I think you’re harping on this figure because it fits your conclusion.”

      11 specifically mentions an observed 28:1 conversion ratio, which is 3.5%.

      “harping” – lol. I mentioned it as the lower range of conversion, and then mentioned how much a cup of carrots would convert to at that lower range.

      “This is a much more in-depth article by the National Institutes of Health regarding vitamin A conversion. It is very clear from the research overall presented here that plant sources of vitamin A are sufficient. http://ods.od.nih.gov/…/VitaminA-HealthProfessional/”

      This article fall victim to the exact conversion miscalculations that the original letter you linked me to points out. It claims that one sweet potato contains 1,400 mcg RAE per serving, and that the rda is 900 mcg RAE, but then converts the sweet potato RAE incorrectly to 28,000 UI and overestimates the RDA score fourfold. It should say that it meets 150% of the RDA, not 561%. No doubt they utilized the flawed USDA database that the letter you posted points out.

      “I hope you dig deep – beyond what Taubes presented in his saturated fat section of Good Calories, Bad Calories, which is so pathetically researched and manipulated I wouldn’t even know where to start to refute it. But I’ll wait until you write your article to comment. ”

      Must be convenient to wave away hundreds of pages of research with a couple of insults.

      “And it’s annoying that you highlight only the studies that seem to fit your conclusion, giving them a much higher weight towards your conclusion (or rather, already dominant position). Here’s just one of them: http://www.ncbi.nlm.nih.gov/pubmed/19500961

      Once again, you post something that supports my claim. This study shows both a) that vegetarians have lower blood DHA, and b) that supplemental ALA does not raise DHA.

      Is this how you do all your research? Man.. it’s almost funny..

      “my bad here – you’re right. I meant to link to another article:
      http://www.redorbit.com/…/ The authors still support eating fish moderately, but that isn’t the point of contention here. It was simply an aside point that excess Omega-3 intake is possible,”

      Of course it’s possible. This study mentions people who are taking high doses of supplements combined with multiple kinds of fortified foods and daily fish. It’s a kind of unlikely scenario, given that most people don’t get enough DHA/EPA.

      “especially when you review the literature that supports the “ALA conversion to EPA / DHA is sufficient” position.”

      But you still haven’t presented ANY of that literature. I can’t find it. I can find that one study you used as a source in your article. I posted 8 studies supporting my position. Please, if the research is out there, point me to it!

  3. says

    I think it’ great that you are writing about these topics, Aaron. I, personally, don’t feel as confident pointing to any one type of diet for people just yet, as I think the comprehensive solid science is still developing on this. I also know that it is entirely possible that the actual answer to what is best or optimal could differ from person to person based on individual nutritional needs, which becomes uber complex research-wise, but I still want to know either way.

    I’ve read Gary Taubes’ books and think it’s fantastic that he’s challenging old paradigms and prompting new research, even though his initial goal was to address weight loss vs general nutrition. I’m especially excited about his new research institute, NuSI, that just launched for the purpose of actively and publicly challenging his own hypothesis with interdisciplinary experts and attempting to get the bottom of healthy/unhealthy causation links: http://nusi.org/ This kind of effort is overdue and the research model they are using could benefit so many areas of health research.

    When I was actively exploring the issue of vegan/vegetarian vs meat diet, I asked a friend of mine who is a bio-chem professor, what her take was on the science argument. She said she’d personally seen cadavers of long-time vegetarians and long-time carnivores and unhealthy organs were represented in both and healthy organs were represented in both. She concluded from this, and other research, that nutrient variety and balance was key and was the only real goal for good nutrition. From that perspective, the meat or no meat question becomes a moral one and can start to resemble an abortion issue relating to consciousness and suffering and where lines should be drawn. (And the arguments get just as heated, as you can imagine. After all, who wants to be seen as an unnecessarily violent person based on a sandwich choice?). Of course, this moral dilemma could be easily and effortlessly resolved by technological advancement such as nanotech, where we wouldn’t have to kill an animal to produce the same nutrients/texture/taste enjoyed by carnivores, so long as this technology is freely accessible.

    The other moral issue is fossil fuel energy and waste related to factory farming that contributes to our overall environmental demise. My avocation of a resource-based economy is my ultimate response to this, but it doesn’t address human health via nutrition.

    In New York, after the 2010 Z Day presentation, I had lunch with Jacque Fresco. I ordered a vegetarian meal and he asked if I was a vegetarian. I said no (I’m not, though a lot of my diet is vegetarian by preference.). He didn’t hear my response and I think he assumed I said I was a vegetarian and immediately went into a story on how even copper has ‘consciousness’ if we were to measure energy feedback while manipulating it. (He used the word consciousness in a facetious way). We didn’t discuss anything more on that topic, but his response leads me to believe that he views the diet choice as a moral vs scientific one. This becomes all the more fun as people cite the studies attempting to quantify the ‘feelings’ and ‘consciousness’ of plant life. There would be all sorts of shade of grey as to what is moral to eat and not eat based on the potential suffering of the endangered life comprising a plant-based salad. ( Leading to questions ala: If a tree falls dead in a forest, and the humans who witness this can’t see or hear any expressions of suffering, did it suffer?)

    Just my thoughts as I contemplate these ideas…

    • aaron says

      Hey Jen, I appreciate the comments. 🙂

      I’m not sure I necessarily recommend a Taubesian kind of diet, or any specific diet really. Basically I just think people should cut out processed foods, refined carbs/sugars, and poor quality foods overall (factory farmed meats, large scale monocrops, etc). Macronutrient ratios I’m not so sure about. I do pretty firmly (obviously, lol) believe that some animal products are good for us, because they contain things plant foods don’t, and I don’t buy the research which blanketly says ‘meat eaters have worse health’, for reasons I’ll go into in another post.

      It really does come down to ethics. And I posted my thoughts on that, which haven’t changed even since I was a vegetarian briefly. It is a heated conversation, especially when you put things as bluntly as I did, but it’s a good conversation to have.

  4. says

    Hi Aaron,

    I just noticed part 2, and it reminded me that I wanted to ask you a few things about part 1:

    1) You wrote that 3% conversion is at the lower end of variability in conversion efficiency for beta-carotene. Wouldn’t this mean that the majority of the population has conversion ratios high enough that they could meet vitamin A requirements from plant sources alone? In the article, you seem to agree that satisfying the vitamin A RDA from beta-carotene alone is doable.

    2) What about vitamin A toxicity? Since vitamin A is a fat-soluble vitamin, the body has no good mechanism for eliminating excessive vitamin A. Beta-carotene avoids this problem because it is a vitamin A precursor. The body will only convert just enough into retinol to meet its needs (assuming there is more than enough beta-carotene in the diet, of course). Vegans use this logic to argue that carotenoids are therefore the preferred and sufficient way to get vitamin A. I would like to hear you response to this.

    3) Vitamin K2 research seems to be in the early stages, judging by the fact that most of your references in that section are observational studies and animal studies. Given the track record of broken promises in focusing on isolated vitamins (first vitamin C, then vitamin E, and now vitamin D), I’m quite skeptical that vitamin K2 will turn out to be a nutrient that bucks this trend. And even if isolated vitamin K2 does turn out to be beneficial, that doesn’t guarantee you will reap the same rewards by eating K2-rich whole foods (meat, dairy, eggs, offal, etc). Other compounds in the whole food could neutralize (or even outweigh) any benefit provided by the K2 content of those foods.

    • says

      To clarify, when I wrote, “In the article, you seem to agree that satisfying the vitamin A RDA from beta-carotene alone is doable,” I mean to say that satisfying the RDA is doable with a conversion ratio around 8% or better, which covers the majority of the population.

    • aaron says

      Hi Will! Appreciate the comments! 🙂

      1 – Yes. There is also the issue of diminishing results – that people tend to convert a smaller percentage of beta-carotene the more of it they eat, but it is definitely possible for most people to hit the RDA from beta-carotene alone on a well planned diet. For others, it seems that it isn’t.

      Please remember that my title of the article is ‘animal foods are necessary for all people in every case’, but ‘animal foods are good for you’ – with the caveat that ‘some animal foods are good for you’.

      2 – I struggled whether to mention vit. a toxicity in this article, because it is a real thing, and I didn’t want to seem intentionally deceptive – but ultimate the topic is better suited to a future planned article which talks about some of the potential negatives of too much animal foods, and helping to curb or eliminate those. I think Chris Masterjon’s work with Vit A+D interactions and Vit D protecting from VIt A toxicity is essential for getting a good grasp on that topic. Great question though I thank you for giving me the chance to clarify.

      3 – I’m curious about this ‘track record of broken promises’ you speak of? It’s not been my reading of the literature. Maybe there was a lot of hype when those vitamins were first discovered that has died down, I’m not sure, but there are major benefits from all three of those vitamins, and deficiency in any of them is bad news.

      I’m going to talk a little more about other factors outweighing these positives in my response to your comment on Part 2, because you mention it there as well.

      • says

        Thanks, Aaron!

        Yes, by “broken promises” I’m referring to the early hype. This wasn’t merely about getting just enough to prevent overt deficiency, but taking higher doses as an optimal strategy for preventing chronic disease. One example would be the antioxidant narrative and the hope associated with supplemental beta-carotene, vitamin C, and vitamin E.

        http://www.hsph.harvard.edu/nutritionsource/antioxidants/

        Much of this hype was based on preliminary evidence (mechanistic studies and animal models), before the results of human clinical trials were in. This appears to be the state of affairs right now for vitamin K2. I think a lot of the benefits currently attributed to vitamin K2 are premature, and are likely to be either smaller than expected or perhaps even non-existent as the reliability of the evidence increases.

  5. A useless article that paints a very bias position like the meat industry would like you to believe. Many fermented foods from countries like China, India and Korea also contain large amounts of K2. Personally, I think if you can not eat natto you deserve weak bones and heart attacks.

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