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.
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
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
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
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.
- Advanced Nutrition and Human Metabolism (5th Edition) pg.381-383 (back)
- Effects of BHA, d-alpha-tocopherol and retinol acetate on TCDD-mediated changes in lipid peroxidation, glutathione peroxidase activity and survival. (back)
- Vitamin A inhibits doxorubicin-induced membrane lipid peroxidation in rat tissues in vivo. (back)
- Vitamin A status in children with asthma. (back)
- Serum vitamin A concentrations in asthmatic children in Japan. (back)
- Antilithogenic and litholytic action of vitamin A vis-a-vis experimental calculi in rats (back)
- Altered lipid catabolism in the vitamin A deficient liver. (back)
- The importance of beta-carotene as a source of vitamin A with special regard to pregnant and breastfeeding women. (back)
- Advanced Nutrition and Human Metabolism (5th Edition) pg.376 (back)
- Estimation of carotenoid accessibility from carrots determined by an in vitro digestion method. (back)
- Bioconversion of dietary provitamin A carotenoids to vitamin A in humans (back)
- Influence of dietary fat on beta-carotene absorption and bioconversion into vitamin A. (back)
- 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)
- Short-term (intestinal) and long-term (postintestinal) conversion of β-carotene to retinol in adults as assessed by a stable-isotope reference method (back)
- Beta-carotene, vitamin A and carrier proteins in thyroid diseases (back)
- Low zinc intake decreases the lymphatic output of retinol in rats infused intraduodenally with beta-carotene. (back)
- Retinol, alpha-tocopherol and carotenoids in diabetes. (back)
- Variability in conversion of β-carotene to vitamin A in men as measured by using a double-tracer study design (back)
- Variability of the conversion of beta-carotene to vitamin A in women measured by using a double-tracer study design. (back)
- Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001) (back)
- carotene in carrots, raw – 7,990mcg converts to approx. 26,000IU (back)
- Oregon State University Vitamin A resource (back)
- Traditional and modern Greenlandic food – dietary composition, nutrients and contaminants. (back)
- Retinol Content of Wild Foods Consumed by the Sahtú (back)
- 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)
- Lipids and vitamin A and E status in vegetarian children (back)
- Vegan Diet and Vitamin A Deficiency (back)
- Joel and Sergine Le Moaligou convicted of causing child’s death (back)
- Nutrient intake and vitamin status of healthy French vegetarians and nonvegetarians. (back)
- Selected Vitamins and Trace Elements in Blood of Vegetarians (back)
- The contribution of β-carotene to vitamin A supply of humans. (back)
- Elucidation of the mechanism producing menaquinone-4 in osteoblastic cells. (back)
- The UBIAD1 prenyltransferase links menaquinone-4 [corrected] synthesis to cholesterol metabolic enzymes. (back)
- Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. (back)
- A high menaquinone intake reduces the incidence of coronary heart disease. (back)
- Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats. (back)
- Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. (back)
- Vitamin K2 Shown to Reverse Arterial Calcifications – NPI center (back)
- Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein. (back)
- VKORC1 haplotypes are associated with arterial vascular diseases (stroke, coronary heart disease, and aortic dissection). (back)
- 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)
- Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women. (back)
- Vitamin K2 improves bone strength in postmenopausal women (back)
- Menatetrenone (vitamin K2) and bone quality in the treatment of postmenopausal osteoporosis. (back)
- Effects of vitamin K2 on osteoporosis. (back)
- Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. (back)
- Combined treatment with vitamin k2 and bisphosphonate in postmenopausal women with osteoporosis. (back)
- 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)
- 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)
- Apoptosis induction of vitamin K2 in lung carcinoma cell lines: the possibility of vitamin K2 therapy for lung cancer. (back)
- Vitamin K2-induced antitumor effects via cell-cycle arrest and apoptosis in gastric cancer cell lines. (back)
- Vitamin K2-induced cell growth inhibition via autophagy formation in cholangiocellular carcinoma cell lines. (back)
- Combined treatment of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis. (back)
- Role of vitamin K2 in preventing the recurrence of hepatocellular carcinoma after curative treatment: a meta-analysis of randomized controlled trials. (back)
- Omega-3 fatty acids and inflammation (back)
- Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. (back)
- n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases (back)
- Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (back)
- Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. (back)
- Omega-3 polyunsaturated fatty acids and immune-mediated diseases: inflammatory bowel disease and rheumatoid arthritis. (back)
- 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)
- Long chain omega-3 fatty acids and cardiovascular disease: a systematic review. (back)
- 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)
- Seafood omega-3 intake and risk of coronary heart disease death: an updated meta-analysis with implications for attributable burden (back)
- Prevention of sudden cardiac death with omega-3 fatty acids in patients with coronary heart disease: a meta-analysis of randomized controlled trials. (back)
- Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease (back)
- N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials (back)
- Omega-3 fatty acids in high-risk cardiovascular patients: a meta-analysis of randomized controlled trials (back)
- n−3 Fatty acids and cardiovascular disease (back)
- Accumulated Evidence on Fish Consumption and Coronary Heart Disease Mortality (back)
- Omega-3 dietary supplements and the risk of cardiovascular events: a systematic review. (back)
- Omega 3 Fatty acids and cardiovascular outcomes: systematic review and meta-analysis. (back)
- Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis. (back)
- 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)
- Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review (back)
- Fish, long-chain omega-3 polyunsaturated fatty acids and prevention of cardiovascular disease–eat fish or take fish oil supplement? (back)
- Quality analysis of commercial fish oil preparations. (back)
- Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements (back)
- Effect of omega-3 dietary supplements with different oxidation levels in the lipidic profile of women: a randomized controlled trial. (back)
- Oxidation of Marine Omega-3 Supplements and Human Health (back)
- Efficiency of conversion of alpha-linolenic acid to long chain n-3 fatty acids in man. (back)
- Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? (back)
- Conversion of alpha-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. (back)
- Polyunsaturated fatty acid status of Dutch vegans and omnivores. (back)
- DHA status of vegetarians. (back)
- Very low n-3 long-chain polyunsaturated fatty acid status in Austrian vegetarians and vegans. (back)
- Fatty acid composition of erythrocyte, platelet, and serum lipids in strict vegans. (back)
- Fatty acid patterns in triglycerides, diglycerides, free fatty acids, cholesteryl esters and phosphatidylcholine in serum from vegetarians and non-vegetarians. (back)
- Long-chain n–3 polyunsaturated fatty acids in plasma in British meat-eating, vegetarian, and vegan men (back)
- Serum fatty acid, lipid profile and dietary intake of Hong Kong Chinese omnivores and vegetarians. (back)
- Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine. (back)
- 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)
- 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)
- alpha-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans. (back)
- 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)
- Dietary intake and adipose tissue level of specific fatty acids in a selected group from the Lower Silesia population. (back)
- Fatty acid composition of subcutaneous adipose tissue and diet in postmenopausal US women (back)
- Docosahexaenoic Acid in Breast Milk Reflects Maternal Fish Intake in Iranian Mothers (back)
- The effects of fish oil supplementation in pregnancy on breast milk fatty acid composition over the course of lactation: a randomized controlled trial. (back)
- Seafood consumption, the DHA content of mothers’ milk and prevalence rates of postpartum depression: a cross-national, ecological analysis (back)
- The influence of a vegetarian diet on the fatty acid composition of human milk and the essential fatty acid status of the infant. (back)
- Maternal docosahexaenoic acid supplementation and fetal accretion. (back)
- Essential fatty acid transfer and fetal development. (back)
- Maternal DHA and the development of attention in infancy and toddlerhood. (back)
- Maternal supplementation with very-long-chain n-3 fatty acids during pregnancy and lactation augments children’s IQ at 4 years of age. (back)