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It's an age old question. Well, no, not really. It's actually just some fuckery that low carb knobs like to talk about. The question is whether or not low density lipoproteins (LDL) are causal of atherosclerotic cardiovascular disease (ASCVD) in the context of low inflammation. Luckily we have plenty of data on this question. So let's dive in.
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Firstly, we have epidemiological data that aims to divide a population up into quartiles related to acute myocardial infarction (AMI) [1](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343474/). These quartiles have varying levels and combinations of exposure to either high LDL, or high C-reactive protein (CRP): high LDL and high CRP, high LDL and low CRP, low LDL and high CRP, and low LDL and low CRP.
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![[Pasted image 20221123154714.png]]
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Looking carefully at this graph, we see that risk is lowest when both LDL and CRP are both low. But risk does go up in the context of low LDL and high CRP as well. The absolute worst situation to be in is with high LDL and high CRP. That group is in its own league in terms of risk.
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So, these data would seem to suggest that, yes, high inflammation does carry an independent risk of increased AMI, and presumably ASCVD. However, let's take another look at the graph. The green line is representing the risk of AMI in the context of high LDL and low CRP. This is the context low carb people love to speculate about, and it shows that LDL carries an independent risk all on its own as well.
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Recently, subgroup analyses on the FOURIER trial have also been done investigating the relationship between inflammation and ASCVD endpoints [2](https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.118.034032). The results essentially show the same thing.
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![[Pasted image 20221123154709.png]]
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Again, we see that having both high LDL and high CRP together yields the worst outcomes, having either elevated in isolation increases risk, and having both as low as possible maximally decreases risk. Now, granted we can't technically call this experimental data as far as CRP is concerned, since this is a post-hoc, observational analysis. Nevertheless, it shows the exact same hierarchy of effect as the epidemiology.
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Here's a representation of the data that is a little easier on the eyes:
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![[Pasted image 20221123154659.png]]
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Now, why isn't inflammation a target for therapy if it's so damn important? Well, the truth is we have attempted to target inflammation. The results have been almost universally unsuccessful [3](https://www.wjgnet.com/2220-6132/full/v8/i1/1.htm)[4](https://pubmed.ncbi.nlm.nih.gov/30560921/). We target LDL specifically because it is the most reliable target for therapy at this time. Interventions aimed to lower LDL reduce the risk of AMI and ASCVD, but interventions aimed to lower inflammation do not.
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**Key points:**
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- LDL and inflammation are both independently causal of ASCVD.
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- Inflammation causes ASCVD in both high and low LDL contexts.
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- LDL causes ASCVD in the context of both high or low inflammation.
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- Interventions to lower inflammation have largely been unsuccessful in reducing the risk of ASCVD.
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- Interventions to lower LDL have been overwhelmingly successful in reducing the risk of ASCVD.
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**References:**
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[1] [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343474/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343474/)
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[2] [https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.118.034032](https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.118.034032)
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[3] [https://www.wjgnet.com/2220-6132/full/v8/i1/1.htm](https://www.wjgnet.com/2220-6132/full/v8/i1/1.htm)
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[4] [https://pubmed.ncbi.nlm.nih.gov/30560921/](https://pubmed.ncbi.nlm.nih.gov/30560921/)
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#patreon_articles
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#disease
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#LDL
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#inflammation
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#cardiovascular_disease
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If you spend much time in the nutrition corner of social media, you may have noticed that there is an enormous amount of talk about nutrient deficiencies. It seems as though everyone is running deficient in something— vitamin D, calcium, zinc, etc. In some cases it may be true, sure. It may also be a decent recommendation to monitor your status of certain problem nutrients. But, did you know there are nutrients you probably never have to worry about?
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I made a couple of interesting discoveries relating to nutrient deficiencies while attempting to research nutrient depletion-repletion studies. As it turns out, just as there are nutrient deficiencies that are relatively common, there are also nutrient deficiencies that almost never happen. There are certain nutrients that are very, very rarely associated with deficiencies.
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Those nutrients are:
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- Vitamin B5
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- Choline
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- Manganese
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- Phosphorus
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Deficiencies of vitamin B5, manganese, and phosphorus have only ever been produced in metabolic wards. Meaning that we've only observed clinical deficiencies of these nutrients when we've locked people up and only feed them diets devoid of those nutrients.
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Deficiencies in choline are somewhat different. We first discovered that choline was required in the diet when patients receiving intravenous nutrition were fed choline-free formulas. That should say something about how common choline deficiencies are likely to be. We had to feed bed-ridden people choline-free diets intravenously to even discover that this nutrient was essential to get in the diet.
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It's been shown that 10% of the population require approximately double the AI of choline if they are deficient in riboflavin. But that's highly conditional and not a general effect. All in all it doesn't seem like choline deficiencies typically present themselves spontaneously in the population. Likely choline isn't much to worry about either. As I discuss [here](https://www.patreon.com/posts/elusive-choline-33684646), choline requirements depend on a large number of other nutritional factors and are incredibly difficult to characterize.
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**Key points:**
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- Deficiencies in vitamin B5, manganese, and phosphorus almost never happen in free-living humans.
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- Deficiencies in choline are difficult to characterize because choline requirements largely depend on overall diet quality.
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#patreon_articles
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#nutrition
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#disease
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#nutrients
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#vitamin_b5
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#choline
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#manganese
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#phosphorus
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Since I escaped the clutches of low carb zealotry, I've warmed up to a lot of conventional ideas about what constitutes a generally healthful diet. I've changed my positions on saturated fat, vegetable oils, sugar, carbohydrates, calories, etc. All of which I've discussed at length on my blogs and social media. I've also changed my views on dietary fibre, despite not really discussing it that much in the past.
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As I write this, I am of the opinion that dietary fibre is critically important for long-term human health, despite it technically not being an essential nutrient. My current diet gives me about 30-50g/day of fibre on average. The DRI for fibre is 38g/day for men and 25g/day for women. But, I was curious to know if there was any evidence that perhaps higher intakes could yield additional benefits.
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I stumbled across this systematic review and meta-analysis of dietary fibre intakes and cardiovascular disease (CVD) and coronary heart disease risk (CHD) [1](https://pubmed.ncbi.nlm.nih.gov/24355537/). As I read through it I was struck by these graphs, which illustrate the estimated effect of dietary fibre intake on CVD and CHD risk.
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![[1-1.jpg]]
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They suggested that we have at least one study (marked as red bars) suggesting that fibre could confer a benefit to CVD and CHD risk reduction all the way up to >60g/day. I'd never heard of intakes that high being studied before.
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I managed to track down the paper [2](https://pubmed.ncbi.nlm.nih.gov/23543118/). The fibre intakes were estimated using two different methods. One method yielded an estimated intake of ~63g/day, and multivariate analyses showed that intakes this high could reduce CVD risk by ~40% and CHD risk by ~30%. Huge numbers.
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In groups whose fibre intakes approximated the DRI, CVD risk was reduced by ~40% yet again, but CHD risk was only reduced by 20%. Still huge numbers, but this could suggest benefits to consuming fibre at levels that exceed the current DRI.
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**Key points:**
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- Meeting the DRI for fibre intake confers consistent benefits to CVD and CHD risk.
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- There is evidence that suggests eating even more fibre could confer additional benefits.
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**References:**
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[1] Diane E Threapleton, et al. Dietary fibre intake and risk of cardiovascular disease: systematic review and meta-analysis. BMJ. 2013 Dec. [https://pubmed.ncbi.nlm.nih.gov/24355537/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898422/)
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[2] Diane E Threapleton, et al. Dietary fibre and cardiovascular disease mortality in the UK Women's Cohort Study. Eur J Epidemiol. 2013 Apr. [https://pubmed.ncbi.nlm.nih.gov/23543118/](https://pubmed.ncbi.nlm.nih.gov/23543118/)
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#patreon_articles
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#nutrition
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#disease
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#fibre
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#cardiovascular_disease
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There are many so-called "optimal" micronutrient ratios that have been described in the literature. However very few of them have any sort of real validation with regards to human physiology, let alone human health outcomes. Often times ratios are simply reflecting having either too much of one nutrient or not enough of another nutrient, and not actually reflecting a particular ratio that nutrients need to be maintained within.
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For example, with the omega-3 to omega-6 ratio, virtually all of the negative associations with a low omega-3 to omega-6 ratio can be explained by having insufficient omega-3 intakes. Rather than higher omega-6 intakes being harmful, the skewed ratio is merely reflecting that one nutrient intake is inadequate. All the ratio does is confuse the issue, because lowering omega-6 to within an "optimal" omega-3 to omega-6 ratio doesn't address the inadequate omega-3 intake.
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I'm usually not a big fan of ratios in nutrition for reasons that I explained in [this](https://thenutrivore.blogspot.com/2020/01/measuring-nutrient-density-calories-vs.html) blog article. Ratios don't give you enough information. Foods that are enormously high in both nutrients could get similar scores to foods that are dismally low in both nutrients. For example, 100/10=10, and 1/0.1=10. Both of these examples give us identical scores, but there is an order of magnitude difference between the input values.
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Nevertheless, the academic debate around these ratios continues. But the least I could do to add some sanity to the debate is to help us visualize the ratios in a more productive way. So I've prepared a series of charts using a selection of common nutrient ratios. The charts are set up to actually tell us which types of foods are highest in whichever nutrient, in order to actually optimize the ratios.
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**Omega-3 vs Omega-6**
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![[Pasted image 20221123151445.png]]
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**Vitamin E vs Polyunsaturated Fat**
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![[Pasted image 20221123151451.png]]
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**Polyunsaturated Fat vs Saturated Fat**
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![[Pasted image 20221123151458.png]]
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**Potassium vs Sodium**
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![[Pasted image 20221123151503.png]]
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**Calcium vs Magnesium**
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![[Pasted image 20221123151508.png]]
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**Calcium vs Phosphorus**
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![[Pasted image 20221123151511.png]]
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**Zinc vs Copper**
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![[Pasted image 20221123151516.png]]
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#patreon_articles
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#nutrients
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#nutrition
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Is it necessary to consume animal foods to meet sufficiency of vitamin A? Some people in the nutrition space seem to think so. Proponents of so-called "ancestral diets" such as Chris Masterjohn and Chris Kresser have been squawking about this idea like a couple of demented parrots for years, but is there any merit to it?
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The argument essentially goes like this:
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There is genetic variation in the activity of the BCO1 enzyme, which is responsible for converting carotenoids into to active form of vitamin A, retinol. Therefore, plant foods are an unreliable source of retinol in those of us with these genetic variants, because they won't be able to convert enough.
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Cool story. It definitely seems as though there could be physiological plausibility for this hypothesis. But, let's see how it plays out in meatspace. No pun intended.
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Right off the bat, we can easily locate research wherein retinol status is ascertained in people with these genetic variants [1](https://pubmed.ncbi.nlm.nih.gov/19103647/). It seems as though even the people with the worst impairments maintain adequate retinol status, despite only getting an average of a measly 133mcg/day of retinol.
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The only thing that appears to change is that the ratio of beta-carotene to retinol, which is increased based on the exact type of genetic variation in the conversion rate. But it doesn't appear as though much else actually changes. In fact, the entire variance in the population sample in this study had fasting plasma retinol within the reference range. The authors themselves commented that all volunteers had adequate serum vitamin A concentrations.
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Additionally, a rather recent study published in 2020 found no differences in retinol status between BCO1 genotypes in a population consuming extremely low amounts of preformed retinol [14](https://pubmed.ncbi.nlm.nih.gov/32560166/). Again, virtually all study participants were within the reference range for plasma vitamin A, and plasma retinol concentrations did not vary between genotypes. In fact, vitamin A deficiency was correlated similarly with lower plasma carotenoid concentrations and plasma retinol concentrations.
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So, it does not actually seem to be the case that having these genetic variants meaningfully affects retinol status. There is a more parsimonious way of reconciling these data, though. It just means the rate of conversion is probably slower. The shape of the conversion curve is likely just longer and flatter in so-called "impaired" genotypes, but it's very likely the case that and the area under that conversion curve is likely the same.
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It's akin to the difference between low glycaemic carbohydrates and high glycaemic carbohydrates when matched for calories. The rates of absorption between the two yield differently shaped curves. The low glycaemic curve is long in duration and low in concentration in the postprandial window, while the high glycaemic curve is short in duration and high in concentration in the postprandial window. However, the area under both of these curves is identical.
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This is likely analogous to the conversion rates between so-called "imapired" genotypes and wildtype genotypes. Those with the so-called "impaired genotypes" are simply converting for longer, but much less at a time, whereas those with the wildtype genotypes are converting for a shorter period of time, but much more at a time. But the total amount converted between the two genotypes is likely close to equivalent.
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But, we can take this a step further and actually see what happens when we try to correct vitamin A deficiency using dietary carotenoids in human subjects [2](https://pubmed.ncbi.nlm.nih.gov/15883432/)[3](https://pubmed.ncbi.nlm.nih.gov/17413103/)[4](https://pubmed.ncbi.nlm.nih.gov/9808223/)[5](https://pubmed.ncbi.nlm.nih.gov/10584052/)[6](https://pubmed.ncbi.nlm.nih.gov/15321812/)[7](https://pubmed.ncbi.nlm.nih.gov/16210712/). On the whole, eating foods rich in carotenoids reliably improves and/or normalizes vitamin A status. Even foods that have been genetically engineered to have higher levels of carotenoids reliably improve vitamin A status in humans [8](https://pubmed.ncbi.nlm.nih.gov/19369372/).
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As a side note, the only cases of vitamin A toxicity (hypervitaminosis A) from whole foods that I could find in the literature involved the consumption of preformed retinol from liver [9](https://pubmed.ncbi.nlm.nih.gov/25850632/)[10](https://pubmed.ncbi.nlm.nih.gov/21902932/)[11](https://pubmed.ncbi.nlm.nih.gov/10424294/)[12](https://pubmed.ncbi.nlm.nih.gov/31089689/)[13](https://pubmed.ncbi.nlm.nih.gov/3655980/). In one case, a child died from consuming chicken liver pate sandwiches. I could find no case reports of vitamin A toxicity related to carotenoids.
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**Key points:**
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- Genetic impairments in the conversion of carotenoids to retinol do not seem to impact retinol status or make deficiency more likely.
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- Dietary carotenoids from whole plant foods can easily maintain adequate retinol status.
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- The only case reports of vitamin A toxicity from whole foods are attributable to liver consumption.
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**References:**
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[1] W C Leung, et al. Two Common Single Nucleotide Polymorphisms in the Gene Encoding Beta-Carotene 15,15'-monoxygenase Alter Beta-Carotene Metabolism in Female Volunteers. FASEB J. 2009 Apr. [https://pubmed.ncbi.nlm.nih.gov/19103647/](https://pubmed.ncbi.nlm.nih.gov/19103647/)
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[2] Paul J van Jaarsveld, et al. Beta-carotene-rich Orange-Fleshed Sweet Potato Improves the Vitamin A Status of Primary School Children Assessed With the Modified-Relative-Dose-Response Test. Am J Clin Nutr. 2005 May. [https://pubmed.ncbi.nlm.nih.gov/15883432/](https://pubmed.ncbi.nlm.nih.gov/15883432/)
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[3] Judy D Ribaya-Mercado, et al. Carotene-rich Plant Foods Ingested With Minimal Dietary Fat Enhance the Total-Body Vitamin A Pool Size in Filipino Schoolchildren as Assessed by Stable-Isotope-Dilution Methodology. Am J Clin Nutr. 2007 Apr. [https://pubmed.ncbi.nlm.nih.gov/17413103/](https://pubmed.ncbi.nlm.nih.gov/17413103/)
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[4] S de Pee, et al. Orange Fruit Is More Effective Than Are Dark-Green, Leafy Vegetables in Increasing Serum Concentrations of Retinol and Beta-Carotene in Schoolchildren in Indonesia. Am J Clin Nutr. 1998 Nov. [https://pubmed.ncbi.nlm.nih.gov/9808223/](https://pubmed.ncbi.nlm.nih.gov/9808223/)
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[5] G Tang, et al. Green and Yellow Vegetables Can Maintain Body Stores of Vitamin A in Chinese Children. Am J Clin Nutr. 1999 Dec. [https://pubmed.ncbi.nlm.nih.gov/10584052/](https://pubmed.ncbi.nlm.nih.gov/10584052/)
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[6] Marjorie J Haskell, et al. Daily Consumption of Indian Spinach (Basella Alba) or Sweet Potatoes Has a Positive Effect on Total-Body Vitamin A Stores in Bangladeshi Men. Am J Clin Nutr. 2004 Sep. [https://pubmed.ncbi.nlm.nih.gov/15321812/](https://pubmed.ncbi.nlm.nih.gov/15321812/)
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[7] Guangwen Tang, et al. Spinach or Carrots Can Supply Significant Amounts of Vitamin A as Assessed by Feeding With Intrinsically Deuterated Vegetables. Am J Clin Nutr. 2005 Oct. [https://pubmed.ncbi.nlm.nih.gov/16210712/](https://pubmed.ncbi.nlm.nih.gov/16210712/)
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[8] Guangwen Tang, et al. Golden Rice Is an Effective Source of Vitamin A. Am J Clin Nutr. 2009 Jun. [https://pubmed.ncbi.nlm.nih.gov/19369372/](https://pubmed.ncbi.nlm.nih.gov/19369372/)
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[9] Yosuke Homma, et al. A Case Report of Acute Vitamin A Intoxication Due to Ocean Perch Liver Ingestion. J Emerg Med. 2015 Jul. [https://pubmed.ncbi.nlm.nih.gov/25850632/](https://pubmed.ncbi.nlm.nih.gov/25850632/)
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[10] E Dewailly, et al. Vitamin A Intoxication From Reef Fish Liver Consumption in Bermuda. J Food Prot. 2011 Sep. [https://pubmed.ncbi.nlm.nih.gov/21902932/](https://pubmed.ncbi.nlm.nih.gov/21902932/)
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[11] K Nagai, et al. Vitamin A Toxicity Secondary to Excessive Intake of Yellow-Green Vegetables, Liver and Laver. J Hepatol. 1999 Jul. [https://pubmed.ncbi.nlm.nih.gov/10424294/](https://pubmed.ncbi.nlm.nih.gov/10424294/)
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[12] Martha E van Stuijvenberg, et al. South African Preschool Children Habitually Consuming Sheep Liver and Exposed to Vitamin A Supplementation and Fortification Have Hypervitaminotic A Liver Stores: A Cohort Study. Am J Clin Nutr. 2019 Jul. [https://pubmed.ncbi.nlm.nih.gov/31089689/](https://pubmed.ncbi.nlm.nih.gov/31089689/)
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[13] T O Carpenter, et al. Severe Hypervitaminosis A in Siblings: Evidence of Variable Tolerance to Retinol Intake. J Pediatr. 1987 Oct. [https://pubmed.ncbi.nlm.nih.gov/3655980/](https://pubmed.ncbi.nlm.nih.gov/3655980/)
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[14] Sophie Graßmann, et al. SNP rs6564851 in the BCO1 Gene Is Associated with Varying Provitamin a Plasma Concentrations but Not with Retinol Concentrations among Adolescents from Rural Ghana. Nutrients. 2020 Jun [https://pubmed.ncbi.nlm.nih.gov/32560166/](https://pubmed.ncbi.nlm.nih.gov/32560166/)
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#patreon_articles
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#nutrition
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#disease
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#vitamin_a
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#nutrients
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#nutrient_deficiency
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#animal_foods
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#clownery
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It has been suggested that a plant-based diet leaves one vulnerable to certain nutrient deficiencies. While I believe that this is true, I also believe that these concerns are incredibly overblown. The typical nutrients of concern are: vitamin B12, vitamin D, calcium, iron, and zinc. However, I'm not actually persuaded that any of these nutrients are uniquely concerning on a vegan diet in the general population.
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Research investigating B12 status in vegans comes up mixed, but in populations wherein supplementation is widely practiced, serum B12 does not significantly differ from that of omnivores [1](https://pubmed.ncbi.nlm.nih.gov/26502280). It is also not clear that merely being vegan makes much of a difference for vitamin D status [2](https://pubmed.ncbi.nlm.nih.gov/19339396). Maintaining adequate calcium status as a vegan is merely about consuming an adequate amount of calcium-rich foods [3](https://pubmed.ncbi.nlm.nih.gov/12491091). Lastly, I'm not convinced that iron and zinc are of general concern. It hasn't been persuasively demonstrated that animal food restriction uniquely predisposes to iron or zinc deficiency [4](https://pubmed.ncbi.nlm.nih.gov/27880062)[5](https://pubmed.ncbi.nlm.nih.gov/23595983).
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Food selection is king. When people are making improper food selections to target these nutrients, of course deficiency can occur [6](https://pubmed.ncbi.nlm.nih.gov/14988640). On a vegan diet, we don't get iron from fruit and vegetables unless we're eating a lot of black olives, haha. Soaked legumes and cooked whole grains would be better choices in that regard.
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However, there is one nutrient that I did stumble across that appears to be consistently problematic across vegan populations. Vitamin B6 deficiency seems to loom over various vegan and vegetarian populations, despite more than adequate intakes [7](https://pubmed.ncbi.nlm.nih.gov/16925884)[8](https://pubmed.ncbi.nlm.nih.gov/16988496)[9](https://pubmed.ncbi.nlm.nih.gov/1797957). There are plausible mechanisms by which vitamin B6 could be limiting on a vegan diet without supplementation, which I write about [here](https://thenutrivore.blogspot.com/2019/05/animal-nutrients-part-1-vitamin-b6.html).
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Essentially, vitamin B6 from plant foods typically comes in the form of pyridoxine glucoside, which is significantly less bioavailable than free pyridoxine or preformed pyridoxal [10](https://pubmed.ncbi.nlm.nih.gov/2843032)[11](https://pubmed.ncbi.nlm.nih.gov/9237945). Some of the only decent non-animal sources of vitamin B6 are avocados, bananas, and perhaps lentils. Not even nutritional yeast, which is usually a B-vitamin powerhouse, has a decent amount of vitamin B6. So, it's slim pickings for adequate sources if you're avoiding animal foods. But this might not be enough. While factoring in bioavailability it would take either four average bananas per day to meet sufficiency for vitamin B6, or four California variety avocados per day. For many people there are barriers to doing either consistently.
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I'm not trying to say that vitamin B6 will necessarily become a problem on a vegan diet. My perspective on this is that those following diets that severely restrict animal foods should probably find it prudent to consider adding vitamin B6 as pyridoxal-5-phosphate to their supplementation regimen as a precaution.
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**Key points:**
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- Vitamin B12, vitamin D, calcium, iron, and zinc aren't overly concerning on vegan diets.
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- Nutritional adequacy on a vegan diet can mostly be met with proper food selection.
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- Vitamin B6 deficiency is very common in both vegan and vegetarian populations.
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- Vitamin B6 from non-animal foods is not particularly bioavailable to humans.
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- Supplementing with vitamin B6 as P-5-P would be prudent on vegan diets.
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**References:**
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[1] R Schüpbach, et al. Micronutrient Status and Intake in Omnivores, Vegetarians and Vegans in Switzerland. Eur J Nutr. 2017. Feb. [https://pubmed.ncbi.nlm.nih.gov/26502280](https://pubmed.ncbi.nlm.nih.gov/26502280/)
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[2] Jacqueline Chan, et al. Serum 25-hydroxyvitamin D Status of Vegetarians, Partial Vegetarians, and Nonvegetarians: The Adventist Health Study-2. Am J Clin Nutr. 2009 May. [https://pubmed.ncbi.nlm.nih.gov/19339396](https://pubmed.ncbi.nlm.nih.gov/19339396/)
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[3] Kathrin Kohlenberg-Mueller and Ladislav Raschka. Calcium Balance in Young Adults on a Vegan and Lactovegetarian Diet. J Bone Miner Metab. 2003. [https://pubmed.ncbi.nlm.nih.gov/12491091](https://pubmed.ncbi.nlm.nih.gov/12491091/)
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[4] Lisa M Haider, et al. The Effect of Vegetarian Diets on Iron Status in Adults: A Systematic Review and Meta-Analysis. Crit Rev Food Sci Nutr. 2018 May. [https://pubmed.ncbi.nlm.nih.gov/27880062](https://pubmed.ncbi.nlm.nih.gov/27880062/)
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[5] Meika Foster, et al. Effect of Vegetarian Diets on Zinc Status: A Systematic Review and Meta-Analysis of Studies in Humans. J Sci Food Agric. 2013 Aug. [https://pubmed.ncbi.nlm.nih.gov/23595983](https://pubmed.ncbi.nlm.nih.gov/23595983)
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[6] Annika Waldmann, et al. Dietary Iron Intake and Iron Status of German Female Vegans: Results of the German Vegan Study. Ann Nutr Metab. 2004. [https://pubmed.ncbi.nlm.nih.gov/14988640](https://pubmed.ncbi.nlm.nih.gov/14988640)
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[7] A Waldmann, et al. Dietary Intake of Vitamin B6 and Concentration of Vitamin B6 in Blood Samples of German Vegans. Public Health Nutr. 2006 Sep. [https://pubmed.ncbi.nlm.nih.gov/16925884](https://pubmed.ncbi.nlm.nih.gov/16925884/)
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[8] D Majchrzak, et al. B-vitamin Status and Concentrations of Homocysteine in Austrian Omnivores, Vegetarians and Vegans. Ann Nutr Metab. 2006. [https://pubmed.ncbi.nlm.nih.gov/16988496](https://pubmed.ncbi.nlm.nih.gov/16988496/)
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[9] N Vudhivai, et al. Vitamin B1, B2 and B6 Status of Vegetarians. J Med Assoc Thai. 1991 Oct. [https://pubmed.ncbi.nlm.nih.gov/1797957](https://pubmed.ncbi.nlm.nih.gov/1797957/)
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[10] R D Reynolds, et al. Bioavailability of Vitamin B-6 From Plant Foods. Am J Clin Nutr. 1988 Sep. [https://pubmed.ncbi.nlm.nih.gov/2843032](https://pubmed.ncbi.nlm.nih.gov/2843032/)
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[11] H Nakano, et al. Pyridoxine-5'-beta--glucoside Exhibits Incomplete Bioavailability as a Source of Vitamin B-6 and Partially Inhibits the Utilization of Co-Ingested Pyridoxine in Humans. J Nutr. 1997 Aug. [https://pubmed.ncbi.nlm.nih.gov/9237945](https://pubmed.ncbi.nlm.nih.gov/9237945/)
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|
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#patreon_articles
|
||||
#nutrition
|
||||
#disease
|
||||
#nutrient_deficiency
|
||||
#nutrients
|
||||
#vitamin_b6
|
||||
#vegan_talking_points
|
||||
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Reference in a new issue