RDA levels vs. WHO vs. Nutrient Balance - potassium, calcium

RDA potassium 4700mg a day, WHO 3500 mg a day ..... Is this because in the US salt intake is so high. I rarely make 4700 but 3500 is very doable without supplementing. My potassium-sodium nutrient balance on Cronometer is usually to the right as I eat few processed foods and a lot of veggies.

RDA Calcium (senior) 1200mg vs WHO 500-700. Once again I find getting 500-700 from food doable but the 1200 requires supplements and, honestly, based on various articles I gather there is not a lot of science behind the 1200. I gave up on it because I saw an increase in BP and Horrific consiption no matter what form of calcium I took. The Calcium Magnesium balance in the meters you get with a gold subscription is usually right in the dark green.

So, how do other people feel about or know about these various values. I know from looking at dog food stuff that values were determined based on a grain based diet for dogs and grains impact mineral absorbtion etc. Where did the RDA values come from? How about the WHO values? How about Cronometer "balance"

Just things I am thinking about. FWIW I do supplement Magnesium. Most soils are very depleted in this one. Don't go overboard but do use it.

Comments

  • I regularly get over 1600mg of calcium from food alone, and I can get over 5500-6000mg of potassium from food alone. So, both are certainly doable, and I'm eating well under 2500 kcal per day these days. It's just about structuring the diet in a way that maximizes nutrient density. It's taken me months to dial in my diet, but I still struggle with thiamine, haha.

    I personally feel as though most of the DRIs are probably set too low, because for better or worse I've bought into Bruce Ames' triage hypothesis, hook, line, and sinker. That, and two or three independent research papers I've read that tried to quantify the daily micronutrient yields of contemporary hunter-gatherer diets had calcium at around ~1900mg and potassium at ~10,500mg. So personally, I consider 4700mg as a bare minimum to shoot for for potassium.

    We have to remember that the DRIs are often set around what is sufficient to prevent acute deficiency syndromes, like for folate. Some DRIs are set based on population serum measurements, like for manganese. We can't assume they tell us anything about chronic deficiency syndromes because there is minimal research on the subject. The current, established estimates are based on populations wherein half of people can be expected to get heart disease, a fourth of people can be expected to get cancer, and a tenth of people can be expected to become insulin-dependent type II diabetics. For some DRIs, I think the bar is set pretty low to start.

    On top of that, there are some DRIs that SHOULD exist, but don't exist. I also think some of the DRIs are currently screwed up, because they prioritize precursor nutrients over the biologically active form. For example, there is a DRI on pyridoxine, but not pyridoxal-5-phosphate. There is a DRI specifically for alpha-linolenic acid, but not DHA and EPA. There is no DRI for arachidonic acid specifically, but there is a DRI for linoleic acid. There is a DRI for "vitamin A", which prioritizes carotenoids and does not specifically target preformed retinol (on the NIH's website, sweet potato is mentioned as having more vitamin A than beef liver, which is total and complete nonsense). The DRI for vitamin K doesn't even make any sense at all right now. Not only is the DRI for vitamin K targeting the precursor nutrient, phylloquinone (K1), it's set too damn low. K1 has <10% bioavailability, which means you need to consume about 1200mcg to get the actual DRI of K1. If you shoot for the 120mcg per day, you're actually only getting 1/10th of the DRI. It's madness. There is a DRI for alpha-tocopherol, but no DRI for gamma-tocopherol, even though we know they both have unique biological activity. There is no DRI for lutein and zeaxanthin, even though it's clear as day that supplementing 6000mcg per day (which is totally within the realm of a nutritional dose) uniquely protects against macular degeneration. There's no DRI for glutathione even though it does survive digestion, and does increase glutathione status in the body. There's no DRI for glycine, even though it's pretty apparent from the literature that we need more (at least 10g) than our bodies are capable of synthesizing. There are TONS of other nutrients that aren't even on the map for investigation by those who establish the DRIs, and it frustrates me to no end. The fact that nearly all of nutrients that are ignored are distinctly animal-derived really makes me feel like there is some veiled vegan agenda behind the official nutrition recommendations we get. /rant

  • If I ate 2500 calories a day I would blow up like an elephant. I have lost a significant amount of weight on an average of 1200 a day and am now "in maintenance" trying to make a balance but it looks like around 1400 -1600 will be my target and I do a combination of walking about 6 miles a day and bodyweight fitness. As a senior citizen all health parameters and blood values are good and my diet is basically whole foods based with a mix of meat and vegetable protein. Very low on added sugar and grain products but not low carb.

    Not sure of any vegan agenda and that is certainly not where I am going but I don't believe there is compelling evidence that we should be eating a paleo-hunter-gatherer diet if that is where you are going. Humanity survived better in agricultural communities and disease, albeit different types of disease, existed in both populations. In all cases, animals are fed nutrient deficient diets designed for rapid growth anymore, hunted animals eat pesticide laden food, and our foods are grown in nutrient deficient soils. We grow a lot of our own food in soil supplemented with compost from rotting old hardwoods and with azomite added.

    The fact that all these organizations and esteemed biochemists disagree on these requirements speaks more to muddying the water than adding clarity to me. Ames seems to be another one for me I have not reviewed his work. (I have degrees in chemistry and in biochemistry so Linus Pauling is a hero of mine, though I certainly don't eat the massive amounts of vitamin C he recommended).

    Found a presentation of Ames tagging to go back -

  • edited November 2018

    Maybe the needed amount for K1 is 12mcg and the scientist take care of that 10% bioavailability and they make the RDA 120mcg.

    I apologise for my misspellings, as English is not my native language.

  • I think absorption is a lot of the equation. Different forms of minerals absorb differently and I know from working with dog stuff that phytates interfere with mineral absorption. You can test blood levels of B12 and D but Calcium is tricky because the body will rob bone to maintain balance in the blood and you are in a heap of trouble by the time your calcium levels are off. That, and various medications can throw things for a loop

  • If I ate 2500 calories a day I would blow up like an elephant. I have lost a significant amount of weight on an average of 1200 a day and am now "in maintenance" trying to make a balance but it looks like around 1400 -1600 will be my target.

    I'm pretty sure you could easily meet the DRI for potassium while staying under 1200-1600 kcal. You could do it by juicing carrots or leafy greens. The juice of about six carrots has about a gram of potassium. That's already 1/5th the DRI for 100 kcal. Add in 100g of spinach and 100g of kale and you're already half way there at around 200 kcal. 250g of sweet potato, 7 oz of chicken breast topped with half a cup of tomato sauce. One large banana as a snack. That's 4.7g of potassium for 900 kcal. Within a 1600 kcal window, you could even double the DRI of potassium at that rate if you wanted to.

    I don't believe there is compelling evidence that we should be eating a paleo-hunter-gatherer diet if that is where you are going.

    No, it wasn't where I was going. But contemporary hunter-gathers offer natural experiments that are very supportive of Bruce Ames' hypothesis. Despite the fact that Ames' does not advocate for an ancestral diet of any sort, his theories certainly explain a lot of the observations. For example, the data I referenced on hunter-gather micronutrient intake was collected on contemporary hunter-gathers from around 1900-1997. That anthropological data was used to estimate their daily micronutrient intakes, and then used to create averages. Bruce Ames posits that the body will prioritize pathways in the body that maximize short-term survival/reproductive fitness at the expense of long-term health if nutrients are scarce. In every rigorous experiment performed to test this hypothesis (at least in animals) on different nutrients, it held true. But, it seems as though it may also hold true for humans. Contemporary hunter-gathers routinely demonstrate to us that nutrient intakes far exceeding the current DRIs are inversely associated with degenerative diseases, cardiovascular disease, diabetes, etc. Even if they have no lifespan advantage, they certainly seem to have a healthspan advantage.

    So, I'm not saying that we should eat a "paleo-hunter-gatherer" diet, because I don't even know what that means. But, I think targeting nutrient density is a worthwhile principle that we can extract from those hunter-gathers, and we can readily apply it to our lives. Personally, generally speaking I don't see an obvious downside to this.

    Humanity survived better in agricultural communities and disease, albeit different types of disease, existed in both populations.

    Well, as far as I can tell it seems as though humanity has traded healthspan for the sake of economic convenience. It's much cheaper to live off of sugar, flour, and oil. So, most people eat just that, for both money and time saving. But, again, I'm not suggesting that we go back to eating the way people ate before agriculture. I'm saying we need to leverage nutrient density as much as we can, regardless of how we source our food. What I'm suggesting is a principle, it's not a literal prescription for a specific diet.

    I'd admit that those hunter-gatherers had way more infections, parasites, and sometimes a broken bone was a death sentence. However, despite modern medicine being really, really good at dealing with this acute medical emergencies, it has largely failed to deal with chronic medical emergencies. The natural experiments show us that a life largely free of those chronic issues is possible, at least in theory.

    The fact that all these organizations and esteemed biochemists disagree on these requirements speaks more to muddying the water than adding clarity to me. Ames seems to be another one for me.

    I think most of the disagreements are methodological. Some people believe the DRIs should be set two standard deviations above an average serum concentration of a given nutrient across a population. Some people believe that it is largely impossible to ascertain what is optimal because the RCTs required to suss out the information would be unethical and too costly. I fall into the latter camp. A huge percentage of the disagreements between scientists in nutrition is based solely on what constitutes legitimate evidence, and what methods are legitimate. I think it's perfectly reasonable to turn to natural experiments (like hunter-gatherers) if RCTs are just too hard, epidemiology is just too weak, and animal studies can't be extrapolated to humans reliably. There are populations out there who are testing many of our hypotheses for us, and I think it's worthwhile to extract whatever information we can from them.

    Maybe the needed amount for K1 is 12mcg and the scientist take care of that 10% bioavailability and they make the RDA 120mcg.

    I doubt it, since it takes a pharmacological dose of 1200mcg of phylloquinone to even generate a meaningful effect from the nutrient in vivo. By meaningful, I mean getting phylloquinone to do anything that all of the K2 subforms can also do. Those effects start at around a 1200mcg dose, and don't really become robust until you get to somewhere around a 40mg dose. Which is no longer nutritional, it's pharmaceutical. Meanwhile, nutritional doses (200mcg) of MK-4 and/or MK-7 generates effects on all of the relevant tissues pretty much immediately. This suggests to me that merely targeting "vitamin K" as the DRI is insufficient. Vitamin K1 needs to be deprioritized, and vitamin K2 needs to have its own DRI.

  • edited November 2018

    So, if I eat a bunch of greens every day it's useless for vitamin K, because it's too little ? :/

    I apologise for my misspellings, as English is not my native language.

  • edited November 2018

    It's not useless, because K1 does have biological activity. It just doesn't do everything that K2 can do at much lower doses. You need to get K1 up to pharmacological doses to even begin to see it do what K2 can do. I think the best approach is to eat a diet that pools as many K2 sub-forms, and as much K1, together as possible. Meat, cheeses, natto or other fermented foods, and eggs should all take priority over leafy greens if your goal is to get vitamin K. But leafy greens should be eaten as well, because K1 isn't useless.

    Vitamin K is actually a classification of nutrients. There are about 15-20 different forms. Only three forms have really been studied in humans well; K1, MK-4, and MK-7. However, we know of at least four or five sub-forms of K2 that have unique biological activity; MK-4, MK-7, MK-10, and MK-11. We just don't have any dosing studies or outcome data on those yet. So, if you're particularly risk averse like myself, I'd get a diet that is rich in as wide a variety of menaquinones as possible, and pile greens on top of that.

  • Hello!
    First, the requirement for potassium is an AI (adequate intake) and not an RDA. An AI is set when there isn’t enough research to determine the amount of a nutrient that is essential for various age groups. Most experts agree that the AI set by the Institute of Medicine is excessive; it was based on limited data to off-set the intake of sodium. I 100% agree that meeting the WHO’s recommendation for potassium is acceptable.

    The RDA for calcium is fairly new (established in 2011) and it was determined based on the amount needed for bone health and calcium retention. Now, as we know, bone health is influenced by the quality of our diet and technically, those eating more plant-based have a more alkaline diet so would be fine with a slightly lower intake of 700-800 mg (under age of 50 – women). Post-menopausally, we begin to break down bone mass quicker than it can be maintained, which is why calcium needs jump up to 1200 mg. Again, if you are eating a more plant-based diet and have a bone scan confirming healthy bones, you may be able to consume slightly under this. But if there is a risk of osteoporosis or osteopenia is present, higher calcium (between 1200-1400 mg) is needed.

    Other nutrients, including phosphorus, sodium, vitamin K, magnesium, protein, etc. can influence bone health as well. With regard to magnesium, I would just focus on hitting the RDA, which is easy to do if you regularly eat pulses.

    Also, regarding RDAs, we need to keep in mind how they are established. An EAR (or estimated average requirement) is the intake of a nutrient that will meet 50% of the needs of a population of a defined age and gender. An RDA is 2 standard deviations above the EAR and will meet 97-98% of the needs of a population. EARs are only established if there is ample research (I’m talking multiple systematic reviews and meta-analyses with rigorous research protocols and controlled setting). EARs/RDAs shouldn’t change unless there are ample and equally rigorous studies to suggest doing so.

    Lastly, in regard to vitamin K, the scientific evidence on the necessity of K2 is unclear. If we consider vegans, who have little to no intake of K2 (and would just absorb bacteria-produced K2), there doesn’t seem to be any known or proven negative health outcomes of a supposed vitamin K2 deficiency. As such, I think we need to be careful in generalizing the essentiality of nutrients until objective scientific data grants as the ability to do so.

    Kind regards,

    Susan Macfarlane, MScA, RD
    Registered Dietitian Nutritionist
    cronometer.com
    As always, any and all postings here are covered by our T&Cs:
    https://forums.cronometer.com/discussion/27/governing-terms-and-disclaimer

  • ...those eating more plant-based have a more alkaline diet so would be fine with a slightly lower intake of 700-800 mg (under age of 50 – women) ... if you are eating a more plant-based diet and have a bone scan confirming healthy bones, you may be able to consume slightly under this.

    The relative pH of your diet has nothing to do with mineral loss from, or mineral deposition into, bone. Yes, low pH conditions in the extracellular environment modulates the rate of bone resorption, but this is primarily for supporting calcium homeostasis in response to exercise. It isn't a consequence of the diet unless the diet itself is creating a metabolic acidosis (like with nutritional ketosis or severely over-consuming protein). During exercise, the relative acid load in your blood is increased. Metabolites like lactate, urea, and acetoacetate will necessarily lower blood pH, and are all a consequence of exercise. This signals to osteoclasts to undergo bone resorption to maintain Ca homeostasis. When researchers make the leap from "low pH in the micro-environment causes bone resorption" to "the acid load of the diet causes bone resorption", they're making an invalid inference.

    The myth that the vegan diet is "alkaline" comes from a single small (poorly controlled) study that indicated that omnivores had a higher PRAL and excreted more calcium in the urine. There are any number of things that could explain this phenomenon, given the level of confounding in the study and the small sample size. Everything from protein restriction in the vegans, to protein excess in the omnivores, to mineral status/balance, etc. Maybe vegans do need less calcium, who knows. But it's not clear that the mechanisms that lead to the unique calcium sparing are at all desirable. Especially if it means you need to under-consume protein in order to attain it.

    Other nutrients, including...vitamin K...can influence bone health as well.

    Yes. But K2 is the precise nutrient you want to consume to inhibit bone resorption and facilitate bone remineralization. Osteoblasts secrete osteocalcin, which is carboxylated by vitamin K2 (primiarly MK-7). This action actually tells osteoclasts to stop bone resorption, and tells osteoblasts to rebuild it. After the osteocalcin has been used it is converted to undercarboxylated osteocalcin, which acts as a hormone in the body to support exercise capacity, sex hormone secretion, and insulin sensitivity.

    So, there is a beautiful synergy between calcium, K2, and exercise. Exercise triggers the process of bone resorption, K2 moderates it, and undercarboxylated osteocalcin is released as a consequence to further support the exercise capacity. But, this doesn't happen unless K2 status is optimal, as K1 doesn't support this process at all. You can convert K1 to MK-4, but MK-4 is primarily supporting vitamin-K dependent processes in the soft tissue, not so much the bone. Research currently indicates that your need for K2 far exceeds the body's capacity to synthesize it from K1. It also indicates that there is a need for variety in K2 sub-forms

    Lastly, in regard to vitamin K, the scientific evidence on the necessity of K2 is unclear. If we consider vegans, who have little to no intake of K2, there doesn’t seem to be any known or proven negative health outcomes of a supposed vitamin K2 deficiency. As such, I think we need to be careful in generalizing the essentiality of nutrients until objective scientific data grants as the ability to do so.

    I mean, we can split hairs about what constitutes "legitimate scientific data". Some of the DRIs have astonishingly little data behind them, like manganese or vitamin B5. Far less data than what is available for vitamin K2. There is plenty of wonderful mechanistic detail that has been worked out for K2, and every scrap of evidence appears to cohere. The only difference is that there is no clear acute deficiency syndrome associated with K2 deprivation. This is where me and the Institute of Medicine diverge philosophically. I think the prevention of chronic deficiency syndromes is equally as important as preventing acute deficiency syndromes. The IoM feels differently. Personally, I think we will one day expand the range of what we consider to be essential nutrients based on long-term health in addition to short term health.

    In the observational literature, K2 intake is universally inversely associated, in a dose-dependent manner, with soft-tissue calcification. In animal models, knocking out the gene responsible for converting K1 to K2 in the context of a K2 deficient diet facilitates soft tissue calcification and osteoporosis. K1 alone does nothing to stop it. In vivo, K2 activates matrix-GLA-protein and directs calcium away from soft tissue and toward bone. K2 also activates osteocalcin to rebuild the bone with the calcium delivered by matrix-GLA-protein. The evidence is almost complete, and everything makes sense. There are several large RCTs that are currently ongoing to test these mechanisms in free-living humans, but directionally the literature is VERY persuasive that K2 (at least both MK-4 and MK-7) are necessary for proper calcium homeostasis long-term. Even if your arteries don't harden over night by not eating enough K2, it doesn't make it non-essential. It just means that our criteria for determining what is indeed essential isn't currently calibrated properly.

    (and would just absorb bacteria-produced K2)

    If you're referring to K2 produced by the human gut, this is also a myth. Just like in any other cell, bacteria store their K2 in their membranes and organelles. You'd actually have to digest your own gut bacteria in order to liberate the K2 and absorb it. The data on the whole is that humans derive little to no K2 from our gut bacteria.

  • But then how can we survive if K2 is so important in our bodies and no food contain it and K2 from gut it's a myth ? :(

    I apologise for my misspellings, as English is not my native language.

  • edited November 2018

    Many foods contain crazy high amounts of K2. Natto has around 900mcg of MK-7 per 100g serving. So, even eating a little tiny bit of it will give you more than enough MK-7. Pork contains ridiculously high amounts of MK-4, MK-10 and MK-11. Certain types of cheeses contain crazy high amounts of K2, mostly as MK-8 and MK-9. Poultry livers contain really high amounts of MK-4. Eggs contain marginal amounts of K2 as MK-4. Sauerkraut and Kimchi do as well, but even less than eggs. It would be relatively easy to work at least 200mcg of different K2 sub-forms into your diet.

    One of the limitations with K2 content measurements in food is that researchers aren't even looking. There are plenty of food analysis studies looking for MK-4 and MK-7 content of food. But, there are fewer studies looking for MK-8 and MK-9, and even fewer studies looking for MK-10 and MK-11. The problem is that nobody has actually just decided to measure the total menaquinone content of different foods. Sometimes there are also menaquinones in foods that we didn't know existed.

    It's HIGHLY likely that most of the foods we consider good sources of K2 are actually much richer than we think they are, merely because they've never had their total menaquinones measured before. For example, for years it was established that Jarlsberg cheese had around 60mcg of K2 per 100g serving. However, they discovered a special type of K2 in the cheese called MK-9(4H). Including this menaquinone, Jarlsberg cheese has closer to 140mcg of K2 per 100g serving. If you count K2 toward the RDA for vitamin K, 100g of Jarlsberg cheese gives you around 116% of the daily value. I mean, that's a lot of cheese, haha. But, even 30g of Jarlsberg, 3 eggs, a little chicken liver, or just a tablespoon of natto will give you the RDA. Personally, I take a natto supplement to a total of 200mcg of K2 every day. But I also eat a wide range of K2 containing foods.

  • Wow, I didn't know that ! :astonished: Thanks for the info !
    I do eat cheese, pork, liver and egs... but fermented soy it's not common in our country. :( Too bad.
    So, Vitamin K from Cronometer refers only to K1 ?

    I apologise for my misspellings, as English is not my native language.

  • edited November 2018

    The DRI for vitamin K set by the Institute of Medicine doesn't make any distinction between K1 and K2, but they place priority on K1 in terms of their recommendations. As for Cronometer, there will be K1 and K2 data in their food databases, but it will be horribly incomplete. For a lot of foods that I regularly eat I had to make custom foods entries that include the K2 data.

  • I'll also point out that veganism has been associated with ischemic heart disease in some of the prospective literature. A condition that vitamin K2 deficiency could actually explain, as ischemic heart disease manifests itself as arterial calcification the vast majority of the time.

  • I checked the Natto food from Cronometer and they reports 23 mcg for vitamin K. So I gues that this is K1, because Natto has 900 mcg ok K2.

    I apologise for my misspellings, as English is not my native language.

  • The K2 content of natto in Cronometer's databases is incomplete. Every independent analysis I've seen says around 900mcg to 1100mcg total menaquinones. https://honey-guide.com/2014/03/10/menaquinones-k2-and-phylloquinone-k1-content-of-animal-products-and-fermented-foods/

  • Hi @BRBWaffles

    The reference for those eating a plant-based diet requiring lower calcium needs comes from the WHO. It’s not referring to calcium deposition into bone, but rather total retention by the body (i.e. lower calcium loss in the urine). I also think we need to be careful not to focus too much on one single nutrient when it comes to discussing the overall health of an entire body system or organ. The take home message regarding calcium (to keep things simple for anyone reading this) is that calcium is an important component of bone health. Minimum amounts are necessary to prevent osteoporosis but the exact level of intake needed to maintain bone health throughout life is still controversial and may depend on individual lifestyle factors and genetics.

    I also wrote a blog post on PRAL and alkalinity (you can find it on the Cronometer blog); the whole acid/ash theory isn’t very strong when you consider the impact of foods within the body.

    I love your detailed mechanistic explanation of the way K2 works on bone health. It’s clear that you read a lot of nutrition research and have a solid understanding. But if I can offer one small piece of advice it would be to start with mechanistic and cellular studies and to continue to expand your research to include epidemiological studies. As a healthcare professional (and very humbly speaking on behalf of nutrition researchers) it’s unethical and unscientific to create nutrition guidelines, recommendations, and policies without have the rigorous data to back up such recommendations. Since the Cronometer forum is public platform that incorporates the nutrition needs of diverse populations, any recommendations that I make need to be credible and factual. And as I’m sure you’ve learned, 90% of studies published either provide us with useless information or have flawed methods that it’s necessary to take them with a grain of salt. (Whenever I review research, I consider the GRADE approach, the hierarchy of literature, the confounders that were not considered, and the methods/measurements that were used; doing this can be time consuming but helps you to appreciate that just being published doesn’t mean a study is any good. Also, you can consider a journal’s impact factor; < 6 is suggestive of lower quality research).

    I do agree that there is a lack of data behind some of the DRIs; in these cases, very conservative recommendations are made that consider human safety.
    I also read A LOT of research on veganism (as I’m a research consultant in the field) so you’d have to share the study you’re referring to where it is linked to ischemic heart disease. The only risk of heart disease for vegans is homocysteine and methylmalonic acid. Adequate B12 supplementation prevents this.

    Happy to clarify anything mentioned here!

    Kind regards,

    Susan Macfarlane, MScA, RD
    Registered Dietitian Nutritionist
    cronometer.com
    As always, any and all postings here are covered by our T&Cs:
    https://forums.cronometer.com/discussion/27/governing-terms-and-disclaimer

  • I do agree that there is a lack of data behind some of the DRIs; in these cases, very conservative recommendations are made that consider human safety. I also read A LOT of research on veganism (as I’m a research consultant in the field) so you’d have to share the study you’re referring to where it is linked to ischemic heart disease. The only risk of heart disease for vegans is homocysteine and methylmalonic acid. Adequate B12 supplementation prevents this.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191896/

    Skip ahead to Table 4. Veganism was actually associated with an increase in cardiovascular disease and ischemic heart disease mortality among women. However, the opposite was true for men. Whereas pescatarianism was

    But, to be clear, I don't think this is a cause and effect relationship. I may think veganism is silly, reckless, and needlessly restrictive to the point of bordering on a sort of religious fanaticism. However, I don't think veganism causes IHD and CVD mortality to increase in women and decrease in men, haha. But, I think it's totally plausible that this reflects things that may have been missing from the diet, and perhaps those things affect one sex more than the other. Perhaps it's iron. Anemia is an independent risk factor for CVD, and iron inadequacy is certainly more problematic for women than men.

    But if I can offer one small piece of advice it would be to start with mechanistic and cellular studies and to continue to expand your research to include epidemiological studies.

    I have.

    https://www.ncbi.nlm.nih.gov/pubmed/15514282

    In their multivariate analyses, K2 presented itself as an independent variable that was inversely associated with CVD. But K1 wasn't.

    https://www.ncbi.nlm.nih.gov/pubmed/27927636

    This last study doesn't speculate much about what aspect of natto was so uniquely beneficial. High quality soy protein was associated with a reduction in CVD and IHD, but natto consumption knocked it out of the park. Maybe it just means that soy consumption is a marker of good lifestyle habits, and natto is merely an extension of that. Maybe it's totally the healthy-user bias. But it's also very plausible that it was the menaquinone content of natto that offered the unique benefit.

    https://www.ncbi.nlm.nih.gov/pubmed/19179058

    https://www.ncbi.nlm.nih.gov/pubmed/27640076

    https://www.ncbi.nlm.nih.gov/pubmed/18722618

    And there are also RCTs beginning to tease out this effect:

    https://www.ncbi.nlm.nih.gov/pubmed/25694037

    More rigorous RCTs are under way:

    https://www.ncbi.nlm.nih.gov/pubmed/29561783

    https://www.ncbi.nlm.nih.gov/pubmed/26516910

  • Thanks for sharing this study. I took a look at the methods and unfortunately, there are a number of limitations that significantly impair our ability to deduce any good conclusions.

    First, the use of Adventist populations has been criticized. In general, these populations are mostly vegetarian, don’t drink, don’t smoke, and have healthy approaches to stress-management (which is why they are one of the Blue Zones). When comparing healthy vegan Adventists to healthy non-vegan Adventists, there really isn’t going to be stark differences in outcomes and this population simply doesn’t reflect the way most of the population eats and lives.

    In addition, they classified vegans and vegetarians in the way I hate most – FFQ. Furthermore, there was no attempt to qualify the type of diet individuals ate. In present day, with veganism on the rise, it’s so important for research articles to consider the nutrient intake of vegans in order to differentiate those eating whole-food, plant-based from “junk food vegans”.

    Regarding the outcomes of the study, technically a “vegetarian-style” diet (since they grouped dietary groups together – another pet peeve ) was associated with a lower risk of all-cause mortality. And when you look at death rates, vegans had the second lowest death rate, compared to pescatarians, which is interesting.

    Lastly, we need to consider who the reference population is, non-vegetarians. Veganism wasn’t associated with death from heart disease, but based on these findings alone (again a healthy vs. a healthy population) veganism wasn’t always as good as the other dietary patterns in lowering death risk. But compared to non-vegetarians it is.

    If I were reporting on this study to an authoritative body, my conclusion would be very conservative and likely state that “vegetarian-type dietary patterns are associated with a lower risk of mortality compared to non-vegetarian dietary patterns among Adventist population groups”. Beyond that, there’s little we can conclude.

    Also, to play devil’s advocate, when you say:

    “But, to be clear, I don't think this is a cause and effect relationship. I may think veganism is silly, reckless, and needlessly restrictive to the point of bordering on a sort of religious fanaticism.”

    It doesn’t really sound like you are dietary agnostic. 😉 Which is totally fine! We all have our biases when it comes to diet. And while I am very much pro-vegan, I do think there are other healthy ways of eating.

    Now, onto the vitamin K battle!

    So I don’t necessarily think what you are arguing is incorrect, but we may need more convincing data in order to change current recommendations for the general population. I think where recommendations will start will be with at-risk populations (i.e. those with osteopenia/osteoporosis).

    While I don’t have time to review the studies you shared, what I’m thinking of doing on the blog is a summary of each of the essential nutrients; highlighting the DRIs, as well as current controversies and new research. The research you shared will certainly be useful when I get to vitamin K.

    Keep up the great work!

    Susan Macfarlane, MScA, RD
    Registered Dietitian Nutritionist
    cronometer.com
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  • It doesn’t really sound like you are dietary agnostic.

    I'm mostly agnostic to subjects of legitimate controversy in the literature, when the costs and benefits of certain foods or diets are genuinely ambiguous. In those cases, I have an innocent-until-proven-guilty approach and don't worry about it. However, I do not have the same view of veganism. I think it's completely unambiguous that veganism is inherently reckless, if not outright dangerous.

    The only reason it has the political and academic traction that it does is because it appeals to idealistic left-wing moral principles that just so happen to be popular at this moment in history. I think if people weren't so ideologically motivated, a critical examination of human physiology and genetic variation would have landed veganism in the bin a long time ago. It's only real life-line is that it's fashionable at the moment.

    One could easily retort with "well, I know lots of vegans who are thriving". Which sounds convincing and meaningful at first. But, in reality all it really demonstrates is that if you get enough people to self-select a vegan diet, you'll get some for whom it works well enough. It doesn't speak to the many people who assuredly tried veganism and were actually harmed by it. So, I don't buy into the appeals to self-selected populations of any sort. They weren't randomized to veganism, so it tells us nothing about its viability. When people are randomized to veganism, as can be found on PubMed, there are rarely adherence rates above 50% or 60% among studies that rigorously track it.

  • @BRBWaffles

    As mentioned, I've spent a lot of time researching veganism as I'm a research analyst on the topic in my other job. I promise that if I come across something in the research or in my clinical practice that suggests vegans are at an increased risk of mortality/morbidity, I will be sure to let you know. :wink:

    Kind regards,

    Susan Macfarlane, MScA, RD
    Registered Dietitian Nutritionist
    cronometer.com
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  • I doubt that very much. I provided you with that precise data, and you dismissed it. If you read PubMed with a critical eye, you'll find animal food abstinence is associated with a whole host of pathologies. Everything from chronic peripheral neuropathy, permanent CNS trauma, to even blindness. The data exists, and is easy to find. The problem is confirmation bias keeps one from accepting the data as a representation of a potential danger. Instead, the most ideologically committed vegans typically just shrug it off and speculate that those who experienced harm from the diet merely did it wrong. I don't buy it.

    I had a vegan MD at one point mention to me that it was unambiguous that veganism was dangerous. But he was vegan purely for moral reasons, and claimed that he would accept his likely early morbidity because it wasn't worth the "murder". To this date he's the only honest vegan I've ever met.

  • edited November 2018

    First, the use of Adventist populations has been criticized. In general, these populations are mostly vegetarian, don’t drink, don’t smoke, and have healthy approaches to stress-management (which is why they are one of the Blue Zones). When comparing healthy vegan Adventists to healthy non-vegan Adventists, there really isn’t going to be stark differences in outcomes and this population simply doesn’t reflect the way most of the population eats and lives.

    Who criticised the cohort selection?

    Butler et al. (2007) state that for North-American Adventists populations about half eat a diet similar to the general population (46.8% non-vegetarian). That isn't that a good comparison? Butler et al. (2007) also consider the low levels of drinking and smoking to be a strength rather than a limitation because it eliminates those habits as confounding. Seems reasonable.

    Butler, T. L., Fraser, G. E., Beeson, W. L., Knutsen, S. F., Herring, R. P., Chan, J., . . . Jaceldo-Siegl, K. (2008). Cohort Profile: The Adventist Health Study-2 (AHS-2). International Journal of Epidemiology, 37(2), 260-265. doi:10.1093/ije/dym165

    Edit: Also, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986422/ tend to agree but, as expected, caution about extending any conclusions to more general groups. But that's a limitation for any cohort study really.

    #moredotsthanadalmatian

  • edited November 2018

    Hello,

    If you're interested, this is a good article that points out some of the issues with studying Seventh Day Adventist populations: https://www.ncbi.nlm.nih.gov/pubmed/25149402

    Overall, findings from this population are not necessarily duplicated in other cohorts.

    While I do agree that a tightly controlled cohort is useful if you want to say look at a nutrient level, it's not as beneficial when you are looking at chronic disease risk, as the generalizability is severely limited.

    The other thing I would be cautious of is looking at studies with early vegan population groups. The diet of a vegan in 2007 is very different from that in 2018; some nutrients have increased, but others have decreased.

    At the end of the day, we have enough information and literature to show that a well-planned vegan diet can meet the nutrient needs of individuals at various stages of the life cycle. This doesn't mean that everyone needs to go vegan but it gives peace of mind to those that are interested in doing so. :)

    Kind regards,

    Susan Macfarlane, MScA, RD
    Registered Dietitian Nutritionist
    cronometer.com
    As always, any and all postings here are covered by our T&Cs:
    https://forums.cronometer.com/discussion/27/governing-terms-and-disclaimer

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