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...The most northern is Sardinia, Italy and even there one can get good sun exposure much of the year, suggesting high vitamin D levels could be an essential factor in longevity.

 

Yes, Sardinia, even though not a southerly region, tend to be sun-scorched

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Btw, do you  recall what Rhonda recommends in regards to K2 supplementation ?  

 

 

Sibiriak, I found the relevant transcript from the Tim Ferris podcast, although strictly it refers to Rhonda's personal regime. I don't know why she takes MK4, presently there are mixed Mk4 + MK7 supplements. If I remember well, MK4 has a short life in the system.

 

 

Another supplement that I take every other day is vitamin K2 which is found in fermented foods particularly natto but also in organ meat. This is thought to be a good one to take with vitamin D since both are involved in calcium homeostasis. I usually take 100 micrograms in the form of menaquinone otherwise known as MK4.

 

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  • 3 years later...

It seems like levels much over 40-50 ng/mL increase risk, based on what I am reading nowadays.

See also this:

Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study

Compared with controls, the offspring of nonagenarians who had at least one nonagenarian sibling had a reduced frequency of a common variant in the CYP2R1 gene, which predisposes people to high vitamin D levels; they also had lower levels of vitamin D that persisted over the 2 most prevalent genotypes. These results cast doubt on the causal nature of previously reported associations between low levels of vitamin D and age-related diseases and mortality.

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Ron, that's a very old study in the world of vitamin D research (2012). Lots has come out since then.

There remains disagreement about the exact optimal level. Many knowledgeable doctors & researchers quote 40-60ng/ml. Few to no people advocate 30ng/ml as better than 40ng/ml though some claim that 40 should be the upper end of the optimal range, but most of the uncertainty and debate is about where the upper end of optimal range is. As the reverse-J-shaped curve Michael R posted on the 1st or 2nd page of this thread in 2016-2017 showed, the steepness of the all-cause mortality graph is lower in the higher blood level direction than the lower level, so it makes sense there is more debate about the upper end of the optimal range. And there may be tradeoffs such as increases in some kinds of mortality vs decreases in others.

But it's also important to note that there is ample evidence that low vitamin D levels worsen COVID-19 and in fact lots of evidence that vitamin D supplements directly help against this virus (more than others) and good mechanism arguments as well (including direct action against the virus particles). For a review, see my review http://agingbiotech.info/vitamindcovid19/ or its 1-pager summary: http://agingbiotech.info/vitamindcovid19facts/

So here in the year 2020 the optimal blood vitamin D (25OHD) range has probably temporarily shifted to a higher range than the previous optimal due to a higher short-term risk from COVID-19.

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By thefind Rhonda Patrick 

On 6/9/2017 at 4:30 PM, Sibiriak said:

Thanks mccoy!

I was able to trace Rhonda's supplement, it is Thorne vitamin D/K2, ordered one bottle and it is very convenient, comes in drops. Pretty expensive but supposedly good quality studd.

image.png.1aabec5bcaa0ffc0521fcc6c64e99616.png

 

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Thanks Mccoy,

 
Serving Size: Two Drops
Servings Per Container: 600
  Two Drops Contain: %Daily Value
Vitamin D (as Vitamin D3) (1,000 IU) 25 mcg 125%
Vitamin K (as Vitamin K2 (Menatetrenone))† 200 mcg 167%

Daily Value (DV)
†MK4

Other Ingredients

Medium chain triglyceride oil, mixed tocopherols.

I see that the Thorne product uses the MK4 form of K2.  There's been good deal of discussion about the distinct bioactivities,  bioavailability  and relative merits of MK7 vs MK4 which I'm sure you are familiar with,  so I won't go into that. 

There does seem to be agreement  that standard MK4 dosages need to be much greater than equivalent MK7 dosages  which suggests that the 200mcg MK4 dosage is quite low and perhaps completely ineffective.   (Many studies use MK7 dosages of 180-360 mcg/day,  while major MK4 studies have used 45 mg/day.)

Personally,  I  prefer to have my Vit. D and K2 supplements separate  so I can adjust levels individually.   Currently, I'm taking MK7  and a vegan form of D3 (more expensive!).   I've considered an MK7/MK4 combination or "full spectrum" K2 supplement, but haven't gone that route so far.

 I base my Vit D  supplementation on blood tests,  aiming for ~ 40ng/ml.   I don't get to much sun, so I definitely must supplement.

Edited by Sibiriak
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Yes, the MK4 form is probably less desirable than the MK7 form but my suspicion (gathered after some research) is that the importance of the K2 vitamin may be overestimated and that the body may be using MK1, phylloquinone = simple K vitamin to manufacture MK7.

The above being said, I still take MK7 pills, but saw no noticeable differences from my previous amounts, much smaller than the accepted minimum requirement of about 80 ug/d.

The precautionary principle rulez...

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On 7/30/2020 at 11:25 AM, kpfleger said:

Ron, that's a very old study in the world of vitamin D research (2012). Lots has come out since then.

There remains disagreement about the exact optimal level. Many knowledgeable doctors & researchers quote 40-60ng/ml. Few to no people advocate 30ng/ml as better than 40ng/ml though some claim that 40 should be the upper end of the optimal range, but most of the uncertainty and debate is about where the upper end of optimal range is.

I agree with much of what you wrote and my personal doctor subscribes to 30-40 (I've been generally hovering around 30 but lately upped my intake of D and now I am at 46, so I am reducing it a bit).

But I read the study I posted a bit differently.  It seems to indicate to me that there are long-lived people who are naturally predisposed to low levels of vitamin D.  Wheather these people live longer because of the lower vitamin D levels or despite of it, is a different question.  It may simply be the case that people with the common variant in CYP2R1 who have low vitamin D levels are adversely affected by such lower levels, while those with reduced frequency are not.

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  • 2 years later...

Almost three years later, I still don't know how I feel about supplementing with vitamin D 🤔

Vitamin D Pills Don’t Prevent Bone Fractures, Osteoporosis: Study
 

Quote

 

As The New York Times reports, bone fractures and osteoporosis now join the list of several other vitamin D supplement use cases that the VITAL study has debunked. For example, earlier analyses of the data found that the supplements don’t protect against developing cancer or cardiovascular disease, fallscognitive declinemigrainesstrokemacular degeneration, or joint pain—nor did it reduce body weight or BMI.

Even though the supplements are taken by millions of Americans, according to the Times, some experts who reviewed the data now say it’s not worthwhile to do so without specific reason, such as an extreme deficit.

 

 



But, there is this one (although, anazingly, it doesn't adjust for education level, or even for transient supplementation seemingly):

Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status
 

Quote

Across all formulations, vitamin D exposure was associated with significantly longer dementia-free survival and lower dementia incidence rate than no exposure (hazard ratio = 0.60, 95% confidence interval: 0.55–0.65). The effect of vitamin D on incidence rate differed significantly across the strata of sex, cognitive status, and APOE ε4 status.



And finally, here is a discussion of both sides:
 

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That study from VITAL data that showed no benefit for fracture risk came out half a year ago The editorial that accompanied it was unbelievable and the study itself did not conform to reasonable guidelines for studies of nutrient (as published by Heaney 8 years ago). In particular, the VITAL subjects started with plenty high vitamin D levels at baseline.

Several people wrote rebuttal pieces to that study right after it came out. I collected at least 4 of them and wrote a thread here summarizing them and other points (including the link to the Heaney guidelines study I just mentioned) here: 

 

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If I try really hard I can sort of understand how it's easy to be confused because despite the overwhelming data over years & years and countless studies, there are still somehow big vitamin D skeptics who partially feed of the fact that some of the vitamin D advocates go to far & exaggerate the positive data. And it's not helped by journalists who want to write sensationalist articles.

But if you actually read the literature and think carefully about what data there is, what you see is huge amount of data showing that vitamin D levels are important, supplementation seems to be beneficial when levels are low and supplementation is daily (not giant doses then stopped for a long time), and direct sun probably has other benefits too. The problem is that then 1 popular article comes out and some subset of people just forget all the prior info for some reason.

To continue to feel that it's ambiguous whether vitamin D insufficiency is important just seems head-in-the-sand to me at this point.

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I can easily imagine a completely legit set of cases when vitD supplementation is not helping with fracture risks, vitD helps to get more calcium absorbed and less being lost. If a person has enough calcium fed back into bone remodelling process without this, in many cases seems a "backup" way - then yes, such a low impact thing will not be visible in the highly complex "aggregate" parameter as fracture risk, which itself is measured as a proxy due to impossibility to measure it directly anyhow.

So nothing wrong, there could be such cases and it is expected and explainable with accumulated knowledge.

My own case was like this.

I discovered my calcium at a higher normal which is not really normal as many people are mentioning, I was able to lower it with 5000ku of d3 daily and increasing the daily intake of calcium to 1300-1600mg/day (plants sources, so no idea how much of it is absorbed). The thing that looked paradoxically for me at the beginning of debug is that both things have to be done, when I was on 600-800mg/day vitD supplementation was less effective and serum calcium was higher - body just used pth to "suck" more of it from bones because of not enough intake so a backup route was not able to help with it.

Sometimes, very rare I feel small sand being urinated but I don't have an unpleasant feeling of small stones being formed periodically like it was before my current regimen.

Actually, the same thing - stones are more likely to be formed when calcium intake is too low rather then normal-high is described in the "Nutrition Therapy for Urolithiasis" https://link.springer.com/book/10.1007/978-3-319-16414-4

 

So depending on calcium intake and a lot of personal things it could be possible to run without supplements if the rate of remodelling is lower and the influx of calcium is sufficient. In other words, from fracture perspective both answers are right - just becasue of "too many moving parts" in the calcium homeostasis equation.

 

From bones perspective it seems a serie of 3-4 tests of calcium (better ionized), pth and vitD (better "converted" if available and not too expensive) should be done to understand the own strategy on this topic. For me it took almost 2 years to learn my case, since I had no single good source of explanations, so I moved in the dark with it.

 

Also vitD has another roles, especially in things related to immunity. They are not well studied due to complexity, my IMHO is that it is a good idea to have a good vitD status before the infection attack, vitD can be "loaded" with high doses to get rid of bad status but this is not helping fast enough when a person is already severely deseased (early covid studies and older influenza confirmed this). An indirect thing in this area - depletion of vitD in people after mid-heavy infectious deceases recovery, so it seems being used for something.

 

Br,

Igor

 

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I had run across a vitamin D population study from Japan, which claims that a large portion of the Japanese are deficient based on the 20 ng/ml guidelines:

The prevalence of vitamin D insufficiency (serum 25(OH)D3; 12 ng/ml (30 nmol/L) ≤ and <20 ng/ml (50 nmol/L))/deficiency (<12 ng/ml) was 47.7% in summer and 82.2% in winter.

Conversely, North Americans, who take vitamin D more frequently, are much less likely to be deficient. Yet life expectancy in NA is far lower than in Japan (I realize that this is broad brush and there are many other differences). But my point is that perhaps the push for higher D intake in the West has something to do with the fact that vitamin D supplementation (virtually all produced in China) is a $1.9 billion industry, expected to double in the next decade.

See also this from the Harvard Health blog:

Vitamin 😧 What’s the "right" level?

Quote

 

... I spoke with osteoporosis expert Dr. Joel Finkelstein, associate director of the Bone Density Center at Massachusetts General Hospital, whose research in this field spans over three decades. He agreed with the authors of the NEJM article that we are currently over-screening for vitamin D deficiency, and overtreating people who are getting enough vitamin D through diet and sun exposure. "Vitamin D has been hyped massively," he states. "We do not need to be checking the vitamin D levels of most healthy individuals."

He points out that from an evolutionary standpoint, it doesn’t make sense that higher vitamin D levels would be beneficial to humans. "Vitamin D is actually quite hard to find in naturally occurring food sources," he points out. "Yes, we can get vitamin D from the sun, but our bodies evolved to create darker skin in the parts of the world that get the most sun. If vitamin D is so critical to humans, why would we evolve in this way, to require something that is hard to come by, and then evolve in such a way as to make it harder to absorb?"

 

 

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On 3/24/2023 at 8:14 AM, Ron Put said:

I had run across a vitamin D population study from Japan, which claims that a large portion of the Japanese are deficient based on the 20 ng/ml guidelines:

The prevalence of vitamin D insufficiency (serum 25(OH)D3; 12 ng/ml (30 nmol/L) ≤ and <20 ng/ml (50 nmol/L))/deficiency (<12 ng/ml) was 47.7% in summer and 82.2% in winter.

Conversely, North Americans, who take vitamin D more frequently, are much less likely to be deficient. Yet life expectancy in NA is far lower than in Japan (I realize that this is broad brush and there are many other differences). But my point is that perhaps the push for higher D intake in the West has something to do with the fact that vitamin D supplementation (virtually all produced in China) is a $1.9 billion industry, expected to double in the next decade.

See also this from the Harvard Health blog:

Vitamin 😧 What’s the "right" level?

 

The anthropology evidence is clear we have lighter skin in order to produce more vitamin D in northern latitudes. Melanins in dark skinned humans protect them from the year round bombardment of intense sunlight. They produced plenty of D and didn’t need light skin in spite of the melanin which was needed to prevent severe skin damage

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  • 1 month later...
2 hours ago, Amar said:

Hi. Could anyone share the studies on the time it takes for the levels to deplete without any supplementation?

It is not possible to answer on such a question in so generalized way - too many moving parts, e.g. not only race, age, health condition, daily d / precursor income (+fats in the diet), accute/chronic infection but also the rate of its usage and pathways involved are changing with its availability - the body shuttles it to more important areas when there is low availability.

Also there seems interplay with a and k2 body statuses.

Also different tissues have different vitD receptor eagerness (also there are known genetic differences in this area).

Also it does not travel easily between the tissues (e.g. no matter how high it is set with supplements in blood not all tissues will be optimally saturated that way).

So the process is not linear.

 

Also serum analysis available widely is a proxy that is not reliable in many situations, it measures a precursor of a real molecule in charge that is derived also based on many moving parts (e.g. ca levels and pth). And the well known published values are known rather for caucasians, other ancestries have it different.

 

I would rather go from assessing practices/recommendations in selecting personal strategy, e.g. "Vitamin D Deficiency in Adults: When to Test and How to Treat" (Mayo Clin Proc. • August 2010;85(8):752-758 • doi:10.4065/mcp.2010.0138 ) or, if a deeper dive is needed some huge books are available, e.g. Elsevier "VITAMIN D VOLUME 1: BIOCHEMISTRY,
PHYSIOLOGY AND DIAGNOSTICS" + "VITAMIN D VOLUME 2: HEALTH, DISEASE AND
THERAPEUTICS" or similar foliants, there are a lot of publications (but we are still far away from understanding all the things surrounding this topic due to its position in the kinetics of our biology).

 

But if some values are still interested I intuitively assess them as weeks-months to get lower than 20 ng/ml if 30 is selected as a lower normal (which is disputable on its own) in the northern areas w/o any supplementations.

In my case (midage, male, caucasian):

- 1 month to drop from 40 to 30 supplementing with 2000U daily at the very end of the dark season (april-may) - here 2000U was enough in the previous months to stay above 30, thus I run on a summer accumulated in addition with such supplementation

- 1.5 months to drop from 27 to 17 without supplement and with negligible intake from seafood - september-november - here the case was not preceeded by any supplementation but summer was not so far and I was not sick with something in between.

 

I also can say one more interesting thing - after a whole year supplementation 8000 every second day (or 5000 a day) I still saw a remarkable speedup in nails and hair growth happening in the first sunny days when I got a natural "loading" of it via tissues, it was a bit surprising for me. Without supplementing I experienced this effect usually after some weeks from the first strong sun, with supplements my body is able to produce this effect with the very first sunny days, almost immediately.

 

Br,

Igor

Edited by IgorF
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  • 4 weeks later...

I recall that this may have been posted before somewhere, but it's worth noting to keep things in perspective:

Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study

Abstract

Background: Low levels of 25(OH) vitamin D are associated with various age-related diseases and mortality, but causality has not been determined. We investigated vitamin D levels in the offspring of nonagenarians who had at least one nonagenarian sibling; these offspring have a lower prevalence of age-related diseases and a higher propensity to reach old age compared with their partners.

Methods: We assessed anthropometric characteristics, 25(OH) vitamin D levels, parathyroid hormone levels, dietary vitamin D intake and single nucleotide polymorphisms (SNPs) associated with vitamin D levels. We included offspring (n = 1038) of nonagenarians who had at least one nonagenarian sibling, and the offsprings' partners (n = 461; controls) from the Leiden Longevity Study. We included age, sex, body mass index, month during which blood sampling was performed, dietary and supplemental vitamin D intake, and creatinine levels as possible confounding factors.

Results: The offspring had significantly lower levels of vitamin D (64.3 nmol/L) compared with controls (68.4 nmol/L; p = 0.002), independent of possible confounding factors. There was no difference in the levels of parathyroid hormone between groups. Compared with controls, the offspring had a lower frequency of a genetic variant in the CYP2R1 gene (rs2060793) (p = 0.04). The difference in vitamin D levels between offspring and controls persisted over the 2 most prevalent genotypes of this SNP.

Interpretation: Compared with controls, the offspring of nonagenarians who had at least one nonagenarian sibling had a reduced frequency of a common variant in the CYP2R1 gene, which predisposes people to high vitamin D levels; they also had lower levels of vitamin D that persisted over the 2 most prevalent genotypes. These results cast doubt on the causal nature of previously reported associations between low levels of vitamin D and age-related diseases and mortality.

Edited by Ron Put
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The article is interesting but there is maybe something peculiar in the numbers.

I'm not familiar with the nmol/L unit, so I converted the numbers into ng/mL. The results, from nmol to ng:

  • 64.3 nmol/L = 25.8 ng/mL
  • 68.4 nmol/L = 27.4 ng/mL

Please check if that's accurate.

So the average difference between the nonagenarians offspring and control is absolutely trivial, less than 2 ng/mL. It may even be in the order of the analytical error.

The conclusion should have sounded that the levels are equal to all practical effects, and yes, if the results are reliable vitamin D would not seem to constitute a longevity parameter.

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Very weak observational study to put against the huge body of work (hundreds to thousands of papers) showing causality via RCTs, well worked out biological mechanisms, and Hill's Criteria of causation (the same criteria used to show smoking causes cancer, for which RCTs are clearly considered unethical).

For just a small sample of some of the ways in which low vitamin D levels are likely to hasten aging (and therefore lower longevity) see this short thread: 

 

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kpfleger, I too agree on the necessity to evaluate all a priori  knowledge.

What impressed me negatively in that article is that they called a significant difference what is a actually a 6% difference, which is conceptually more trivial than significant. Even if statistically significant, to all practical purposes I would regard the two groups as equal in vitamin D serum values.

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On 6/6/2023 at 1:40 PM, kpfleger said:

Very weak observational study to put against the huge body of work (hundreds to thousands of papers) showing causality via RCTs

Karl, these are strong and categorical statements, but I have to respectfully disagree that the issue is so cut and dry. 🙂

While industry has been pushing tests and supplementation, most professional bodies do not appear to subscribe to the thesis that a vast number of the population is deficient to the point where it is detrimental.

Population data does not support your claim, or is contradictory. at best Most people live perfectly healthy lives at the low end of the established minimum values (15 µg in Europe and about 15 in the US).

Hundreds or thousand of shoddy papers are not proof, at least in my opinion, but also according to plenty of experts in the field. We saw this with Covid and masking.

Here is something from Harvard (I believe it was posted before):

"Dr. Finkelstein and his colleagues published a study of over 2,000 perimenopausal women who had been followed for almost 10 years, and they found that vitamin D levels less than 20 were associated with a slightly increased risk of nontraumatic fractures. They concluded that because few foods contain vitamin D, vitamin D supplementation is warranted in women at midlife with levels less than 20 ng/mL. "For perimenopausal women or other groups of people with higher fracture risk, certainly a level of 20 or above is ideal," and he adds: "For the vast majority of healthy individuals, levels much lower, 15, maybe 10, are probably perfectly fine, and so I would say I agree with what the authors of the New England Journal perspective article are saying."

All that said, most experts, including Dr. Finkelstein, agree we should be checking vitamin D levels in high-risk people — those most at risk for a true deficiency. These include people with anorexia nervosa, people who have had gastric bypass surgeries, who suffer from other malabsorption syndromes like celiac sprue, or who have dark skin, or wear total skin covering (and thus absorb less sunlight). In addition, certain populations will require that vitamin D level of 20 ng/ml or higher. This can include perimenopausal women, people diagnosed with osteopenia (reduced bone density, but not osteoporosis) and osteoporosis or other skeletal disorders, as well as pregnant and lactating women. All of these groups should be screened and treated as appropriate."

And here is what AMA-ASSN has to say:

"Caution is warranted given the surprising lack of effects, or sometimes even harmful effects, found in large, long-term trials of other previously promising nutrients and hormones, such as antioxidants and hormone replacement therapy. It is likely that greater vitamin D exposure will benefit at least some in the population, but more research is needed. Conclusions: While the associations between vitamin D and various disease outcomes appear promising, clinical trials have yet to prove that vitamin D is causally related to most of these outcomes. More long-term, well-designed studies, including large intervention trials, are needed across all life stage and racial and ethnic groups to better understand vitamin D’s role in disease prevention, to determine the optimal doses and serum 25(OH)D levels, and to fully elucidate the potential for adverse outcomes at various intakes. Nevertheless, physicians should consider measuring the serum concentration of 25(OH)D in patients at risk of vitamin D deficiency and counsel those with deficient or insufficient levels on ways to improve their vitamin D status."

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It's well known that there is much skepticism about vitamin D from official bodies and many experts and at the same time much of the negativity is based on misunderstanding of failed vitamin D RCTs, most of which failed due to supplementing people who were already sufficient or supplementing with too-low amounts to move deficient people high enough for clinical relevance. So it's easy to find failed RCTs but hard to find any failed RCTs that correctly test the hypothesis that moving people from deficiency (<20ng/ml to sufficiency (>30ng/ml as recommended by the Endocrine Society and the large body of research showing immune system relevance above this level) improves outcomes. And it's easy to find poor op-eds from those that don't appreciate that. It's also easy to find lots of people saying that caution is warranted until large RCTs prove benefit, but this is silly as keeping controls deficient to do a proper trial would be unethical, which is why Bradford Hill's criteria of causation were used to prove the most likely causal importance of smoking for cancer---no large RCTs were conducted for that.

Despite the controversy, there are plenty of cut-and-dried facts about vitamin D that it is hard to deny, and that consequently justify strong categorical statements such as the one I made earlier:

(1) The deficiency rates are crazy high, way higher than any other micronutrient and way higher than the rule-of-thumb RDA target of 2.5% of population. (RDAs are supposed to be set so that compliance with the min rec gets 97.5% of population to avoid deficiency.) My calculations based on 3 published peer reviewed papers suggests ~50% of global population is deficient at the 20ng/ml level (and roughly 3/4 have less than the Endocrine Society rec): 

(2) The RDA was set too low by at least 5x (more straightforwardly by closer to 10x) due to a statistical mistake made in the 2010 IoM report. This is peer reviewed and published and not contradicted by the IoM (now called NAM): See https://pubmed.ncbi.nlm.nih.gov/25333201/ & https://www.mdpi.com/2072-6643/7/3/1688/htm 

(3) It is incontrovertible that low vitamin D status is a significant risk factor for Covid, a fact that does not require RCTs to prove but has been almost completely ignored by public health officials during the entire pandemic.

One can argue about how much data truly justifies that D supplements would help various conditions for which there is a lot of suggestive evidence, but the balance of evidence combined with rudimentary decision theory makes it absolutely clear that for almost every condition for which vitamin D deficiency correlates with higher incidence or worse outcomes (which includes too many conditions to list, including most of the biggest health burden conditions society faces) the good evidence suggesting that vitamin D status <20ng/ml (deficiency) is more likely to provide good health outcomes than levels above this threshhold is essentially zero. Clinical medicine doesn't like to approve new pharmaceutical agents based on "balance of evidence" arguments---for that medicine requires overwhelming evidence based on large well-conducted RCTS. But for the question of what levels to shoot for of a naturally occurring substance the decision-theoretic question of which range is likely to minimize long-term risks and optimize long-term health is reasonable and even essential. On that question, accumulated data & biological understanding overwhelming favor avoiding deficiency, to the extent that this simple statement of the issue is pretty cut-and-dried.

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