Thursday, January 10, 2008

Vitamin D

On the last post I mentioned the Kitavans and their tendency to eat fish as their primary source of protein. Fish comes bundled with omega three fatty acids and I would suggest that this is a major contributor to their overall health.

The other highly relevant substance for human health is vitamin D. This is not really a food related vitamin or even a vitamin at all, as we make it ourelves. I think it's probably impossible to improve on Vieth's early summary except to say every paper published on vitamin D shows that it is critical to avoiding heart disease, cancer, multiple autoimmune diseases plus type 2 diabetes. And anything else you care to mention I guess.

How much D is needed for health? Vieth's abstract sums it up in these terms:

"Except in those with conditions causing hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D concentrations <140 nmol/L, which require a total vitamin D supply of 250 µg (10000 IU)/d to attain. Published cases of vitamin D toxicity with hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intake of 1000 µg (40000 IU)/d. Because vitamin D is potentially toxic, intake of >25 µg (1000 IU)/d has been avoided even though the weight of evidence shows that the currently accepted, no observed adverse effect limit of 50 µg (2000 IU)/d is too low by at least 5-fold."

So Vieth is pushing for 10,000 iu/d. Six egg yolks provide about a third of the Fitday RDA (recently increased to 10 µg or 400 iu). Half an hour's sun bathing provides Vieth amounts. But even when the sun does shine in January there is no UVB in the UK. So 10,000 iu of oil based D3 it is during the Winter.

I was curious as the the probable vitamin D status of the Kitava natives studied by Lindeberg. They maintain their insulin sensitivity throughout their lives and vitamin D is crucial for this. Lindeberg didn't measure D3, so I've had to have a guess. Kitava is just off of the equator. My guess is that there is probably about 12 hours of sunshine per day many days of the year. I wondered how pigmented the Kitavans were and how much clothing they wore. These are primary determinants of vitamin D3 synthesis.

Putting "Kitava" in to a google image search brought this up as the first hit. Humans are mammals. Please do not click on the following link if you are offended by the direct proof of this. It's to do with feeding babies.

Kitava native

I would guestimate 10,000 iu/d D3, most days of her life.

That's my Winter supplement sorted out. Summer time I'd opt for the Kitava solution.



Anonymous said...

The Kitavans also eat coconut, from what I've read. Consider the health benefits of coconut oil. The virgin coconut oil is best, then macadamia oil, and cocoa butter (1, 2, and 3% PUFAs, respectively). Palm oil, and olive oil are higher in PUFAs. They are better used infrequently, if at all. I'm not big on eating nuts and seeds. Ruminant animals are better.

It's possible that PUFAs increase a person's need for Vitamin D, while saturated fats decrease it. At any rate, limiting PUFAs seems to offer similar benefits to Vitamin D.

Anonymous said...

Sorry, the link died recently. Here is another copy of the article.

More information on Mead oil

Also, search for "mead acid" to see more about the benefits of low-PUFA intake (so-called EFAD).

G said...

Hi Peter -- You've got AMAZING posts! They've helped me understand a lot of biochemistry behind nutritional modifications for various disease states. Your wit always blows me away. I find it really funny that poor studies are bashed globally... the net is so powerful and awesome.
My cat recently passed away -- I wish I found you sooner. Do you supplement your cats? any extra fish oil or vit D?
Thank you! g

Peter said...

Cats are difficult re vit D, they make it with sunlight and break it down immediately. They appear to be diet dependent and mouse content, eight per day, appears to be about right. I can't find out what that should be!!!!!! Also I think there may well be sense in bruce's thoughts on excess PUFA increasing need for D. There is way too much PUFA even in LC cat food. My cats eat raw mince, raw chicken wings, occasional cans of pilchards/sardines. Very hard to know their D status as the measurement is not available in the UK, though it can, at a significant cost, can be gotten by shipping the blood to the USA. USA does somethings really well. Pubmed is number 1.


PS the last cat I blood sampled (the cat is allergic to EVERYTHING) was hypovitaminaemic for D but trying to find a dose rate which will not cause hypercalcaemia is a bit of a nightmare. Guessing at 200iu/d, checking calcium fortnightly and will re measure D in 6 months. Tailing off its steroids as and when I can. Owners won't rawfeed and that would not really address to XS omega 6s anyway....

G said...

I agree the excess omega-6s in the cat diet is a 'killer'(just as it is for humans). I think Tiger (my cat who passed away) should've had an all protein diet. We moved 2yrs ago and he did have a steady diet of mice for a short period but alas the neighborhood decided to start a mouse abatement program. His sister is doing well (just lonely). I've seen some frozen rabbit at the grocery store -- maybe I'll grind it for her once a week for a nice treat. :)


Anonymous said...

Some interesting article regarding fish oil

Peter said...

Hi Hela,

I gather Ray Peat doesn't like PUFA.... Too much info to take in at one sweep but I have his viewpoint in mind.


Ken said...

Lean phenotype and resistance to diet-induced obesity in VDR knockout mice correlates with induction of uncoupling protein-1 in white adipose tissue

"how pigmented the Kitavans were and how much clothing they wore. These are primary determinants of vitamin D3 synthesis.

Only in brief periods of time. In practice, even for the very darkest of people living in Britain, it doesn't make much of a difference to their Vitamin D levels how dark their skin is. A study under natural conditions in Birmingham, England, revealed comparable increases in 25-OHD levels after the summer sunshine from March to October in groups of Asians, West Indians and Caucasoids … This absence of a blunted 25-OHD response to sunlight in the dark-skinned West Indians at high northerly latitudes (England lies farther north than the entire United States of America except for Alaska) proves that skin colour is not a major contributor to vitamin D deficiency in northern climes.

Asians have got rickets in the UK but that was nutritional rickets due to their traditional diet not how dark their skin was (not very, compared to West Indians)

[Robins, A.H. (1991). Biological perspectives on human pigmentation. Cambridge Studies in Biological Anthropology, Cambridge: Cambridge University Press.]

Sunbath in the British summer sun and you will make 20,000IU in less that 20 minutes. This can be stored and would have to see you through the UVR- less winter

Kitvians have evolved to deal with all year rounds Vitamin D synthesis from the all year round UVR. After making 20,000 IU which takes them about an hour synthesize stops.

Question: if Vitamin D is so very good for you and northern Europeans have evolved where it is absent for half the year why do they shut off synthesis after this limit of 20,000 IU is reached? They ought to have evolved to make all they can while the sun shines and then store for the winter.

The Pharmacology of Vitamin D If one looks at the system of vitamin D metabolism in Figure 2 from the perspective of a system
designed to control something, it becomes clear that this is a system better designed to cope with an abundance of supply, not a lack of it. The flow of vitamin D toward 25(OH)D is remarkably inefficient, with most bypassing
it. Furthermore, there is no way to correct for deficiency of vitamin D, other than to redirect utilization of 25(OH)D toward 1,25(OH)2D production, which is the pathway most acutely important for life. That is, when supplies of
vitamin D are severely restricted, its metabolism is directed only toward the maintenance of calcium
homeostasis. To expand on the point that the system of vitamin D metabolism is effectively a designed for adjusting for higher inputs, not lower inputs, I offer the example of an air-conditioner system. Air conditioners are designed to compensate for excessive heat, but they are a useless way to compensate for a cold environment.

So if evolution limits Vitamin D I am wondering why you are not.

Ken said...

At the first step synthesis in the skin Vitamin the D is limited to 20,000.

The flow of vitamin D toward 25(OH)D is remarkably inefficient, with most bypassing it.

It could be explained that the metabolism of people in cold countries is still adapted to the high UVR environment where humans evolved, However, if true this ought to make the efficiency of the first step (synthesis in the skin) imperative for North Europeans in particular. They have to go 6 months without.

Ken said...

Kitavan's skin colour is nothing to do with the amount of UV they are exposed to, other islanders in the region are extremely dark skinned.
Coconut diesel

Kitava native I would guestimate 10,000 iu/d D3, most days of her life.

Agreed, but I suspect taking that amount of D in pills is going to enter the blood stream in an abrupt way, a rather unnatural way not like the way UVR synthesized vitamin D enters the blood of Kitvians. Take a look at this please:-

In a more recent study by Wortsman et al. (11), the capacity of the skin to produce vitamin D was not altered in obesity. However, the increase in serum vitamin D3 after sun exposure was 57% less in obese compared with nonobese subjects. The increase in serum vitamin D3 after oral supplementation was similar in obese and nonobese subjects. This supports the hypothesis of a decreased release of endogenously produced vitamin D into the circulation due to more storage in sc fat in obese subjects (11). Adiposity in Relation to Vitamin D Status and Parathyroid Hormone Levels: A Population-Based Study in Older Men and Women

Peter said...

Hi Ken,

Complex comments need more time to think than one liner replies. I note from the abstract of Wortman's paper that they found a similar relationship between BMI and both the concentration of D3 after irradiation or oral D2. The two phrases of interest are:

"BMI was inversely correlated with serum vitamin D3 concentrations after irradiation (r = -0.55, P = 0.003) and with peak serum vitamin D2 concentrations after vitamin D2 intake (r = -0.56, P = 0.007)"

Same correlation coefficient and same p value


"Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D3 from cutaneous and dietary sources because of its deposition in body fat compartments"

Note there is no restriction as to which the body fat compartments.

The concept of D3 rising in the blood after D2 supplementation is strange. I don't think D2 can be converted to D3 and the abstract does not say that which is claimed in the text you cite...

Re skin colour and D3 production. As there does appear to be an upper limit to D3 production after which break down of preD3 limits the excess, I can accept that skin colour becomes less and less important as sunlight becomes more and more available.

There is certainly an hypothesis that skin pigmentation is there to limit UV destruction of folate rather than limiting D3 production.

If I could get 20,000 iu per day every day by sunlight exposure for six months each year I would try skipping my oral D3 gelcaps. But 10,000 iu per day all year seems a very reasonable compromise compared to 20,000 iu for half the year (if I could remotely get that sun exposure, which I can't).

I would accept that intervention trials with oral D3 are needed before the hupla about D3 is confirmed, but I would want a serious reason not to supplement before halting on the basis of a non physiological route of administration.

So in answer to your question from first comment: If Vitamin D is so very good for you and northern Europeans have evolved where it is absent for half the year why do they shut off synthesis after this limit of 20,000 IU is reached? They ought to have evolved to make all they can while the sun shines and then store for the winter.

The text which follows the question answers this. Evolution has not adapted. Our metabolism expects 20,000 iu per day and can cope with this even if limited to only 6 months rather than 12 months each year. On less than 20,000 iu/day there is a redirection towards calcium homeostasis because without this we would die. On 400iu/d we don't die, just get the gamut of problems currently associated with vitamin D3 deficiency.

As the italicised texts states:

"To expand on the point that the system of vitamin D metabolism is effectively... designed for adjusting for higher inputs, not lower inputs..."

If we walked out of Africa 60,000 years ago I think it's perfectly reasonable to assume our bodies have not been able to adapt to current inputs of D3 and going back to putting a high input in to a system which expects a high input seems perfectly reasonable. The system is designed for a high input, use one.

Do you see any great advantage to limiting D3? I'm not a VDR knockout mouse, fascinating though these animals are...


BTW the other thing which has crossed my mind on several occasions is that D3 may be much less important under carbohydrate restriction than when living on starches, but I've not had the time or papers available to follow this idea through. None of the long time LC eaters suggest D3 supplementation. There aren't many starches in northern Scotland, ditto sunbathing. I'm not closed to this idea, but I'm not driven to experiment along that line myself...

Ken said...

Thanks for a very comprehensive response to all my points, sorry if they were a bit convoluted.

1)We have a limit so that UVB-on-the-skin-synthesis of vitamin D ceases after 20,000IU which needs 20 minutes sunshine.
(the sun heating the skin triggers the breakdown of 'D', I am not certain about this but I think sunbathing while turning every 20 min may provide more)

2)The system of vitamin D regulation is inefficient but very good at dealing with excess amounts.

3)Exposed skin is 50% less efficient at making 'D' by the end of summer because it gets a tan.

Taken together with the fact that humans had been under natural selection in northern Europe for a awful long time with the same long UVB-less time these facts lead me to think that the amount of UVB that we get in northern Europe is sufficient for optimum health. There has been no modifyng of our bodies for maximizing vitamin D because the amount synthesised (and stored) in spring and summer with UVB exposure is more than enough for the best of health; especially if one is not obese and sunbathes regularly.

I dont think that it is beneficial to take 10,000 IU throughout the UVB-less months. However as " the system of vitamin D metabolism is effectively designed for adjusting for higher inputs," it probably does no harm.

You mentioned the theory that Folic Acid is destroyed by UV(A) 5-Methyltetrahydrofolate inhibits photosensitization reactions and strand breaks in DNA
Branda and Eaton reported a significant decrease of folate in plasma from psoriasis patients treated with methoxalen phototherapy. They also found loss of folate in plasma exposed ex vivo to UVA. They suggested that "Prevention of ultraviolet photolysis of folate and other light sensitive nutrients by dark skin may be sufficient explanation for maintenance of this characteristic in human groups indigenous to regions of intense solar radiation." (11) . Our results demonstrate that the photolysis of folate observed in their study was not due to the intrinsic photolability of 5-MTHF but instead may have been mediated by the methoxalen.../
We demonstrate that 5-methyltetrahydrofolate (5-MTHF, the predominant folate in plasma) is also a potent, near diffusion limited, scavenger of singlet oxygen and quencher of excited photosensitizers. Both pathways result in decomposition of 5-MTHF, although ascorbate can protect against this loss. In the absence of photosensitizers, 5-MTHF is directly decomposed only very slowly by UVA or UVB. Although synthetic folic acid can promote DNA damage by UVA, submicromolar 5-MTHF inhibits photosensitization-induced strand breaks. These observations suggest a new role for reduced folate in protection from ultraviolet damage and have bearing on the hypothesis that folate photodegradation influenced the evolution of human skin color.—

To me that suggests the theory is wrong.

Peter said...

Yes, figure 2 in the results is quite convincing. Any theories as to why we are pigmented and why we tan? To reduce excessive D3 production seems unlikely as there does seem to be a limit as to how high this can go. Just to stop us burning?

Stefansson describes life of the traditional Inuit as largely topless in Winter, when the housing was very warm, but not outdoors in the Summer. There clearly is a lot of UVB about in the Arctic in Summer as they used wooden slitted snow goggles for eye protection. But whole to half body exposure is not something I've come across in any account. Fish was a staple for months at a time on occasions though, some D3 there.

Do you have any thoughts on meat based diets vs D3 requirements? Is high D3 intake a patch on junk food? Modern salads and brightly coloured veggies being included in the latter.


PS, re 10,000 iu; yes, I'd basically decided it was not likely to be toxic while I kicked the above ideas around in my head, without getting anywhere much...

Ken said...

Pigmentation varies for the reasons given here in my opinion. SEXUAL SELECTION AND HUMAN GEOGRAPHIC VARIATION"
"Among early modern humans, a woman would face stronger competition for a mate the
further away she was from the equator. Men were less available because they 1) hunted over longer distances that increased male mortality proportionately and 2) were less able to offset the resulting man shortage through polygyny. The longer the winter, the costlier it became to provision a second wife and her children, since women could not gather food in winter. Women competed the most for mates in the 'continental Arctic,' where wandering herds were the main food source.

why we tan? Just to stop us burning?
Probably, the erythemal (burning) UV exposure that is UVB gets through pale skin easily and reddens it, if the sexual selection theory is correct red skin would be bad, According to Loan et al (2007)"In humans, the adult male is ruddier in complexion than the adult female and male hormones greatly increase blood circulation in the skin’s outer layers. Testosterone influences erythropoiesis during male puberty and a decline of testosterone with aging increases the risk of anemia. Furthermore, men with hypogonadism or those taking anti-androgenic drugs frequently have anemia. These data are consistent with a testosterone-dependent ruddiness of the male complexion, as seen in many other species where red coloration acts as a signal of male dominance." a tan would be better than the 'boiled lobster' look for a woman.

Stefansson describes life of the traditional Inuit as largely topless in Winter, when the housing was very warm, but not outdoors in the Summer. There clearly is a lot of UVB about in the Arctic in Summer as they used wooden slitted snow goggles for eye protection. But whole to half body exposure is not something I've come across in any account.
That is a very good point, I had assumed they wore a minimum of clothing in the summer. I suppose that the amount of vitamin D they synthesized on the face, hands and any other exposed skin was enough, still a bit surprising to me though. Another indication that a little sun goes a very long way perhaps.

The idea that non -nutritional rickets was easy to get is difficult to leave behind but it realy was a rare disease, virtually nonexistant I think:- Know Your Pathology: Osteomalacia and Rickets However, rhe rarity of this disease in the past is attested by the few cases described even in exhaustive studies of human remains prior to the Medieval period.

Do you have any thoughts on meat based diets vs D3 requirements? Is high D3 intake a patch on junk food? Modern salads and brightly coloured veggies being included in the latter.
Food sources of 'D' (liver, fish) are slight compared to what the sun makes. I think that obesity from junk food and just junk causing insulin resistance increases inflamation so if vitamin D really does modulate the immune system larger amounts might be called for than when eating a meat based diet.

Ken said...

I have had a rethink on vitamin D for a person who is not at all overweight

Vitamin D 'insufficiency' (putatively due to living at a high high latitude)as the cause of a myriad of diseases is being given ever more credence in the medical world. The public has it hammered into its mind by journalists quoting epidemiologists that vitamin D is vitally necessary for health and in short supply away from the equator.

The availability of berries to be gathered along with the fattened prey animals being more easily hunted must have made summer a time when an excess of calories was being ingested and hence a time when bodyfat was increasing. Summer would certainly be a time when vitamin D was synthesized in excess of requirements. It is known that vitamin D is stored in the body fat.

"Food scarcity is endemic among Arctic groups. Typically, food crises occur over yearly and generational cycles".

Presumably winter would be such a time, if so it would also be a time when the bodyfat added to in the summer was used up. Hence there may be an additional benefit to the breakdown and metabolism of adipose tissue in the UVB-less months of winter inasmuch as this also results in the stored vitamin D being released to supply the bodies requirements though the UVB-less months - precisely when it is needed.

Agriculture probably shoud not be expected to have changed this system much, seasonal fluctuations in bodyfat along with food scarcity may have been less dramatic but winter was a time of hunger well into historical time in northern Europe

The relevance of this to modern claims of Vitamin D 'insufficiency' is that for today's people there are no periods of food scarcity and hence adipose tissue fails to release its stores of vitamin D . Scots whose high rates of disease at a high latitude make them the best example of the vitamin D insufficiency theory are more obese than anyone but Americans.
Seasonal variance of 25-(OH) vitamin D in the general population
Vitamin D insufficiency in southern Arizona
Prevalence of vitamin D insufficiency in obese children and adolescents.
Body fat and vitamin D status in black versus white women.
Body fat content and 25-hydroxyvitamin D levels in healthy women.

So for someone who is not experiencing enough of a calorific deficit in the winter to induce the metabolism of their fat stores (which may contain a large amounts of vitamin D) ingesting a substantial quantity of 'D' in a capsule might well be very beneficial.

. said...

Great book from a cholesterol skeptic:

Vitamin D and Cholesterol: The Importance of the Sun [Hardcover], David S. Grimes