Monday, December 07, 2009

Vitamin D and UV fluctuations (2)

EDIT: I feel I should just add that a number of factors came together for these last two posts. Vieth's article from Ted crystalised it. I'd been thinking about JK and vitamin D for some time and Ken supplied, years ago, several interesting papers and ideas on D3 and skin colour. I think he's talking sense.

I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control.

By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few).

For reasons which will become clearer I am far more interested in what is happening at the lower levels of vitamin D availability, rather than any toxicity from high dosages.

There was a problem of clinical rickets and osteomalacia in children and women of Asian and Middle Eastern origin in Glasgow from the 1960s onwards. The problem centres around gross deficiency of vitamin D, with 25(OH)D in the plasma sitting around 20nmol/l. Some of these people develop full blown rickets or frank osteomalacia, some don't. Dunnigan appears to have spent most of his career on this problem. A simple vitamin D deficiency does not seem to be adequate for rickets, though it is required.

Here's what Dunnigan has to say on the subject:

"The discovery of late rickets and osteomalacia in the Glasgow Muslim community in 1961 (Dunnigan et al. 1962) was followed by a study of 7 d weighed dietary intakes in rachitic and normal Muslim schoolchildren and in a control group of white schoolchildren (Dunnigan & Smith, 1965). Surprisingly, the dietary vitamin D intakes of rachitic Asian children, normal Asian children and Glasgow white children were similar. The higher fibre and phytate intakes of the Asian children were not considered aetiologically significant. Studies of daylight outdoor exposure showed no significant differences between the summer and non-summer exposures of rachitic and normal Muslim schoolchildren or between Muslim and white schoolchildren (Dunnigan, 1977). These patterns of daylight outdoor exposure did not conform to the Muslim ‘purdah’ stereotype, although sunbathing was unknown in the Asian community. It was also evident that many Glasgow white schoolchildren went out relatively little, even in fine weather, in a form of ‘cultural purdah’. Similar patterns of apparently adequate daylight outdoor exposure were noted in Asian women with privational osteomalacia wearing Western dress in London (Compston, 1979). These observations did not support the hypothesis that Asian rickets and osteomalacia resulted from deficient exposure to UVR or from deficient dietary vitamin D intake relative to white women and children in whom privational rickets and osteomalacia were unknown outside infancy and old age."

What appears to make a difference in his book is meat:

"Where UVR is limited by latitude and urbanization, the prevalence of privational rickets and osteomalacia is determined by dietary factors. Limited UVR is necessary but insufficient to induce ‘cases’ of privational rickets or osteomalacia unless the diet deviates from the Western omnivore pattern. This diet is characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals. The Western omnivore diet provides complete protection from privational rickets and osteomalacia from infancy to old age at the low levels of dietary vitamin D intake which characterize the largely unfortified British diet and at the levels of casual exposure to UVR experienced in the high latitudes of the UK. An omnivore Western diet will not prevent hypovitaminosis D at very low or zero UVR exposure levels; by inducing mild secondary hyperparathyroidism this may contribute to the risk of type two osteoporosis in old age. As the dietary pattern moves from omnivore to vegetarian, rachitic and osteomalacic risk rise synergistically with falling exposure to UVR (Fig. 1). UVR exposure levels associated with Asian rickets and osteomalacia in the UK are similar to the casual daylight exposure levels of a substantial proportion of the urban white population. Dietary risk factors for privational rickets and osteomalacia are independent of the low vitamin D content of most foods and appear to result from interactions between constituents of animal foods (predominantly meat and meat products) and the intermediary metabolism of endogenously-synthesized vitamin D."

Dunnigan feels the evidence from Glasgow suggests that an animal based diet largely protects against bone based effects of gross 1,25(OH)2D deficiency in the plasma. Supplementary vitamin D does also work, but was only transiently taken up by the Asian community.

"The provision of free vitamin D supplements in 1979 in an effort to reduce the prevalence of Asian rickets in the city is not responsible for this trend (Dunnigan et al. 1985). Supplement uptake declined rapidly within a few years of the onset of the campaign and vitamin D supplements are now rarely consumed by Asian schoolchildren and women (Henderson et at. 1989)."

Omnivory was taken up with westernisation of the diet. Along with the disappearance of rickets there was noted the arrival of appendicitis, an excellent confirmation of the switch in diet pattern.

From all of this I would deduce that, under marginal levels of UVB in Glasgow, the primary determinant of gross clinical expression of deficiency of vitamin D is vegetarianism. There is a protective effect of meat consumption. McDonalds will do. So might reindeeer meat in the Magdalenian Basin 18,000 years ago.

Which brings me to human migration out of the tropics and in to temperate areas. We came out of Africa and across central Russia about 60,000 years ago. During/since that time we northerners have lost our bulk melanin pigment layer, except for a faint induced tinge after summer sun exposure, which presumably acts to blunt excessive vitamin D production. If we can lose our sunscreen, yet still put up a temporary sunshade of a tan, do we really need 10,000iu per day year round?

Vieth argues for generous supplementation. I cannot see any argument against maintaining modest yet minimally variable levels, based on his own hypothesis. Modest UVB exposure with a meat based diet might well be adequate.

I would then tend to leave the vitamin D paradox as a suggestion that the role of vitamin D in cancer might need re evaluating. I am quite well convinced from the Glasgow experience that catastrophic vitamin D deficiency can be largely be ameliorated by eating meat. Can "suboptimal" vitamin D deficiency relating to cancer and CVD also be optimised by eating meat? Supplementing just 100iu/d sorts out rickets but the same effect can be achieved with the occasional burger.

Most of us who have ended up on low carbohydrate eating did not think it up for ourselves. There are shoulders on which we still try to scramble. For me it was Atkins, Yudkin, Lutz, Groves and especially Kwasniewski. No one was or is advocating 10,000iu/d of vitamin D. They were/are all advocating a diet based on meat and animal fat. These pioneers did not have the EBCT tracking which is available to many of us nowadays, but their clinical experience, with all of the caveats that that needs, is that LC, animal fat based diets reverse CVD.

I can see that aiming for a middle to upper lab range is a reasonable hedging of bets. I'm not sure it is needed unless you come from a history of vegetarianism or persist in the consumption of whole meal flour, especially if coupled with near complete UV avoidance. Never forget that much of the data on vitamin D supplementation comes from a population crushed under the Food Pyramid or its derivatives, an eating plan which almost seems to have been designed to maximise disease. Vitamin D might well help under these situations, but what of those of us who eat Food?

It seems like humans can get away with vegetarianism in the tropics. Move north and you need to eat meat.



Anne said...

Your post reminds me of what Dr David Grimes wrote in Dr Davis's Heartscan blog about fish and vitamin D and how Scots and Inuits had enough D when they ate plenty of fish but not when they changed their diets:


alex said...

Good Point. Vitamin D and Rickets have less relationship that expected, mice with "null-VDR", that have no way to metabolize Vitamin D, did not develop rickets as long as they got enough calcium and phosphat.

See point 8 in:

And i assume that eating enough meat will provide enough phosphat.

Regarding your comment on Vitamin D and Cancer, see this excellent paper from Oxford Journals:

happy lecture,


LeenaS said...

Peter, your view agrees very much with my experience.

For the first 40 years I literally shunned the sun, due to very serious pollen allergies, which appeared in March - i.e. before the real sun even kicked in here (southern Finland). And I stayed in until fall frost cleaned the air, but then the sun was gone, too. If I tanned any then, it would peel off in two days, always - except for one year on the other side of Atlantic and with pollen unknown to my immune system. And yes, I was sickly with allergies, sensitivities, flues and other inflammations most times - but had no rickets (maybe thanks to the minor amounts of butter and cheese that I had then - and vitamin supplements were were given as kids... and the real milk which was available then?)

For the last 9+ years I've not had much more sun, but the diet has changed. From harlf vegetarian grain diet it changed into one low in cereal fibre and high (or higher still) in butterfat and animalfats. No vitamin D pills but I've finally learned to "supplement" with daily egg yolks, too.

... and behold, the allergies and flues and imflammations are no more. And I tan now; its not dark but it comes easily and it does not wear off like it did before.

Regards and thanks!

caphuff said...

thanks for this very fascinating post.

Peter said...

Hi Anne, that's a very reasonable level of 25(OH)D. The question to me is if it could be maintained by meat eating without the fish/D3 content, ie with daily beef. And if it couldn't be maintained, would that actually matter if it was on a LC diet.... But as soon as you start to include rice and particularly chapatis made with high extraction ratio flour, D would probably become crucial...

Alex, nice link, more recent than those cited by Vieth and the paradox continues. Meat is pretty reasonable for phosphate and what there is is bioavailable.

LeenaS, over the years I've done LC with rapid gravitation to JK, then added mega dose C (OMG, I just remembered I actually did juicing for a few weeks they decided to get back to my OD roots, pun intended) and found I was not quite so healthy, especially skin wise, now a year of high D and a tail down to low D (after an over-high lab result) and I see no worsening of anything. I might post about my now resolved finger arthritis some time, but anyway, it's gone... I'm still doing fish oil.

Caphuff, I just keep wondering....


Kennedy said...

I had the same line of thought too.

I think rather the Tanning helps protect Folate being destroyed than curbing excessive D3 production, or some sort of balance depending on demand.

blogblog said...

One of my university lecturers F.E.G (Frank) Harrap did some very important research on phytates in the late 1950s. He once told me that there was an epidemic of rickets in Britain during WW2 when large amounts of bran was added to white bread as an extender. The flour was fortified with very finely ground chalk. This eliminated the problem. The cause of the rickets was later found to be due to phytates preventing calcium absorption.

Peter said...

Blogblog, I certainly have heard of the Dublin experience with high extraction ratio flours. I remember my baker in Norfolk telling me he was very dubious about the benefits of wholemeal bread on that basis. Of course I didn't believe a word of it! I was in to whole grains in those days.

Kennedy, I've read the paper on folate but I think other commenters didn't feel this held water. Dunno!

Justin said...

"It seems like humans can get away with vegetarianism in the tropics. Move north and you need to eat meat."

This conclusion has some interesting implications. Take vegetarian Indians who immigrated to the United States. I happen to know a number of Indians who immigrated -- my wife's parent's generation. Many, many of them have suffered from cancer or diabetes. What is going on here? And could it be somehow tied to a vegetarian life in sunny India protecting against these ailments but a similar diet in North America being deadly?

Nigel Kinbrum BSc(Hons)Eng said...

Justin said...
"I happen to know a number of Indians who immigrated -- my wife's parent's generation. Many, many of them have suffered from cancer or diabetes. What is going on here?"

Looks like hypovitaminosis D to me. Dark skin + Northern Latitude -> insufficient D3 synthesis in skin.

Hypovitaminosis D -> increased risk factor for diabetes & cancer etc.

Peter said...

Justin and Nigel,

As far as I have looked there is only clear data on rickets; in India sunshine gives adequate D to cope with vegetarianism. With reduced sunshine vegetarianism is a good trigger for rickets, as per Glasgow.

Once you get up to higher levels of D, above rickets threshold, we are in to speculation. But for avoiding diabetes and cancer, both conditions of hyperinsuliaemia, I would want to see a marked effect on insulin resistance... Ultimately I would be suspicious that anyone going the diabetes/cancer route is cooking their liver with fructose. After that hyperinsulinaemia is needed for normoglycaemia. If the pancreas loses and cannot sustain adequate hyperinsulianemia, you get diabetes. If it wins you get cancer. They're both hyperinsulinaemia driven. Does D make enough difference to insulin levels to stop this, or does it stop the initial fatty liver in the face of fructose? These are the questions that matter to me.

If D is just tinkering with the cancer threshold in the face of continued hyperinsulinaemia, it just looks like a sticking plaster to me...


gunther gatherer said...


"Does D make enough difference to insulin levels to stop this, or does it stop the initial fatty liver in the face of fructose?"

In light of this question, would you say the Kitavans are keeping their insulin low despite their 70% starch diet through continuous exposure to the sun? I don't know how much meat they get either, but I suppose it's quite a bit less than what we get in Europe.

If your "as you go north, you need more meat" approach is true, we'd probably see hunter gatherers eating less meat by the equator. This means more carbs in their diet. Does anyone know if this checks out?

I suppose you can also extrapolate and say the less meat in the HG diet, the darker the people (because they are most likely in the sun all the time).

Are there any cases of renal stones or hypercalcinuria with the Maasai, who eat lots of meat AND live under the hot sun? If this theory is true, they would show some overdose of vitamin D, no? Or perhaps with extremely dark skin this isn't the case...

blogblog said...

Due to differences in pigmentation the darkest skinned people need about 45x as much UV as exposure as light-skined to produce the same amount of vitamin D.

People from southern India or Afro-Carribean people are in reality wearing natural Factor 30 sunblock all year round. They are never going to get adequate UV exposure in Britain. In the USA "typical" African Americans living above 40'N latitude are unable to synthesise sufficient Vitamin D a at any time of the year.

Melanin isn't to stop excess vitamin D production - this is self-limiting. Melanin is to stop serious sunburn and skin cancers.

I live in Brisbane Australia - 27'S latitude. This equates to 4'S latitide in mid-summer. In summer the average northern European in Brisbane will get sunburnt in less than 10 minutes. Few northern European children would survive to adulthood if they had to live here as naked hunter-gatherers.

notrace said...
This comment has been removed by the author.
notrace said...

I was looking around for skin help and came across a reference to 1,25 Vit D being made in the skin from cholesterol and UVB. Could extra cholesterol from a meat\animal fat be contributing to Vit D efficacy?

Bodo Lehmann, Peter Knuschke, Michael Meurer
Department of Dermatology, Carl Gustav Carus Medical School, Dresden University of Technology, Dresden, Germany

Calcitriol [1,25(OH)2D3], the hormonally active form of vitamin D3 (D3) is produced in both renal and extrarenal tissues. Our findings demonstrate that physiological doses of UVB radiation at 300 nm induce the conversion of 7-dehydrocholesterol (7-DHC) via preD3 and D3 into calcitriol in the pmol range in epidermal keratinocytes. The hydroxylation of photosynthesized D3 to calcitriol is strongly suppressed by ketoconazole, a known inhibitor of cytochrome P450 mixed function oxidases. The UVB-induced formation of calcitriol in human skin is demonstrable in vivo by the microdialysis technique. These results suggest that human skin is an autonomous source of hormonally active calcitriol.

Gyan said...

Vegetarianism does not exist among Muslims. Was meat very expensive in 1960s Glasgow?
Or were the rickets cases Hindu?
Meat is normally cooked in oil in India. Maybe PUFA is confounding factor with meat-eating rickets-having Muslims?

Re: whole wheat flour (atta in Hindi), is phytate significant disrupter of VD3 or not?. Or is there some other component of atta?

Perhaps British cow-milk is not good source of VD3 and Indian cow/buffalo milk is?

Gyan said...

Didnt the Europeans used to eat huge amounts of wheat bread till recent times?

Like of order of 1 to 1.5 kgs per day.
This is what I have read about French and Russian peasantry. Perhaps I am entirely mistaken and it should be 150 g/day?

A wheat chapati is pretty light. I think 3 chapatis (that comprise a full Indian meal) total only 75-100 g.

Jocelyn said...

Might be onto a winner here - this could explain the devastating effects on health of immigrants moving to western nations. Maybe its not the switch in diet but the latitude that has them at far greater risk of cancer & diabetes. It's their lack of vit D synthesis.
A possibility and probably just another peice of the puzzle.

Peter, your post near the top was a little confusing, are you saying you developed a skin condition after you adopted LC?

Peter said...

Gunther, I've not chased the studies on equatorial diets but there is far more scope for starches here. Certainly HLA B27 is selected against in equatorial latitudes and becomes progressively commoner as you go north. That's a negative selection pressure by starch. I suspect the Maasai are adequately pigmented to control their D levels appropriately and they are still living where they evolved, though obviously milk is a quite recent introduction...

I had wondered about Kitava, D and starches, but you could equally argue modest fructose, maximum starch and fish here.

Blogblog, I am assuming that in pre sunscreen days caucasians managed with hand and face exposure in tropical Aus without significant solar burns. If hands and face can adapt why can't the rest of the body? Not all tropical dwellers have negroid levels of pigment.

Notrace, I'm not so sure on this one, it is a cholesterol precursor which forms preD3 under UVB and the more cholesterol you deliver from the liver/diet I guess the lower the level of intermediaries of the synthetic pathways there would be... Dunnigan looks to be an epidemiologist rater than a biochemist as nuts and bolts are thin on the ground in the papers. Had to look hard for the actual 25(OH)D levels for rickets... Very interesting about extra-renal 1,25(OH)2D formation.

Gyan, I butchered huge sections out of the post, all of which are in the download of Dunnigan's review. He does discuss the role of high extraction flours and rickets from unleavened bread (phytic acid rich) under marginal calcium status. Another gift from wheat.

He covers "sunshine rickets" from the Middle East (High D3, low calcium, high phytate) before he goes on to Hindus.

What I couldn't find is whether meat eating in the Hindus actually raised the 25(OH)D levels in the blood or merely allowed more effective use of what little was present. Several of the older papers are free to download but not the more recent ones.

The European bread was fermented, often lactofermented for days, which would destroy a significant amount of the phytate. Unleavened bread is far more of a problem. Again we are in the calcium deficiency rickets rather than vitamin D deficiency and I can't see what high phytate diets do to blood vitamin D level.


No, I had the most awful acne as a teenager and persisted with low grade acne problems on my back, shoulders, chest and face in to adulthood. This 90% resolved on LC and near 100% resolved on gluten elimination. On mega dose C there was a minor relapse and the spots tended to linger for far longer than during LC before before megadosing. I stopped mega dosing unless I needed a relatively non toxic anti inflammatory, but for me to mega dose is now very rare. I do still get occasional spots but nothing like pre LC days or while I was on high dose C. I suspect C may do more good if you are on a carb based diet...

For cancer and diabetes I would be looking for insulin dysregulation. I'm waiting to see what D does here.


blogblog said...

"Blogblog, I am assuming that in pre sunscreen days caucasians managed with hand and face exposure in tropical Aus without significant solar burns. If hands and face can adapt why can't the rest of the body? Not all tropical dwellers have negroid levels of pigment."

Most older Australians have substantial sun damage to the face and hands. Virtually everyone I know aged over 65 has had some form of treatment for pre-cancerous skin lesions.

Visiting Scandinavian, British and Canadian women often look far younger than their Australian counterparts due to a lack of sun damage to their skin.

Most of the less-pigmented societies living in the tropics traditionally avoided the sun at all costs. In Vietnam and southern China the people wore long pants, long sleeves and huge hats. A suntan was considered extremely bad.

Nigel Kinbrum BSc(Hons)Eng said...

Peter said...
"For cancer and diabetes I would be looking for insulin dysregulation. I'm waiting to see what D does here."

See Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction.

Max said...

After reading the link supplied by Alex and the opposing Vitamin D led by Trevor Marshall, seems information is getting confusing

This statement from the site

"In an effort to curb chronic disease, well-intentioned researchers are promoting vitamin D, a substance that, according to recent molecular modeling research, can act as an immunosuppressive steroid"

What's your thoughts on this Peter?

Jordan said...

Many studies were done on Jews from Yemen who emigrated to Israel in the early 1950s. In Yemen, rickets was rampant, but heart disease, cancer and diabetes were unknown. Rickets was cured quickly upon arrival to Israel, but autopsies on people who died in auto crashes showed no clogging of the arteries for these Jews originally from Yemen. Their children who had lived in Israel their whole lives, however had the heavy clogging similar to most Israelis who had come from Europe. Not much of a difference in latitude...

Gyan said...

Muslim children ate more wheat and less milk than lacto-vegetarian Hindus.

There is association of greater osteomalcia with greater lentil consumption in lacto-veg Hindu women. Mysterious.

But why he says that phytate is not significant?

Sven said...

@gunther gatherer:

You wrote (a couple of weeks ago) that your body temperature rose while eating a hf/lc-diet. That´s interesting because my experience is quite different. My basal temperature dropped to 35,5 degrees Celsius after about 2 1/2 years on a JK-like diet. I suppose because there is no hunger while eating loads of fat my caloric intake dropped too much. After adding lunch back into my schedule and upping carbs (100-150g/day) my basal temp is now in the 36,0-36,3 range. I don´t know if it´s calories or carbs. I suppose the former, but I am not sure.
What about your caloric intake after starting lc? Did it go up our down? How many meals do you eat per day? What is your macro-ratio?

Dr. B G said...


It is interesting that you noticed mild acne flares with high vitamin C. Mark Sisson at one of his recent talks at Crossfit gyms said that vitamin C competes w/insulin on the insulin receptors... (he was talking about how important it is to control insulin for longevity). I should've asked b/c now I can't find anything on it.

Have you heard of this?

Your post is excellent!!! I've been wondering about: Cholesterol, collagen, calcium and C (vitamin C) and D. Can't seem to live well constitutionally without these. It appears the body is pretty ingenious about endogenous and exogenous sourcing of vitamin D over the millenium.


gunther gatherer said...

Hi Sven.

My diet hasn't changed very much in the last 2 years since I started PETER'S VERSION of the JK diet religiously. That means especially that I took out all grains and mostly replaced them with more animal fat if possible. I'd say I eat anywhere between 2500 and 3000 kcal a day.

I don't exercise, but I do practice intermittent fasting by waiting until 4:00 pm to eat almost every day. The eating period stops about 2 hours afterward because I stuff myself, but I would eat more if I could! I'd say macros are 80% animal fat, about a palm-sized chunk of meat, and I don't count the carbs because they're basically a handful of nuts. I also take cold showers sometimes as a method of hormesis.

Basically, if you haven't taken out grains and are still eating gluten, there's a good chance your thyroid is being suppressed, which would definitely lower your body temp. If you add carbs to try to raise your bodytemp, make sure they are paleo. My carb sources are usually nuts and maybe 80% chocolate. Not to mention the few carbs in my high-fat yogurts, etc.

Hope that helps!

Justin said...


Have you posted anywhere what the results of going this route have been?

As it is, I've been ramping up my fat intake (over protein) over the past week and a half while also doing daily IF -- 16 hour fasts, 8 hour eating windows (usually a late lunch around 2 - dinner at 7:30 or 8 and then maybe some form of dessert).

So far, noticed a clear impact on appetite suppression during the eating window though I usually get hungry by around noon or 1pm. Been practicing LC/paleo since Feb. 2008, so this is more an experiment with higher fat intake than anything else.

Sven said...


>I'd say I eat anywhere between >2500 and 3000 kcal a day.

Has your pre paleo caloric intake been the same (higher/lower)?

>Basically, if you haven't taken >out grains and are still eating >gluten, there's a good chance >your thyroid is being suppressed,

My carb sources have been (as they are now) primarily potatoes, rice and dairy (cream, no milk). My gluten intake has been minimal and way below what I consumed pre LC. Gluten can´t be the reason.

gunther gatherer said...


The diet alone took me from 79kg. to 70kg. in about 12 weeks, with liberal cheating on my part because I was still experimenting and got a lot of things wrong. In other words, it took me a long time to get things right.

IF and hormesis techniques took me from there to 65kg.

Besides the weight loss, there've been numerous improvements in my overall health over the 2 years since, namely more energy, better sleep, more equalized mood and better handling of stress, resolution of prostate problems and midnight urination, Reynaud's (though hands and feet get cold in winter still), rectal itch, acne, hair loss problems, thyroid levels went to normal and trigs and CRP are great. Peter and I have also discussed off-blog whether a kidney stone incident was actually a stone I had for years that the OD SHRANK so it could finally pass down the ureter.

Unfortunately I'm too shy to have my own blog about this, so I hope you'll believe all this. If not, just try for yourself and please post your results.

gunther gatherer said...


Pre-paleo was definetely LESS caloric intake per day, WITH exercise. I don't understand how the gluttony and sloth theory of obesity just refuses to die. I have to add though that I did binge at least once a week.

I forgot to mention to Justin that another result of this plan was complete resolution of eating disorder symptoms and binging. I just don't have the insatiable urge anymore.

Try adding some iodine as a supplement. This could immediately correct your thyroid problem. Most westerners are woefully deficient in iodine due to modern agricultural techniques which deplete the soil of nutrients, not to mention added fluoride in water and heavy metals in food which supplant iodine in the body because they are chemically lighter.

Justin said...


Thanks for the info -- if you don't mind my asking, how tall are you?

I'm about 5'11" and I went from 183 to 165 in the span of a couple months back in 2008 doing IF and low-carb'ing. Subsequently I got into CrossFit and put on some muscle and ratcheted back up over 170. Nowadays I am around 175 and all attempts to get back under 170 have been thwarted.

Incidentally, I think I may have gotten too concerned with protein intake over fat intake, so I'm trying to ratchet fat up a lot more and keep my protein in check (a la OD -- or close to it maybe 1.2 OD on protein). So far, it seems I've expereinced some appetite suppression that just wasn't there when I'd consume more protein and less fat. Seems the lack of fat made me have more cravings.

So we'll see how this OD tweak goes!

gunther gatherer said...


I'm 5'9. Started doing OD at 36 (was paleo for 2 years before) and just turned 39.

Unless you're trying to build muscle, you should probably keep to Kwasniewski's protein limits at 1g per kg ideal bodyweight. In other words, if you're hoping to get to 165 lbs, that's 75g protein a day. Anything more than that will raise insulin more than you want.

Please post your progress so we can get a group picture of general results.

blogblog said...

re gunther-gatherer:

"Unless you're trying to build muscle, you should probably keep to Kwasniewski's protein limits at 1g per kg ideal bodyweight. In other words, if you're hoping to get to 165 lbs, that's 75g protein a day. Anything more than that will raise insulin more than you want."

I disagree. You can't effectively combine low protein and low carbohydrate because of the constant metabolic conflict between protein synthesis and maintaining blood glucose. 70g of protein a day is probably adequate if you are you are eating 300g of carbohydrate as well.

Traditional Inuit diets contained 4-5g/kg/day of protein. The Masai diet is high in both protein and lactose.

If you see old photos of traditional HGs as you will notice the males are nearly always quite muscular.

Wild mammals typically obtain around 3-5g/kg/day of protein from their diet or gut fermentations.

gunther gatherer said...

Let me refrase. Unless you're trying to build muscle AND are exercising with intense lifting, I wouldn't recommend going over JK's limits, regardless of what HGs may do.

Blogblog, this is an ongoing conflict on this blog between what is tried and tested by HGs and what JK recommends and our own experience with his diet. I'm not sure how much protein is ideal, I'm just following his guidelines.

Sven said...


>Pre-paleo was definetely LESS >caloric intake per day, WITH >exercise.

For me it´s the other way around. I suppose the caloric drop brought my thyroid problems.

>Try adding some iodine as a >supplement.

I started supplementing iodine a couple of months ago. Besides raising my TSH I haven´t felt any effects.

Justin said...

I regularly workout -- say at least 3X week -- intense weight lifting or bodyweight exercises (pull-ups, ring push-ups or dips, etc.).

The limited protein intake is really interesting to me.

My personal experience is that keeping protein high (say 1gm protein per pound of weight) while limiting carbs and having moderate fat (all in an effort to lean out past a certain point) inevitably leads to eating a lot more protein -- say snacking on beef jerky and pork rinds (for example). I'm guessing the excess protein is triggering insulin which triggers hunger. Fat blunts that effect*.

I think my chief obstacle at this point is ascending the learning curve for how to ramp up fat intake and minimize protein. I'm so accustomed to having high protein meals (usually 2x/day). At present, I'm relying on heavy whipping cream, throwing out egg whites, using a lot of butter, and eating cheese. Any good ideas for ramping this up out there? I do love bacon :) but maybe that would be out of line?

Forgive this question, but what's the take on alcohol in OD?

* It seems I've read conflicting views on which blunts hunger more -- fat or protein. Seems its fat in my experience.

gunther gatherer said...


I say just try the OD as given by JK and see how you feel. I can almost guarantee your hunger pangs will subside by subbing fat for protein/carbs. If you think you're getting too scrawny after a few months, you can always push protein up a few grams.

Don't forget jerky and pork rinds have lots of salt, which will show up on the scale as water retention. You should probably read Peter's "What I eat" blog entries thoroughly to get ideas of how he manages to do all this. I guess a little bacon for flavor won't kill you. Peter eats it too (to flavor the liver dishes).

In other words, maybe go by the book for the next couple months and then adjust the macro ratios for your personal aesthetic or health needs.

I personally don't think a high protein diet is good either for the kidneys or the liver, and it definitely raises insulin. This is one of the founding principles of the OD.

gunther gatherer said...

Sorry, I should say try the OD as given by JK and tweaked by Peter. That is, no grains, some vit D and omega 3, etc. You know the rest...

Justin said...

Thanks for bearing with me and apologies to Peter for hijacking your comments!

Ken said...

Excellent post.

Re. European bread
What caused the rickets epidemic? .

Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry.

"These data support the concept of stable patterns of gene transcription unique to a geographic ancestral lineage. Differences in expression of several carbohydrate metabolism genes suggest both genetic and transcriptional mechanisms contribute to these patterns and may play a role in exacerbating the disproportionate levels of obesity, diabetes, and cardiovascular disease observed in Americans with African ancestry".

I'm wondering about mtDNA, hunter gatherers in Europe would have been adapted to eating a diet very low in carbohydrates.

The end of he ice age and the later switch to agriculture may have disadvantaged many of the European 'low-carb' hunter gatherer mtDNA lines to the extent of them disappearing over thousands of years. European mtDNA that is around today may well have been rare in the ice age. It might be that today European mtDNA is more adapted to eating carbohydrate than it was way back in the Magdalenian.

'Mitochondrial DNA haplogroups and type 2 diabetes: a study of 897 cases and 1010 controls' "[...]
it is shown that European mtDNA haplogroups are unlikely to play a major role in the risk of developing the disorder."

'Mitochondrial haplogroup N9a confers resistance against type 2 diabetes in Asians'

'Women with mitochondrial haplogroup N9a are protected against metabolic syndrome'

'Mitochondrial DNA adaptations in living human populations' (John Hawkes).

"The occurrence of potentially adaptive mtDNA mutations appears to have been quite a common event throughout human prehistory, because today's haplogroups appear to be separated by many mutations that are adaptive in different contexts."

Bryan - oz4caster said...

Hi Peter,

Hope you're enjoying your new location. Very interesting post as usual. It reminded me of a related post by Loren Cordain where he theorizes how Europeans got their white skin. In it he says:

"Nutritional scientists have known forever and a day that excessive consumption of whole grain cereals severely impairs vitamin D metabolism and can lead to the bone disease, rickets. In fact, as far back as 1918, before vitamin D was discovered, a scientist in England by the name of Mellanby routinely induced experimental rickets in puppies by feeding them an oat diet."

You can read the entire newsletter article here:
A 10,000 Year Old Riddle of Bread and Milk Solved


blogblog said...

in some parts of northern Europe agriculture is basically only a century old. Stefansson noted that when his parents lived in Iceland in the mid 19th century that bread was only eaten a few times a year. The traditional Icelandic diet was almost entirely comprised of meat, fish and fermented milk products.

Being of northern European origin I find I can't tolerate more than 30g/day of carbohydrate.

blogblog said...


This is just another one of Cordain's half-baked ideas based on a limited and very selective reading of the scientific literature. He is an obscure physical education professor who dabbles in nutrition. Despite what some of Cordain's supporters may claim he has no real academic reputation as a researcher. His work is certainly not cited in any important nutrition or exercise physiology textbooks.

Cordain doesn't seem to understand that there has been a massive amount of historically recent migration - far too recent for substantial evolutionary adaptation:

- the Bantu people of southern Africa migrated from the tropics less than 300 years ago. This is why the people of southern Africa are back.

- Northern India was invaded by light skinned Eurasians.

- the people of South East Asia are historically recent migrants from the far north. This is why tropical Vietnam is populated by pale skinned people.

There has also been a vast amount of intermarriage. For example the majority of modern Australian aborigines have a very significant European heritage.

Cordain also ignores the fact that hunter-gathers spend nearly all their time outside and wear very little clothing. This means they need far more pigmentation to protect against sunburn and skin cancers. People in agricultural societies tend to spend more time under shelter and often wear far more clothing. Traditional Arabs would completely cover their faces and bodies to avoid the sun. In tropical Vietnam the people are lightly pigmented. But they also wear clothing that eliminates most sun exposure.

blogblog said...
This comment has been removed by the author.
blogblog said...

Jared Diamond has by far the simplest and probably most plausible reason for global variations in skin colour. He believes that peoples preference for certain physical characteristics and cultural biases is far more important than beneficial adaptations to the local environment - the Peacock's Tail Paradox. [Logically a peacock would have dull plumage and a small tail to help protect against predators. However peahens prefer males with huge tails and showy plumage.]

The de-pigmented people of northern Europe are descended from a very small number of individuals. It is a quite possible that these blue-eyed blondes and redheads preferred each other as sexual partners. Once their numbers reached a critical mass of a few dozen they could form their own tribes. It is then just a matter of time for these people increase to millions.

Diamond talks about how the Fore people of the New Guinea highlands consider their women to be exceptionally beautiful. However the Fore think the neighbouring tribes are less attractive. The Fore consider European women to be hideously ugly with "yellow hair like dead grass and white skin like ghosts." Fore people have very dark skin despite living in a thick rainforest with very little sun exposure. However their extreme cultural distaste for pale skin would eliminate any possible benefit of less pigmented skin.[I know of a white geologist who suffered severe vitamin D deficiency working in the New Guinea highlands due to a lack of sunlight.}

Local conditions can often be largely overcome by behavioural changes. Australians of northern European origin simply use sunscreen and seek shade rather than relying on melanin.

Bryan - oz4caster said...


Cordain is not one of my favorite health and diet authors, as I think he is off track in supporting a low-fat and low-saturated fat diet. However, I do think he has some interesting ideas and I am not going to belittle him because he has "no real academic reputation" as a researcher. I have great respect for Anthony Colpo, who has "no real academic reputation" as a researcher and little respect for T Collin Campbell who has a "real academic reputation". Logic and science should be the judge of ideas, not reputation.

My reference to Cordain's recent newsletter article in the context of this post is more about the evidence that diets high in whole grain may disrupt vitamin D metabolism and make it easier to achieve vitamin D deficiency. I think his theory about the involvement of whole grains and milk in shaping skin color of northern Europeans is intriguing, though I don't have the scientific background to fully assess his logic. The theory that you mentioned by Jared Diamond strikes me as being rather racist and not very plausible considering how readily people tend to mix when they meet. The U.S. is a prime example of a cultural and racial melting pot. Even Europe is much more diverse than it used to be a couple hundred years ago.

Jürgen said...

Hi Peter,

I love your site a lot, I already pulled tons of valuable information from there!

Now I would like to hear your comments to this one
I’ve found today, and which irritates me quite a bit.

It shows a significant decrease in bone mineral density and bone mineral content in children under a ketogenic diet after 15 month.

Thank you

Nigel Kinbrum BSc(Hons)Eng said...

Having taken a peek at Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet, I think the answer lies in the sentence:-
"Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D."

So the statements:-
"The mechanism is unclear. Further studies are needed." and "The KD resulted in progressive loss of BMC." leads me to suspect a lack of working brain cells in the people that published the above study.

blogblog said...

Bryan said:

"The theory that you mentioned by Jared Diamond strikes me as being rather racist and not very plausible considering how readily people tend to mix when they meet. The U.S. is a prime example of a cultural and racial melting pot. Even Europe is much more diverse than it used to be a couple hundred years ago."

The theory is far more plausible than most others and has nothing to do with racism.

In traditional tribal societies everyone is closely related and they look very similar. The neighbouring tribes speak a different language and are often mortal enemies. In many traditional societies all marriages are arranged. In situations like this there is very little opportunity for any social interaction between different groups. So people will naturally be attracted to people who seem familiar and safe and see strangers as potential enemies.

People who grow up in a multicultural society are far more open to marrying partners from different ethnic different groups. People who spend their early childhood in monocultures are far less likely to marry someone from a different ethnic group. This is probably an issue of unfamiliarity rather than racism. If you grow up with children from a different ethnic group you don't see them as "foreign".

Diamond mentioned a study of Chinese Americans living in San Francisco. The children who grew up in Chinatown only married other ethnic Chinese. Those Chinese Americans who grew up in the suburbs rarely married Chinese people.
This is despite the fact that as adults both groups interacted widely with non Chinese people.

blogblog said...

Dietary changes can't explain blonde hair or blue eyes. The Japanese have similar low levels of melanin as northern Europeans but have black hair and brown eyes. Hair doesn't produce vitamin D and the contribution from the iris is negligible.

The Japanese eat polished white rice which doesn't contain phytates.

Ken said...

John Hawks quotes a Science article:-
'The agricultural revolution favored people lucky enough to have gene variants that helped them digest milk, alcohol, and starch. Those mutations therefore spread among farmers. But other populations remained more carnivorous, such as the Saami of frigid northern Norway, whose ancestors herded reindeer. Among Saami ancestors, genes to digest meat and fat efficiently were apparently favored. One gene variant, for example, makes living Saami less likely to get uric acid kidney stones—common in people who eat high-protein diets—than are people whose ancestors were vegetarian Hindus and lack this gene variant, says geneticist Mark Thomas of University College London (UCL).' Here.

He remarks:

"There is an unresolved tension in the article: Is there a better diet for everyone? Clearly some populations have undergone large recent diet changes with bad consequences; the same bad outcomes occur in some people despite possibly adapting to new diets for thousands of years. And yet, every metabolic or diet-related syndrome is variable, and we know that some genes related to digestion and metabolism have rapidly changed. "Westernization" is not as simple as it seems, nor is agriculture (or, for that matter, pastoralism) -- and the responses to each vary for stochastic reasons in different populations."

Peter Frost says

"The Inuit have made the transition from a low to high carbohydrate diet in two or three generations. There have been negative effects, and I don't want to minimize them, but the most serious ones seem to be due to overeating.

There seems to have been a period of a thousand years or so when the northward movement of hunter-gatherers stalled. There may have been trade between the two groups and this may have allowed some hunter-gatherers to become habituated to cereal foods.""

blogblog said...

I'm of northern European ancestry. I can eat as much meat and hard cheese as I like and never feel unwell. I drink whole cream by the cupful with no digestive symptoms. I often eat 300-400g of fat a day with no problems. However a tiny amount of bread, fruit or vegetables wreaks havoc on my digestion. As little as 100g of carbohydrate will make me sick for 4-5 days.

Thankfully I live in Australia where meat and dairy is very affordable and abundant. I have decided my only overseas holiday options are New Zealand, Mongolia, Argentina and Lappland.

Peter said...

Hi Nigel,

I think we are still observational here. Again, the intervention studies will no doubt be coming in soon. Until they do we don't know whether low D is possibly caused by living on Fanta with its associated obesity and the rest of the metabolic syndrome.

Max, I think that Trevor Marshall is struggling to account for the benefits seen in intervention trials in a similar way to how Vieth is looking to explain the negative associations in observational trials. Life becomes much simpler if you regard vitamin D as being important under certain conditions, in particular as an agent to ameliorate pro inflammatory states, rather than a panacea in its own right. This would lead me to suspect a benefit if you live on bagels deep fried in partially hydrogenated soya oil but it may have far less detectable benefit on a diet based around saturated fat and normoglycaemia. I don't see anyone looking in this area.

Jordan, The Yemeni Jews and CVD has been looked at in the context of both sugar and omega 6 PUFA, I believe. Both increase on the move to Israel.


I suspect he may be talking about amounts, but if not, I would disagree. I feel the Muslim situation is closer to "sunshine rickets" without the sunshine. The Hindu situation is far more interesting.

G, No I haven't. The C people suggest C lowers insulin resistance a little but I've not got a lot in the way of refs for this.

I have to wonder whether the TYP observation of marked regression of plaque with D supplementation are purely D related or are associated with a drift away from vegetarian leanings towards more fat acceptance, more LC acceptance, possibly more meat acceptance. Dr D did have quite strong pro vegetarian leanings which are happily far less evident nowadays. The big problem with an approach like TYP is that it is multiple interventions. Generally pretty good interventions, but it is then hard to tease out what might be happening... Certainly from just reading Dr D's blog!

Gunther and Sven, not much to add really except that under hard exercise JK does allow more carbs, which would probably have a protein sparing effect. Or, to cite Sonksen, higher insulin inhibits protein catabolism, helping you keep what you have produced, so might conceivably increase muscle mass at a given level of amino acid through put.

Ken, I'm sure there are multiple metabolic adaptations to sustained nutrient sources. What I like about the OD is that it is so similar to starvation, which I suspect is a highly conserved metabolic ability.

Brian and Blogblog, Cordain has so many cookie ideas that we have to accept that some of them will be correct, I just can't tell unless they are totally dumb, like putting his name as middle author of a paper suggesting we all need to be statinated down to a cholesterol of 70mg/dl. We've discussed this before and I've seen rumours that Cordain is less saturophobic than in the past but he has a long way to go in my book.

Nigel, Yes the KD is very extreme compared to the OD and in the full text papers you never actually get to see what was fed to the children. Clearly a diet producing 20% incidence of renal stones and occasional death from pancreatitis has a long way to go. This paper shows no problem with ordinary ketogenic diet:

and this one shows bone loss and increased Ca excretion, however there was significant weight loss which reduces bone density, unlike the situation on the KD where children are trying to grow...

So my comment would be to be careful with the KD as it stands.

Ken, my biggest problem with Peter Frost's comment is that the most serious problems of the Inuit seem to come from over eating. This is simply a way of describing the phenomenon of people being always hungry as they are squirrelling away dietary calories as fat so need extra to run their metabolism. Why? certainly not greed and certainly not over eating... I'm back on insulin again, and diseases.


Ken said...

"What I like about the OD is that it is so similar to starvation, which I suspect is a highly conserved metabolic ability".

That is a very good point which I hadn't thought of.

It has set me wondering about the duration of periods of OD 'starvation', sure winter would have been a time of hunger until recently but the availability of food including carbs would always be greater in summer. Mimicking starvation for a few months of the year with OD is going to be good but 24/7 year after year ?

blogblog said...


I assume that humans in cold regions had a feast-famine metabolism like bears. It certainly would be desirable to enter winter with 10-20kg of body fat. Death by starvation at age 15 will have a much greater natural selection effect than Type 2 diabetes at age 65.

A psychiatrist friend suggested to me that seasonal affective depression may be an evolutionary adaptation to conserve energy in people living at high latitudes . Not wanting to much anything except rest and sleep all winter will certainly save a lot of energy.

Dr. B G said...

Actually I think we are a lot like bears... they are omnivorous predators too typically consuming high amounts of dietary n-3.

And prone to alopecia like humans (thanxxx Dexter) from grains/gluten other nutritional deficiencies and omega-6 toxicities:

Peter said...

G, wow, looks like gluten to me! But no one would be feeding a bear on whole grains... Would they?

Ken and Blogblog,

The idea of seasonal nutrition with strict LC in the Winter and more fruit, maybe starches, nuts (omega 6s) and vitamin D during late summer is an attractive idea. I believe Susan Allpost has ideas along these lines, even if I've been told she is a bit of a saturophobe, maybe ought to do some reading...


TedHutchinson said...

25-Hydroxyvitamin D3 is an agonistic vitamin D receptor ligand
25-Hydroxyvitamin D(3) 1alpha-hydroxylase encoded by CYP27B1 converts 25-hydroxyvitamin D(3) into 1alpha,25-dihydroxyvitamin D(3), a vitamin D receptor ligand.

25-Hydroxyvitamin D(3) has been regarded as a prohormone.

Using Cyp27b1 knockout cells and a 1alpha-hydroxylase-specific inhibitor we provide in four cellular systems, primary mouse kidney, skin, prostate cells and human MCF-7 breast cancer cells, evidence that 25-hydroxyvitamin D(3) has direct gene regulatory properties.

The high expression of megalin, involved in 25-hydroxyvitamin D(3) internalisation, in Cyp27b1(-/-) cells explains their higher sensitivity to 25-hydroxyvitamin D(3).

25-Hydroxyvitamin D(3) action depends on the vitamin D receptor signalling supported by the unresponsiveness of the vitamin D receptor knockout cells.

Molecular dynamics simulations show the identical binding mode for both 25-hydroxyvitamin D(3) and 1alpha,25-dihydroxyvitamin D(3) with the larger volume of the ligand-binding pocket for 25-hydroxyvitamin D(3).

Furthermore, we demonstrate direct anti-proliferative effects of 25-hydroxyvitamin D(3) in human LNCaP prostate cancer cells.

The synergistic effect of 25-hydroxyvitamin D(3) with 1alpha,25-dihydroxyvitamin D(3) in Cyp27b1(-/-) cells further demonstrates the agonistic action of 25-hydroxyvitamin D(3) and suggests that a synergism between 25-hydroxyvitamin D(3) and 1alpha,25-dihydroxyvitamin D(3) might be physiologically important.

In conclusion, 25-hydroxyvitamin D(3) is an agonistic vitamin D receptor ligand with gene regulatory and anti-proliferative properties.

Bear in mind that at 40ng/ml 100nmol/l there was no measurable anti proliferative action.

Vitamin D supplementation during lactation to support infant and mother.shows @ 58.8ng/ml=147 nmol/l human breast milk flows replete with D3. Lowest incidence of chronic disease is also associated this level.

It will be interesting to see what the MP lobby make of these new findings?

Ken said...

More new findings for you Ted!

Introduction of oral vitamin D supplementation and the rise of the allergy pandemic.

Arterial calcifications and increased expression of vitamin D receptor targets in mice lacking TIF1α.
"Interestingly, the calcifying arteriopathy of TIF1α-null mutant mice shares features with the human age-related Mönckeberg's disease and, overall, the TIF1α-null mutant pathological phenotype supports the hypothesis that aging is promoted by increased activity of the vitamin D signaling pathway."

Population differences in vitamin D metabolism. (Scroll down a bit)

Several thousand IU a day in the UVB-less months is not a lot in comparison to what one would get from summer sun, but it is still a lot to be ingesting day in day out for months on end. The 'D' enthusiasts' rationale for supplementation:-
"[...] posits vitamin-D metabolism as a ‘given’ that human skin color has to adjust to, when in fact this metabolic pathway is just as amenable to natural selection as everything else".

A thousand generations of humans in Northern Europe were naturaly selected for maximum fitness in UVB-less winters. It follows that the vitamin D system in their descendants is calibrated and optimized for the summer rise and winter fall in vitamin D levels at northern latitudes. I trust evolution to find the 'sweet spot' for the vitamin D system , ie the setting that keeps me healthy (and looking that way) for as long as possible.

'Evolutionary flaws - or are they?' ( G. Cochran)
"You see, although wandering into suboptimal solutions is certainly possible, you can be sure to see slick, polished, tested and robust implementations of those basically suboptimal designs. Almost always, given an environment that isn't too different fron the ancestral one, those designs will work just as well as they can, which is usually pretty damn well. And if they work well in anyone, you should expect to see them work well in almost everyone."

In 'Serum vitamin D and risk of prostate cancer in a case-control analysis' (2009) it is stated that:-
"No significant association was found between 25-hydroxyvitamin D and risk of prostate cancer (highest vs. lowest quintile: odds ratio = 1.28, 95% confidence interval: 0.88, 1.88; P for trend = 0.188). Subgroup analyses showed no significant heterogeneity by cancer stage or grade, age at diagnosis, body mass index, time from blood collection to diagnosis, or calcium intake. In summary, the results of this large nested case-control study provide no evidence in support of a protective effect of circulating concentrations of vitamin D on the risk of prostate cancer".
Casts a lot of doubt on Vieth's hypothesis I think.

TedHutchinson said...

How strong is the evidence that solar ultraviolet B and vitamin D reduce the risk of cancer?
An examination using Hill's criteria for causality William B Grant

This has a section on prostate cancer and vitamin d incidence that may help you understand the overall relationship.

Ken said...

Grant himself admits the data on prostate and some other cancers are mixed, moreover he does not suggest supplementation yet, he wants more research.

"Nonetheless, additional randomized, controlled trials are warranted to further examine the link between vitamin D and cancer incidence, survival and mortality."

Maybe some cancers are prevented with higher D but I bet other unpleasant ilnesses are made more likely. Grant's presentation of the data contains an implicit false premise inasmuch as he
" posits vitamin-D metabolism as a ‘given’ that human skin color has to adjust to, when in fact this metabolic pathway is just as amenable to natural selection as everything else".

I'm willing to accept there might be advantages to getting extra UVB / vitamin D, but I keep coming back to the same point. Evolution could have, and surely would have, given us all much higher levels and D storage for winter if it was an unalloyed benefit.

It is clear to me that there is some kind of trade off between beneficial and deleterious effects. The real limit on vitamin D is our physiology not the latitude. When you raise 'D' levels artificially - and thousands of IU/day are indeed unnatural - you move out of the 'sweet spot' and into the danger zone.

mutant pathological phenotype supports the hypothesis that aging is promoted by increased activity of the vitamin D signaling pathway..