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It seems that sedentary lifestyle, poor diet and lack of exposure to sunlight is taking its toll on the last generation of Britons: rickets are on the rise again, causing a debate on whether to implement laws forcing food companies to supplement their products with vitamin D. Ol' good cod liver oil is also being missed.
According to Times Online, some 50% of British adults have vitamin D deficiency in winter and spring, one of six severely so. People of "Asian" origin and in particular those who cover much of their body because of religious reasons (read: Muslims particularly) are at increased risk.
The article also blames television and videogames for this epidemic.
Sources: The Register, Times Online.
12 comments:
"People of "Asian" origin and in particular those who cover much of their body because of religious reasons (read: Muslims particularly) are at increased risk.
No, allow me to elucidate. :-
"Undoubtedly, lighter skin allows more UV-B into the skin. As Robins (1991, pp. 60-61) notes, black African skin transmits three to five times less UV than does European skin. But is this a serious constraint on vitamin D production? Apparently not. Blood metabolites of vitamin D show similar increases in Asian, Caucasoid, and Negroid subjects when their skin is either artificially irradiated with UV-B or exposed to natural sunlight from March to October in Birmingham, England (Brazerol et al., 1988; Ellis et al., 1977; Lo et al., 1986; Stamp, 1975; also see discussion in Robins, 1991, pp. 204-205)."
Vitamin D and UV fluctuations(2).
" '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. [cereals seem to increase vitamin D requirements by decreasing calcium absorption and by shortening the half-life of the main blood metabolite of vitamin D (Pettifor, 1994; see <a Href="http://paleodiet.com/phytic.txt>Paleodiet</a>).]
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.'
Dunnigan appears to have spent most of his career on this problem. [He} 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. What appears to make a difference in his book is meat:
Cont.
'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.' "
What caused the rickets epidemic? .
" [T]he evidence points to a highly localized origin, essentially southwest England in the early 17th century. Rickets was completely new to observers at the time, including the College of Physicians president Francis Glisson. In 1650, he wrote..."
Pigmentation and Vitamin D Metabolism in Caucasians: Low Vitamin D Serum Levels in Fair Skin Types in the UK.
"[T]his study shows that fair skin types within a Caucasian population in the UK are most at risk of vitamin D deficiency. This ... may result from genetic differences in vitamin D metabolism in subjects with fair skin compared to those with darker skin. A study of more than 1000 subjects in France linked fair skin to low vitamin D"
Sun avoidence?; I can tell you that very very few people in Britain avoid the sun, quite the opposite.
Now fair skin lets in more UV but that's not why white skin evolved it was actually SEXUAL SELECTION. Higher vitamin D levels are an undesirable side effect which causes a problem. hence a significant minority of whites have special adaptations to reduce these levels. This is in addition to a vitamin D synthesis limit that kicks in after a mere 20 minutes sunshine remember.
"Europeans [are] genetically polymorphic in their ability to maintain blood levels of vitamin D? At least two alleles reduce the effectiveness of the vitamin-D binding protein, and their homozygotes account for 9% and 18% of French Canadians (Sinotte et al., 2009).+
Why are Europeans white?
"Do we know when Europeans became white? This change has been roughly dated at two gene loci. At SLC45A2 (AIM1), Soejima et al. (2005) have come up with a date of ~ 11,000 BP. At SLC24A5, Norton and Hammer (2007) suggest a date somewhere between 12,000 and 3,000 BP. These are rough estimates but it looks like Europeans did not turn white until long after their arrival in Europe. As a Science journalist commented: “the implication is that our European ancestors were brown-skinned for tens of thousands of years” (Gibbons, 2007)."
So you're telling me that the only use of white skin (increasing vit. D synthesis) is not of any use at all? What's then: a genetic defect?
Sorry, I don't believe a word (and please try to be shorter in your comments, with less quotes and more going to the grain).
Also don't you wonder why all concentration of rickets, including historical epidemics, is concentrated in the European North, where sunlight is low? These epidemics, whatever the detail of their causes are clearly putting pressure in the population to lighten their skin... or to eat a lot of fish.
Skin color is the only human variable trait I know that has a very clear adaptative value: it is there for a reason and that reason is the balance between solar protection and vitamind D synthesis.
Sorry if I overstepped the mark with overlong quotes.
You're sticking to William Charles Wells' idea. It was a good one in it's day but time has passed it by.
Dunnigan knows everything there is to know about rickets in Britain, he says its occurence in Asians is due to not eating meat (Hindus?), rather than having dark skin. There are lots of black Africans in Scotland and there has never been rickets among them.
John Snow (of cholera fame) published On the adulteration of bread as a cause of rickets in 1857.
"Dr. Snow observed that the illness was most frequent in London and the south of England where industrial bakeries used alum to make bread look whiter. It was rare in the north where bread was normally home-baked"
Why is "all concentration of rickets, including historical epidemics,.. concentrated in the European North"? Well the south of Europe gets a lot more UV so yes it may prevent people with weird diets getting rickets. With the origin of white skin are not talking about today or the 17th century but evolutionary time when nobody was a vegetarian or eating alum adulterated bread. However, white skin did NOT stop a very high proportion of the British population getting rickets in the 17 century, if their skin was evolved to prevent rickets then why did it suddenly stop working in the 17th century?
Doesn't that suggest a new factor entered the equation?
While I agree people with meat free diets may be more likely to get rickets in Northern Europe the lesser UV at high latitude is a contributary factor not the main one.
The adulteration of bread started in England for historical reasons, if latitude is the main determinant of getting rickets Southern England (four hundred miles to the south of Glasgow) is an unlikely place to find it appearing first. And why was it new to them in the early 17th century?; England was in the same place it always was so the amount of UV it got hadn't changed in the 17th century.
Skin color is the only human variable trait I know that has a very clear adaptative value: it is there for a reason and that reason is the balance between solar protection and vitamind D synthesis
Yes that is true but most peoples in the world from reindeer hunting Siberians to !Kung Bushmen are a sort of light brown that does not change very much from one extreme of UV to the other. UV radiation is a selective pressure but it's not a very strong one.
The extremes of skin, ie white and black are not the result of the same process of selection that has produced the Siberians or the !Kung.
Men are darker than women; north Europeans are lighter than south Europeans; are they are less masculine than South Europeans?
In the G spot post French people are scoffing at the lack of hetrosexual sexual passion of the male British northern Europeans. Maybe they're right!
Phosphates are widely available in all kind of foods. Phosphates are seldom, if ever, a nutritional lack. Excess of phosphates instead is very common, causing an imbalance with calcium and the production of kidney stones, osteoporosis and even cancer.
Lack of phosphates instead may cause problems in muscles, blood and brain. But not in bones.
So I don't think that your alternative makes any sense: all breads are high in phosphates (organic ones more but also in vitamins) and all the "explanation" seems extremely speculative.
As you know fish in particular has loads of vitamin D and that distorts the picture. Also we don't yet understand well how the pigmentation components of East Asian (or Khoisan) types work. We know that they use different genes than West Eurasians and that they are extremely well protected against skin cancer, hence same color may be a misleading element.
When in this article they say "Asians", they seem to mean primarily South Asians, not Chinese.
Men are darker than women...
Which makes total sense because men don't get pregnant nor lactate. Appropriate levels of vitamin D in children, since the womb, are crucial for proper development, notably of the brain, as I have discussed elsewhere. naturally children are normally lighter than adults of either sex. This happens even among our cousins of the Pan genus: young chimpanzees are white, while old chimpanzees are black.
(In the UK 'Asians' means Pakistanis, Indians and Bangladeshis)
People from tropical countries do not handle UV and vitamin D synthesis the same as those from northern Europe, the natural optimum level, the homeostasis of the blood level of vitamin D is different. People from Northern Europe have higher levels than those from South Asia (or the Middle East or Africa) see also Black-White Differences in Cancer Risk and the Vitamin D Hypothesis
Please bear in mind that the data was the same for antioxidants; low levels were found to be strongly associated with disease. When they did the trials, lo and behold, their hapless human guinea pigs started to die, the excess was so great in several cases that the trials were halted.
The evidence against antioxidant (and other vitamin) supplementation has been mounting up inexorably, what makes you think vitamin D will be different?
Implicit in the talk of vitamin D insufficiency is that there is a best vitamin D level applicable to everyone and everyone should supplement until it is reached. I just doesn't work that way, levels reached by supplementation do not bring the expected benefits for antioxidants ect. It will take longer for the deleterious effect of vitamin D supplementation to be discovered because it mimics aging and aging is a subtle process.
The end result will be the same: benighted amateur nutritionists putting their lives into fast forward.
I think that you are defending here some pet theory by that Pete Frost guy, who wants to attribute skin color differences not to selection but to some other weird reason. I just don't believe on that shit and I'm beginning to suspect he has a racist agenda.
So enough. And I tell you seriously: this is not the place for racist ideologies. I'm sure that there are many ghettoes in the Internet for people who sponsors racism but this is not among them.
Vitamin D Production after UVB Exposure Depends on Baseline Vitamin D and Total Cholesterol but Not on Skin Pigmentation
"The increase in 25(OH)D level after UVB exposure was negatively correlated with baseline 25(OH)D level (P<0.001) and positively correlated with baseline total cholesterol level (P=0.005), but no significant correlations were found with constitutive or facultative skin pigmentation. In addition, we paired a dark-skinned group with a fair-skinned group according to baseline 25(OH)D levels and found no differences in 25(OH)D increase after identical UVB exposure."
Vitamin D, Adiposity, and Calcified Atherosclerotic Plaque in African-Americans
"... positive associations exist between 25-hydroxyvitamin D and aorta and carotid artery CP in African-Americans. The effects of supplementing vitamin D to raise the serum 25-hydroxyvitamin D level on atherosclerosis in African-Americans are unknown. Prospective trials are needed to determine the cardiovascular effects of supplemental vitamin D in this ethnic group"
Seasonal Genetic Influence on Serum 25-Hydroxyvitamin D Levels: A Twin Study
"In conclusion, our results indicate that approximately half of the variation in serum vitamin D status during the summer season is explained by genetic factors. The winter season variation in serum levels can mainly be explained by shared environmental influences, i.e. solar altitude. These findings suggest that genetic factors play a major role in the generation of vitamin D in the skin and should encourage further research aiming at the identification of these factors."
Plasma 25-hydroxyvitamin D and prostate cancer risk: The Multiethnic Cohort.
. "When clinically defined cutpoints were used, there was no increased risk for the lowest 25(OH)D concentration (OR for <20 versus 30-<50ng/ml=1.10, 95% CI=0.68-1.78), while there was a suggestive increased risk for higher concentrations (OR for 50ng/ml=1.52, 95% CI=0.92-2.51).
Nutritional rickets: still a problem for the pediatric population
"Nutritional rickets is still prevalent in many parts of the developing world and is re-emerging in developed countries. Although vitamin D deficiency plays a central role in the pathogenesis of this disease, calcium deficiency and genetic factors may also cause or contribute to the development of rickets. This review will focus on the classical form of nutritional rickets, in other words, vitamin D-deficiency rickets"
From the PLoS ONE article (Snellman et al.): "Vitamin D deficiency is common, especially among people in defined risk groups, such as the elderly living in nursing homes, obese persons, those normally veiled and dark-skinned people".
"In conclusion, our results indicate that approximately half of the variation in serum vitamin D status during the summer season is explained by genetic factors. The winter season variation in serum levels can mainly be explained by shared environmental influences, i.e. solar altitude".
The others don't seem very relevant, right?
OK maybe you're right and the solar altitude in northern Europe makes it more likely that for a multi ethnic population with extremely low UV exposure Middle Eastern or African people would get rickets before a white European person. And if somone has rickets there is no argument about it.
However the report in the post is about 'Vitamin D deficiency' which is a very different thing to rickets.'Vitamin D deficiency' is diagnosed by the level of calcidiol (25-hydroxy-vitamin D) in the blood and nothing else. This standard is under 32 ng/mL or 75nmol/l yet half of tanned outdoors types do not attain that level.
Low Vitamin D Status despite Abundant Sun Exposure (that's their title)
"In a study from south India, levels below 50 nmol/L were found in 44% of the men and 70% of the women. The subjects are described as “agricultural workers starting their day at 0800 and working outdoors until 1700 with their face, chest, back, legs, arms, and forearms exposed to sunlight” (Harinarayan et al., 2007). In a study from Saudi Arabia, levels below 25 nmol/L were found in respectively 35%, 45%, 53%, and 50% of normal male university students of Saudi, Jordanian, Egyptian, and other origins (Sedrani, 1984)."
The criterion for vitamin D sufficiency is really high, so high 50% of British adults don't attain it, not because they are not in the sun but because:-
"our results indicate that approximately half of the variation in serum vitamin D status during the summer season is explained by genetic factors"(Snellman)
In other words the 50% with low levels have them as a result of Europeans' naturally selected genetic make up interacting with the northern European environment: it preserved in half of Europeans a genetic propensity to have a lower D level than current medical opinion says is healthy.
"tropical humans seem to compensate by converting more vitamin D into its active form. Although a single UV-B exposure produces less vitamin D3 in black subjects than in whites, the difference narrows after liver hydroxylation to 25-OHD and disappears after kidney hydroxylation to 1,25-(OH)2D. The active form of vitamin D is thus kept at a constant level, regardless of skin color (Matsuoka et al., 1991, 1995)."
Here
For humans of tropical origin who have naturally very low vitamin D wherever they are even when they live close to the equator, it is dangerous to force their 25-OHD up to the level of 'sufficiency' and beyond. This level is higher than half of whites living at a European latitude attain; for people of tropical origin in can only damage their health.
Surely this is relevant:-
Vitamin D, Adiposity, and Calcified Atherosclerotic Plaque in African-Americans
"... positive associations exist between 25-hydroxyvitamin D and aorta and carotid artery CP in African-Americans. The effects of supplementing vitamin D to raise the serum 25-hydroxyvitamin D level on atherosclerosis in African-Americans are unknown"
and this:-
Plasma 25-hydroxyvitamin D and prostate cancer risk: The Multiethnic Cohort.
. "When clinically defined cutpoints were used, there was no increased risk for the lowest 25(OH)D concentration (OR for <20 versus 30-<50ng/ml=1.10, 95% CI=0.68-1.78), while there was a suggestive increased risk for higher concentrations (OR for 50ng/ml=1.52, 95% CI=0.92-2.51)".
Well, the debate on which is the optimal vitamin D level and if overdose of vitamin D might be dangerous (most vitamins, incl. vit. D, have overdose levels, which are no doubt dangerous) is different from the more than likely fact that pigmentation is directly related, at least in West Eurasia, to adaptation for increased metabolic production of vit. D in the skin, specially in winter.
It still stands that is most likely that families that have recently migrated to Northern Europe from tropical areas (particularly) and are not used to the climatic influence on vitamin D metabolism and all the implications this has for health, specially among children, are likely to cause unwillingly harm to their children by not providing them with the nutritional supplements needed and/or encouraging increased outdoors activities all year long. After all, we are so well adapted to our respective climatic strips that we would not think about that unless health care experts address the matter.
Similarly I imagine that this ignorance on how vitamin D is metabolized was important in the process of colonization of Eurasia, causing diverse health problems that put much pressure on pigmentation and whatever other genetic factors related to vitamin D metabolism. And that's surely the reason that we have so many shades of color. This pressure might have been less intense on peoples who ate lots of fish, which is about the only nutritional input that can partly replace skin metabolism of vitamin D.
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