In a study from Hawaii, vitamin D status was assessed in 93 healthy young adults who were visibly tanned and averaged 22.4 hours per week of unprotected sun exposure, with 40% reporting no use of sunscreen. Yet their mean vitamin D level was 79 nmol/L and 51% had levels below the recommended minimum of 75 nmol/L (Binkley et al., 2007).
These results are consistent with those of a study from Nebraska. The subjects were thirty healthy men who had just completed a summer of outdoor activity, e.g., landscaping, construction, farming, and recreation. One subject used sunscreen regularly and sixteen others sometimes or rarely. Their mean vitamin D level was initially 122 nmol/L. By late winter, it had fallen to 74 nmol/L (Barger-Lux & Heaney, 2002).
A study from south India found levels below 50 nmol/L 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).
These studies lead to two conclusions. First, sun exposure seems to produce vitamin D according to a law of diminishing returns: the more we expose ourselves to the sun, the less the vitamin D in our bloodstream increases. Perhaps frequent sun exposure results in less being produced in the skin and more being broken down in the liver. This might explain why intense sun exposure leads to a lower vitamin D level in Hawaiian subjects than in Nebraskans. In the latter group, vitamin D production may be ‘calibrated’ to provide a reserve for the winter months.
Second, to stay above the recommended minimum of 75-150 nmol/L, we must take supplements in the form of vitamin pills or fortified foods. Sun exposure is not enough. Yet even dietary supplementation seems to be countered by some unknown mechanism within the body:
… what effect does a 400 IU/d dose of vitamin D for an extended time (months) have in adults? The answer is little or nothing. At this dose in an adult, the circulating 25(OH)D concentration usually remains unchanged or declines. This was first shown in both adolescent girls and young women. … mothers who were vitamin D deficient at the beginning of their pregnancies were still deficient at term after receiving supplements of 800-1600 IU vitamin D/d throughout their pregnancies. (Hollis, 2005)
The assembled data from many vitamin D supplementation studies reveal a curve for vitamin D dose versus serum 25-hydroxyvitamin D [25(OH)D] response that is surprisingly flat up to 250 μg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D concentrations exceed 100 nmol/L, a total vitamin D supply of 100 μg (4000 IU)/d is required. (Vieth, 1999)
Only mega-doses can overcome what seems to be a homeostatic mechanism that keeps bloodstream vitamin D within a certain range. Indeed, this range falls below the one that is now recommended. Curious isn't it? Why would natural selection design us the wrong way?
Perhaps ancestral humans got additional vitamin D from some other source, such as the food they ate. In the diets of hunter/gatherers and early agriculturalists, fatty fish are clearly the best source, as seen when we rank the vitamin D content (IU per gram) of different foods (Loomis, 1967):
Halibut liver oil : 2,000-4,000
Cod liver oil : 60-300
Milk : 0.1
Butter : 0.0-4.0
Cream : 0.5
Egg yolk : 1.5-5.0
Calf liver : 0.0
Olive oil : 0.0
Yet fatty fish were unavailable to many ancestral humans, if not most. And again, when vitamin D enters the blood from our diet, it seems to be limited by the same homeostatic mechanism that limits entry of vitamin D from sun-exposed skin.
It looks like natural selection has aimed for an optimal vitamin D level substantially lower than the recommended minimum of 75-150 nmol/L. This in turn implies some kind of disadvantage above the optimal level. Indeed, Adams and Lee (1997) found evidence of vitamin D toxicity at levels as low as 140 nmol/L. But this evidence is ridiculed by Vieth (1999):
The report of Adams and Lee, together with its accompanying editorial, suggest that serum 25(OH)D concentrations as low as 140 nmol/L are harmful. This is alarmist. Are we to start avoiding the sun for fear of raising urine calcium or increasing bone resorption?
These side effects may or may not be serious. But there are others. High vitamin D intake is associated with brain lesions in elderly subjects, possibly as a result of vascular calcification (Payne et al., 2007). Genetically modified mice with high vitamin D levels show signs of premature aging: retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism, and short lifespan (Tuohimaa, 2009). Vitamin D supplementation during infancy is associated with asthma and allergic conditions in adulthood (Hyppönen et al., 2004)
In this, vitamin-D proponents are guilty of some hypocrisy. They denounced the previous recommended level, saying it was just enough to prevent rickets while ignoring the possibility that less visible harm disappears only at higher intakes. Yet the current recommended level ignores the possibility that less visible harm appears below the level of vitamin D poisoning.
This being said, the pro-vitamin-D crowd may still be partly right. The optimal level might now exceed the one the human body naturally tends to maintain. With the shift to industrial processing of cereals, we today consume more phytic acid, which makes calcium unusable and thus increases the body’s need for vitamin D. We have, so to speak, entered a new adaptive landscape and our bodies have not had time to adapt.
Or they may be completely wrong. Frankly, I’m not reassured by the pro-vitamin-D literature. It strikes me as being rife with loosely interpreted facts, like the correlation between cancer rates and distance from the equator (and hence insufficient vitamin D). Cancer rates also correlate with the presence of manufacturing, which is concentrated at temperate latitudes for a number of historical and cultural reasons, notably the absence of slavery and plantation economies.
Then there’s this gem:
The concentrations of 25(OH)D observed today are arbitrary and based on contemporary cultural norms (clothing, sun avoidance, food choices, and legislation) and the range of vitamin D intakes being compared may not encompass what is natural or optimal for humans as a species (Vieth, 1999)
Actually, cultural norms are much more heliophilic today than during most of our past. In a wide range of traditional societies, people avoided the sun as much as possible, especially during the hours of peak UV (Frost, 2005, pp. 60-62). Midday was a time for staying in the shade, having the main meal, and taking a nap. Nor is there reason to believe that sun avoidance and clothing were absent among early modern humans. Upper Paleolithic sites have yielded plenty of eyed needles, awls, and other tools for making tight-fitting, tailored clothes (Hoffecker, 2002).
Heliophilia is the historical outlier, not heliophobia. It was the sunshine movement of the 1920s that first persuaded people to cast off hats, cut down shade trees, and lie on beaches for hours on end. This cultural revolution was still recent when Noël Coward wrote his 1931 piece ‘Mad Dogs and Englishmen’:
In tropical climes there are certain times of day
When all the citizens retire to tear their clothes off and perspire.
It's one of the rules that the greatest fools obey,
Because the sun is much too sultry And one must avoid its ultry-violet ray.
The natives grieve when the white men leave their huts,
Because they're obviously, definitely nuts!
Mad dogs and Englishmen go out in the midday sun,
The Japanese don’t care to, the Chinese wouldn’t dare to,
Hindus and Argentines sleep firmly from twelve to one
But Englishmen detest a siesta.
In the Philippines there are lovely screens to protect you from the glare.
In the Malay States there are hats like plates which the Britishers won't wear.
At twelve noon the natives swoon and no further work is done,
But mad dogs and Englishmen go out in the midday sun.
References
Adams, J.S., & Lee, G. (1997). Gains in bone mineral density with resolution of vitamin D intoxication. Annals of Internal Medicine, 127, 203-206.
Barger-Lux, J., & Heaney, R.P. (2002). Effects of above average summer sun exposure on serum 25-hydroxyvitamin D and calcium absorption, The Journal of Clinical Endocrinology & Metabolism, 87, 4952-4956.
Binkley N, Novotny R, Krueger D, et al. (2007). Low vitamin D status despite abundant sun exposure. Journal of Clinical Endocrinology & Metabolism, 92, 2130 –2135.
Frost, P. (2005). Fair Women, Dark Men. The Forgotten Roots of Color Prejudice. Cybereditions: Christchurch (New Zealand).
Harinarayan, C.V., Ramalakshmi, T., Prasad, U.V., Sudhakar, D., Srinivasarao, P.V.L.N., Sarma, K.V.S., & Kumar, E.G.T. (2007). High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians, American Journal of Clinical Nutrition, 85, 1062-1067.
Hoffecker, J.F. (2002). Desolate Landscapes. Ice-Age Settlement in Eastern Europe. New Brunswick: Rutgers University Press.
Hollis, B.W. (2005). Circulating 25-Hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake, Journal of Nutrition, 135, 317-322.
Hyppönen, E., Sovio, U., Wjst, M., Patel, S., Pekkanen, J., Hartikainen, A-L., & Järvelin, M-R. (2004). Infant Vitamin D Supplementation and Allergic Conditions in Adulthood. Northern Finland Birth Cohort 1966, Annals of the New York Academy of Sciences, 1037, 84–95.
Loomis, W.F. (1967). Skin-pigment regulation of vitamin-D biosynthesis in man, Science, 157, 501-506.
Payne, M.E., Anderson, J.J.B., & Steffens, D.C. (2008). Calcium and vitamin D intakes may be positively associated with brain lesions in depressed and non-depressed elders, Nutrition Research, 28, 285-292.
Tuohimaa, P. (2009). Vitamin D and aging, Journal of Steroid Biochemistry and Molecular Biology, 114(1-2), 78-84.
Vieth, R. (1999). Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety, American Journal of Clinical Nutrition, 69, 842-856.