Inuit and vitamin D

Inuit mothers (Wikicommons - Ansgar Walk) - Inuit have low levels of vitamin D. Does this mean they're not getting enough? Or have their bodies adapted to an environment where it cannot easily be made in the skin or obtained from the diet?

Inuit people have "insufficient" vitamin D, even among those who eat a traditional diet and live a traditional lifestyle. There are consequently moves afoot to remedy this insufficiency by providing vitamin D supplements. In my opinion, this is a response to a largely nonexistent problem and will probably have adverse consequences.

My arguments are explained in an article I have just published in Inuit Studies. Here is the abstract:

Inuit have vitamin D blood levels that generally fall within the range of insufficiency, even when they live on a traditional diet of fish and game meat. Without this vitamin, bones soften and become deformed, a condition called rickets in children and osteomalacia in adults. Until recent times, however, this condition was much rarer among Inuit than among non-Inuit, even when the latter included people living near Inuit communities under similar conditions of climate and housing. This rarity was attributed to extended breastfeeding and a high-meat/low-cereal diet. The situation subsequently reversed, with Inuit becoming more at risk of developing rickets, first in Labrador during the 1920s and later elsewhere. To reduce this excess risk, researchers have recommended vitamin D supplementation, arguing that breast milk has too little vitamin D and that even a traditional diet cannot provide the recommended daily intake. We should ask, however, whether the problem is definitional. Inuit may have lower levels of vitamin D because they need less, having adapted culturally and physiologically to an environment where this vitamin is less easily synthesized in the skin. These adaptations include a diet that enhances calcium bioavailability (by means of ß-casein in breast milk, certain unknown substances in meat, and absence of phytic acid), as well as genetic changes that enable vitamin D to be used more efficiently. Although Inuit are today more at risk of developing rickets than are non-Inuit, this excess risk is nonetheless small and seems to have a dietary cause-namely, early weaning and abandonment of a high-meat/low-cereal diet.

Please feel free to offer comments or criticisms.

Reference

Frost, P. (2018). To supplement or not to supplement: are Inuit getting enough vitamin D? Études Inuit Studies 40(2): 271-291.

https://www.researchgate.net/publication/329450593_To_Supplement_or_Not_to_Supplement_Are_Inuit_Getting_Enough_Vitamin_D

Who gets to write history?

History is written by the survivors – Max Lerner

I prefer Lerner’s version to Churchill’s History is written by the victors. Opinions will survive as long as the group that holds them, and such a group may disappear for reasons besides defeat through conflict. Often, the group is temporary by nature.

Remember this when reading about how the sunshine movement eradicated rickets and tuberculosis—the two long-running epidemics of the Western world. This is a history written by those who kept making their case long after others had lost interest. To quote a Sailerism: History is written by those who write … and write … and write.

Here is how the sunshine movement is usually presented:

In the nineteenth century, different physicians advocated ‘heliotherapy’ as a means to treat rickets and kill the microbes that cause tuberculosis. They were ignored, except by a few nudists and health faddists. Then, two events broke the barrier to public acceptance. One was the Spanish flu of 1918-1919, which showed the need for strong measures to keep microbes from spreading. The other, in 1919, was the discovery that ultraviolet light can cure rickets by releasing a chemical into the bloodstream, later identified as vitamin D. Heliotherapy thus gained in popularity and by the late 1920s sunbathing had become widespread. Meanwhile, tuberculosis and rickets steadily declined until both virtually disappeared.

This narrative leaves out a key detail. The sunshine movement had little effect on the prevalence of either tuberculosis or rickets. Through the 1920s and 1930s, there was only a gradual decline in the incidence of tuberculosis, as part of a downward trend that began in the nineteenth century and that probably was due to stricter segregation of tubercular patients in hospitals and sanatoria. Steep decline began later—after the Second World War (Wilson, 1990). Much of the credit goes to the discovery of antimicrobial drugs like isoniazid, rifampicin, and streptomycin. Just as important was the overall rise in the standard of living, particularly among urban workers. As the population became better nourished and as overcrowded tenements gave way to suburban homes, microbes could not spread so easily to weakened hosts.

Nor was rickets much affected. In Dundee, Scotland, its incidence among children held steady from 1925 to 1935 and then dropped abruptly, apparently after the introduction of a ‘milk in schools’ scheme in 1934 and then greater provision of free meals to needy children. This drop preceded vitamin D fortification of milk and infant cereals (Stewart et al., 1964). In the United States, rickets was deemed as late as 1940 to be “still probably the most common disease of early childhood” (Harrison, 1966). In Sweden, it still afflicted most fetuses and newborns during the early 1950s (Sydow et al., 1956).

By this time, many medical researchers had concluded that the cause could not be lack of sun. A Swedish autopsy study found that rickets in fetuses and newborns showed no significant correlation with the mother’s vitamin D status during pregnancy, as indicated by her consumption of vitamin D supplements or by her degree of sun exposure, i.e., daily walks in the sun, outdoor work, summer holiday in the country, and latitude within Sweden (Sydow et al., 1956). For several research teams, the cause seemed to be substances in commercial bread, like phytic acid, that immobilize calcium and phosphorus within the body (Bruce & Callow, 1934; Harrison & Mellanby, 1939; McCance et al., 1942; McCance & Widdowson, 1942). But fewer and fewer researchers were now interested. Like tuberculosis, rickets too went into a steep decline after the war, eventually becoming a medical oddity by the 1960s (Harrison, 1966).

Meanwhile, interest had been growing in the sunshine movement. It now extended far beyond the medical community, being influential in the fashion industry, the arts and literature, architecture, and the movie industry. It had become a cultural phenomenon, and one that would create much of the look and feel of modern life.

Fashion industry

Gabrielle (Coco) Chanel is usually credited with making suntans popular among women. Certainly, in the late 1920s she was the one who added tanned skin to a new androgynous look, la garçonne, that featured long legs, a flat chest, narrow hips, and large shoulders, like a young boy on the brink of puberty (Andrieu, 2008, p. 73; Bard, 1998; Galante, 1972; Wilson, 1985).

But Coco Chanel simply boarded a bus that was already on the road. As early as 1926, a Connecticut radio station announced: “a coat of tan seems to be the latest style in natural coloring at this season of the year. [It has] been increasing in favor during the last few years” (Nickerson, 1926). Female tanning became fashionable through women acting on their own initiative. Others then saw the market opportunities:

Cosmetics manufacturers took notice of the new acceptability of nonwhite skin and began to produce darker powders, as well as artificial bronzing lotions. By 1929, Jean Patou and Coco Chanel had introduced suntan products, and Helena Rubenstein was selling “Valaze Gypsy Tan Foundation.” Other cosmetics manufacturers were blending powders to be “creamy,” rather than white, and producing “ochre,” “dark rachel,” and “suntan” shades. (Berry, 2000, p. 188)

During this time, skin whiteners became less popular.

Golden Peacock Bleach Cream and other facial bleaches, which were advertised regularly in women’s magazines until the late 1920s, appeared only rarely after the early 1930s, although skin lighteners were still marketed to the African American community. (Berry, 2000, p. 188)

The same trend swept through women’s magazines. By the end of the 1920s, Vogue was telling its readers that “The 1929 girl must be tanned” and “A golden tan is the index of chic” (Vogue, 1929). In the early 1930s, however, these magazines were periodically predicting the end of the suntan fad (Berry, 2000, p. 188). Just as fashion leaders had failed to anticipate this fad, they also misjudged its staying power.

Arts and literature

In the mid-1920s, the sunshine movement spread to artists and literati through multiple points of entry. A key one was the French Riviera (Ash, 1974; Weigtman, 1970).

Among the fashionable, “heliophobia” soon gave way to “heliophilia.” The scene of this minor revolution was the French Riviera—specifically the beach of La Garoupe at Cap d’Antibes—and its chief ideologist was Gerald Murphy [an ex-pat American artist].

… It was the Americans—Cole Porter and the Murphys—who first “discovered” the Riviera as a summer resort. The Murphys began to clear La Garoupe of its layer of seaweed and persuaded the proprietor of the Hotel du Cap to remain open during the summer months … The cultivators of the simple, the connoisseurs of the primitive, formed a new elite comprised of Americans, artists and the more unconventional members of the aristocracy. Among others, the Hemingways, the Fitzgeralds, the Picassos, the Legers and the Count and Countess Etienne de Beaumont, all joined the Murphys at Cap d’Antibes in the summer. It was this elite, with some assistance from Coco Chanel, that raised the suntan to the level of higher fashion. (Ash, 1974)

Andrieu (2008, p. 73) and Weigtman (1970) describe how French writers of the 1920s placed favorable references to tanned skin in their works, associating it with lead characters and positive qualities. Similar placement appears in F. Scott Fitzgerald’s The Great Gatsby (1925). Miss Jordan Baker has "sun-strained eyes," a "slender golden arm," a "brown hand," a "golden shoulder," and a "face the same brown tint as the fingerless glove on her knee” (Fitzgerald, 1992, pp. 15, 47, 57, 84, 185).

Architecture

The sunshine movement brought a new urban landscape by moving buildings further back from the street, limiting their height, and spacing them further apart. Windows also became bigger and more numerous. Meanwhile, modernist architects looked to tuberculosis sanatoria and ocean liners to make their creations more open to the sun and air. They introduced such features as the flat roof, the balcony, and the roof or garden terrace “on which elegant Jazz age young women, dressed in patio-pyjamas, could sunbathe on chaises longues” (Campbell, 2005).

These signatures of modernism marked the design of public housing and, especially, schools, whose population was thought to be most at risk for tuberculosis and rickets:

By the late 1920s, the therapeutic qualities of sunlight were widely recognised, and its use was extended in sunshine schools and open-air clinics to the more general treatment of sickly, TB-prone and crippled children, many of them drawn from the slums. Progressive schools like Bedales early encouraged sunbathing; St Christopher School, Letchworth, installed vita glass; and pictures of Pinehurst School show the children running about naked. (Twigg, 1981)

In general, traditional architecture was seen not simply as old-fashioned but as unhealthy. This gave a revolutionary urgency to the thinking of modernists, like the Swiss architect Le Corbusier:

But when it comes to a question of demolishing rotten old houses full of tuberculosis and demoralizing, you hear them cry, “What about the iron-work, what about the beautiful old wrought-iron work.” (Campbell, 2005)

Such demolition was considered necessary to build a healthier society. “Sunlight stood for the new society of light”:

Houses in the garden cities were oriented towards the sun. Architecture in the interwar years pursued light to an almost obsessive degree. It came to be the emblem of a cluster of reforms in the 1920s aimed at making Britain a better, healthier, cleaner place to live.

… Just as the antiseptic qualities of sunlight had been observed through its action on mouldy, damp objects, so the sunlight for this post-Victorian generation could be made to shine on the dank, rotten and hidden aspects of the Victorian world. (The thirties saw the full flood of anti-Victorianism) This could mean the slum houses and sick children, but it also, very frequently, meant sexuality. (Twigg, 1981)

Movie industry

The tanned look entered the movie industry via individual actors and actresses, notably Joan Crawford:

Joan Crawford was credited for spreading the trend among Hollywood flappers—in addition to tanning her face, Crawford browned her body and went stockingless …
(Berry, 2000, p. 188)

She was reportedly told by MGM to stop tanning because it made her look “like a lineal descendent of Sheba.” The movie industry, however, soon realized there was a market for dark skin as an item of sexual interest. The 1930s thus saw a spate of Hollywood films featuring Latin lovers, Arab sheikhs, and South Seas beauties (Berry, 2000, pp. 110-111).

No one fully understood this phenomenon. Described as a quest for the exotic, one might doubt the exoticism of stars and starlets who were just a darker version of the European phenotype. Nonetheless, through productions like South Pacific (1949), this faux interracialism would help pave the way for the real thing after the war.

Perhaps white Americans were motivated to sexualize dark skin by a ‘rare color effect’ such as exists with differing shades of hair color. The rarer brunettes are, the more they excite sexual interest in men (Anon, 2008; Thelen, 1983). Or perhaps the motivation lay at another level of male sexual response. If women evolved a lighter complexion and other paedomorphic features as a way to inhibit male aggression and stimulate feelings of care, a darker skin tone could exert sex appeal on a more aggressive and less empathetic level (Frost, 2007; Guthrie, 1970).

Social conformity and status competition

Cultural change involves not only leaders but also followers. As more and more people sported tans, the new look tended to spread simply through social conformity and status competition:

The appearance of medical articles that begin to deal with tanning as not directly related to a “cure” shows that the acquisition of the suntan, at least among certain sections of society, was already desirable. In addition the change toward a more positive view of the suntan was to articulate well with other social changes taking place, particularly as related to travel, in the early twentieth century. The idea of health travel was established, with many invalids seeking the sun cure in sanatoria. However, the wealthy invalid was able to travel further — to locations where they could be assured of receiving sunlight, such as the Swiss Alps or the Mediterranean. (Carter & Michael, 2003, p. 269)

The cosmetic aspects of a suntan were not originally much to the fore; during the 1920s tanning was regarded as only a side effect and not spoken of with special favour. By the 1930s, however, the naturist magazines were praising the look of bronzed skin. The fashion spread beyond these circles, to the cosmopolitan and wealthy. By the 1930s the Riviera season had reversed from being winter to summer. The seaside, from being a place for bathing and for sea air became somewhere for taking off your clothes and lying in the sun; the resorts began to publish their sunshine figures; and by the mid 1930s the major cosmetic houses were producing suntan creams. A suntan became associated with youth, health and vigour, qualities that the thirties found particularly attractive sexually. (Twigg, 1981)

During the 1930s, the popularity of suntanning and nudity reached a peak, intellectual and social benefits were said to accrue from sun-exposure, and it was felt to be “imperative” for the successful executive to be tanned, as this indicated “superior physique, intelligence, and moral character.” (Koblenzer, 1998)

Conclusion

The sunshine movement was able to impose its world view—and its version of history—by winning over the creators of modern culture: artists, writers, actors, architects, and fashion designers. This victory, if we can use the term, was achieved not in the narrow realm of medical debate but in the larger one of cultural production. In truth, there was no victory because there was no battle. The ‘other side’ lost interest in explaining the tuberculosis and rickets epidemics once these had subsided. They moved on to other things.

The ‘victors’ had an unforeseen ally: a sensual, if not sexual, fascination with dark skin. By arming young men and women with a medical alibi, the sunshine movement unwittingly opened up a dimension of sexual attraction that had lain unexploited. There had, in fact, been a taboo against sexualizing dark skin, partly because of the racial connotations and partly because dark complexions among white Americans had traditionally been viewed as unfeminine for women and as hypermasculine for men.

Another ally, widespread in the twentieth century, was a belief in change and in the urgency of change. It is probably no coincidence that many sunshine advocates, like the architect Le Corbusier, saw themselves as radicals. The movement likewise had more success in pushing its agenda in the Eastern bloc, as seen in the mass relocation of working families to modernist housing projects, in State-sponsored vacations at Black Sea resorts, and in the DDR’s mass administration of vitamin D megadoses to children.

References

Andrieu, B. (2008). Bronzage. Une petite histoire du Soleil et de la peau, CNRS Éditions.

Anon. (2008). Maxim's audience prefers brunettes; distribution is bimodal. Gene Expression, July 6, 2008.

Ash, J. (1974). The meaning of suntan, New Society, August, pp. 278-280.

Bard, C. (1998). Les garçonnes. Modes et fantasmes des Années folles. Paris: Flammarion.

Berry, S. (2000). Screen Style. Fashion and Femininity in 1930s Hollywood, Minneapolis: University of Minnesota Press.

Bruce, H. & Callow, R. (1934). Cereals and rickets. The role of inositolhexaphosphoric acid, Biochemical Journal, 28, 517-528.

Campbell, M. (2005). What tuberculosis did for modernism: The influence of a curative environment on modernist design and architecture, Medical History, 49, 463-488.

Carter, S. & Michael, M. (2003). “Here comes the sun: Shedding light on the cultural body”, in: H. Thomas & J. Ahmed (ed.) Cultural Bodies: Ethnography and Theory, pp. 260-282, Wiley-Blackwell.

Fitzgerald, F.S. 1992. The Great Gatsby. New York: Collier Books.

Frost, P. (2007). Comment on Human skin-color sexual dimorphism: A test of the sexual selection hypothesis, American Journal of Physical Anthropology, 133, 779-781.

Galante, P. (1972). Les années Chanel. Paris: Mercure de France.

Guthrie, R.D. (1970). Evolution of human threat display organs, Evolutionary Biology, 4, 257-302.

Harrison, D.C., & Mellanby, E. (1939). Phytic acid and the rickets-producing action of cereals, Biochemical Journal, 33, 1660-1680.

Harrison, H.E. (1966). The disappearance of rickets, American Journal of Public Health, 56, 734-737.

Koblenzer, C.C. (1998). The psychology of sun-exposure and tanning, Clinics in Dermatology, 16, 421-428.

McCance, R., & Widdowson, E. (1942). Mineral metabolism of dephytinized bread, Journal of Physiology, 101, 304-313.

McCance, R., & Widdowson, E. (1942). Mineral metabolism of healthy adults on white and brown bread dietaries, Journal of Physiology, 101, 44-85.

Nickerson, E.C. (1926). Nature's Cosmetics, Bulletin sanitaire 26(5), 134-140.

Stewart, W.K., Mitchell, R.G., Morgan, H.G., Lowe, K.G., & Thomson, J. (1964). The changing incidence of rickets and infantile hypercalcaemia as seen in Dundee, The Lancet, 283(7335), 679-730.

Sydow, G.V., Ranström, S., Berezin, D., & Axen, O. (1956). Histological findings characteristic of rickets in foetuses and young infants, Acta Paediatrica, 45, 114-138.

Thelen, T.H. (1983). Minority type human mate preference. Social Biology, 30, 162-180.

Twigg, J. (1981). “Sunlight & nature” in: The Vegetarian Movement in England, 1847-1981: A study in the structure of its ideology, Doctoral thesis presented to the London School of Economics, University of London. http://www.ivu.org/history/thesis/sunlight.html

Vogue (1929). June 22, pp. 99, 100.

Weightman, J. (1970). The solar revolution. Reflections on a theme in French literature, Encounter, December, pp. 9-18.

Wilson, E. (1985). Adorned in Dreams: Fashion and Modernity, London: Virago.

Wilson, L.G. (1990). The historical decline of tuberculosis in Europe and America: Its causes and significance, Journal of the History of Medicine and Allied Sciences, 45, 366-396.

What caused the rickets epidemic?

The English, like other Western nations, were once plagued by rickets—a softening of the bones leading to fractures and deformity, particularly in children. Initially rare, it became much more frequent after 1600 and had reached epidemic levels by the turn of the 20th century (Gibbs, 1994; Harrison, 1966; Holick, 2006; Rajakumar, 2003). A survey at the Great Ormond Street Hospital found symptoms of rickets in one out of three children under 2 years of age and another one at Clydeside, in 1884, found symptoms in every child examined (Gibbs, 1994). Elsewhere during the late 19th century, in Boston and Leiden (Netherlands), autopsy studies showed rickets in 80-90% of all children (Holick, 2006).

The currently accepted explanation was developed in the late 1880s by Dr. Theobald Palm. For Palm, rickets seemed to correlate with lack of sun. The illness was more common in northwestern Europe, particularly England, where sunlight was naturally weaker. It was also more common in urban areas where “a perennial pall of smoke, and ... high houses cut off from narrow streets a large proportion of the rays which struggle through the gloom” (Hardy, 2003). His hypothesis was strengthened in 1919 by the finding that ultraviolet light can cure rickets by releasing a chemical, eventually identified as vitamin D, that provides us with calcium and phosphorus from food passing through the gut (Gibbs, 1994). Such health benefits, together with the anti-microbial action of UV light, led to the ‘sunshine movement’ of the 1920s—a vast effort to boost sun exposure by redesigning our clothes, our streets, parks, and buildings, and even our notions of fun and recreation. This movement gave us much of the look and feel of modern life.

By the mid-20th century, rickets was again rare, thus vindicating not only UV therapy but also the view that lack of sun had been the cause (Harrison, 1966). This view nonetheless remains unproven. Although vitamin D does help the body absorb more calcium and phosphorus, no one knows for sure whether the epidemic was due to low levels of this vitamin. That kind of blood test did not exist yet. People may have developed rickets because something was immobilizing calcium or phosphorus in their bodies. They would have then required more vitamin D. This possibility is hinted at by Harrison (1966):

… a number of cases are on record of children with marked rickets who have received an amount of vitamin D ordinarily sufficient to prevent rickets and who do not have manifestations of intestinal malabsorption. When these children are given increased amounts of vitamin D, several thousand units per day, the biochemical manifestations of vitamin D effect result, and roentgenograms show healing of the rickets. The basis for this increased requirement is not known.

At the height of the epidemic, one physician did suggest that something was immobilizing phosphorus in people with rickets. Dr. John Snow (1857) 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. He reasoned that this alum combined with phosphorus in the body to form insoluble aluminum phosphate, thus depleting the reserves of phosphorus needed for strong bones.

Snow pointed out that London bakeries would add about one and a half ounces of alum per four pounds of loaf. Since manual laborers met 70% of their energy requirements by eating bread, they would have been ingesting 20 g of alum daily or 4 g of aluminum hydroxide (Dunnigan, 2003). A recent case study describes an infant who developed rickets after consuming 2 g of aluminum hydroxide (via antacids) per day over five to six weeks (Pattaragarn & Alon, 2001). There have been many other reports of antacid-induced rickets (Boutsen et al., 1996; Cooke et al., 1978; Pivnick et al., 1995; Shetty et al., 1998; Spencer & Kramer, 1983).

Snow’s hypothesis was forgotten and has been dusted off only in recent years (Dunnigan, 2003; Hardy, 2003; Paneth, 2003). This renewed interest is partly due to the realization that rickets can be caused not only by lack of vitamin D but also by ingested substances that make phosphorus or calcium unusable. Alum is one, as seen in reports of rickets induced by antacids. Another is phytic acid in cereal grains (Sandberg, 1991). The acid binds to calcium and makes it unavailable to the body, as shown when dogs develop rickets on an oatmeal diet (Harrison & Mellanby, 1939). It is this calcium depletion, via food like unleavened bread or chapatti, that now causes rickets in the Middle East and South Asia (Berlyne et al., 1973; Harinarayan, Ramalakshmi, Prasad, Sudhakar, Srinivasarao, Sarma, & Kumar, 2007).

We may never disprove the view that lack of sun caused the rickets epidemic of a century ago. But we can point to some inconsistencies. First, rickets was much less frequent in northern England and absent in northwest Scotland—the area of Great Britain with the weakest solar UV (Gibbs, 1994). Second, it was not really a disease of cities with dark narrow streets and smoke-filled skies, as Snow (1857) himself observed.

The usual causes to which rickets are attributed are of a somewhat general nature, such as vitiated air, want of exercise and nourishing food, and a scrofulous taint. These explanations, however, did not satisfy me, as I had previously seen a good deal of practice in some of the towns in the north of England, where the over-crowding and the other evils above mentioned were as great as in London, whilst the distortion of the legs in young children was hardly present; moreover, I noticed that the most healthy-looking and best-nourished children often suffered most from curvature of the bones of the legs, owing to their greater weight; and I afterwards found that this complaint was quite common in the villages around London as well as in the metropolis itself.

Lack of sun also fails to explain why the epidemic initially broke out within a small geographic area. Indeed, the 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:

The disease became first known as near as we could gather from the relation of others, after sedulous inquiry, about thirty years since, in the counties of Dorset and Somerset … since which time the observation of it hath been derived unto all the southern and western parts of the Kingdom. (Gibbs, 1994)

Gibbs (1994) attributes this rapid growth to that of England’s home-based textile industry, which by 1600 had become the main export. “Whole families worked from before dawn until after dusk in their homes and, whether the children were too young to work or old enough to assist in home production, they would have lived their lives predominantly indoors.” This explanation is hard to accept because textile cottage industries developed primarily in the midlands and around London. The southwest trailed the rest of England in this regard. In addition, family workshops were normally off-limits to children below the age of apprenticeship. Such children would have been left with elderly relatives or told to play outside.

But there may have been an indirect link with the growth of England’s textile industry, namely the parallel growth in the use of alum to fix the colors of cloth. Until the ban on alum imports in 1667, when newly exploited Yorkshire shales became the main source, England imported this substance from the Italian Papal States (Balston, 1998; Jenkins, 1971). The port of entry would have been Bristol—in Somerset county, southwest England. This may have been where English bakers first learned to whiten bread with alum.

When did bakers stop using alum? The practice seems to have died out after the turn of the century with tougher enforcement of food adulteration statutes in the United Kingdom and elsewhere (Kassim, 2001). By the mid-20th century, “the use of alum in bread was only occasionally encountered” (Hart, 1952). Eliminating this additive from bread probably did much to eliminate rickets. Probably just as important was the decreasing importance of bread in working class diets, as a result of increasing affluence.

But this is not what the history books say. As Steve Sailer tells us, history is written by those who like to write, and much more has been written about the sunshine movement and its presumed benefits for humanity.

References

Balston, J. (1998). “In defence of alum – 2. England”, In: The Whatmans and Wove Paper: Its invention and development in the West, West Farleigh.

Berlyne, G.M., Ari, J.B., Nord, E., & Shainkin, R. (1973). Bedouin osteomalacia due to calcium deprivation caused by high phytic acid content of unleavened bread, The American Journal of Clinical Nutrition, 26, 910-911.

Boutsen, Y. Devogelaer, J.P., Malghem, J., Noël, H., & Nagant de Deuxchaisnes, C. (1996). Antacid-induced osteomalacia, Clinical Rheumatology, 15, 75-80.

Cooke, N., Teitelbaum, S., & Aviol, L.V. (1978). Antacid-induced osteomalacia and nephrolithiasis, Archives of Internal Medicine, 138, 1007-1009.

Dunnigan, M. (2003). Commentary: John Snow and alum-induced rickets from adulterated London bread: an overlooked contribution to metabolic bone disease, International Journal of Epidemiology, 32, 340-341.

Gibbs, D. (1994). Rickets and the crippled child: an historical perspective, Journal of the Royal Society of Medicine, 87, 729-732.

Hardy, A. (2003). Commentary: Bread and alum, syphilis and sunlight: rickets in the nineteenth century, International Journal of Epidemiology, 32, 337-340

Harrison, D.C., & Mellanby, E. (1939). Phytic acid and the rickets-producing action of cereals, Biochemical Journal, 33, 1660-1680.

Harrison, H.E. (1966). The disappearance of rickets, American Journal of Public Health, 56, 734-737.

Hart, F.L. (1952). Food adulteration in the early twentieth century, Food Drug Cosmetic Law Journal, 7, 485-509.

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.

Harrison, H.E. (1966). The disappearance of rickets, American Journal of Public Health, 56, 734-737.

Holick, M.F. (2006). Resurrection of vitamin D deficiency and rickets, The Journal of Clinical Investigation, 116, 2062-2072.

Jenkins, R. (1971). “The alum trade in the fifteenth and sixteenth centuries, and the beginnings of the alum industry in England,” in: Links in the history of engineering and technology from Tudor times: the collected papers of Rhys Jenkins, pp. 193-203, Newcomen Society (Great Britain), Published by Ayer Publishing.

Kassim, L. (2001). The co-operative movement and food adulteration in the nineteenth century, Manchester Region History Review, 15, 9-18.

Paneth, N. (2003). Commentary: Snow on rickets, International Journal of Epidemiology, 32, 341-343.

Pattaragarn, A., & Alon, U.S. (2001). Antacid-induced rickets in infancy, Clinical Pediatrics, 40, 389-393.

Pivnick, E.K., Kerr, N.C., Kaufman, R.A., Jones, D.P., & Chesney, R.W. (1995). Rickets secondary to phosphate depletion: a sequela of antacid use in infancy. Clinical Pediatrics, 34, 73-78.

Rajakumar, K. (2003). Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective. Pediatrics, 112, 132-135.

Sandberg, A.S. (1991). The effect of food processing on phytate hydrolysis and availability of iron and zinc. Advances in Experimental Medical Biology, 289, 499-508.

Shetty, A.K., Thomus, T., Rao, J., and Vargus, A. (1998). Rickets and secondary craniosynostosis associated with long-term antacid use in an infant. Archives of Pediatrics & Adolescent Medicine, 152, 1243-1245.

Snow J. (1857). On the adulteration of bread as a cause of rickets. Lancet, ii:4–5. (Reprinted in International Journal of Epidemiology (2003), 32, 336–337.)

Spencer, H., & Kramer, L. (1983). Antacid-induced calcium loss, Archives of Internal Medicine, 143, 657-659.

Vitamin D and skin color. Part II

Is white skin an adaptation to the cereal diet that Europeans have been consuming for the past five to seven thousand years?

When early Europeans switched from hunting and gathering to cereal agriculture, the new diet may have provided less vitamin D (i.e., from fatty fish), which the body needs to metabolize calcium and create strong bones. There would thus have been stronger selection for endogenous production of vitamin D in the skin’s tissues. Since such production requires UV-B light and since melanin blocks UV, this selection may have favored a lighter skin color (Sweet, 2002). In addition, 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 Paleodiet).

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).

The vitamin D hypothesis also implies that European skin turned white almost at the dawn of human history. Cereal agriculture did not reach northern Europe until some 5,000 years ago and, presumably, the whitening of northern European skin would not have been complete until well into the historical period. Is this a realistic assumption, given the depictions of white-skinned Europeans in early Egyptian art?

References

Brazerol, W.F., McPhee, A.J., Mimouni, F., Specker, B.L., & Tsang, R.C. (1988). Serial ultraviolet B exposure and serum 25 hydroxyvitamin D response in young adult American blacks and whites: no racial differences. Journal of the American College of Nutrition, 7, 111-118.

Ellis, G., Woodhead, J.S., & Cooke, W.T. (1977). Serum-25-hydroxyvitamin-D concentrations in adolescent boys. Lancet, 1, 825-828.

Lo, C.W., Paris, P.W., & Holick, M.F. (1986). Indian and Pakistani immigrants have the capacity as Caucasians to produce vitamin D in response to ultraviolet radiation. American Journal of Clinical Nutrition, 44, 683-685.

Pettifor, J.M. (1994). Privational rickets: a modern perspective. Journal of the Royal Society of Medicine, 87, 723-725.

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

Stamp, T.C. (1975). Factors in human vitamin D nutrition and in the production and cure of classical rickets. Proceedings of the Nutrition Society, 34, 119-130.

Sweet, F.W. (2002). The paleo-etiology of human skin tone. Backintyme Essays.

Skin color and vitamin D

Differences in human skin color are commonly explained as an adaptive response to solar UV radiation and latitude. The further away from the equator you are, the weaker will be solar UV and the less your skin will need melanin to prevent sunburn and skin cancer.

A variant of this explanation involves vitamin D, which the body needs to make strong bones and which the skin produces with the help of UV-B. The further away from the equator you are, the lighter your skin will be to let enough UV-B into its tissues for vitamin D production. Or so the explanation goes.

To test this hypothesis, Osborne et al. (2008) measured skin color and bone strength in a hundred white and Asian adolescent girls from Hawaii. Skin color was measured at the forehead and the inner arm. Bone strength was measured by section modulus (Z) and bone mineral content (BMC) at the proximal femur. A multiple regression was then performed to investigate the influences of skin color, physical activity, age, ethnicity, developmental age, calcium intake, and lean body mass on Z and BMC. Result: no significant relationship between skin color and bone strength.

Is there, in fact, any hard evidence that humans vary in skin color because they need to maintain the same level of vitamin D production in the face of varying levels of UV-B? Robins (1991, pp. 204-205) found the data to be unconvincing when he reviewed the literature. In particular, there seems to be little relationship between skin color and blood levels of 25-OHD—one of the main circulating metabolites of vitamin D:

The vulnerability of British Asians to rickets and osteomalacia has been ascribed in part to their darker skin colour, but this idea is not upheld by observations that British residents of West Indian (Afro-Caribbean) origin, who have deeper skin pigmentation than the Asians, very rarely manifest clinical rickets … Moreover, artificial irradiation of Asian, Caucasoid and Negroid subjects with UV-B produced similar increases in blood 25-OHD levels irrespective of skin pigmentation … 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.

The higher incidence of rickets in British Asians probably has less to do with their dark color than with their systematic avoidance of sunlight (to remain as light-skinned as possible).

Skin color and natural selection via solar UV

Solar UV seems to be a weak agent of natural selection, be it through sunburn, skin cancer, or vitamin D deficiency. Brace et al. (1999) studied skin color variation in Amerindians, who have inhabited their continents for 12,000-15,000 years, and in Australian Aborigines, who have inhabited theirs for some 50,000 years. Assuming that latitudinal skin-color variation in both groups tracks natural selection by solar UV, their calculations show that this selection would have taken over 100,000 years to create the skin-color difference between black Africans and northern Chinese and ~ 200,000 years to create the one between black Africans and northern Europeans (Brace et al., 1999). Yet modern humans began to spread out of Africa only about 50,000 years ago. Clearly, something other than solar UV has also influenced human variation in skin color ... and one may wonder whether lack of solar UV has played any role, via natural selection, in the extreme whitening of some human populations.

Indeed, people seem to do just fine with a light brown color from the Arctic Circle to the equator. Skeletal remains from pre-contact Amerindian sites show little evidence of rickets or other signs of vitamin D deficiency—even at latitudes where Amerindian skin is much darker than European skin (Robins, 1991, p. 206).

Why, then, are Europeans so fair-skinned when ground-level UV radiation is equally weak across Europe, northern Asia, and North America at all latitudes above 47º N? (Jablonski & Chaplin, 2000). Proponents of the vitamin D hypothesis will point to the Inuit and say that non-Europeans get enough vitamin D at high northerly latitudes from fatty fish. So they don’t need light skin. In actual fact, if we look at the indigenous peoples of northern Asia and North America above 47º N, most of them live far inland and get little vitamin D from their diet. For instance, although the Athapaskans of Canada and Alaska live as far north as the Inuit and are even somewhat darker-skinned, their diet consists largely of meat from land animals (caribou, deer, ptarmigan, etc.). The same may be said for the native peoples of Siberia.

Conversely, fish consumption is high among the coastal peoples of northwestern Europe. Skeletal remains of Danes living 6,000-7,000 years ago have the same carbon isotope profile as those of Greenland Inuit, whose diet is 70-95% of marine origin (Tauber, 1981). So why are Danes so light-skinned despite a diet that has long included fatty fish?

Skin color and sexual selection via male choice

Latitudinal variation in human skin color is largely an artefact of very dark skin in sub-Saharan agricultural peoples and very light skin in northern and eastern Europeans. Elsewhere, the correlation with latitude is much weaker. Indeed, human skin color seems to be more highly correlated with the incidence of polygyny than with latitude (Manning et al., 2004).

This second correlation is especially evident in sub-Saharan Africa, where high-polygyny agriculturalists are visibly darker than low-polygyny hunter-gatherers (i.e., Khoisans, pygmies) although both are equally indigenous. Year-round agriculture allows women to become primary food producers, thereby freeing men to take more wives. Thus, fewer women remain unmated and men are less able to translate their mate-choice criteria into actual mate choice. Such criteria include a preference, widely attested in the African ethnographic literature, for so-called 'red' or 'yellow' women — this being part of a general cross-cultural preference for lighter-skinned women (van den Berghe & Frost, 1986). Less mate choice means weaker sexual selection for light skin in women and, hence, less counterbalancing of natural selection for dark skin in either sex to protect against sunburn and skin cancer. Result: a net increase in selection for dark skin.

Just as weaker sexual selection may explain the unusually dark skin of sub-Saharan agricultural peoples, stronger sexual selection may explain the unusually light skin of northern and eastern Europeans, as well as other highly visible color traits.

Among early modern humans, sexual selection of women varied in intensity along a north-south axis. First, the incidence of polygyny decreased with distance from the equator. The longer the winter, the more it cost a man to provision a second wife and her children, since women could not gather food in winter. Second, the male death rate increased with distance from the equator. Because the land could not support as many game animals per unit of land area, hunting distance increased proportionately and hunters more often encountered mishaps (drowning, falls, cold exposure, etc.) or ran out of food, especially if other food sources were scarce.

Sexual selection of women was strongest where the ratio of unmated women to unmated men was highest. This would have been in the ‘continental Arctic’, a steppe-tundra environment where women depended the most on men for food and where hunting distances were the longest (i.e., long-distance hunting of highly mobile herds with no alternate food sources). Today, this environment is confined to the northern fringes of Eurasia and North America. As late as 10,000 years ago, it reached much further south. This was particularly so in Europe, where the Scandinavian icecap had pushed the continental Arctic down to the plains of northern and eastern Europe (Frost, 2006).

The same area now corresponds to a zone where skin is almost at the physiological limit of depigmentation and where hair and eye color have diversified into a broad palette of vivid hues. This ‘European exception’ constitutes a major deviation from geographic variation in hair, eye, and skin color (Cavalli-Sforza et al., 1994, pp. 266-267).

References

Brace, C.L., Henneberg, M., & Relethford, J.H. (1999). Skin color as an index of timing in human evolution. American Journal of Physical Anthropology, 108 (supp. 28), 95-96.

Cavalli-Sforza, L.L., Menozzi, P., & Piazza, A. (1994). The History and Geography of Human Genes. Princeton: Princeton University Press.

Frost, P. (2006). European hair and eye color - A case of frequency-dependent sexual selection? Evolution and Human Behavior, 27, 85-103

Jablonski, N.G. & G. Chaplin. (2000). The evolution of human skin coloration, Journal of Human Evolution, 39, 57-106.

Manning, J.T., Bundred, P.E., & Mather, F.M. (2004). Second to fourth digit ratio, sexual selection, and skin colour. Evolution and Human Behavior, 25, 38-50.

Osborne, D.L., C.M. Weaver, L.D. McCabe, G.M. McCabe, R. Novotony, C. Boushey, & D.A. Savaiano. (2008). Assessing the relationship between skin pigmentation and measures of bone strength in adolescent females living in Hawaii. American Journal of Physical Anthropology, 135(S46), 167.

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

Tauber, H. (1981). 13C evidence for dietary habits of prehistoric man in Denmark. Nature, 292, 332-333.

van den Berghe, P.L., & Frost, P. (1986). Skin color preference, sexual dimorphism and sexual selection: A case of gene-culture co-evolution? Ethnic and Racial Studies, 9, 87-113.