The spread of acne

I found this article by Loren Cordain et al. while I was looking for something else, and thought I'd point it out:

Acne vulgaris: a disease of Western civilization
Background In westernized societies, acne vulgaris is a nearly universal skin disease afflicting 79% to 95% of the adolescent population. In men and women older than 25 years, 40% to 54% have some degree of facial acne, and clinical facial acne persists into middle age in 12% of women and 3% of men. Epidemiological evidence suggests that acne incidence rates are considerably lower in nonwesternized societies. Herein we report the prevalence of acne in 2 nonwesternized populations: the Kitavan Islanders of Papua New Guinea and the Aché hunter-gatherers of Paraguay. Additionally, we analyze how elements in nonwesternized environments may influence the development of acne.
Observations Of 1200 Kitavan subjects examined (including 300 aged 15-25 years), no case of acne (grade 1 with multiple comedones or grades 2-4) was observed. Of 115 Aché subjects examined (including 15 aged 15-25 years) over 843 days, no case of active acne (grades 1-4) was observed.
Conclusions The astonishing difference in acne incidence rates between nonwesternized and fully modernized societies cannot be solely attributed to genetic differences among populations but likely results from differing environmental factors. Identification of these factors may be useful in the treatment of acne in Western populations.

The observations are well-summarized there in the abstract. The introduction points out in addition other populations where acne was apparently rare or absent before Westernization, including Inuit and Okinawan peoples. Also, acne is less prevalent in more rural samples of mixed-ancestry populations, such as Peruvians or South Africans.

In the context of an apparent increase in acne with the introduction of urbanization and Westernized diet, the paper suggests that acne mainly results from diet, in particular depending on the insulin response. This mechanism is a bit involved, so if you are interested, you should refer to the paper.

The journal accompanied that article with an editorial, which notes the interest of recent research into links between obesity, insulin resistance and hyperandrogenism.

This is a great couple of paragraphs:

Cordain et al (1) suggest that diet-induced hyperinsulinemia elicits endocrine responses that may affect the development of acne through mediators such as androgens, insulinlike growth factor (IGF) 1, IGF binding protein 3, and retinoid signaling pathways. The role of diet in endocrine activity is supported by the observation that improvements in nutrition have been linked to an earlier onset of sexual maturation and the development of acne in young girls and boys. Numerous studies have shown that improvements in general nutrition in girls have led to an earlier onset of menses and that menses is delayed in girls with low body fat such as athletes and ballet dancers. (7) In 1970, the mean age of onset of menarche in the United States was 12 years compared with age 16 years for girls in 1835. (8) Of interest is the observation that the mean age of onset of menarche in the Kitavan population is 16 years, which is significantly older than girls in westernized societies. In a 5-year longitudinal cohort study of 439 black girls and 432 white girls in Cincinnati, Ohio, Lucky et al (9) demonstrated that those with severe comedonal acne had a significantly earlier age of onset of menarche and higher serum levels of dehydroepiandrosterone than girls with mild comedonal acne. This study demonstrated that the early development of comedonal acne might be one of the best predictors of later, more severe disease. In a similar 5-year longitudinal study of 219 black and 249 white early adolescent boys in Cincinnati, black boys had higher pubertal maturation scores than white boys of the same age. (10) The prevalence and severity of acne correlated well with advancing pubertal maturation. Is the late onset of menarche in Kitavan girls "protective" against the development of acne or severe acne? Although Cordain et al do not present data regarding the age of sexual maturation of the Kitavan or Aché boys, is it also possible that their relative lack of acne might relate to a later age of pubertal maturation and sebaceous gland exposure to higher circulating levels of androgen?
If acne results from hyperinsulinemia, as proposed by Cordain et al,1 one would expect that obese individuals, who are relatively chronically insulin resistant, would have a higher prevalence of acne. Bourne and Jacobs (11) evaluated 2720 military recruits for obesity and the presence of acne and noted an association between the 2 in the older recruits (ages 20-40 years) but not in those in the age range of 15 to 19 years. This observation suggests that the presence of acne in a younger population may be associated with factors other than obesity or insulin resistance. In fact, serum levels of IGF-1 are highest during periods of the adolescent growth spurt and taper off in the 20s, which coincides with the pattern in the peak incidence of acne. (12) Insulinlike growth factor 1 functions similarly to insulin in that it can promote the growth of keratinocytes and sebaceous glands. It is possible that that the effects of the hyperinsulinemia on acne in obese adolescents may be overshadowed by the effects of high levels of circulating IGF-1. As pointed out by Cordain et al, acne has been associated with elevated serum levels of IGF-1 in adult women with acne. (13) All adolescents, including the Kitavan and Aché, would experience increases in IGF-1 during adolescence, so increases in IGF-1 alone cannot explain the presence of acne.

Yes, IGF-1 is the tiny dog gene, in case you're wondering what kind of search led me to this!

The editorial is receptive but still skeptical of the diet-acne link proposed by Cordain et al.:

Although Cordain et al. (1) make a strong argument for the role of diet in acne, we believe that it is difficult to dissociate environmental factors such as diet from genetic factors in their study. The Aché and Kitavan people live in closely knit communities, and therefore genetic factors may play a role in the relative lack of acne in these populations. Several studies point to an association of genetic factors with acne, including studies that demonstrate variations in the prevalence of acne among ethnic groups and the high degree of concordance of acne in twins. (15-19)

There are a number of later references that cite the paper by Cordain et al., if you're interested in following up -- a link between acne and diet has always been problematic, but this is probably more or less because expression of the disease also depends on several genetic factors that are difficult to untangle.

References:

Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. 2002. Acne vulgaris: a disease of western civilization. Arch Dermatol 138:1584-1590.

Thiboutot DM, Strauss JS. 2002. Diet and acne revisited. Arch Dermatol 138:1591-1592. Abstract