The role of diet in clinical and endocrine manifestations of acne vulgaris

Variations in acne prevalence worldwide have prompted researchers to question the natural development of the disease. Although acne is common in Western societies, this disorder remains absent in primitive societies existing on traditional food patterns and is observed only in low frequencies in societies with moderate intakes of Westernised foods. Recent observational reports suggest that the absence of acne in these societies may be due to environmental factors, mainly local diets, which are devoid of high glycaemic index carbohydrates. High glycaemic carbohydrates have been implicated in acne aetiology because of their ability to increase insulin demand and other factors associated with insulin resistance. Clinical and experimental evidence suggests that insulin can promote the bioavailability of insulin-like growth factor-1 (IGF-1) and androgens, by decreasing IGF-binding protein-1 and sex hormone binding globulin (SHBG) levels respectively. This hormonal response may in turn promote unregulated tissue growth (follicular epithelial growth) and androgen-mediated sebum production, two factors responsible for acne proliferation. The overall aim of the present work was to investigate the effect of a low glycaemic diet on the severity of acne symptoms and endocrine variables associated with insulin resistance. This involved the recruitment of young male acne sufferers for a 12 week randomised controlled dietary intervention trial. The experimental treatment was a low glycaemic load diet, which mimics the diets of the acne-free populations, and the control situation was a typical high glycaemic load Western diet. Acne lesion counts were assessed at monthly intervals throughout the study and hormonal variables associated with acne were measured at the study’s termination. This investigation found that a low glycaemic load diet significantly reduced acne lesion counts when compared with a conventional high glycaemic load Western diet. The lessening of acne severity may be explained by improvements in metabolic-endocrine parameters following the dietary intervention. The experimental diet reduced insulin resistance and androgen bioavailability, and increased levels of SHBG and IGF binding protein-1, when compared to controls. However, these changes may also relate to modest weight loss which concurred with the reduction in glycaemic load. Post hoc analysis revealed that the effect of the low glycaemic load diet on acne and certain endocrine variables (insulin sensitivity, SHBG and androgen bioavailability) was lost after statistically adjusting for weight loss. Although this study could not determine an aspecific effect of a low glycaemic load diet from that of weight loss, these findings are consistent with earlier suggestions of the association between hyperinsulinemia and acne