The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides

Summary

Background

Dietary factors have long been implicated in acne pathogenesis. It has recently been hypothesized that low glycemic load diets may influence sebum production based on the beneficial endocrine effects of these diets.

Objective

To determine the effect of a low glycemic load diet on acne and the fatty acid composition of skin surface triglycerides.

Methods

Thirty-one male acne patients (aged 15–25 years) completed sebum sampling tests as part of a larger 12-week, parallel design dietary intervention trial. The experimental treatment was a low glycemic load diet, comprised of 25% energy from protein and 45% from low glycemic index carbohydrates. In contrast, the control situation emphasized carbohydrate-dense foods without reference to the glycemic index. Acne lesion counts were assessed during monthly visits. At baseline and 12-weeks, the follicular sebum outflow and composition of skin surface triglycerides were assessed using lipid absorbent tapes.

Results

At 12 weeks, subjects on the experimental diet demonstrated increases in the ratio of saturated to monounsaturated fatty acids of skin surface triglycerides when compared to controls [5.3 ± 2.0% (mean ± S.E.M.) vs. −2.7 ± 1.7%, P = 0.007]. The increase in the saturated/monounsaturated ratio correlated with acne lesion counts(r = −0.39, P = 0.03). Increased follicular sebum outflow was also associated with an increase in the proportion of monounsaturated fatty acids in sebum (r = 0.49, P = 0.006).

Conclusion

This suggests a possible role of desaturase enzymes in sebaceous lipogenesis and the clinical manifestation of acne. However, further work is needed to clarify the underlying role of diet in sebum gland physiology.

Introduction

Dietary factors have long been implicated in the pathogenesis of acne [1], [2]. It is well known that increased sebum production plays a fundamental role in acne [3] and evidence suggests that dietary manipulation alters sebaceous gland output. Extreme caloric restriction dramatically decreases the sebum excretion rate and these changes can be reversed when a normal diet is resumed [4], [5]. Other studies have demonstrated that increased consumption of dietary fat or carbohydrate increases sebum production [6], and modifications to the type of carbohydrate can also alter sebum composition [7], [8]. Altogether, these studies suggest that the quantity and composition of foods, when changed significantly, may affect underlying mechanisms involved in sebum production.

Evidence suggests that diet may be an important source of substrate for the synthesis of sebaceous lipids [1]. Human sebum is comprised mainly of triglycerides (40–60%), wax esters (19–26%) and squalene (11–15%), with some cholesterol and cholesterol esters [9], [10], [11]. These lipids can be synthesized from a variety of sources (e.g. glucose, acetate, and fatty acids) which serve to donate two carbon fragments [12], [13]. However, some dietary lipids (especially fatty acids) can also pass unchanged from the circulation to the sebaceous cells. It is presumed that undifferentiated cells of the sebaceous gland acquire the dietary lipids whilst in the basal layer exposed to the circulation [14]. This notion is supported by the observation that sebum contains linoleic acid, an essential fatty acid that cannot be synthesized in vivo and therefore must be obtained from the diet.

The triglyceride fraction of sebum is presumably responsible for acne development [15], [16]. Bacteria can hydrolyze sebaceous triglycerides [17], liberating the fatty acids which can penetrate the follicular wall and become incorporated into the metabolism of the surrounding epidermis. The application of free fatty acids on rabbit ears or hairless mice has been shown to induce hyperkeratinization and epidermal hyperplasia similar to that seen in comedo formation [15], [18]. However, the hyperkeratotic effect may not be a feature of all fatty acids, as recent evidence suggests that only monounsaturated fatty acids (MUFAs) stimulated the morphological changes whereas saturated fatty acids (SFAs) have little effect [15]. Human sebum is known to contain a high proportion of MUFAs, with a characteristic double bond at the Δ6 position rather than at the standard Δ9 position [16]. The most abundant of these is sapienic acid (16:1Δ6), which is formed by the Δ6 desaturation of palmitic acid (16:0) [19]. Sapienic acid is unique to human sebum and has not been identified in other human tissues or in sebaceous gland secretions of other animals [16]. It is presumed that this fatty acid may play a role in acne pathogenesis, however its role is not well defined [20].

In the present study, we examined the influence of diet on the fatty acid composition of skin surface triglycerides. Recent evidence suggests that low glycemic load diets may affect sebum production based on the beneficial hormonal effects of these diets [21]. The glycemic load may be interpreted as a measure of the blood glucose and insulin-raising potential of the diet, as it represents the rate of carbohydrate absorption (indicated by the glycemic index) and the quantity of carbohydrate consumed [22]. Previous studies indicate that the dietary manipulation of the quality and quantity of carbohydrates can affect the composition of fatty acids in sebum [7], [8]. A relative excess of dietary carbohydrate (500 g/day) can increase the proportion of 16:1 in sebum, however the effect on the other fatty acids of sebum is varied depending on the type of carbohydrate used [7], [8]. Based on these observations, one can speculate that the composition of fatty acids in sebum may vary with alterations in the dietary glycemic load. Therefore, the objective of the present study was to determine the effect of a low glycemic load diet on acne and the fatty acid composition of skin surface triglycerides.