The constant friction caused by protective devices such as a helmet, shoulder pads or pillows will make acne management futile and may be counted as one of acne causes. Cosmetic face friction as a cosmetic care becomes more and more fashionable, which may lead to exogenous acne in those without any history of acne . Athletes may be more prone to acne due to combating pressure and friction, which is more known as acne mechanica .
Compelling evidence exists that high glycemic load diets may be viewed as what causes acne . Foods with significant sugar content and other carbohydrates yielding high glycemic loads affect serum insulin and insulin-like-growth-factor-1 (IGF-1) levels, both of which promote increase production of available androgens and the subsequent development of acne . In addition, dairy products can change the hormonal levels. The natural function of mild being to stimulate growth, it contains anabolic steroids as well as true growth hormones and other growth factors . Insulin sensitivity and sex-hormone-binding globulin (SHBG) are directly correlated, such that falls in insulin sensitivity increase the free androgen index (FAI) [preziosi].
The intake of abundant hypoglycemic carbohydrate-rich foods and high consumption of mild and dairy protein such as whey protein [*] predominantly during puberty, a period of high insulin/IGF1 signaling, may over-activate mTORC1, which enhances sebocyte growth and proliferation and SREBP-1 (Sterol regulatory element binding protein-1), the key transcription factor of lipid biosynthesis, mediated sebaceoous lipogenesis . Individuals with higher serum level of linoleic acid, ω-6, and alpha linolenic acid, ω-3, have been found less prone to keratinocyte tumors such as squamous cell carcinoma and basal cell carcinoma, a fact which may shed light on contribution of diet, omega-3 and omega-6 poly unsaturated fatty acids to comedogenesis and acne causes in less differentiated overly proliferated cells.
There is substantial epidemiological and biochemical evidence supporting the effects of milk and dairy foods and products as enhancers of insulin-IGF1 signaling, counted as one of likely acne causes, leading to its aggravation. Moreover, milk signaling potentiates the signaling effects of hyperglycemic carbohydrates. By the same token, the branched chain essential amino acid, BCAA, leucine, abundant in whey protein, commonly consumed by athletes, and enhanced IGF-1 by diary products sensed and integrated by mTORC1 and cause its activation, which, in turn, activates the transcription factor, SREBP, and thereby by merit of sebaceous lipogenesis may be counted toward acne causes.
On the other hand, leucine can be directly converted to free fatty acids and sterols within sebocytes for lipid synthesis. Wheat protein (7%) contains half as much leucine as whey protein (14%). Signaling pathways in acne mediated by high glycemic load and diary products. Note how high insulin/IGF1 activates mTORC1 .
These findings shed new light on the role of milk signaling during adolescence and may explain the observed association of severe acne and increased risk of prostate cancer later in life by a common mode of signal transmission .
Acne is rather universal in adolescent population within western societies while its frequency in certain remote islands appear to be nearly rare. Role of hereditary can not be disregarded in acne vulgaris as differences in prevalence across various geographical areas has been observed. This in part can be attributed to the distinct dietary choices, environmental variations as well as heterogeneity in genetic makeup . Examination of dietary habits and patterns in multifarious societies is a valuable means to elucidate diet-acne link .
A significant linear relationship between acne prevalence and number of cigarettes smoked daily was obtained (P<0.001) in a study done by Ring J et al to evaluate contribution of smoking to acne causes. In addition, a significant dose-dependent relationship between acne severity and daily cigarette consumption was shown by linear regression analysis  . Comedonal postaldolescent acne appears as the most frequent clinical form of postadolescent acne and seems to be strictly correlated with cigarette smoking .
Within the dermatology community, a general consensus has emerged that a poor or ambiguous association exists between diet and the etiology of acne vulgaris for more than twenty years  . Role of hereditary has been reported by several studies . However, genetic factors may not fully account for this influence and environmental contributions especially through dietary regimens may be considered. Today several studies indicate role of diet induced through modification of genetic expression . Surge of insulin and IGF1 following consumption of certain diets leads to depletion of transcription factor FoxO1, which is activatory for acne target genes and one of mechanism by which acne causes exert, at molecular level, their leverage.
High glycemic diet, dairy products and animal protein has been recognized as affecting this expression through activation of IGF-1/insulin, which, in turn, influence mTORC1 . Transcriptor factor sterol regulatory element binding protein-1 (SREBP-1) is influenced by mTORC1. This pathway leads to pathogenesis in sebaceous glands and more synthesis of free fatty acids, with well known role in acne vulgaris pathogenesis.
In comparison diets high in saturated fat have been associated with increase in IGF-1 and androgens . Moreover, composition of fatty diet is of significance. Omega-3 fatty acids show decrease in pro-inflammatory pathways and IGF-1 . IGF-1 is comedogenic by activation of nuclear transcription factors such as FoxO1 and mTORC1 which directly affect genes influencing acne through androgen receptor trans activation, increase in sebaceous gland secretions and follicular inflammation.
Influence of dietary changes in activation of mTORC1. Reduction in high glycemic food diet, dairy preparations and foods rich in animal protein (leucine) changes this pathway. Effect of isotretinoin, benzoyl peroxide on attenuation of mTORC1 is demonstrated .