Acne vulgaris: The metabolic syndrome of the pilosebaceous follicle

Acne and nutrition: hypotheses, myths and facts

“…An in vitro study showed that forkhead box transcription factor (FoxO)‐1 activity was reduced in sebaceous glands through an increase in insulin and IGF‐1 levels in SZ95 sebocytes proposing that FoxO1 principally might be involved in the regulation of growth‐factor‐stimulatory effects on sebaceous lipogenesis and inflammation in the pathological condition of acne . Moreover, insulin and IGF‐1, both stimulated by milk products and whey protein intake, have been shown activating the PI3K/Akt pathway which plays a key role in the sebaceous lipogenesis being of critical importance in the pathogenesis of acne . FoxO transcription factors are inhibitors of mTORC1 activity .…”

The effect of milk consumption on acne: a meta‐analysis of observational studies

“…Although the same positive association was found among the American and European population, no association was found in Asia, Africa and South America. 31,36 The increased mTORC1 signalling promotes sebaceous lipogenesis, 37 increases the synthesis of gonadal and androgen, enhances the bioactivity of androgen and stimulates the androgen receptor signalling, 35 all of which contribute to acne pathogenesis critically. Although several cohort and case-control studies have been performed, few randomized controlled trials and systematic studies have been conducted.…”

Complementary and alternative therapy for pediatric acne: A review of botanical extracts, dietary interventions, and oral supplements

“…While acne is extremely common in westernized societies, the absence of acne among adolescents and young adults of Papua New Guinea and Paraguay has sparked interest in dietary and lifestyle factors affecting acne . Acne has been proposed to represent metabolic syndrome of the pilosebaceous unit due to increased insulin and insulin‐like growth factor‐1 (IGF‐1) signaling, as well as overactivation of mammalian target of rapamycin complex 1 (mTORC1), playing a key role in the pathogenesis . Increased insulin and IGF‐1 signaling enhance androgen synthesis and androgen receptor activation, as well as activation of AKT and ultimately mTORC1.…”

“…Increased insulin and IGF‐1 signaling enhance androgen synthesis and androgen receptor activation, as well as activation of AKT and ultimately mTORC1. Activation of mTORC1 results in activation of sterol response element binding factor 1 (SREBP1), a lipogenic transcription factor, which promotes the formation of free fatty acids and acts as a pathogen‐associated molecular pattern for activation of toll‐like receptor 2 driven inflammation . A variety of dietary changes may attenuate mTORC1 signaling, including reduced glycemic load, reduced milk consumption, reduced dairy consumption, and reduced intake of saturated fat .…”

“…A variety of dietary changes may attenuate mTORC1 signaling, including reduced glycemic load, reduced milk consumption, reduced dairy consumption, and reduced intake of saturated fat . Additionally, certain supplements and dietary factors may inhibit mTORC1 signaling, including epigallocatechin‐3‐gallate (green tea), resveratrol, omega‐3 fatty acids, and vitamin D …”