Epigenetics, Diet & Acne

Avoiding habits that elevate growth factors (or growing out of puberty) changes expression of genes involved in acne.

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J Dtsch Dermatol Ges. 2010 Feb;8(2):105-14. doi: 10.1111/j.1610-0387.2010.07344.x.

FoxO1 - the key for the pathogenesis and therapy of acne?

[Article in English, German]

Melnik BC.

Source

Department of Dermatology, Enviromental Medicine and Health Theory, University of Osnabrück, Germany. melnik@t-online.de

Abstract

Five main factors play a pivotal role in the pathogenesis of acne: androgen dependence, follicular retention hyperkeratosis, increased sebaceous lipogenesis, increased colonization with P. acnes, and inflammatory events. This paper offers a solution for the pathogenesis of acne and explains all major pathogenic factors at the genomic level by a relative deficiency of the nuclear transcription factor FoxO1. Nuclear FoxO1 suppresses androgen receptor, other important nuclear receptors and key genes of cell proliferation, lipid biosynthesis and inflammatory cytokines. Elevated growth factors during puberty and persistent growth factor signals due to Western life style stimulate the export of FoxO1 out of the nucleus into the cytoplasm via activation of the phos-phoinositide-3-kinase (PI3K)/Akt pathway. By this mechanism, genes and nuclear receptors involved in acne are derepressed leading to increased androgen receptor-mediated signal transduction, increased cell proliferation of androgen-dependent cells, induction of sebaceous lipogenesis and upregulation of Toll-like-receptor-2-dependent inflammatory cytokines. All known acne-inducing factors exert their action by reduction of nuclear FoxO1 levels. In contrast, retinoids, antibiotics and dietary intervention will increase the nuclear content of FoxO1, thereby normalizing increased transcription of genes involved in acne. Various receptor-mediated growth factor signals are integrated at the level of PI3K/Akt activation which finally results in nuclear FoxO1 deficiency.

So, they name 

5 major factors in the pathogenesis of acne:

androgen dependence, follicular retention hyperkeratosis, increased sebaceous lipogenesis, increased colonization with P. acnes, and inflammatory events.

All those factors are related to a relative deficiency of the nuclear transcription factor FoxO1.

Nuclear FoxO1 suppresses androgen receptors, genes involved in cell proliferation and lipid biosynthesis. and inflammatory cytokines.

Elevated growth factors due to puberty OR Western diet and lifestyle decrease Fox01

This leads to increased androgen receptor sensitivity, increased cell proliferation, and increase in inflammatory cytokines. I have to look into what 'induction of sebaceous lipogenesis' means, exactly.

Retinoids, antibiotics work by increasing FoxO1 and so will dietary interventions. I.e. avoiding high glycemic and insulinotropic diet habits.

'thereby normalizing increased transcription of genes involved in acne' - in other words, it changes genetic expression or 'flips some genetic switches'.