Dairy and Acne

Mechanisms

Acne, or as it is technically called Acne Vulgaris, has historically been linked to dairy (being the most commonly reported dietary association with acne[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15394875|title=The acne problem|published=1949 Dec|authors=ROBINSON HM|journal=South Med J]).

Acne can be furthered and made worse by excessive insulin secretion[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/21335995|title=Evidence for acne-promoting effects of milk and other insulinotropic dairy products|published=2011|authors=Melnik BC|journal=Nestle Nutr Workshop Ser Pediatr Program] and appears to also be exacerbated by IGF-1[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/10465280|title=Growth hormone and insulin-like growth factors have different effects on sebaceous cell growth and differentiation|published=1999 Sep|authors=Deplewski D, Rosenfield RL|journal=Endocrinology] and Glucose-dependent insulinotropic polypeptide (GIP). In the case of IGF-1, there are repeated correlations between those with acne and higher serum IGF-1 concentrations.[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/7608381|title=Elevated serum insulin-like growth factor-1 (IGF-1) levels in women with postadolescent acne|published=1995 Apr|authors=Aizawa H, Niimura M|journal=J Dermatol][reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15781674|title=Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women|published=2005 Mar|authors=Cappel M, Mauger D, Thiboutot D|journal=Arch Dermatol]

These systemic factors appear to be induced following dairy consumption with insulin, IGF-1,[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15054433|title=High intakes of skimmed milk, but not meat, increase serum IGF-I and IGFBP-3 in eight-year-old boys|published=2004 Sep|authors=Hoppe C, Mølgaard C, Juul A, Michaelsen KF|journal=Eur J Clin Nutr] and GIP (which acts to further induce insulin[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/22647249|title=The insulinogenic effect of whey protein is partially mediated by a direct effect of amino acids and GIP on β-cells|published=2012 May 30|authors=Salehi A, Gunnerud U, Muhammed SJ, Ostman E, Holst JJ, Björck I, Rorsman P|journal=Nutr Metab (Lond)]) being increased to levels greater than that of an equicaloric portion of meat (as a comparative protein source).

When looking at serum anabolic factors, dairy protein appears to induce some of these factors to a greater degree than other protein sources

Insulin and IGF-1 both act upon the insulin receptor, the typical signalling pathway includes signalling via PI3K to mTOR/Akt which then induces nuclear ejection of FOX01.[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/20151947|title=FoxO1 - the key for the pathogenesis and therapy of acne|published=2010 Feb|authors=Melnik BC|journal=J Dtsch Dermatol Ges]

This nuclear ejection of FOX01 tends to be seen as anabolic, as the presence of FOX01 in the nucleus per se is anti-anabolic and ejection hinders its actions.[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15817464|title=Glucose-dependent insulinotropic polypeptide (GIP) stimulation of pancreatic beta-cell survival is dependent upon phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signalling, inactivation of the forkhead transcription factor Foxo1, and down-regulation of bax expression|published=2005 Jun 10|authors=Kim SJ, Winter K, Nian C, Tsuneoka M, Koda Y, McIntosh CH|journal=J Biol Chem][reference|url=http://www.ncbi.nlm.nih.gov/pubmed/20394627|title=Is nuclear deficiency of FoxO1 due to increased growth factor/PI3K/Akt-signalling in acne vulgaris reversed by isotretinoin treatment|published=2010 Jun|authors=Melnik BC|journal=Br J Dermatol][reference|url=http://www.ncbi.nlm.nih.gov/pubmed/20930691|title=The role of transcription factor FoxO1 in the pathogenesis of acne vulgaris and the mode of isotretinoin action|published=2010 Oct|authors=Melnik BC|journal=G Ital Dermatol Venereol] By facilitating anabolic signalling FOX01 ejection can augment androgen-dependent or insulin-receptor (mTOR dependent) anabolism, both the androgen pathway[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/17300229|title=Testosterone metabolism to 5alpha-dihydrotestosterone and synthesis of sebaceous lipids is regulated by the peroxisome proliferator-activated receptor ligand linoleic acid in human sebocytes|published=2007 Mar|authors=Makrantonaki E, Zouboulis CC|journal=Br J Dermatol] and the mTOR/Akt pathway (downstream of the insulin receptor)[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/17989724|title=IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway|published=2008 May|authors=Smith TM, Gilliland K, Clawson GA, Thiboutot D|journal=J Invest Dermatol] increase sebaceous lipogenesis (production of lipids in sebocytes, these cells being skin cells that have a high likelihood of acne production) and activation of the mTOR/Akt pathway can augment androgen signalling.[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/17202144|title=Insulin-like growth factor 1/insulin signaling activates androgen signaling through direct interactions of Foxo1 with androgen receptor|published=2007 Mar 9|authors=Fan W, Yanase T, Morinaga H, Okabe T, Nomura M, Daitoku H, Fukamizu A, Kato S, Takayanagi R, Nawata H|journal=J Biol Chem]

Anything that activates mTOR/Akt can plausibly increase the efficacy of androgen signalling. Activation of the insulin receptor reliably activates mTOR/Akt (and IGF-1 also acts on this receptor) and is thought to be the main player as there are correlations between diet, insulin and IGF-1 (known to reflect the diet), and acne in humans

Interventions

A few studies have claimed that reducing total insulinogenic secretions of the diet (limiting grains and dairy) would be beneficial in acne control[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/20107753|title={Acne vulgaris. Role of diet}|published=2010 Feb|authors=Melnik B|journal=Hautarzt][reference|url=http://www.ncbi.nlm.nih.gov/pubmed/19709092|title=Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris|published=2009 Oct|authors=Melnik BC, Schmitz G|journal=Exp Dermatol] or at least that the link between dairy and acne requires more investigation.[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/23210645|title=Epidemiology of acne vulgaris|published=2012 Dec 4|authors=Bhate K, Williams HC|journal=Br J Dermatol][reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15692488|title=Acne and milk, the diet myth, and beyond|published=2005 Feb|authors=Danby FW|journal=J Am Acad Dermatol]

When looking at surveys, there does appear to be an increased risk of acne associated with dairy products although the relative risk ratios (ranging from 1.12[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/15692464|title=High school dietary dairy intake and teenage acne|published=2005 Feb|authors=Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD|journal=J Am Acad Dermatol]-1.44 depending on dairy product or 1.10-1.19[reference|url=http://www.ncbi.nlm.nih.gov/pubmed/18194824|title=Milk consumption and acne in teenaged boys|published=2008 May|authors=Adebamowo CA, Spiegelman D, Berkey CS, Danby FW, Rockett HH, Colditz GA, Willett WC, Holmes MD|journal=J Am Acad Dermatol]) appears to be weak.

There is a plausible link between dairy consumption and acne but correlational research does not fully support this link; studies tend to be conducted in adolescents (rather than adults) and the results are not too in favor of a strong link; perhaps weak at best

There appears to be a more reliable link between IGF-1 per se than dairy products per se, and although the latter may spike the former current (limited) research does not support a strong relation between dairy and acne

Dairy By-products?

As both whey protein and casein protein are dairy byproducts, and thus can spike insulin and GIP levels, they are theoretically able to also induce acne.