So, what do we really know about acne?
Well for one, we know that it’s a common human skin disease characterized by red scaly skin, black heads, white heads and other forms of blemishes. We also know that the idea that “acne is generally expected to spontaneously regress during the late teenage or early adulthood years” is a complete and utter lie… at least in North America.
There are many people still suffering from acne in their 30s, 40s, and beyond.
Acne affects more than 85% of adolescents and, as many of us have noticed, often continues will into adulthood[i].
Despite this knowledge, the truth is there are relatively few studies in the literature that address adult acne. And, while acne may seem like a mild inconvenience to some (usually those not suffering from it) the importance of providing treatment for adults is heightened by the fact that acne that persists for long periods is more likely to lead to scarring[ii], and because there is an association between the prevalence of severe long-lasting acne and increased risk of prostate cancer later in life[iii].
Most of our interest in acne is cosmetic. Most of us spend a considerable amount of time every week trying to keep our bodies looking young. From lifting heavy weights to keeping our waistline in check, the pursuit of a youthful looking body is never ending.
But the first line of defense in looking younger is your skin. Your skin tells all. Based on this reason alone, it’s worth taking a closer look at acne.
While the exact cause of acne is still elusive, accumulating evidence suggests that the nutrient-activated mTOR signaling pathway plays a pivotal role in its pathogenesis (remember mTOR is everywhere, not just in muscle). Since mTOR is involved in the pathogenesis of acne, then we need to look at what things affect mTOR and see if we can draw a relation between them- mTOR and acne.
Elevated IGF-1 is a strongly connected to mTOR activation and it is also a phenomenon that has been observed in adult women and men with acne. [iv]
IGF-1 is a hormone similar in molecular structure to insulin. It plays an important role in childhood growth and continues to have anabolic effects in adults. It is available on the black market, and is a drug of choice among elite bodybuilders; however interestingly, both fasting and weight training increase Growth Hormone levels without increasing IGF-1 levels, but more on that later…
Clinically, IGF-I has been shown to correlate with acne lesion counts in adult women and significantly higher IGF-I levels have been described in women suffering from acne compared with control subjects with little to no acne[v],[vi],[vii].
In fact, IGF-1 seems to have a closer connection to acne during puberty then the often-accused testosterone does. Acne incidence more closely corresponds to the changing course of IGF-I levels than to changes in plasma androgens. This is because IGF-I levels peak during late puberty and gradually decline until the third decade [viii].
So from the available research it seems as though we have a link between mTOR, IGF-1 and acne. Interestingly, it seems as though we have possible mechanisms as well.
Through a complicated multistep pathway involving the activation of mTOR, IGF-1 induces something called SREBP-1[ix] and SREBP-1 activation in turn results in increased sebaceous lipogenesis and sebum output[x]. (This isn’t really anything you have to know, it’s just always good to know that there is a possible mechanism behind our theories…)
This link between acne and IGF-1 also gives us some possible explanation of the link between acne and cancer as the IGF-1 signaling pathway plays a role in the development of some cancers [xi]. Studies have shown that chronically increased levels of IGF-1 lead to increased growth of existing cancer cells [xii].
So if there is a link between mTOR, IGF-1, and acne- is this information we can use to actually lessen the amount of acne we have?
We’ve long known, or at least speculated, about the link between diet and acne. From chocolate to pizza grease, just about everything labeled “bad for you” has been linked to acne at one time or another. This includes the consumption of dairy foods.
Interestingly, the link between acne and dairy was recognized as early as 1885 and dairy (and other dietary) restriction was part of standard dermatologic therapy for acne through the first half of the 20th century [xiii]
A 1949 study reported 1925 patients who kept food diaries and found that milk was the most common food implicated in acne flares [xiv].
So there’s a possible correlation between milk and acne, as well as Acne and IFG-1/mTOR, but is there a correlation between Milk and IGF-1/mTOR?
Turns out there is.
High milk consumption (especially skim milk) increases IGF-1 levels 10% to 20% in adults and 20% to 30% in children. [xv]
Milk and other dairy products raise IGF-1 levels more than dietary protein found in meat [xvi].
Milk contains carbohydrates, and drinking milk raises both glucose and insulin levels. What makes milk special is that the increase in insulin is actually three to six times what would be expected or predicted from the carbohydrate load in the milk serving [xvii]. This is true for skimmed and full-fat milk, but not for cheese [xviii].
A glass of milk added to a low glycemic index meal can boost the insulin response 300%, to the level produced by a high glycemic index meal. [xix]
Diets composed of foods with a high glycemic index produce hyperglycemia, reactive hyperinsulinemia (high insulin), and increased formation of IGF-1.
So there’s a link between having chronically high IGF-1 levels, high insulin levels, high blood glucose levels, dairy protein, and acne.
So it seems pretty cut and dry… except, as with everything to do with the human body… it’s not.
Most of the research on milk and acne seems to come from one specific group of researchers, and has been refuted by others.
In the study The role of diet in acne: facts and controversies the authors state “on the basis of the existing evidence, is that the association between dietary dairy intake and the pathogenesis of acne is slim.” [xx]
So as with all things science, there are conflicting opinions, but that being said, to date the connection between milk, IGF-1, and acne seems to be your best bet.
Observational studies, including one case–control study [xxi] and two large and well controlled prospective cohort studies [xxii],[xxiii] have demonstrated an association between cow’s milk intake and acne prevalence and severity
These findings are supported by previous population-based studies [xxiv] in which areas with minimal consumption of dairy products had a very low acne prevalence.
So instead of arguing the ins and outs of scientific findings, let’s just do this: if you are suffering from acne you could try lowering your intake of dairy proteins and see if it helps.
It doesn’t seem like you have to lower overall protein intake in as much as you simply need to reduce your dairy intake (not eliminate it) for a month or two and see if it helps.
This may include your post workout shakes.
In unpublished research, acne was worsened in teenaged boys and in mature 40ish men who are consuming casein- and whey-containing protein powder “shakes” (author’s unpublished observations) [xxv]. And if you want to get really nit-picky, it seems like it’s the casein portion of milk more than it is the whey portion that increases IGF-1 [xxvi].
Other things you could try include reducing overall calorie intake and losing weight, as acne seems to be related to being overweight. In fact, if the connection between overweight, mTOR activation, IGF-1 production and calorie intake is true, then you may want to try intermittent fasting as way to combat your acne.
Short periods of fasting have been shown to lower mTOR activity, bioavailable IGF-1, radically decrease serum insulin levels, and lower blood glucose levels, plus, since you’re fasting, you won’t be consuming any dairy.
Finally, many of the current so called “super foods” such as resveratrol from grapes and red wine, epigallocatechin gallate from green tea, geneistein from soy, Diindolylmethane from broccoli, curcumin, and caffeine all seem to involve some amount of mTOR inhibition, either directly or indirectly [xxvii],[xxviii],[xxix],[xxx],[xxxi],[xxxii],[xxxiii],[xxxiv].
As you probably know, I’m not a big believer in super foods; but since you’re experimenting, you may as well see if including any of these into your diet helps.
Personally, I’d bet on the fasting over the super foods 😉
PS – I know there is a small subset of people out there that are going to look past all of the acne info and only see the ‘mTOR is bad’ part…, which is entirely untrue. It’s not bad, it just doesn’t need to be on ALL THE TIME. Let it take a break every once in a while.
[i] James WD. Clinical practice: acne. N Engl J Med 2005;352: 1463-72.
[ii] Layton AM, Henderson K, Cunliffe WJ. A clinical assessment of acne scarring. Clin Exp Dermatol 1994;4:303-8.
[iii] Sutcliffe S, Giovannucci E, Isaacs WB, Willett WC, Platz EA. Acne and risk of prostate cancer. Int J Cancer 2007; 121:2688-92.
[iv]Aizawa H, Niimura M. Elevated serum insulin-like growth factor-1 (IGF-1) levels in women with postadolescent acne. J Dermatol. 1995 Apr;22(4):249-52.
[v] Cappel M, Mauger D, Thiboutot D. Correlation between serum levels of insulin-like growth factor 1, dehydroepidandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Arch Dermatol 2005;141:333-8.
[vi] Deplewski D, Rosenfield R. Growth hormone and insulin-like growth factors have different effects on sebaceous cell growth and differentiation. Endocrinology 1999;140:4089-94.
[vii] Aizawa H, Niimura M. Elevated serum insulin-like growth factor-I (IGF-I) levels in women with postadolescent acne. J Dermatol 1995;22:249-52.
[viii] Smith C, Dunger D, AJK W, Taylor A, Perry L, Gale E, et al. Relationship between insulin, insulin-like growth factor I, and dehydroepiandrosterone sulfate concentrations during childhood, puberty and adult life. J Clin Endocrinol Metab 1989;68: 932-7.
[ix] Foretz M, Pacot C, Dugail I, Lemarchand P, Guichard C, Le Lièpvre X, Berthelier-Lubrano C, Spiegelman B, Kim JB, Ferré P, Foufelle F. ADD1/SREBP-1c is required in the activation of hepatic lipogenic gene expression by glucose. Mol Cell Biol. 1999 May;19(5):3760-8.
[x] Smith TM, Gilliland K, Clawson GA, Thiboutot D.IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway. J Invest Dermatol. 2008 May;128(5):1286-93.
[xi] Braun S, Bitton-Worms K, LeRoith D. The link between the metabolic syndrome and cancer. Int J Biol Sci. 2011;7(7):1003-15.
[xii] Arnaldez FI, Helman LJ. Targeting the insulin growth factor receptor 1. Hematol Oncol Clin North Am. 2012 Jun;26(3):527-42, vii-viii.
[xiii] Bulkley LD. Acne, Its Etiology, Pathology and Treatment. New York: G.P. Putnam?s Sons; 1885
[xiv] H.M. Robinson The acne problem South Med J, 42 (1949), pp. 1050–1060
[xv] Hoppe C, Mølgaard C, Juul A, Michaelsen KF. High intakes of skimmed milk, but not meat, increase serum IGF-I and IGFBP-3 in eight-year-old boys. Eur J Clin Nutr. 2004 Sep;58(9):1211-6.
[xvi] Hoppe C, Mølgaard C, Vaag A, Barkholt V, Michaelsen KF.High intakes of milk, but not meat, increase s-insulin and insulin resistance in 8-year-old boys. Eur J Clin Nutr. 2005 Mar;59(3):393-8.
[xvii] Ostman EM, Liljeberg Elmståhl HG, Björck IM. Inconsistency between glycemic and insulinemic responses to regular and fermented milk products. Am J Clin Nutr. 2001 Jul;74(1):96-100.
[xviii] Holt SH, Miller JC, Petocz P. An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr. 1997 Nov;66(5):1264-76.
[xix] Darwiche G, Ostman EM, Liljeberg HG, Kallinen N, Björgell O, Björck IM, Almér LO. Measurements of the gastric emptying rate by use of ultrasonography: studies in humans using bread with added sodium propionate. Am J Clin Nutr. 2001 Aug;74(2):254-8.
[xx] Batya B. Davidovici, Ronni Wolf The role of diet in acne: facts and controversies Clinics in Dermatology Volume 28, Issue 1, January–February 2010, Pages 12–16
[xxi] Adebamowo CA, Spiegelman D, Danby FW, et al. High school dietary intake and teenage acne. J Am Acad Dermatol 2005; 52: 207–211.
[xxii] Adebamowo C, Spiegelman D, Berkey CS, et al. Milk consumption and acne in teenaged boys. J Am Acad Dermatol 2008; 58: 787–793.
[xxiii] Adebamowo C, Spiegelman D, Berkey CS, et al. Milk consumption and acne in adolescent girls. Dermatol Online J 2006; 12: 1–13.
[xxiv] Cordain L, Lindeberg S, Hurtado M, et al. Acne vulgaris: a disease of Western civilization. Arch Dermatol 2002; 138: 1584–1590.
[xxv] Danby FW. Nutrition and acne. Clin Dermatol. 2010 Nov-Dec;28(6):598-604.
[xxvi] Hoppe C, Mølgaard C, Michaelsen KF. Cow’s milk and linear growth in industrialized and developing countries. Annu Rev Nutr. 2006;26:131-73. Review. Erratum in: Annu Rev Nutr. 2007;27:ix.
[xxvii] Zhou H, Luo Y, Huang S. Updates of mTOR inhibitors. Anticancer Agents Med Chem 2010; 10: 571-581
[xxviii] Brito PM, Devillard R, Nègre-Salvayre A, Almeida LM, Dinis TC, Salvayre R, Augé N. Resveratrol inhibits the mTOR mitogenic signaling evoked by oxidized LDL in smooth muscle cells. Atherosclerosis 2009; 205: 126-134
[xxix] Zhang Q, Kelly AP, Wang L, French SW, Tang X, Duong HS, Messadi DV, Le AD. Green tea extract and (-)-epigallocatechin-3-gallate inhibit mast cell-stimulated type I collagen expression in keloid fibroblasts via blocking PI-3K/AkT signaling pathways. J Invest Dermatol 2006; 126: 2607-2613
[xxx] Van Aller GS, Carson JD, Tang W, Peng H, Zhao L, Copeland RA, Tummino PJ, Luo L. Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. Biochem Biophys Res Commun 2011; 406: 194-199
[xxxi] Beevers CS, Chen L, Liu L, Luo Y, Webster NJ, Huang S. Curcumin disrupts the mammalian target of rapamycin-raptor complex. Cancer Res 2009; 69: 1000-1008
[xxxii] Kong D, Banerjee S, Huang W, Li Y, Wang Z, Kim HR, Sarkar FH. Mammalian target of rapamycin repression by 3,3’-diindolylmethane inhibits invasion and angiogenesis in platelet-derived growth factor-D-overexpressing PC3 cells. Cancer Res 2008; 68: 1927-1934
[xxxiii] Banerjee S, Kong D, Wang Z, Bao B, Hillman GG, Sarkar FH. Attenuation of multi-targeted proliferation-linked signaling by 3,3’-diindolylmethane (DIM): from bench to clinic. Mutat Res 2011; 728: 47-66
[xxxiv] Reinke A, Chen JC, Aronova S, Powers T. Caffeine targets TOR complex I and provides evidence for a regulatory link between the FRB and kinase domains of Tor1p. J Biol Chem 2006; 281: 31616-31626