Acne Originates in the Gut

No acne vulgaris in non-westernized cultures (Staffan Lindeberg, Kitava Study)

The conventional wisdom is that the common skin disorder acne vulgaris develops when sebaceous (oil) glands attached to the hair follicles are stimulated at the time of puberty by elevated levels of male hormones. This increased oil production starts a cascade of events that result in inflammation and proliferation of Propionibacterium acnes.
However, I believe gut dysbiosis and increased intestinal permeability (AKA leaky gut) are the root causes of acne vulgaris – and the scientific studies supporting this notion are now piling up.



Is there any epidemiological evidence to suggest that a western lifestyle promotes higher acne incidence rates?

In westernized societies, acne vulgaris is a nearly universal skin disease. However, epidemiological studies show that acne is almost unheard of in non-westernized populations (1-3).
“The astonishing difference in acne incidence rates between nonwesternized and fully modernized societies cannot be solely attributed to genetic differences among populations but likely results from differing environmental factors” (1).
It’s unlikely that the absence of acne in non-westernized cultures results from genetic resistance to acne. People with similar ethnic backgrounds living in more westernized settings maintain considerably higher acne incidence rates (1, 2).

Hyperinsulinemia and insulin resistance are often suggested to be important factors, and a low glycemic-load diet is often suggested as a potential treatment (1). While it seems that insulin could play a role, alterations in the gut microbiome and gut-derived inflammation are probably the main factors involved.

Which mechanisms are involved?

Several factors contribute to gut dysbiosis, and the following seems to be the most important in connection with acne:

  • Antibiotics: Alter the gut flora which studies have shown may never recover.
  • Other drugs: Several drugs damage the gut microbiota and intestinal lining.
  • Grains: Antinutrients and high-density carbohydrates have been linked to gut dysbiosis and leaky gut.
  • Sugar: A diet high in refined sugars alter gut flora composition.
  • Simplified diet: Besides grains and sugar, common staple foods in the western diet include low-fat dairy and vegetable oils. Most food items are refined, pasteurized, and processed.
  • Excessive hygiene and fear of “germs”
  • Hereditary factors: Microorganisms are passed on from mother to child during birth, breastfeeding, and other types of contact. The child also comes in contact with bacteria from other family members.

These “triggers” almost exclusively appear in westernized societies, and they appear in abundance. Grains have also been a part of the diet in some healthy non-westernized societies. However, they put far more emphasis on making the foods easier to digest in the sense that seeds, grains and nuts were soaked, sprouted, fermented and/or naturally leavened to neutralize naturally occurring antinutrients (2).

The intestinal barrier is the main interface between us and the external envornment, and most of our immune system is located in the gut. A healthy gut flora consists of hundreds of different species of microorganisms, and the dialogue between host and bacteria at the mucosal interface plays an essential part in the development of a competent immune system (4).

When there’s a continued interaction with one or more of the factors listed above, poor gut health is established. In mild-moderate cases there’s a loss of diversity, unhealthy gut flora composition and increased intestinal permeability. Moderate-severe cases are characterized by more severe cases of gut dysbiosis and leaky gut.

Altered gut flora and increased intestinal permeability cause systemic inflammation throughout the body (8). Studies have shown that acne patients are under significant systemic inflammation and oxidative stress (6).
Free radicals cause oxidative damage to sebum, and the oxygen content is reduced. This oxidation changes sebum in a way that it becomes a more suitable environment for P. Acnes. The bacteria get a chance to multiply and eventually lesions appear (6).

Are there any studies done one the connection between gut and skin?

In 2011, Whitney P. Bowe and Alan C. Logan published a paper where they reviewed the connection between acne and the gut (8). Some of the important information:

  • Gastrointestinal symptoms such as constipation, halitosis, and gastric reflux are more common in acne sufferers.
  • Hypochlorhydria is common in acne sufferers. Hypochlorhydria is a significant risk factor for small intestinal bacterial overgrowth which again has been linked to increased intestinal permeability
  • Studies have shown increased intestinal permeability in patients with acne vulgaris
  • A Russian investigation reported that 54% of acne patients have marked alterations to the intestinal microflora
  • Probiotics have shown potential in acne treatment
  • Probiotics can help in regulation of insulin levels.
  • The loss of bifidobacteria by poor dietary choices – high fat, sugar – leads to increased intestinal permeability, encroachment of LPS endotoxins through the intestinal barrier, which in turn leads to low-grade inflammation, oxidative stress, insulin resistance and sickness behavior. In humans, probiotic administration may diminish systemic access of gut-derived LPS endotoxins and reduce reactivity to such endotoxins
  • We know that the typical Western diet, high in sugar and fat, devoid of fiber, the very one correlated with risk of acne, is associated with lower levels of Lactobacillus and Bifidobacterium

One study also showed a statistically significant difference in the prevalence of gastrointestinal symptoms (halitosis; gastric reflux; abdominal bloating; constipation) between patients with and without sebaceous gland diseases (7).

Why does acne coincide with hormonal changes?

Acne development usually coincides with the increased androgen production during puberty. Hormonal changes during menstrual cycle, pregnancy, drug use etc. have also been linked to increased acne formation.

To say that acne is due to changes in puberty suggests that acne can be a normal part of healthy development. This seems very unlikely, since acne vulgaris is unheard of in many non-westernized societies (1-3).

The increased activity of sebaceous glands elicited by androgens during puberty is important in the development of acne. People who get acne are under systemic inflammation and oxidative stress and cannot cope with these changes. Increased sebum production probably results in more oxidative damage and more P. Acnes in the pores.

Hormonal changes and increased sebaceous gland activity are a natural part of human development and only contribute to acne formation when there’s some other underlying issue. Some researchers have speculated that the increased oxidative stress and inflammation in acne patients are caused by the elevated sebum production. However, other studies suggest that the inflammation is closely linked to leaky gut and endotoxemia.

When acne appears, the underlying gut issues might have been present for some time. Even sometimes from birth. When there’s an increased sebum production associated with hormones, the low-grade inflammation caused by leaky gut and gut dysbiosis manifests itself as acne (8).

Other factors can also worsen acne severity during periods of hormonal change:

  • Candida Albicans
    The pathogenicity of Candida Albicans is closely related to hormonal changes and imbalances. Both natural and induced hormonal changes decrease the resistance to candida (19). In combination with a western diet, possibly antibiotics and other factors, this hormonal change can contribute to an altered gut flora.
  • Insulin resistance during puberty
    Recent international studies show that acne is associated with increased consumption of highly palatable, sweet, fried, calorie-rich foods with low nutrient density. It is well documented that a period of insulin resistance occurs during puberty, and this might contribute to decreased tolerance towards the traditional western diet (8).

Why is acne hereditary?

Studies have demonstrated that hereditary factors are important in determining susceptibility to acne (15, 16). However, one small study done on twins concluded that “sebum excretion is under genetic control and the development of clinical lesions is modified by environmental factors” (17).

Since acne doesn’t appear in the early years of life it’s difficult to know if acne is due to genetics or if it’s caused by some other factor. Families with a history of acne might have different dietary habits than families with little to no history of acne.
Micobes pass on from mother to newborn during birth and breastfeeding. The newborn also comes in contact with microbes through other family members. Dysfunctional gut flora is hereditary!

How does antibiotics work against acne?

It seems ironic that antibiotics work against acne when it’s one of the drugs you definitely want to avoid. Some antibiotics have shown to be effective against acne, but the results are usually short-term. Also placebo has to be considered as an important factor (18).

“The mechanism(s) of action of oral antibiotics in acne remains a mystery – is it a systemic effect against P. acnes, an anti-inflammatory influence, ability to lower sebum free fatty acids, or via antioxidant activities. Could it be due to the influence of antibiotics on the gut microbiota, which in turn improves glycemic control and decreases LPS endotoxin encroachment into the periphery?” (8)

Studies done on acne and diet have shown varying results; why?

Studies done on acne and diet have focused on low-glycemic load diets, omega-3, probiotics, and milk consumption.

Low-glycemic load and omega-3

Results: Most newer studies show that omega-3 and low glycemic load-diets improve symptoms in acne vulgaris patients. However, total remission is rarely seen (9-14).

A diet based on low glycemic load foods will definitely help most cases of acne by regulating insulin (1, 8) and improving gut health. Also, omega-3 is anti-inflammatory..

Why it doesn’t work 100%:

  • Most of the studies have very little focus on the types of foods included and their effect on the gut flora and intestinal lining.
  • There’s no regulated intake of beneficial bacteria or prebiotics that will improve gut flora.
  • Food intolerance is closely connected to the gut microbiome. These studies take little to no account of individual food intolerances.
  • Dietary changes are often not enough to treat gut dysbiosis and leaky gut.


Results: Several large studies have linked dairy consumption with acne (8).

None of the studies have made a positive correlation between fermented dairy and acne. Regular milk contains hormones and growth factors like IGF-1.
“Acne is certainly driven by insulin-like growth factor I (IGF-I), and IGF-I can be absorbed across colonic tissue. Therefore, it is interesting to note that probiotic bacteria (Lactobacilli in particular) utilize IGF-I during the fermentation process when added to milk, with a resultant 4-fold lower level of IGF-I in fermented vs. skim milk” (8)

The fact that milk consumption aggravates acne is consistent with the theory that acne is caused partly by increased intestinal permeability. With increased intestinal permeability the intestinal absorption of certain components in dairy products would be enhanced.


Results: Fermented dairy and probiotic supplements have shown promising results in acne treatment (8).

Why it doesn’t work 100%:

  • No other dietary changes except probiotics!
  • Only a couple of new strains of bacteria are administered.
  • In some cases of moderate-severe gut dysbiosis it could be necessary to reduce the numbers of overgrowing microorganisms before new strains manage to populate the gut.


Eating a traditional diet with plenty of probiotics and prebiotics should significantly improve most cases of acne vulgaris. Other measures, such as introducing an entirely new ecosystem of bacteria in the gut with advanced probiotics could be necessary in severe cases of gut dysbiosis.


  1. Antibiotics and/or other drugs, simplified diet, grains, sugar, excessive hygiene, poor hereditary gut flora, and other factors that damage gut microbiota or  increase intestinal permebaility–> dysfunctional gut flora and increased intestinal permeability.
  2. Dysfunctional gut flora and increased intestinal permeability –> systemic inflammation and oxidative stress
  3. Oxidative stress and inflammation –> Acne vulgaris

1: Cordain L, Lindeberg S, Hurtado M, et al. Acne vulgaris: a disease of Western civilization.
Arch Dermatol. 2002 Dec;138(12):1584-90.

2: Price, Dr Weston, A., Nutrition and Physical Degeneration. 6th edition, 14th printing. La Mesa, CA, USA. Price-Pottenger Nutrition Foundation, 2000.

3: Schaefer O. When the Eskimo comes to town. Nutr Today. 1971;68-16

4: Guarner F, Malagelada JR. Gut flora in health and disease. Lancet. 2003 Feb 8;361(9356):512-9.

5: Cordain L. Cereal Grains: Humanity’s Double-Edged Sword
World Rev Nutr Diet. 1999;84:19-73.

6: Research shows inflammation causes acne

7: Zhang H, Liao W, Chao W, et al. Risk factors for sebaceous gland diseases and their relationship to gastrointestinal dysfunction in Han adolescents. J Dermatol. 2008 Sep;35(9):555-61.

8: Bowe WP, Logan AC. Acne vulgaris, probiotics and the gut-brain-skin axis – back to the future?
Gut Pathog. 2011 Jan 31;3(1):1.

9: Smith RN, Mann NJ, Braue A, et al. A low-glycemic-load diet improves symptoms in acne vulgaris patients: a randomized controlled trial. Am J Clin Nutr. 2007 Jul;86(1):107-15.

10: Cordain L. Implications for the role of diet in acne.
Semin Cutan Med Surg. 2005 Jun;24(2):84-91.

11: Thiboutot DM, Strauss JS. Diet and Acne Revisited
Arch Dermatol. 2002 Dec;138(12):1591-2.

12: Spencer EH, Ferdowsian HR, Barnard ND. Diet and acne: a review of the evidence
Int J Dermatol. 2009 Apr;48(4):339-47.

13: Veith WB, Silverberg NB. The association of acne vulgaris with diet.
Cutis. 2011 Aug;88(2):84-91.

14: Logan AC. Omega-3 Fatty Acids and Acne
Arch Dermatol. 2003 Jul;139(7):941-2; author reply 942-3.

15: Goulden V, McGeown CH, Cunliffe WJ.The familial risk of adult acne: a comparison between first-degree relatives of affected and unaffected individuals.Br J Dermatol. 1999;141297-300

16: Ballanger F, Baudry P, N’Guyen JM, et al. Heredity: A Prognostic Factor for Acne
Dermatology. 2006;212(2):145-9.

17: Walton S, Wyatt EH, Cunliffe WJ. Genetic control of sebum excretion and acne—a twin study
Br J Dermatol. 1988 Mar;118(3):393-6.

18: Chiou WL. Oral tetracyclines may not be effective in treating acne: dominance of the placebo effect. Int J Clin Pharmacol Ther. 2012 Mar;50(3):157-61.

19: T.J. Rogers, E. Balish. Immunity to Candida Albicans
Microbiol. Rev. 1980, 44(4):660.

20: McDade, T.W., Rutherford J. , Adair, L, et al. Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood
Published online before print December 9, 2009, doi: 10.1098/rspb.2009.1795


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