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Review paper

The possible role of diet in the pathogenesis of adult
female acne

Krystyna Romańska-Gocka, Magdalena Woźniak, Elżbieta Kaczmarek-Skamira, Barbara Zegarska

Department of Cosmetology and Esthetic Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

Adv Dermatol Allergol 2016; XXXIII (6): 416–420
DOI: 10.5114/ada.2016.63880

Acne in adults is a chronic, increasingly common disease, especially among women. It differs in pathogenesis and
clinical presentation from adolescent acne. Acne in adults is associated with Western diet, defined as high con-
sumption of milk, high glycemic load and high calorie intake. Metabolic signals of this diet result in a significant
increase in insulin/insulin growth factor 1 serum level and consequently in the molecular interplay of mammalian
target of rapamycin complex 1 kinase (mTORC1)/forkhead box protein 1 (FoxO1) mediated nutrient signaling, leading
to increased proliferation of keratinocytes, increased lipogenesis and sebum production and finally to aggravation
of acne.
Key words: female acne, diet, insulin growth factor 1, forkhead box protein 1, mammalian target of rapamycin
complex 1 kinase.

age, female gender and long duration of acne (> 5 years)
Acne in adults is defined as the presence of acne le- [9]. The impairment of quality of life can be alleviated by
sions after the age of 25 years [1]. Acne affects 64% of the appropriate acne treatment [9].
adults in their 20s and 43% in their 30s [2]. It is affecting Studies suggest that components of Western diet,
an increasing number of adults, especially females and particularly dairy products may be associated with acne.
it is observed in up to 54% of women [1, 3]. Acne in adult Acne is absent in populations consuming low glycemic
women, in different age categories, has a significantly load diet and not consuming refined sugars, grains, milk
higher prevalence than acne in adult men [4]. It is more and dairy products [10]. The beneficial therapeutic effects
frequent in African American and Hispanic women than of low glycemic load diet on the clinical course and in-
in Continental Indian, Caucasian and Asian ones [5]. The tensity of acne and sebum production has been demon-
disease is a chronic, relapsing, inflammatory condition strated in several studies [11–13].
and requires long-term treatment [1]. The aim of this review is to highlight that dermatolo-
Two main subtypes of adult acne can be identified: gists treating acne should take into account not only
persistent adolescent acne (80% of cases) and late-onset pharmacological treatment, but also dietary interven-
acne (20% of cases), with first symptoms appearing well tions, because of the beneficial endocrine effects of low
after puberty, usually about the age of 21–25 [6]. Both glycemic load diet [14].
types are frequently associated with inflammation, hy-
perpigmentation and scarring [7]. Women are more dis-
turbed by the disease than men [8]. Acne is an important Clinical presentation
problem because it causes psychological disturbances, Clinical features of adult female acne differ from ado-
in comparison with those among patients with systemic lescent acne [1], with a predominance of inflammatory
diseases, such as diabetes mellitus, asthma or epilepsy lesions such as papules and pustules. Typical features are
[9]. It leads to negative self-esteem and negative body nodules, usually painful, sometimes indolent, of long du-
image. It causes depression symptoms and anxiety. ration, which result in residual hyperpigmentation, local-
A greater impact on quality of life is associated with older ized typically on U-zone: cheeks, peri-oral and lower chin

Address for correspondence: Krystyna Romańska-Gocka MD, PhD, Department of Cosmetology and Esthetic Medicine,
Collegium Medicum, Nicolaus Copernicus University, 5 Kurpińskiego St, 85-096 Bydgoszcz, Poland, phone: +48 605 413 908,
Received: 15.02.2016, accepted: 11.07.2016.

416 Advances in Dermatology and Allergology 6, December / 2016

exacerbating inflammatory acne lesions [7]. growth hormone. in the production of sebum induced by nicotine and a re- duction in the production of vitamin E [25]. Comedo. there is a correlation hormone and melanocortins [32]. such of adolescent patients. P acnes nes may be clinically absent in adults [7]. thus stimu- non-inflammatory adult female acne through an increase lating an increase in sebum production [33]. the failure to respond to many oral antibiotic According to last studies most women have both inflam. may be somewhat different in adult female studies. The premenstrual flare of acne Numerous causalities have been proposed to ex. 37]. mainly closed acne than in controls [35]. is also the time of maximum [19]. with a significantly higher level of IGF1 in women with tor in adult acne when retentional lesions. respectively) [30]. normal androgen levels. cosmetics can be a fac. There is a strong correlation between smoking and androgen-sensitive cell’s androgen receptor. December / 2016 417 . 23]. estrogens. Systemic signs of hyperandrogenemia. 20] but in other studies. courses. 16]. Acne has a multifactorial pathogenesis but the andro- genic stimulation of sebaceous glands is always impor- tant [1]. proved by clinical observations that the puberty period. are numerous and localized specifically on stimulates lipogenesis in sebaceous glands by the in- cheeks and the front head [3].2% of women. However. such as sun powders. The degree of adult acne. glucocorticosteroids. Several studies The involvement of IGF1 in pathogenesis of acne was have shown that cosmetics play an aggravating role [16. insulin-like growth the development of clinical disease is mediated by envi. Even in women with is an inherited disease. petrolatum and certain (SREBP1) [32. is caused by an increase in the testosterone to estro- plain post-adolescent acne. Overstimulated SREBP1 increases vegetable oils [27]. can have their natural effect on 24]. treatment [19–21]. 28]. [34]. The isolated mandibular localization is not and level of sebum secretion does not appear to contrib- the most frequent. Probably. adrenocorticotropic ronmental factors [22]. The role of cosmetics in acne growth factor 1 exacerbations remains controversial. acne severity is similar to that observed in adolescence [17]. 56.. Al. as well as others that aggravating factors are sun exposure and smoking [20. However. Some cosmetic ingredi. 39%. the cosmetic factor is not characterized by a peaking level of androgens. the total amount of sebum and enhances the relative Advances in Dermatology and Allergology 6. acnes matory and non-inflammatory acne lesions [7]. According to different acne course. The androgenic hor- between daily stress and acne severity [3. UV causes Relationship between acne and insulin-like inflammation and generates squalene peroxides which are highly comedonic [26]. Insulin-like growth factor 1 comedones. pattern of acne increases with age. It is probable that acne is a result of keratosis of the pilosebaceous duct [2. studies report a correlation between IGF1 masks and creams not tested as being non-comedonic level and acne lesion counts in adult women together [25]. The possible role of diet in the pathogenesis of adult female acne area [7. after 40 years old [3]. suggests that antibiotic resistance of P. 17. duction of sterol response element-binding protein-1 ents elicit comedones: lanolin. Involvement may induce chronic stimulation of the innate immunity in of non-facial skin is also very common. factor 1 (IGF1). 36. is a part of adult acne [19]. diagnosis [7. 7]. 39–85% of women have worsening of acne in acne than in adolescent acne. it is exacerbated response of the pilosebaceous unit to the very probable that the influence of these factors on the normal circulating androgens [29]. insulin and IGF1. The un- Acne is a multifactorial disease which originates in derlying endocrine disorder is rare in female with adult- the pilosebaceous unit. and should be considered the days before menstruation. reported first-degree family members with acne [3]. 15. Moreover. Important mones present in dairy products. as irregular menstrual cycles or hirsutism. the presence of endocrine condition and need further bacterium acnes. insulin. No clear pattern of endocrine abnormalities has Pathogenesis of adult acne been demonstrated in post adolescent acne [15]. This ute to the different characteristics of late onset acne [15]. Other hormones influencing the sebum production are: though sebum excretion is influenced by genetic factors. observational.8% of them androgen medications are effective treatment for acne. The four obvious factors typical onset acne. acnes lesions [3. in comparison to younger adults (53% vs. Nodules can be present in the upper face There is no difference in microbiology in adult acne in as well and may be present without other inflammatory comparison to adolescent acne. some types of cosmetics are more involved sebum production and the peak in the incidence of acne in the development of acne lesions. It is very probable that acne gen ratio in the luteal phase [31]. The different clinical presentation of acne in women Role of hormones suggests involvement of a different mechanism than that observed in the adolescent group [1]. may indicate pathology are: inflammation. The density of P. especially women aged as a specific problem requiring another approach to over 30 years. which contribute to acne physio. Resistant strains of. affecting only 11. 18]. In a multicenter. increased sebum production and hyper. colonization with Propioni. growth shown as an aggravating factor in adult female patients hormone. are circulating naturally. According to Dreno et al. Additionally. oral contraceptives and anti- non-interventional study of 384 women.

leaving rally containing growth hormones and anabolic steroids. associated with limited or no acne [53]. confirmed that gly- sine adenosine (CA) repeats. high 192–194 fre. remove FoxO1 from the nucleus [33. the 192 bp allele and/or 194 bp allele of the IGF1 promoter dairy and sweets also with obesity and low intake of fish. in which he gene has been reported and a functional relationship correlated the Western diet with the disorder [13]. behind a de-repressed (and therefore active and recep- significantly contribute to high IGF1 signaling [11. and increase androgen bio. and acne [12. Western diet-derived metabolic signals are Effect of Western diet on adult acne sensed by the FoxO1 and mTORC1 The link between acne and Western diet. milk and polymorphic microsatellite composed of variable cyto. natu. The reduction of FoxO1 levels in the nucleus. protein synthesis. cell growth. This polymorphism consists of a highly suming diets without refined sugar. quency was observed in patients with severe acne [39]. the adult acne [40]. Anything that sensitizes of acne. acne [41]. induces cell phoinositol-3-kinase and Akt kinase. all of which play a role in the pathogenesis sors in dairy products [33. [54. Elżbieta Kaczmarek-Skamira. found a close association be- most common allele contains 19 repeats. after binding to its receptors. fish and seafood [48. so that it can be stimulated by androgens. low-glycemic-index foods have the expression of SREBP-1c. phos- togen which. 54–56]. which renders glucose-dependent insulin signaling. one needs to Food with a high glycemic index is rapidly absorbed. The number of CA repeats cemic load plays a substantial role in the pathogenesis of ranges between 10 and 24. 42]. have higher circulating IGF-1 levels. He between IGF1 polymorphism and circulating IGF1 levels demonstrated that acne is absent in populations con- and acne severity. Regular consumption of foods with a high glycemic key transcription factor of lipid synthesis SREBP-1c. In opinion. a potent mi. vegetables and nificantly higher in the acne group than in controls. whereas FoxO1 antagonized to acne [32]. enhanced lipogenesis in SEB-1 sebocytes via activation tration. The carriers of tween moderate to severe acne and high intake of milk. hormonal mediators. Recently. If one wishes to open up the androgen receptor lean meats. Insu- index elevates serum insulin concentration. dairy products [14]. have been demonstrated in several studies [10. sen- Insulin and IGF1 augment sebum production. polymorphism in the promoter of the IGF1 published his first article on diet and acne. Barbara Zegarska amount of monounsaturated fatty acids in sebum. Milk proteins. gen receptor will turn on acne [55]. thus regulatory element binding protein-1 (SREBP-1). Kwon et al. Grossi et al. and to the exogenous androgens and androgen precur- availability. This can be done increases serum glucose levels and stimulates increased by phosphorylating the FoxO1 molecules. acnes colonization and biofilm formation transcription factor of lipid biosynthesis [40]. high insulin-/IGF1 signaling (IIS) on metabolic regulations me- calorie intake high glycemic load and high fat and meat diated by forkhead box protein O1 (FoxO1) and mTORC1 intake. and diminishes the signaling stimulates gene transcription. reduced expression of been shown to increase SHBG and reduce androgen lev. (nutrient-sensitive mammalian target of rapamycin com- 40–42]. inflammation. Phosphorylation is accomplished Although milk has a low glycemic index. 51]. with body mass index (BMI) lower than 18. a key influencing P. adrenal androgen synthesis. by regulation the 52]. cell pro- 418 Advances in Dermatology and Allergology 6. FoxO1. In Mahmood and Bowe’s in all mammalian tissues including sebaceous glands. them soluble and capable of leaving the nucleus. Insulin-like growth insulin sensitivity. In Caucasian population. ribo- expression of pro-inflammatory interleukin-8 and sterol some biogenesis. Cordain [38]. grains. Also. tive) androgen receptor. translation. which sup. and it is expressed its exacerbation to diet [43–47]. raises androgen concentration and contributes of the PI3K/Akt pathway. encourage patients with acne to avoid high glycemic the androgen receptor is repressed by the presence of index food and substitute it for fresh fruits. of insulin or IGF1 and is mediated by two enzymes. Conversely. The intake of fish (1 day/week or more).Krystyna Romańska-Gocka.5 kg/m2 were all predominance of 194 allele. Histopathological and immunohistochemical mTORC1 is a nutrient-sensing kinase that regulates evidence that a low glycemic load diet reduces the size growth and metabolism in all eukaryotic cells. it aggravates by a two-step process that is induced by elevated levels acne by increasing the level of IGF1 [50]. December / 2016 . Studies of diverse populations show that indi. stimulate sitizes the androgen receptor to endogenous androgens. defined as Acne aggravation is a result of upstream activation of high consumption of cow’s milk and dairy products. Thus. vegetables. In addition. 49]. mTORC1 of sebaceous glands. Higher SHBG levels have been associated with lower associated with attenuated IIS [56]. plex 1 kinase) [10. Findings of the studies by Smith have illustrated the androgen receptor and then stimulates that andro- the various interactions between high glycemic load diet. viduals with acne commonly attribute the condition or FoxO1 is localized on the nucleus. 54]. 56]. so ultimately andro- proliferation and inhibits apoptosis of keratinocytes and gen sensitivity is enhanced by elevated IGF1 and insulin sebocytes and stimulates sebum production [30. Allele 192–194 was sig. current knowledge on this topic is sufficient to the natural resting state of an androgen-responsive cell. Magdalena Woźniak. SREBP-1 should be expected on a low glycemic load diet els. factor 1 suppresses lipid metabolism. lin-like growth factor 1 induced SREBP-1 expression and presses sex hormone-binding globulin (SHBG) concen. 54].

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