Diet in the prevention of hidradenitis suppurativa (acne inversa).

Full control of hidradenitis suppurativa requires the prevention of new lesions. These appear to be induced by a complex series of hormonally driven molecular activities that lead to obstruction of the follicular duct, rupture and destruction of the sebaceous glands, the development of deep dermal sinuses that subsequently rupture to the surface, and production of an invasive subcutaneous mass that is resistant to medical therapy. Preliminary observations suggest that the use of a healthy and fully natural zero dairy and low glycemic-load diet may provide relief from progression of the lesions and possibly prevention of new lesions, even when medications fail.

New and traditional surgical approaches to hidradenitis suppurativa.

When the prevention of new lesions fails and when medical therapy of established and growing lesions is ineffective, surgery is the accepted method of dealing with hidradenitis suppurativa/acne inversa. The rationale and preferred techniques of mini-unroofing using a biopsy punch, deroofing using scissors, electrosurgery or laser, and classical wide excision and closure are discussed. The situation in which incision and drainage is considered for temporary pain relief would be best considered an opportunity for deroofing, as illustrated in the accompanying online videos.

Current concepts in the management of hidradenitis suppurativa in children.

PURPOSE OF REVIEW: This review is intended to provide the background aetiopathogenetic framework upon which management of this disorder can be based, particularly with relation to new concepts of the pathogenesis of the disorder. The emphasis is on the prevention of the disorder's full expression by addressing the metabolic changes that drive the underlying structural damage and the immune system's subsequent reaction to this damage. RECENT FINDINGS: The mechanism by which dietary factors impact on this disease are elucidated, the anatomic defect suspected to be responsible for the disorder is introduced, and an updated flow sheet describing and linking the clinicopathological changes recently described are provided. SUMMARY: Recent work in the understanding of the induction and evolution of the lesions provides a background upon which the preventive regimen and both the medical and surgical approaches can be effectively based.

Hidradenitis suppurativa.

Hidradenitis suppurativa is a chronic relapsing disorder of the folliculopilosebaceous units (FPSUs). Its negative impact on quality of life is extreme, mainly due to the lack of early recognition, accurate diagnosis, and appropriate management. The support structure of the FPSUs is defective. Under the influence of endogenous reproductive hormones, exogenous hormones, androgens and their precursors in dairy products, and other dietary factors, the follicular unit is plugged and distended by retained keratin. Friction, shearing forces, and pressure lead to rupture and leakage of the ductal contents from the weakened FPSU, causing an inflammatory reaction mediated mainly by the innate immune system. Therapy requires patient comprehension and cooperation, counseling, aggressive hormonal and dietary modification, avoidance of the trauma that leads to rupture, active multimodal anti-inflammatory therapy, and early unroofing and debridement. The full therapeutic program is needed to avoid the aggressive surgery required if the condition is not diagnosed early and managed appropriately.

Turning acne on/off via mTORC1.

Over the past 10 years, the increase in comprehension of the mechanisms behind acne has been truly exponential. Starting with the ethnological work of Cordain, accelerated by the epidemiological work of Adebamowo, supported by the clinical trials of Smith and Mann, Kwon, DiLandro and others, the interface of diet and acne is coming into focus. Melnik now presents an exceptional pair of papers that illustrate for dermatologists what translational research is all about. The Western diet, the role of dairy, FoxO1 and mTORC1, the interplay of agonists and antagonists, therapeutics present and future - the jigsaw puzzle is coming together.

Acne: Diet and acnegenesis.

Acne is a manifestation of hormonal overstimulation of the pilosebaceous units of genetically susceptible individuals. Endogenous reproductive and growth hormones, exogenous reproductive hormones, insulin and endogenous insulin-like growth hormone-1, sourced from and stimulated by dairy and high glycemic load foods, all appear to contribute to this overstimulation. A postulated molecular mechanism linking food and acne is reported and integrated into the clinical picture.

Nutrition and acne.

There are significant data supporting the role of diet in acne. Our Western diet includes many dairy sources containing hormones.. The natural function of milk being to stimulate growth, it contains anabolic steroids as well as true growth hormones and other growth factors. The presence of 5α-pregnanedione, 5α-androstanedione, and other precursors of 5α-dihydrotestosterone add to the potency of milk as a stimulant of acne. In addition, foods with significant sugar content and other carbohydrates yielding high glycemic loads affect serum insulin and insulin-like growth factor-1 levels, both of which promote increased production of available androgens and the subsequent development of acne.

Hidradenitis suppurativa.

Hidradenitis suppurativa (HS) is a chronic, inflammatory, scarring condition involving the intertriginous skin of the axillary, inguinal, inframammary, genital, and perineal areas of the body. It is also referred to as acne inversa and Verneuil disease. Follicular occlusion is the primary event in HS. It is now accepted that the first pathogenetic change is in the pilosebaceous follicular ducts, like acne, and so there has been a move to rename this disorder acne inversa. Despite the legitimate argument that hidradenitis suppurativa is a misnomer, the term has become generally accepted.

Nutrition and aging skin: sugar and glycation.

The effect of sugars on aging skin is governed by the simple act of covalently cross-linking two collagen fibers, which renders both of them incapable of easy repair. Glucose and fructose link the amino acids present in the collagen and elastin that support the dermis, producing advanced glycation end products or "AGEs." This process is accelerated in all body tissues when sugar is elevated and is further stimulated by ultraviolet light in the skin. The effect on vascular, renal, retinal, coronary, and cutaneous tissues is being defined, as are methods of reducing the glycation load through careful diet and use of supplements.

New developments in our understanding of acne pathogenesis and treatment.

Interest in sebaceous gland physiology and its diseases is rapidly increasing. We provide a summarized update of the current knowledge of the pathobiology of acne vulgaris and new treatment concepts that have emerged in the last 3 years (2005-2008). We have tried to answer questions arising from the exploration of sebaceous gland biology, hormonal factors, hyperkeratinization, role of bacteria, sebum, nutrition, cytokines and toll-like receptors (TLRs). Sebaceous glands play an important role as active participants in the innate immunity of the skin. They produce neuropeptides, excrete antimicrobial peptides and exhibit characteristics of stem cells. Androgens affect sebocytes and infundibular keratinocytes in a complex manner influencing cellular differentiation, proliferation, lipogenesis and comedogenesis. Retention hyperkeratosis in closed comedones and inflammatory papules is attributable to a disorder of terminal keratinocyte differentiation. Propionibacterium acnes, by acting on TLR-2, may stimulate the secretion of cytokines, such as interleukin (IL)-6 and IL-8 by follicular keratinocytes and IL-8 and -12 in macrophages, giving rise to inflammation. Certain P. acnes species may induce an immunological reaction by stimulating the production of sebocyte and keratinocyte antimicrobial peptides, which play an important role in the innate immunity of the follicle. Qualitative changes of sebum lipids induce alteration of keratinocyte differentiation and induce IL-1 secretion, contributing to the development of follicular hyperkeratosis. High glycemic load food and milk may induce increased tissue levels of 5alpha-dihydrotestosterone. These new aspects of acne pathogenesis lead to the considerations of possible customized therapeutic regimens. Current research is expected to lead to innovative treatments in the near future.

Acne, dairy and cancer: The 5alpha-P link.

A potent link to dairy seems to exist for three hormone-responsive glands. Acne, breast cancer and prostate cancer have all been linked epidemiologically to dairy intake. Although mechanisms postulated here remain to be accurately defined, the likely link involves Insulin-like Growth Factor-1 as a general stimulant, synergized by the steroid hormones present in milk. The IGF-1 may be either absorbed from milk, or stimulated by its ingestion, or both. The 5alpha-reduced compound 5alpha-pregnanedione (5alpha-P) present in milk is a direct precursor of dihydrotestosterone and may act through that pathway in prostate cancer, but 5alpha-P has also recently been shown to be capable of inducing estrogen receptors in breast cancer cells, upregulating cancer cells' sensitivity to estrogen. The introduction of exogenous hormones and growth factors into tissues that have not evolved defensive feedback inhibition of their corresponding endogenous sources is postulated as a direct stimulatory threat to these organ systems, whether for hyperplasia or neoplasia.

Diet and acne.

Acne is caused by the action of dihydrotestosterone, derived from endogenous and exogenous precursors, likely acting synergistically with insulin-like growth factor-1. These sources and interactions are discussed. Both a mechanism of action and recommended dietary changes that limit ingestion and production of these hormones are proposed.

Milk consumption and acne in teenaged boys.

OBJECTIVE: We sought to examine the association between dietary dairy intake and teenaged acne among boys. METHODS: This was a prospective cohort study. We studied 4273 boys, members of a prospective cohort study of youths and of lifestyle factors, who reported dietary intake on up to 3 food frequency questionnaires from 1996 to 1998 and teenaged acne in 1999. We computed multivariate prevalence ratios and 95% confidence intervals for acne. RESULTS: After adjusting for age at baseline, height, and energy intake, the multivariate prevalence ratios (95% confidence interval; P value for test of trend) for acne comparing highest (>2 servings/d) with lowest (<1/wk) intake categories in 1996 were 1.16 (1.01, 1.34; 0.77) for total milk, 1.10 (0.94, 1.28; 0.83) for whole/2% milk, 1.17 (0.99, 1.39; 0.08) for low-fat (1%) milk, and 1.19 (1.01, 1.40; 0.02) for skim milk. LIMITATIONS: Not all members of the cohort responded to the questionnaire. Acne assessment was by self-report and boys whose symptoms might have been part of an underlying disorder were not excluded. We did not adjust for steroid use and other lifestyle factors that may affect occurrence of acne. CONCLUSION: We found a positive association between intake of skim milk and acne. This finding suggests that skim milk contains hormonal constituents, or factors that influence endogenous hormones, in sufficient quantities to have biological effects in consumers.