Acne vulgaris causes
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Acne develops as a result of blockages in follicles. Hyperkeratinization and formation of a plug of keratin and sebum (a microcomedo) is the earliest change. Enlargement of sebaceous glands and an increase in sebum production occur with increased androgen (DHEA-S) production at adrenarche. The microcomedo may enlarge to form an open comedo (blackhead) or closed comedo (whitehead). Increased sebum production provides an environment for the overgrowth of Propionibacterium acnes. Bacterial overgrowth of Propionibacterium acnes can cause inflammation, leading to inflammatory lesions (papules, pustules, or nodules) in the dermis around the microcomedo or comedo, which may result in scarring or hyperpigmentation.
There are many misconceptions and myths about acne.
Exactly why some people get acne and some do not is not fully known. It is known to be partly hereditary. Several factors are known to be linked to acne:
- Family/Genetic history. The tendency to develop acne runs in families. For example, school-age boys with acne have other members of their family with acne. A family history of acne is associated with an earlier occurrence of acne and an increased number of retentional acne lesions. 
- Hormonal activity, such as menstrual cycles and puberty. During puberty, an increase in male sex hormones called androgens cause the glands to get larger and make more sebum. 
- Stress, through increased output of hormones from the adrenal (stress) glands.
- Hyperactive sebaceous glands, secondary to the three hormone sources above.
- Accumulation of dead skin cells.
- Bacteria in the pores, to which the body becomes 'allergic'. Propionibacterium acnes (P. acnes) is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing. 
- Skin irritation or scratching of any sort will activate inflammation.
- Use of anabolic steroids.
- Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
- Exposure to high levels of chlorine compounds, particularly chlorinated dioxins, can cause severe, long-lasting acne, known as Chloracne.
- Exposure to certain drugs and chemical compounds, including narcotics (opiates and opioids), especially when taken intravenously
Several hormones have been linked to acne: the androgens testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), 17-hydroxyprogesterone, as well as insulin-like growth factor 1 (IGF-I). In addition, acne-prone skin has been shown to be insulin resistant.
Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adults may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing's syndrome. Menopause-associated acne occurs as production of the natural anti-acne ovarian hormone estradiol fails at menopause. The lack of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne climacterica in this situation).
A recent study, based on a survey of 47,335 women, did find a positive epidemiological association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese and cream cheese. The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine IGF-I) present in cow milk. Though there is evidence of an association between milk and acne, the exact cause is unclear. Most dermatologists are awaiting confirmatory research linking diet and acne but some support the idea that acne sufferers should experiment with their diets, and refrain from consuming such fare if they find such food affects the severity of their acne.
Seafood often contains relatively high levels of iodine. Iodine is known to make existing acne worse but there is probably not enough to cause an acne outbreak. Still, people who are prone to acne may want to avoid excessive consumption of foods high in iodine.
High Carbohydrates/High GI
It has also been suggested that there is a link between a diet high in refined sugars and other processed foods and acne. The theory is that rapidly digested carbohydrate food such as white bread and refined sugars produces an overload in metabolic glucose that is rapidly converted into the types of fat that can build up in sebaceous glands. According to this hypothesis, the startling absence of acne in non-westernized societies could be explained by the low glycemic index of these cultures' diets. Others have cited possible genetic reasons for there being no acne in these populations, but similar populations shifting to these diets do develop acne. Note also that the populations studied consumed no milk or other dairy products. Further research is necessary to establish whether a reduced consumption of high-glycemic foods (such as soft drinks, sweets, white bread) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons. Avoidance of 'junk food' with its high fat and sugar content is also recommended. On the other hand there is no evidence that fat alone makes skin oilier or acne worse.
The University of Pennsylvania and the US Naval Academy conducted experiments that fed subjects chocolate or a bar with similar amounts of macronutrients (fat, sugar etc.) and found that consumption of chocolate, frequent or not, had no effect on the developing of acne. 
A 2005 systematic review found "surprisingly little evidence exists for the efficacy or lack of efficacy of dietary factors, face-washing and sunlight exposure in the management of acne." A study in November 2006 in Australia gave a 50% reduction in 12 weeks in mild-moderate facial acne by introducing its subjects to a high protein, low GI diet. 
The American Medical Association says chocolate does not contribute to acne. 
A recent study shows that a diet high enough in sugars triggers the liver to convert these sugars into lipid; as a side-effect this stops production of sex hormone binding globulin- a chemical which reduces the level of testosterone in the blood. Since high testosterone levels generally trigger acne, the researchers believe that this can be a cause.
Vitamins A and E
Studies have shown that newly diagnosed acne patients tend to have lower levels of vitamin A circulating in their bloodstream than those that are acne free. In addition people with severe acne also tend to have lower blood levels of vitamin E.
Acne is not caused by dirt. This misconception probably comes from the fact that blackheads look like dirt stuck in the openings of pores. The black color is simply not dirt but compact keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining the duct to separate and flow to the surface in the sebum created there by the body.
Causes by Organ System
|Cardiovascular||No underlying causes|
|Chemical / poisoning||Dioxins, Industrial exposure to halogenated hydrocarbons|
|Dermatologic||Chloracne, Skin irritation or scratching|
|Drug Side Effect||17-hydroxyprogesterone, antiepileptics, bromides, Cidofovir, Dactinomycin, dehydroepiandrosterone sulfate (DHEAS), Desogestrel and Ethinyl Estradiol, dihydrotestosterone (DHT), Eflornithine, Estradiol valerate and estradiol valerate/dienogest, Ethynodiol diacetate and ethinyl estradiol, Fluoxymesterone, gefitinib, Goserelin, iodides, isoniazid, Ivacaftor, leflunomide, lithium, low Vitamin A levels, low Vitamin E levels, methyltestosterone, nabumetone, Nafarelin, Oxandrolone, oxcarbazepine, phenytoin, pramipexole, prednisolone, steroids, testosterone, Chlorides
|Ear Nose Throat||No underlying causes|
|Endocrine||Congenital adrenal hyperplasia, Cushing's syndrome, increased androgen production, insulin-like growth factor 1 (IGF-I), polycystic ovary syndrome, Dioxins|
|Environmental||Increased stress levels|
|Gastroenterologic||No underlying causes|
|Genetic||Genetic, congenital adrenal hyperplasia|
|Hematologic||No underlying causes|
|Iatrogenic||No underlying causes|
|Infectious Disease||Propionibacterium acnes infection, Staphylococcus epidermidis|
|Musculoskeletal / Ortho||No underlying causes|
|Nutritional / Metabolic|
|Obstetric/Gynecologic||Menstrual cycles, oral contraceptives, pregnancy, Dioxins|
|Opthalmologic||No underlying causes|
|Overdose / Toxicity||No underlying causes|
|Psychiatric||No underlying causes|
|Pulmonary||No underlying causes|
|Renal / Electrolyte||No underlying causes|
|Rheum / Immune / Allergy||Dioxins|
|Trauma||No underlying causes|
|Urologic||No underlying causes|
|Miscellaneous||No underlying causes|
Causes in Alphabetical Order
- A diet high in glycemic index foods and dairy products
- Congenital adrenal hyperplasia
- Consumption of cottage cheese and cream cheese
- Consumption of partially skimmed milk
- Cosmetic agents
- Cushing's syndrome
- Dehydroepiandrosterone sulfate (DHEAS)
- Desogestrel and Ethinyl Estradiol
- Dihydrotestosterone (DHT)
- Increased androgen production
- Increased stress levels
- Industrial exposure to halogenated hydrocarbons
- Insulin-like growth factor 1 (IGF-I)
- Low Vitamin A levels
- Low Vitamin E levels
- Menstrual cycles
- Oral contraceptives
- Polycystic ovary syndrome
- Propionibacterium acnes infection
- Skin irritation or scratching
- Staphylococcus epidermidis
- Simpson, Nicholas B.; Cunliffe, William J. (2004). "Disorders of the sebaceous glands". In Burns, Tony; Breathnach, Stephen; Cox, Neil; Griffiths, Christopher. Rook's textbook of dermatology (7th ed. ed.). Malden, Mass.: Blackwell Science. pp. pp. 43.1-75. ISBN 0-632-06429-3.
- F. Ballangera, P. Baudrya, J.M. N'Guyenb, A. Khammaria, B. Dréno Heredity: A Prognostic Factor for Acne 5/2/2005
- US Dept Health and Human Services January 2005
- National Guideline Clearinghouse 11/12/2007
- Adebamowo CA, Spiegelman D, Danby FW, Frazier AL, Willett WC, Holmes MD (2005). "High school dietary dairy intake and teenage acne". J Am Acad Dermatol. 52 (2): 207–14. PMID 15692464.
- Fries JH (1978). "Chocolate: a review of published reports of allergic and other deleterious effects, real or presumed". Ann Allergy. 41 (4): 195–207. PMID 152075.
- Danby FW (2007). "Acne and iodine: Reply". J Am Acad Dermatol. 56 (1): 164–5. PMID 17190637.
- Loren Cordain, et al. "Acne Vulgaris - A Disease of Western Civilization" Arch Dermatol. 2002;138:1584-1590. Observation
- Smith R, Mann N, Makelainen H, Braue A, Varigos G (2004). "The effect of short-term altered macronutrient status on acne vulgaris and biochemical markers of insulin sensitivity". Asia Pac J Clin Nutr. 13 (Suppl): S67. PMID 15294556.
- Anderson, Laurence. 2006. Looking Good, the Australian guide to skin care, cosmetic medicine and cosmetic surgery. AMPCo. Sydney. ISBN 0-85557-044-X.
- "Sweet news about chocolate". usaweekend.com. 1998-06-05. Retrieved 2007-05-27.
- Magin P, Pond D, Smith W, Watson A (2005). "A systematic review of the evidence for 'myths and misconceptions' in acne management: diet, face-washing and sunlight". Fam Pract. 22 (1): 62–70. PMID 15644386.
- RMIT acne study
- JAMA Patient Page - Acne
- Naweko San-Joyz (April 11, 2007). "How Does Vitamin A Prevent Acne Outbreaks?". American Chronical. Retrieved 2007-09-17.
- El-Akawi Z, Abdel-Latif N, Abdul-Razzak K (2006). "Does the plasma level of vitamins A and E affect acne condition?". Clin. Exp. Dermatol. 31 (3): 430–4. doi:10.1111/j.1365-2230.2006.02106.x. PMID 16681594.