Acne Cream Rosacea
Acne vulgaris (commonly called acne) is a common skin condition, caused by changes in the pilosebaceous units, skin structures consisting of a hair follicle and its associated sebaceous gland via androgen stimulation. It is characterized by noninflammatory follicular papules or comedones and by inflammatory papules, pustules, and nodules in its more severe forms. Acne vulgaris affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back. Severe acne is inflammatory, but acne can also manifest in noninflammatory forms. Acne lesions are commonly referred to as pimples, blemishes, spots, zits, or acne.
Acne is most common during adolescence, affecting more than 85% of teenagers, and frequently continues into adulthood. The cause in adolescence is generally an increase in male sex hormones, which people of both genders accrue during puberty. For most people, acne diminishes over time and tends to disappear—or at the very least decrease—after one reaches one's early twenties. There is, however, no way to predict how long it will take to disappear entirely, and some individuals will continue to suffer well into their thirties, forties and beyond.
The face and upper neck are the most commonly affected, but the chest, back and shoulders may have acne as well. The upper arms can also have acne, but lesions found there are often keratosis pilaris, not acne. Typical acne lesions are comedones, inflammatory papules, pustules and nodules. Some of the large nodules were previously called "cysts" and the term nodulocystic has been used to describe severe cases of inflammatory acne.
Aside from scarring, its main effects are psychological, such as reduced self-esteem and, according to at least one study, depression or suicide. Acne usually appears during adolescence, when people already tend to be most socially insecure. Early and aggressive treatment is therefore advocated by some to lessen the overall impact to individuals.
Terminology
The term acne comes from a corruption of the Greek άκμή (acne in the sense of a skin eruption) in the writings of Aëtius Amidenus. Used by itself, the term "acne" refers to the presence of pustules and papules. The most common form of acne is known as "acne vulgaris", meaning "common acne". Many teenagers get this type of acne. Use of the term "acne vulgaris" implies the presence of comedones.
The term "acne rosacea" is a synonym for rosacea. Chloracne is associated with chlorine toxicity.
Causes of acne
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). Whiteheads are the direct result of skin pores becoming clogged with sebum, a naturally occurring oil, and dead skin cells. In these conditions the naturally occurring largely commensal bacteria Propionibacterium acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules, or nodules) in the dermis around the microcomedo or comedo, which results in redness and may result in scarring or hyperpigmentation.
Primary causes
The root causes of why some people get acne and some do not are 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 often have other members in their family with acne as well. 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 follicular glands to get larger and make more sebum.
- Inflammation, skin irritation or scratching of any sort will activate inflammation. Anti-inflammatories are known to improve acne.
- Stress, through increased output of hormones from the adrenal (stress) glands. While the connection between acne and stress has been debated, scientific research indicates that “increased acne severity” is “significantly associated with increased stress levels.” The National Institutes of Health list stress as a factor that “can cause an acne flare.” A study of adolescents in Singapore “observed a statistically significant positive correlation…between stress levels and severity of acne.”
- Hyperactive sebaceous glands, secondary to the three hormone sources above.
- Accumulation of dead skin cells that block or cover pores.
- Bacteria in the pores. Propionibacterium acnes (P. acnes) is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing.
- Use of anabolic steroids.
- Any medication containing lithium, barbiturates or androgens.
- Exposure to certain chemical compounds. Chloracne is particularly linked to toxic exposure to dioxins, namely Chlorinated dioxins.
- Exposure to halogens. Halogen acne is linked to exposure to halogens (e.g. iodides, chlorides, bromides, fluorides).
- Chronic use of amphetamines or other similar drugs.
Several hormones have been linked to acne: the androgens testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), 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 adult women 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).
Diet
Chocolate
The popular belief that consumption of chocolate can cause acne is not supported by scientific studies. As discussed below, various studies point not to chocolate, but to the high glycemic nature of certain foods containing simple carbohydrates as a cause of acne. Chocolate itself has a low glycemic index
Milk
Recently, three epidemiological studies from the same group of scientists found an 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 insulin-like growth factor 1 (IGF-1)) or even iodine present in cow milk.
Carbohydrates
The long-held belief that there is no link between diets high in refined sugars and processed foods, and acne, has recently been challenged. The previous belief was based on earlier studies (some using chocolate and Coca Cola) that were methodologically flawed. The recent low glycemic-load hypothesis postulates that rapidly digested carbohydrate foods (such as soft drinks, sweets, white bread) produce an overload in blood glucose (hyperglycemia) that stimulates the secretion of insulin, which in turn triggers the release of IGF-1. IGF-1 has direct effects on the pilosebaceous unit (and insulin at high concentrations can also bind to the IGF-1 receptor) and has been shown to stimulate hyperkeratosis and epidermal hyperplasia. These events facilitate acne formation. Sugar consumption might also influence the activity of androgens via a decrease in sex hormone-binding globulin concentration.
In support of this hypothesis, a randomized controlled trial of a low glycemic-load diet improved acne and reduced weight, androgen activity and levels of insulin-like growth factor binding protein-1. High IGF-1 levels and mild insulin resistance (which causes higher levels of insulin) had previously been observed in patients with acne. High levels of insulin and acne are also both features of polycystic ovarian syndrome.
According to this hypothesis, the absence of acne in some non-Westernized societies could be explained by the low glycemic index of these cultures' diets. It is possible that genetic reasons account for there being no acne in these populations, although similar populations (such as South American Indians or Pacific Islanders) 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, or treatment that results in increased insulin sensitivity (like metformin) can significantly alleviate acn
