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Introduction
Acne is a common skin disorder affecting the face, neck, chest
and back affecting 70% to 80% of young adults. Though not physically
disabling, acne can cause severe emotional stress due to permanent
facial scarring and due to its persistence. Additionally, it occurs
during adolescence - a difficult period of growth and development
for any young adult. Appropriate treatment can improve the lives
of affected individuals dramatically.
The primary lesions of acne are the comedones. Comedones are
plugs of sebum and keratin lodged in the follicular ducts. These
comedones are non-inflammatory, but if they rupture the follicular
wall, an inflammatory reaction to the sebum produces papules,
pustules and cysts. The anaerobic bacteria, propionibacteria,
inhabiting the microenvironment of the follicle, also promote
non-inflammatory lesions into inflammatory lesions. The immune
system recognizes the bacteria in the ruptured hair follicles
and responds to them to try and destroy the bacteria. These inflammatory
lesions may produce scars if the inflammation is intense enough.
The question is, what causes the increased production of sebum
and why does this eventually lead to acne? Several factors may
be involved.
Androgens
Numerous studies have shown that androgens are a major factor
in the production of acne. Most androgens are produced by the
gonads and adrenal glands, but some are also produced locally
within the sebaceous glands from the adrenal precursor hormone
called DHEA.
Though the cellular or molecular mechanism by which androgens
stimulate sebum production is not fully understood it is well
known that major androgens, like testosterone, interact with the
sebaceous glands through androgen receptors. These androgen receptors
are located on cells of the basal layer of the sebaceous glands
and the outer root sheath keratinocytes of the hair follicle.
The important role of androgens in stimulating sebum production
is shown by the following five pieces of clinical evidence:
- The development of early acne in the prepubertal period occurs
with higher serum levels of DHEAS, a precursor of testosterone.
- Androgen-insensitive
subjects lacking functional androgen receptors do not produce
sebum and do not develop acne.
- Androgen producing tumors of
the ovary or adrenal glands are often associated with acne.
- Systemic
administration of testosterone and DHEAS increases the size
and secretion of sebaceous glands.
- Severe acne is often associated
with higher serum androgen levels.
It is therefore clear that hormones are involved in acne development.
Stress induced acne
In women, onset of acne coincides with menarche but its prevalence
varies widely. An interesting development has been the identification
of low grade persistent acne in women over 25 years of age, some
in their forties. This is believed to be due to stress induced
secretion of adrenal androgens. Emotional stress has been anecdotally
linked to acne though an objective assessment has been lacking
until recently. The latest studies on stress induced acne do show
a statistical correlation.
Growth hormones in acne
Growth hormone is produced by the pituitary glands and acts on
the liver and peripheral tissues to stimulate the production of
insulin growth factor (IGF) also known as somatomedians. IGF comes
in two forms, the more prevalent IGF-1 and also IGF-2. IGF is
a known promoter of keratinocyte activity. IGF-1 can promote increased
sebaceous gland oil production. Because of this property, growth
hormone may be involved in acne development. Acne is most widespread
during adolescence when growth hormone secretion and IGF-1 serum
levels are at their highest. Also, IGF-1 molecules can be produced
locally within the skin where they can interact with the IGF receptors
on the sebaceous glands to increase sebum production. Consequently,
the growth that occurs in teens may contribute to the development
of acne
Diet as a cause of acne
Diet as a cause of acne has traditionally been dismissed as myth.
However, the near absence of acne in non-westernized cultures
and the presence of acne in western or westernized cultures suggests
that diet and the environment could be causes. One study suggests
that the high glycemic diets of the West could cause acne by producing
hyperinsulinemic states.
Genetic factors
Another factor, facial oiliness or seborrhea, is believed to
be a pre-condition for acne. The degree of oiliness that an individual
experiences may be partly due to their genetic make up. It seems
likely that some genes code for a higher level of sebaceous gland
activity and oil production. Genes may also play a role in the
nature of the sebum that is produced. Some genes code for higher
levels of cholesterol production. Cholesterol is a relatively
sticky molecule. When there is more cholesterol produced by the
sebaceous glands, the oils and dead cells from the hair follicle
canal are more likely to stick together and form the nucleus of
a sebum plug.
Seborrhea most commonly occurs on the face, but with the exception
of isotretinoin, no other drug is able to inhibit sebum production.
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