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1. How Hormones Affect Acne
Acne is a skin condition that occurs when your hair follicles become
plugged with oil and dead skin cells. Acne most commonly appears on your
face, neck, chest, back and shoulders. Acne can be distressing and
annoyingly persistent. Acne lesions heal slowly, and when one begins to
resolve, others seem to crop up.
Acne is a condition of the skin that shows up as different types of bumps.
These bumps can be blackheads, whiteheads, pimples, or cysts. Teens get
acne because of the hormonal changes that come with puberty.
Acne formation process and the role of hormones
Excessive sebum production is perhaps the key characteristic of acne.
Sebum production in the skin is handled by cells known as sebocytes. They
are a bit like water balloons in that they gobble fatty acids and grow bigger
and bigger. Once they mature they make their way into the hair canal where
they burst and spill the sebum. Hormones stimulate the growth of
sebocytes and thus sebum production.

2. Blockage of the hair canal (follicle) by
dead skin cells is another key
characteristic of acne. Cells known as
keratinocytes are the most common cells
in the outer layer of the skin. They form
the walls of the hair canal. In a healthy
skin they die and separate and are
pushed out of the skin by the growing hair. In an acne-prone skin this
process goes haywire for two reasons.
• Excess growth of skin cells.
• Condition known as hyperkeratinization. Keratin is a protein that
binds these cells together, and when you have too much of keratin the
bonds between the cells are stronger. So when the cells die they are
more likely to stick together and block the hair canal.
There’s a good reason to believe hormones affect both of those. It’s known
that hormones accelerate the growth of skin cells (thus more dead skin cells
to eliminate), and researchers suspect that hormones up-regulate keratin
levels (and thus hinder separation of dead skin cells). Once the hair canal is
blocked by a sticky mixture of sebum and dead skin cells it starts to swell as
more and more dead skin cells are pushed into the area. Oxygen levels
plummet at the blocked pore, and this creates an ideal environment for P.
Acnes bacteria to thrive.
Inflammation results as the immune system attacks the bacteria in the
blocked pore. Acne patients have markedly stronger inflammatory
response to acne bacteria than people with healthy skin.
To summarize, hormones affect all the primary causes of acne: sebum
production, skin cell growth and separation and inflammation.
The culprits: Insulin, IGF-1 and androgens
Now that we understand how hormones affect acne, let’s see which
hormones are to blame. This discussion could get very complicated very
quickly, as different hormones have somewhat different effects on different

3. cell types in the skin. But we don’t have to
worry about what. So, in the interest of
keeping things simple we can say that the
primary hormones behind acne are:
• Insulin is a storage hormone (among other things). It takes glucose
(sugar) and amino acids (protein) from bloodstream to the cells.
Eating carbohydrates and protein (to lesser extent) will cause insulin
levels to increase.
• Insulin like growth factor 1 (IGF-1) is a growth hormones. It often
goes hand in hand with insulin, so anytime insulin increases so does
IGF-1.
• Androgens are male sex hormones, of which testosterone is the best
known. Other acne-relevant hormones are dihydrotestosterone
(DHT) and dehydroepiandrosterone (DHEAS).
Here’s how these hormones affect Acne:
IGF-1 stimulates the growth of sebocytes and thus increases sebum
production. One study demonstrated correlation between IGF-1 levels and
facial sebum production.
• Make skin cells grow faster
• Stimulate the synthesis of androgens in the testes and ovaries
• Make the skin more sensitive to androgens
So while insulin and IGF-1 act on the skin directly their primary effect on
acne comes from the fact that they multiply the effect of androgens.
Hormones affect all the steps in the acne formation process. They increase
sebum production and skin cell growth, hinder separation of dead skin cells
and increase inflammation.
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