although considered a male hormone, is also present in women. It is estimated
that only 30% of testosterone in women is produced
in the ovary while the rest is derived in the transformation of adrenal
androgen precursors like dehydro epiandrosterone (DHEA) andandrostenedione
that wanes proportionally with age. The exact roles played on pattern baldness in women of the over production of androgen, androgen activity,
and androgen receptors, are still unclear.
The enzyme that is responsible for the metabolism of testosterone into
Dihydrotestosterone of DHT is the5 -reductase. DHT binds itself in the
androgen receptor with five times tenacity than that of testosterone and
DHT is more potent than testosterone in its ability to downstream activation.
The only logical way to treat pattern baldness is to block the involvements
of androgen receptors and 5a-reductase. Several agents had been used to
block these mechanisms which resulted in varying success rates in men
and women. The studies eventually lead to the development with a combination
of an anti-androgenic progestogen with estrogen - an agent that produces
both androgen receptor antagonism and decrease skin 5a-reductase activity.
The major advantage of this combination over the treatment regimens in
women is its contraceptive effect that safeguards the possibility of feminization
of a male fetus.
Different mechanisms by which contraceptive pills block androgens
- Progesterone is a potent inhibitor of 5 -Reductase activity and androgen
receptor binding. Birth control pills can be used to treat pattern baldness in women since they are known to inhibit the production of
androgens in the woman’s ovaries, including testosterone.
that are found in oral contraceptives in the market have a closer
structural relationship in testosterone and estrogen than
it is with progesterone. (Progestins are the synthetic form of the
female sex hormone called progesterone). These pills induce developments
characteristics (androgenic), female characteristics (estrogenic),
or estrogen-inhibiting activities. Progestin was found to act as antagonist
or agonist depending on its inherent androgenic properties, and
easily compete with testosterone and DHT for androgen-receptor binding.
- Some potent orally active progestogens are Chlormadinone acetate,
cyproterone acetate and dienogest – all of which has antiandrogenic
instead of partial androgenic activity. They block the androgen
organs at the same time reducing the activity of skin 5a-reductase
in sebaceous glands and hair follicles. Aside from their function
Chlormadinone acetate and cyproterone acetate also functions as
suppressor of gonadotropin secretion reducing the ovarian and adrenal
- The release of egg from the ovary in females can
be suppressed with oral contraceptive pills, diminishing the production
Studies on levels of sex-hormone binding globulin or SHBG (a glycoprotein
that is synthesized by the liver and is the most important protein for
androgen binding) shows that it inversely co-relates with the severity
of the alopecia. The binding affinities differ in androgens and estradiol,
although the more potent ones are bound in the plasma to SBHG, example
of which is the affinity of androgens which is three times stronger in
DHT and nine times stronger in estradiol. Elevation in testosterone level
was found to cause SHBG synthesis to increase activity of 5 -Reductase
and decrease enzymes that are responsible for the metabolism of testosterone
to DHT. Since estrogens decreases the amount of free testosterone as it
increases SHBG, oral contraceptive pills with estrogen make the sex hormones
unavailable for conversion to DHT.
Combined oral contraceptive pills
Combination of estrogen and progestin in a combined oral contraceptive
(COC) pills may help decrease the central androgen production in the adrenals
and ovaries. The estrogen component found in the formulations of these
COC pills is usually ethinyl estradiol in various dosages as the progestin
varies widely with its androgenic capabilities from pill to pill.
The action of COC causes a sharp decrease in the adrenal androgen production
very much like those seen with estrogen alone. These COC increases the
plasma level of 17-hydroxycorticosteroid, decreases the excretion rate
of cortisol, and increases the plasma levels of the corticosteroid binding
protein called transcortin. Cortisol is a steroid hormone that is released
from the adrenal cortex in response to adrenocorticotrophic hormone (ACTH),
after which the liver and the other tissues metabolizes cortisol to inactivate
products like 17-hydroxycorticosteroids, which are then excreted from
the body by urine. Adrenal function is indexed through the excreted 17-hydroxycorticosteroids
COC pills that contains 2mg of chlormadinone acetate or cyproterone acetate
plus 30 or 35µg of ethinyl estradiol improved the resolution of
seborrhoea in 80 percent of users; improved acne condition in 59–70
percent; treated hirsutism in 36 percent; and advanced improvements on
androgen-related alopecia in up to 86 percent.
Side effects of oral contraceptive pills
Results on experiments suggests that there are no specific adverse effects
for using oral contraceptive pills although some women complained of headaches,
breast tenderness and nausea. Oral contraceptive pills are generally tolerated
and these drugs have no clinically relevant effects on metabolic functions,
liver functions, and bodyweight, and have rare effects on mood and libido.
The possibility of the involvement of contraceptive pills in increasing
the risk of breast cancer is still a controversial issue.
Some authors opined that COC pills have potential serious side effects
in the body like venous thromboembolism (occlusion of a blood vessel due
to a fibrinous clot), stroke, and myocardial infarction (heart attack).
High doses of ethinyl estradiol promote high risks of these side effects.
Individuals with hypertension, diabetes, and migraine headaches and in
individuals who smoke cigarettes have higher probability of contracting
stroke and myocardial infarctions.