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Baldness Biology
 Male pattern baldness overview
 Female pattern baldness overview
 Male pattern baldness presentation
 Female baldness presentation
 Hair fiber in pattern baldness
 Hair follicles in pattern baldness
 Androgen hormones in men
 Androgen hormones in women
 Androgen receptors in baldness
 5 alpha reductase in baldness
 Inflammation in baldness
 Genetics in pattern baldness
 Diseases associated with baldness
 Pattern baldness in children
Baldness Treatments
 Minoxidil for pattern baldness
 Minoxidil for female baldness
 Minoxidil for male baldness
 Finasteride for male baldness
 Finasteride for female baldness
 Tretinoin for pattern baldness
 Diazoxide for pattern baldness
 Ketoconazole for pattern baldness
 Antiandrogens for pattern baldness
 Contraceptives for female baldness
 Spironolactone for female baldness
 Flutamide for female baldness
 Cyproterone acetate for baldness

Testosterone, 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.
  • Progestins 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 of male 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 it can 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 receptors intarget organs at the same time reducing the activity of skin 5a-reductase in sebaceous glands and hair follicles. Aside from their function stated, Chlormadinone acetate and cyproterone acetate also functions as suppressor of gonadotropin secretion reducing the ovarian and adrenal androgen productions.
  • The release of egg from the ovary in females can be suppressed with oral contraceptive pills, diminishing the production of androgens of the ovaries.

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 in urine.

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.

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