Androgenic hair loss in women
Androgenic alopecia in women


Androgenic alopecia is an androgen dependant type of hair loss that involves recession of hair at the temples to form a characteristic “M” patter.  Hair also thins at the crown area near the top of the head.  This type of hair loss can range from mild to severe.  The number of hair follicles remain the same, though some may be dormant while androgenic alopecia is active.

In women, the extent of hair loss is generally less than in men.   In women, hair tends to become thinner all over the head but often there is still a clear pattern of hair loss evident at the temple and crown.

It has been assumed that the hormonal basis for androgenic alopecia is similar in women and men, though the hyperandrogenic symptoms may not correlate with high levels of androgens in the body [1].

Androgenic alopecia in men is associated with cardiovascular disease, insulin resistants and a higher body mass index (BMI).  In women, this form of hair loss is linked to polycystic ovary syndrome (PCOS) and endometriosis.


Women normally notice hair thinning over the frontal area first, the rest of the scalp becomes more visible thereafter. Over time, the thinning usually develops in a patterned fashion.  The most pronounced thinning is seen over the frontal and parietal scalp area, and greater hair density is found over the occipital scalp.

Women typically retain a rim of hair along the frontal hairline, even when the scalp is visible behind the hairline.  Miniaturised hairs (the shorter and thinner hairs of various lengths and diameter) are the hallmark of androgenic alopecia and result from the shortening of growth phase and reduction in hair fibre size.

Increased spacing between hairs makes the central parting appear wider over the frontal scalp compared to the occipital scalp.  Less commonly, hair density appears normal at the scalp (proximal) area, but the hair no longer grows to its previous length, resulting in wispy ends; in this case, the shortening of the anagen phase progresses more rapidly than the reduction in thickness of the hair fibre.

The patient may note that her ‘ponytail’ is smaller in girth and the hair is cut to shorter lengths to give a fuller appearance. She may feel that her hair does not grow at all.

Female hair loss

The Savin scale. The Savin scale measures overall thinning of the crown scalp, and consists of 8 crown density images reflecting a range from no hair loss (stage I-1), to mild (stages I-2, I-3, I-4 to severe hair loss (stages II-1, II-2, III, advanced).


Blood tests are used to identify whether the patient is suffering from true androgenic hair loss or female pattern hair loss.  Female pattern hair loss presents with the same clinical features as androgenic alopecia, but there is not always evidence of elevated androgens in the serum.  Blood tests do not measure the level of testosterone upregulated to DHT, so DHEA can be evaluated with testosterone.

Free / Total testosterone. Androgenic alopecia implies a dependence on increased expression of androgens, but female androgenic alopecia does not require an absolute elevation of androgens in the blood.  The majority of women with androgenic alopecia have no clinical or biochemical evidence of elevated androgens.  However, a subset of women with androgenic alopecia do, and women with concomitant symptoms of hirsutism (excess body and facial hair), adult acne, and irregular periods, should be screened for excess testosterone.

Dehydroepiandrosterone sulfate. This test is often done for women who show signs of having excess male hormones. Some of these signs are hair loss, excess facial and body hair growth, oily skin, acne, irregular periods, or problems becoming pregnant.

Sex Hormone-Binding Globulin (SHBG). Most testosterone is bound to sex hormone-binding globulin protein and is not active. If you have a low level of sex hormone-binding globulin, you may have a high level of free testosterone in your bloodstream.  Low levels of SHBG are associated with obesity, stress and high levels of cortisol.

Ferritin / Serum Iron / TIBC.  Iron deficiency contributes to hair loss and can be identified by two methods: serum ferritin or serum iron, and TIBC (total iron binding capacity).  Low ferritin levels are diagnostic of an iron deficiency.  However, low iron stores in patients with chronic disease may not be detected as ferritin is an acute phase reactant, and active inflammatory disorders and infections increases iron storage.  The elevation in these situations give a false reading of normal or high iron stores. Iron deficiency is associated with low serum iron, and a relatively high TIBC, with a low percentage of saturation.

Vitamin D. Androgenic alopecia is associated with low levels of vitamin D and other fat-soluble vitamins.  A higher level of vitamin D receptors are found in patients with low levels of vitamin D. Although vitamin D is commonly referred to as a ‘vitamin’ it is a biological response-modifying steroid hormone  and now understood to be one of the most influential steroid hormones in the body.  Vitamin D has emerged as the second most important nutrient (after iron) in healthy body functioning.

Cholesterol / Triglycerides. An abnormal lipid profile can contribute to hair loss.  Cholesterol helps to repair and heal your body; you will produce more if there is a great deal of inflammation occurring in your body. So, any factor that would raise inflammation, can raise your cholesterol too. A high level of triglycerides can indicate poor sugar regulation, or the start of insulin resistance.  Cholesterol is a precursor to testosterone and oestrogen, so high levels of cholesterol will increase levels of DHT.


Most women with androgenic hair loss show no other clinical or biochemical evidence of androgen excess. The family history of women with androgenic alopecia is not as straightforward as those of men with similar pattern hair loss.  Regardless of the origin, the hair follicle’s sensitivity and follicular changes in androgenic alopecia in males and females appear the same.  There is a final common pathway of follicular miniaturisation.

This includes:

  • Progressive reduction of the time the hair follicle spends in anagen phase.
  • A prolonged period before anagen starts after the hair has been shed.
  • Hair follicles gradually reducing production of terminal hairs resulting in slow growing hair and less scalp coverage.

Excess androgens are synonymous with excessive secretion of androgens; indirect evidence of the existence of hirsutism (excess hair on face and body), severe acne, irregular menstrual cycles, and / or high serum testosterone, free testosterone, or DHEAS.  Less than 40% of women with androgenic alopecia display hyperandrogenism in blood tests.


Androgenic alopecia responds well to a combination of hair loss therapy that includes the use of topical phytoestrogens and minoxidil and nutritional therapy (zinc, B complex vitamins, antioxidants and fatty acids, iron).  Depending on the severity of hair loss, graded by the Savin scale, hair loss typically takes around 6 months to respond to therapy.


  1. Norwood OT. Incidence of female androgenetic alopecia (female pattern alopecia). Dermatologic Surgery. 2001 Jan;27(1):53-4.
  2. Futterweit W, Dunaif A, Yeh HC, Kingsley P. The prevalence of hyperandrogenism in 109 consecutive female patients with diffuse alopecia. Journal of the American Academy of Dermatology. 1988 Nov 1;19(5):831-6.