Female pattern hair loss not always Genetic

As a Trichologist specialising in female hair loss since 1999, I’ve treated thousands of women across the world for thinning scalp hair density.

The trends I’ve observed in many women has led me to believe – despite prevailing medical opinion – there are two forms of so-called ‘genetic, hereditary or pattern’ thinning in females.

‘True ‘genetically inherited female androgenic alopecia – or female pattern thinning – is manageable but not ‘curable’. Put simply – this is because female pattern thinning is an ‘inherited’ condition from the mother – so there’s nothing’ to cure.

Genetically inherited female androgenic alopecia is an autosomal recessive hereditary trait affecting numbers of women within an extended family. The woman will recount a family history of her mother, grandmother/s, sisters, aunts or female cousins with a comparable thinning hair problem. These women tend to exhibit the condition after puberty or in their early twenties, particularly following childbirth.

It’s long been known that female pattern hair loss is a similar but clinically separate condition from that of male genetic balding. Whilst the hormonal conversion of Dihydrotestosterone (DHT) in ‘androgen sensitive’* hair follicles across the top of the scalp occurs in both males & females – the hair follicles in women are randomly affected – thus thinning of the scalp hair occurs rather than complete baldness. Unlike males, afflicted women also generally retain their frontal hairline margin (albeit with some hairline recession).

The majority of women presenting with pattern hair thinning exhibit (what I term) ‘acquired’ pattern scalp hair thinning – the result of metabolic homeostasis compensation mechanisms by the body, from cascading metabolic/hormonal and sometimes nutritional disturbance within a number of body systems.

These women may be any age & relating a common history of lethargy; body skin, scalp & hair may be dry OR oily –sometimes with T-zone acne ‘breakouts; menstrual difficulties, pre-menstrual mood disorders, weight gain, diminished libido, sleep disturbance or headaches. Thyroid function testing** and/or salivary hormone profiles (SHP) will often be ‘outside range’, with elevated Testosterone (TT) and/or DHEA – the Adrenal gland endeavoring to stimulate thyroid function.

A dual presentation of ‘pattern’ AND ‘diffuse’ scalp hair density thinning will be evident in some women.

Careful evaluation of the Client’s history and associated symptoms should be undertaken to exclude diffuse Alopecia areata – which presents in a similar way but is a condition of autoimmune origin.

The research of Dr. John Lee –Australia’s most prolific thyroid researcher – advocates that in pre-menopausal women particularly – the geneses of these problems are frequently found in deficient iron storage (termed ‘ferritin’) or other nutrient disturbance that ‘drive’ metabolic functioning.
Iron, Vitamin D, Iodine, Zinc & Selenium – are some of the most essential nutrients for metabolic function.
Adequate iron storage is essential to ‘furnace’ intracellular energy output, from which adenosine tri-phosphate (ATP) is produced. To generate sufficient & quality ATP, a Ferritin of 120-150ug/L (within a usual reference range of 20-300ug/L) is essential for optimal metabolic & liver detoxification functioning in a younger adult person***.

Both metabolic (thyroid) activity & Phase II liver detoxification pathways are ATP dependant.

An ATP-deprived liver is ‘sluggish’ & readily overloaded when a woman is taking hormone therapy (contraceptive or HRT medication), consumes some daily alcohol, caffeine or nicotine. These combined substances occupy the total capacity of the liver’s Phase I detoxification pathway, & the liver’s ability to process other substances such as the body’s own hormone by-products or other toxins is progressively impaired – ultimately resulting hormonal disturbance & cellular toxicity.

Iron ‘switches on’ on ALL other body systems + functions – hence its fundamental importance (Lee: 2006).

Older post-menopausal women (>65+) will often show a decline in overall scalp hair density as well as pattern thinning. This is in part due to the ageing process and post-menopausal decline in female and metabolic (thyroid/adrenal) hormones. They are frequently Vitamin D (or other nutrient) deficient and a blood pathology baseline should always be assessed.

A variant of ‘pattern’ thinning sometimes seen in Women of post-menopausal age**** is frontal hairline margin regression; usually accompanied by bilateral recession at the temples – with or without fibrosing (a form of skin ‘scarring’ which progressively destroys underlying skin appendages – hair follicles, sweat + oil glands). This condition may be of autoimmune origin.

Females (and males) of different racial or ethnic groups may show variations in presentation or ‘focus’ of thinning: Anglo-Saxon females mostly reveal thinning from behind the frontal hairline margin.

Women of Asian heritage will have decreased hair density across the top of the scalp as multiple hair shaft-producing follicles limit the number of hair shafts produced. Androgenic thinning in others may be more apparent around the crown or as bilateral recession at the temples.

In the very complex way body systems influence & compensate for each other, weaker male hormones – partly produced in the adrenal glands – are up-converted to Testosterone (TT), and used as an auxiliary ‘fuel source’ to ATP in an attempt to stimulate thyroid-metabolic function. In pattern thinning, some of this Testosterone is further up-converted to DHT which has a miniaturising influence on ‘androgen-sensitive’ hair follicles across the top of the scalp.

There are more than 20 known reasons why the female body will reveal increased Testosterone levels. (ARL/Healthscope Laboratories: 2005)

Compensatory Adrenal output and lowered TT production can be achieved by providing the body with the basic nutrients (Iron, Vitamin D, Iodine, and Zinc) and restore metabolic homeostasis. In some individuals medication to support the thyroid-adrenal axis/ other hormonal pathways may also be required.
Latest research has shown a significant catalyst for DHT-induced hair loss is Transforming Factor Beta 1. TGF Beta 1 induces follicle cell apoptosis (cell death) and premature scalp hair balding. The amino acid Taurine is a potent inhibitor of Transforming Factor Beta 1 and an especially effective biologic ‘anti-ageing’ amino acid at therapeutic doses (600mg). It provides anti-fibrotic properties; helps prevent macular degeneration and – in the treatment of ‘pattern’ hair loss in both sexes – is a TGF Beta 1 conversion blocker.

Increased facial or body hair (hypertrichosis) often accompanies pattern scalp hair thinning because follicles across the top of the scalp are androgen sensitive – causing follicle miniaturisation & hair shaft thinning (vellus hairs), whilst facial/body hair is male hormone (androgen) dependant – leading to increased hair growth in these areas. Other symptoms may include acne, oily/greasy T-zone or scalp, mood disturbance – especially irritability and menstrual irregularities (as previously mentioned).

‘Pattern’ thinning may also present from the hormonal consequences of being overweight, refined food diets and decreasing physical activity*****. At the heart of this is elevated blood Insulin levels (hyperinsulinaemia) – and its disordering effects on Oestrogen-Testosterone ‘aromatization’; hormone carrier proteins, and the delicate balance of hormones within the body. Specific blood and/or Saliva hormone testing should be done to evaluate these areas.

Finally, stress as a cause for hair loss is often prematurely diagnosed by some practitioners, who are either unsure of what to look for or what to ask. Nevertheless severe or protracted stress from emotional, physical, chemical, or dietary causes can wreak havoc on many of the body’s vital hormones.

Adrenal gland production of Cortisol is raised in times of acute stress. When this is prolonged, excess Cortisol affects production of the hormones themselves & their target tissue sensitivity. Hormones that regulate ovarian/testicular function (gonadatrophins) in the respective sexes are decreased – resulting in lowered oestrogen in women & decreased testosterone in males.

The pituitary gland’s production of growth & thyroid stimulating hormones are blocked by the indirect influences of excess Cortisol, diminishing & disordering the conversion of the thyroid hormones from active to inactive.******

Adrenal hormone production (including Cortisol) cannot be sustained at elevated levels indefinitely, and ultimately results in adrenal fatigue or adrenal ‘burnout’. Low Cortisol levels adversely influence thyroid function – particularly with a concomitant Vitamin D deficiency (<50nmol/L). Symptoms of low Iron, Cortisol, and hypothyroidism are all similar in presentation.

Successfully treating women for hair loss problems requires careful review of their medical, nutritional, hormonal & lifestyle history undertaken in an organised & sequential way. The ‘ONE TREATMENT FITS ALL’ approach adopted by commercial hair loss centres RARELY EVER yields results for complex female scalp hair loss conditions.

Specific baseline blood & functional pathology (where appropriate) should be undertaken before deciding on a treatment regime. This will provide a clearer representation of what other areas are influencing the primary problem, & treating the cause of the condition rather than just ‘band-aiding’ the symptoms can then be undertaken.

Copyright Anthony Pearce 2006 (Fully revised March 2015)
*Male hormones are collectively termed androgens
**TSH, T4, T3 REVERSE T3 (rT3), Thyroid antibodies and TSH thyroid receptor antibodies (TRA) IF REQUIRED (not usually 1st encounter unless history or symptoms of hyperthyroidism)
***A ferritin of around 90-120ug/L is adequate for a child of senior primary school age or a post-menopausal woman
****or women who’ve undergone hysterectomy or premature menopause
*****See article – ‘Insulin-induced’ pattern hair loss at this website
******Thyroxin (t4) ‘corrupts’ to Reverse T3 (rT3) in place of converting to the active thyroid hormone (t3) – rT3 is DE-activated t4 – a biologic “blank”.