As a Trichologist specialising in female hair loss since 1999, I’ve treated thousands of women across the world for their thinning scalp hair density concerns.
The trend I’ve observed – despite prevailing medical opinion – there are two formsof so-called ‘genetic, hereditary or pattern’ thinning in females.
True genetically inherited female androgenic alopecia – or female pattern thinning – is quite 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 diminishing of the scalp hair density occurs rather than complete baldness. Unlike males, pre-disposed women also generally retain their frontal hairline margin (albeit with some hairline recession).
The management of inherited female androgenic thinning is (or should be) identical to other forms of female hair loss. Identifying contributing factors from nutrient, metabolic or hormonal disturbance, treating the underlying disorder/s and supporting the hair.
Once underlying influences have been stabilised, scalp hair will be supported and can be further focused on with appropriate topical therapies.
My experience suggests 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; Polycystic ovarian syndrome (PCO-s) or elevated Prolactin levels will often show as pattern scalp hair thinning or acne breakouts with increased facial/body hair or other symptoms related to increased androgen levels.
Affected women may be of any age; relating a common history of lethargy, skin, scalp or 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.
Comprehensive thyroid function testing (1) and/or salivary hormone profiles (SHP) will often not be within acceptable (high or low) in a compensatory reaction or as a secondary consequence in maintaining body homeostasis.
A dual presentation of ‘pattern’ AND generalised 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 geneses of these problems are commonly found in nutrient disturbance which are required to fuel metabolic functioning (Lee: 2007). Iron, Vitamin D, Iodine, Zinc & Selenium are regarded as the most essential nutrients for metabolic functioning.
Adequate Ferritin (iron stores) are essential to furnace intracellular energy output, from which adenosine tri-phosphate (ATP) is produced. To generate sufficient & quality ATP, a Ferritin of 100-150ug/L (within a usual reference range of 20-300ug/L) is essential for optimal metabolic & liver detoxification functioning in a younger adult person (2).
Metabolic (thyroid) activity & Phase II liver detoxification pathways are ATP dependent.
In pattern thinning presentations, 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 expression can be achieved by providing the body with the basic nutrients (Iron, Vitamin D, Iodine, and Zinc) to restore metabolic homeostasis.
In some individuals, medication to support the thyroid-adrenal axis/ other hormonal pathways may also be required.
An ATP-deprived liver is generally sluggish in function, and readily overloaded when a woman is taking hormone therapy (contraceptive or HRT medication), consumes daily alcohol, caffeine or nicotine.
These combined substances occupy the total capacity of the liver’s Phase I detoxification pathway and the liver’s ability to process other substances, such as the body’s own hormone by-products or other toxins – ultimately resulting hormonal disturbance and/or cellular toxicity.
Post-menopausal women (>55+) 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 a receding frontal hairline margin – 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.
Women of African or South Sea Islander heritage should be carefully assessed to exclude traction alopecia or chemical-mechanical damage to the frontal hairline margin, which can be mistaken for androgenic pattern hair loss.
Increased facial or body hair (hypertrichosis) sometimes accompanies pattern scalp hair thinning because follicles across the top of the scalp are androgen sensitive – causing follicle miniaturisation and diminished hair shaft diameter (termed: vellus hair).
Facial and body hair however is male hormone (androgen) dependent – 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).
Women will frequently report annoying scalp sensations: a ‘burning’ scalp, tender and painful scalp, generalized irritation of the scalp, itching; or a tactile ‘crawling’ feeling that moves across the top of the scalp. These symptoms may be caused by hormonal fluctuations or increased adrenal hormone surges with stress, or disturbances which drive inflammatory response such as Insulin Resistance or Gut dysbiosis.
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.
Many in orthodox Dermatology still appear to regard ALL follicle miniaturisation & vellus hair presentation as ‘genetic’. Note: biopsy confirmation is NOT a diagnosis of ‘genetic’ hair loss – rather a confirmation of follicle miniaturisation and vellus hair presence.
Other causes for this (as stated above) tend to be discounted or unexplored, and the Client is either advised to “live with it” or offered prescription drugs such as Minoxidil, Spironolactone or other hormonal therapy as a life-long treatment option.
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 protractedstress 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 and their target tissue sensitivity. Hormones that regulate ovarian/testicular function (gonadatrophins) in the respective sexes are decreased – resulting in lowered oestrogen in women or decreased testosterone in males.
The pituitary gland’s production of growth and thyroid stimulating hormones are blocked by the indirect influences of excess Cortisol, diminishing & disordering the conversion of the thyroid hormones from active to inactive (3).
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 where this is accompanying Vitamin D deficiency (<51 nmol/L). Symptoms of low Iron, Cortisol, or hypothyroidism are often initially 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 FIXES ALL’ approach adopted by commercial hair loss centres (and even orthodox medicine) RARELY EVER yields results for complex female scalp hair loss conditions.
Specific baseline blood or functional pathology (where appropriate) should be undertaken before deciding on a treatment regime. This will provide a clearer picture 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.
- Complete thyroid panel: TSH, T4, T3, Thyroid antibodies and Reverse T3 or TSH-thyroid receptor antibodies where appropriate.
- Ranges may vary between Pathology Services; a Ferritin of >85ug/L for effective thyroid function (Chan: 2014)
- T3 is corrupted to Reverse T3 (rT3), which is DE-activated T4 – a biologic ‘blank’.
Copyright Anthony Pearce 2006 (Revised December 2019)