- Is pattern thinning always ‘genetic’?
Two decades in to the 21st century the average consumer might be perplexed that female scalp hair loss remains poorly understood by many in orthodox medicine.
Those seeking answers are invariably given the diagnosis of ‘genetic’ hair loss – even where there is no family history. This is promptly followed by a prescription for one or two outdated blood pressure drugs – one to suppress the woman’s androgen (1) production, and the other to help stimulate follicle hair growth – both on the scalp and body because an oral medication is not targeted.
The experience and clinical observations of this writer has been few women exhibit true genetically-inherited androgenic scalp hair thinning. What it is medicos and dermatologists are seeing is follicle miniaturisation leading to ‘vellus’ hair production through the androgen-sensitive area of the scalp. This all-to-common transformation occurs as a result of homeostatic compensatory measures or as a consequence of metabolic disturbance such as Insulin Resistance.
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.
There are more than 20 known reasons why the (female) body will reveal increased TT levels (ARL/Healthscope Laboratories: 2005).
In pattern thinning, some TT is further up-converted to DHT which can have a miniaturising influence on ‘androgen-sensitive’ hair follicles across the top of the scalp. I have termed this ‘acquired pattern thinning’.
Whilst there are texts filled with hair loss and scalp conditions; the common ones are:
1. Generalised (diffuse) scalp hair thinning as the name implies loss of scalp hair density appears evenly distributed throughout the scalp. Generalised thinning tends to appear slowly over time; it’s reported 20% of volume is lost before it becomes apparent to the individual. Nutrient-metabolic disturbance or the adverse effects of certain medication or hormone therapy are the common causes.
2. Telogen Effluvium (TE) is the diagnostic term to describe the rapid and excessive shedding of follicle scalp hair following illness or febrile fevers. TE is now held to be a non-specific reaction to a wide variety of physiological and/or emotional stressors that synchronise up to 60% of scalp hair follicles into a premature termination of ‘anagen’ phase, followed by the telogen shedding phase one – three months after. Some common initiators of TE are:
- Acute illness – particularly when accompanied high febrile states (elevated body temperature); vomiting and diarrhoea – especially from contaminated food/water.
- Surgical or extensive dental procedures – particularly when substantial blood loss or intra-operative complications have occurred.
- Severe Allergic reactions from any source, but most commonly from chemicals applied to the scalp.
- The commencement or cessation of certain medication such as synthetic hormonal therapy (contraceptives or HRT) taken orally, injected or implanted. Any prescription medication has the potential to trigger a TE episode, but other common drugs are thyroid medication, anti-cholesterol drugs (Statins); anti-androgen medication, anti-convulsant/mood stabilising drugs, anti-depressant medication, anabolic steroids.
- Following childbirth, miscarriage or pregnancy termination. Post-partum TE usually commences 8-10 weeks after childbirth, but when it commences and how severe the hair shed depends on individual circumstances with mother and baby.
- Sudden emotional shock or prolonged and unrelenting mental distress
- Rapid weight loss in a short period of time either by ‘crash-diet’ or illness. A dramatic change in one’s diet; any ‘fad’ diet that promotes the exclusive or excluded intake of certain major foods groups, or harsh detoxification diets.
Ordinarily TE is considered a ‘temporary & self-correcting’ form of generalised scalp hair loss but will only fully resolve when nutrient-metabolic support is optimised to support follicle phasing re-set.
3. Alopecia areata (AA): an autoimmune condition where the immune system is activated to attack the hair follicles in predisposed individuals. AA typically presents as patchy, non-scarring circular or oval ‘bald spots’ (termed lesions) which are well defined and appear suddenly. AA may involve the eyebrows, eyelashes, beard, or any other part of the body where hair grows. Nail involvement consisting of ‘pitting’ of the nail is a common feature.
4. Fibrosing or Scarring Alopecia: a variant of pattern thinning observed in post-menopausal females is a slow receding of the entire frontal hairline margins. The skin takes on a ‘scarred’, blanched or discolored, empty appearance known as ‘fibrosing’ where the underlying dermal structure and appendages – hair follicles, sweat and oil glands are progressively destroyed.
Fibrosing alopecia may be autoimmune/polygenic in origin, viz: there are multiplegenetic factors to susceptibility. These factors eventually interact with disturbed physiological functioning to activate the condition in ageing skin.
Scarring alopecias are as the name suggests, destructive skin conditions that almost always result in permanent hair loss to the areas affected. This group are collectively termed ‘cicatricial’ alopecia, and include folliculitis decalvans, pseudopelade, lichen planus, and ‘lupus’ (discoid type). They are considered autoimmune in origin; usually progress slowly but rate of progression may vary.
Folliculitis decalvans – the only pustular scarring condition – is often accompanied by severe inflammatory reaction and pustular eruptions across the crown area of the scalp. Folliculitis decalvans is sometimes mistaken for fungal infection, so a fungal scraping or biopsy should be considered to attain the correct diagnosis. Gut dysbiosis is a major initiator of autoimmune conditions which attack the skin and should always be thoroughly assessed.
Whatever perceived hair loss or scalp condition a Client/Patient presents with, it should not be trivialised or dismissed. Rather a detailed history of their concerns followed by the appropriate pathology testing should be undertaken and assessed.
Only then will underlying causes be evident, allowing ‘targeted’ treatment to correct or control the condition. One dimensional or ‘scattergun’ treatment approaches hoping for a result rarely work – they also waste the Client’s time and money.
- Spironolactone marketed under its various brand names, and oral Minoxidil. Both drugs were initially prescribed for high blood pressure (hypertension). Androgens is the collective term for all levels of male hormone.
Copyright – Anthony Pearce 2019