An increasing problem in the modern age.
From the time I resolved concentrate on female hair loss issues as a professional specialism, I was never convinced – or more honestly asked by my female clients not to be convinced – that pattern hair loss (in women) is always inherited.
After almost 30 years in trichology, I still have the impression many treating Practitioners regard ALL hair loss issues as one single problem. At the very least it’s conveniently divided between ‘genetic’ hair loss and ‘alopecia’; an anti-androgen (1) or other hormone therapy if you have the former – or Cortisone in various modes of delivery for the latter.
From my experience this one-dimensional approach rarely ever works because the body is an incredibly dynamic interplay of many complex factors that are never static.
This simplistic view continues today with hi-profile entrepreneurial Dermatologists marketing ‘hairy pills’ containing a combination of oral Minoxidil and Spironolactone – both outmoded blood pressure drugs, with Spironolactone doubling as a diuretic and an anti-androgen medication.
According to the Australian TGA, use of medicines (such as Spironolactone and oral Minoxidil) outside the specified indication/s or intended purpose is termed ‘Off Label’ use.
‘Off-label’ is used at the discretion of a medical prescriber who is solely responsible for obtaining informed consent from the patient. ‘Informed consent’ means the patient MUST BE notified of all risks or benefits of the ‘off label’ treatment vs other available treatments OR no treatment at all based on individual circumstances. For additional information please read my Facebook post: Treating hair loss – where most get it wrong …
Plainly put women don’t suffer from an ‘anti-androgen drug deficiency’ – but they do commonly experience nutritional deficiency or hormonal-metabolic-autoimmune disturbance – and this should be investigated as a first response.
By following the work of leading medical researchers – whose support and encouragement I’m grateful to receive – I earlier put forward a theory that most pattern hair loss issues in women are due to cascading hormonal-metabolic disturbance – caused by a complex interaction of many factors – resulting in elevated Testosterone levels which the body utilises in its attempt to maintain homeostasis.
My ‘acquired’ pattern hair loss premise was borne out in patient’s pathology results and subsequent (mostly always successful) treatment.
Hyperinsulinaemia, obesity and ‘pattern’ hair loss:
It’s now a given that obesity/morbid obesity (2) is an increasing health problem in modern societies. This gives rise to many potential health problems: Insulin Resistance (aka ‘Metabolic Syndrome’), hypertension, diabetes – or other hormonal-metabolic disturbance, heart disease and orthopaedic problems to list a few.
An increasingly insidious problem related to this is elevated blood Insulin levels – termed Hyperinsulinaemia. Elevated blood Insulin and Glucose levels are at the heart of Metabolic Syndrome, whereby body cells lose their sensitivity to Insulin required for glucose to enter the cell for energy production.
Although a raised BMI is associated with Insulin Resistance, one does not have to be obese or even overweight to be Insulin Resistant.
Insulin activity is also affected by the stress response. Chronic stress with persistent Cortisol elevation may counteract the effects of insulin, resulting in functional insulin resistance (DTI: 2016). The disruptive effects of oestrogen-copper dominance form synthetic hormone therapy can cause a functional insulin resistance also.
It’s still not wholly clear that obesity – particularly truncal obesity – induces hyperinsulinaemia, or vice versa. There is clear evidence to suggest that high sugar, refined carbohydrate diets are the origins of obesity; hyperinsulinaemia is a corollary of both.
Since the introduction in the 1970’s of Fructose (Corn ‘Syrup’) as a (cheaper) sweetening agent to raw sugar in soft drinks and refined foods, it’s estimated that the rate of obesity has risen exponentially. According to US studies Fructose suppresses the action of Leptin (3) and (fructose) is immediately stored adipose ‘fat’ rather than utilised as energy for the body.
Hyperinsulinaemia in younger females is one factor in Polycystic Ovarian Syndrome (PCOS), resulting in pattern scalp hair loss, increased facial/body hair (‘hirsutism’) and reproductive disturbance. One published study (J Steroid Biochemical Molecular Biology: 1995) found obese women with PCOS had similar Total Testosterone levels to slim PCO females – BUT higher Free Testosterone levels – the effects of which can lead to thinning scalp hair and hirsuteness.
Obesity and hyperinsulinaemia leads to a suppression of the hormone ‘carrier’ protein Sex Hormone Binding Globulin (SHBG) – with a reciprocal rise in ‘free’ Testosterone (TT). SHBG is significant because by manipulating SHBG levels, the amounts of available Oestrogen or TT can be controlled.
Sex Hormone Binding Globulin (SHBG) – a brief overview:
SHBG is a glyco-protein produced in the liver, and a 2nd tier ‘reserve storage’ carrier for Oestrogens and Testosterone in the blood. The levels of SHBG – and the hormones they carry – are influenced by a balance of stimulating and inhibiting factors (Baratosy: 2010). These may be dietary, hormonal (including hormonal therapy), nutritional, age, physical/sexual activity, illness or lifestyle determinants – all of which can impinge on Oestrogen-TT ‘bio-availability’.
Causes for elevated SHBG are:
- Oestrogen excess: synthetic oestrogens found in all contraceptives or HRT.
- Medications: anticonvulsants such as phenytoin sodium (Dylantin), Carbamazepine (Tegretol) or thyroxine (T4 thyroid hormone)
- Health issues: liver disease, anorexia or hyperthyroidism.
A raised SHBG may also cause symptoms of low thyroid function because SHBG partly binds + inactivates the thyroid hormone T4 (Thyroxine).
Factors that increase SHBG:
- Thyroid hormone T3
- Oestrogen including Phyto-oestrogens (plant derived such as Dong Quai)
- High fibre; low protein diet
Factors that decrease SHBG:
- Male hormone (termed ‘Androgens’)
- Progesterone (P4) – low P4 is a common concern for peri-menopausal women.
- Cortisol (Stress + anti-inflammatory hormone from our Adrenal Glands)
- High Protein/(good) Fats diet
Effects of Insulin on Testosterone and other hormones:
Explaining the physiology of TT stimulation, production/secretion and control is beyond the scope and intention of this article. I would instead refer the interested reader to an excellent text by Dr. Peter Baratosy – ‘You and Your Hormones’ (Baratosy: 2010). Suffice to say how and where TT is stimulated and produced in females and males varies between genders.
In females – about 50% of TT is produced by the ovaries and 50% by the Adrenal glands. Unlike male TT production, adrenal androgens in females are not regulated by Follicle Stimulating Hormone (FSH) or Luteinizing Hormone (LH). FSH and LH stimulate ovarian TT production – but most is aromatised back to Oestrogen (4).
It’s important to note that in Insulin sensitive females, FSH and acceptable blood concentrations of Insulin (<10 ng/ml) stimulate aromatase activity (i.e.: the conversion of TT back to Oestrogen); higher blood Insulin concentrations (100 ng/ml) does NOT activate aromatase – hyperinsulinaemia (found in PCOS) suppresses aromatase activity (Steroids: 2001).
Insulin resistance of varying degrees are levels <10 mU/L but the optimised target to minimise inflammation is 6-7 mU/L.
Hyperinsulinaemia disorders the negative feedback loop to the brain which monitors TT and Oestrogen blood levels, disrupting FSH (and LH) activity. FSH is stimulated for increased ovarian TT production in response to (perceived) low Oestrogen levels – but aromatase activity is suppressed, and TT levels continue to rise – and negative feedback response-aromatase ‘failure’ disordering continues (Baratosy: 2010).
Scalp hair loss – commonly with an accompanying androgenic follicle miniaturisation and (sometimes) increased facial/body hair and a coarsening of the skin’s pores in the facial T-zone results when TT cannot be aromatised back to Oestrogen and up-converts to Dihydro-testosterone (DHT). DHT is the biologically-active metabolite of TT – and three times more potent. DHT is formed in the hair follicles, adrenal and male reproductive glands; the important factor for causation here is the TT-DHT ratio – more than total or ‘free’ Testosterone per se (Chan: 2011).
Whilst not without their potential problems, TT and DHT are essential for developing sex-specific characteristics throughout a male’s life. It’s preferable for males to minimise aromatase activity and retain TT (Journal of Clinical Endocrinology Metab: 2002) – but elevated levels of these androgens in a female body comes with detrimental consequences.
What to do:
- Trust your innate intuition that ‘you know your body best’.
- Seek out an experienced health practitioner who won’t dismiss your concerns or immediately prescribe ‘drug’ therapy – but will investigate your concerns with appropriate pathology testing and subsequent treatment options.
- Weight loss from caloric restriction can lower blood Insulin; increase SHBG and decrease Free TT. Eliminating refined carbohydrate/hi-sugar foods is crucial to reducing hyperinsulinaemia. One Canadian study (Journal of Clinical Investigations: 2007) found that when sugar (as monosaccharides) was converted to fatty acids (lipids) – this lipogenesis reduced the liver’s capacity to produce SHBG.
**Current research: according to Dr. Joanna McMillan (2017) and Dr. Michael Moseley, an 800 calorie per day diet formulated and undertaken with strict medical or dietitian supervision can reverse Insulin Resistance (and even non-insulin dependent diabetes [NIDD)). A meagre 800 calorie per day diet is not sustainable long term, but purely used as a short-term driver for metabolic change.
- Increase your physical activity with regular and varied forms of exercise; what you like to do and what’s appropriate for your tolerance and age.
- Eat a wholesome diet of good protein, ALL forms and colors of vegetables, some fruits and small servings of complex carbohydrates. Hydrate well; moderate alcohol intake, don’t smoke cigarettes or take illicit drugs.
- Look to minimise any situation causing continued or unnecessary stress in your life. If unavoidable look to balance these stressors with meditation, yoga, exercise, support groups or personal leisure activities etc.
- Sufficient and quality sleep is essential; judicious sunlight exposure during the day to maintain adequate Vitamin D levels (5)
- I am able to offer my clients a sophisticated ‘all-in-one’ nutrient therapy (powder) formulated to:
- The client’s pathology results.
- Gender and age.
- Weight + height (in elderly and children).
- Condition being treated for.
Nutrient therapy complex + Inositol powder formulation is specifically for insulin resistance/inflammatory process. Inositol promotes:
- Insulin sensitivity; aids in stabilising diabetes (Type I + II). (Type I (IDD) diabetes should discuss with their Doctor before taking).
- As a nutrient therapy treatment for Polycystic Ovarian Syndrome (PCO/s).
- Aids in reducing thyroid antibodies in autoimmune thyroiditis (Dr. Isabella Wentz: 2018)
- Believed to have an inhibiting effect on malignant cell mutation. Recommended for those recovering from any form of cancer, malignancy or those with a strong family history of malignancy (Chan: 2019 – unpublished research).
- Healthy ovarian function + ovum (egg) quality in females.
- Supports balanced hormone levels.
- Mediates cell hormonal, neurotransmitter and growth factor signalling in mammals.
- De-alkalising properties helps decrease inflammatory process – particularly from excess insulin within the body.
- Additional iron, spirulina, zinc or Vitamin D can be added or omitted as required.
What is Inositol: (Myo)-Inositol is natural carbohydrate sugar found in the brain and tissues of all mammals. Inositol is an extremely versatile, effective and safe nutrient with many proven applications. Unlike many medications Inositol has no known side effects when used appropriately.
The Many Causes for Elevated Testosterone Levels in Females:
- Anti-male hormone therapy or medication.
- ’Morbid obesity’ means DOUBLE the person’s normal body weight (height to weight ratio).
- Leptin (from the Greek leptos meaning ‘thin’) is the ‘satiety hormone’ – produced in fat cells and aids in body weight control and energy utilisation + expenditure.
- By the enzyme ‘Aromatase’; mainly found in ‘fat’ cells of both sexes.
- Read articles at this website on Vitamin D and ‘Melatonin – the essential night tonic’.
Writer’s note: Hyperinsulinaemia, obesity + TT-Oestrogen aromatase disordering may cause pattern hair loss in males also AND reduces efficacy of treatment therapies in both sexes. A dual presentation of ‘pattern’ AND ‘diffuse’ scalp hair density thinning will be evident in some women. Sometimes the hair loss picture is purely ‘diffuse’ (i.e.: from all over the scalp).
Copyright Anthony Pearce 2012 (revised December 2020)