Insulin-induced ‘pattern’ hair loss

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 20 years in this field, 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* or other hormone therapy if you have the former – or Cortisone in various modes of delivery for the latter.

This perception is further facilitated when hi-profile Dermatologists here in Australia accept funding from drug companies to ‘prove’ female hair loss can be eradicated by the taking of an outmoded blood pressure drug that doubles as a diuretic and an anti-androgen* medication.

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.

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 privileged to receive – I earlier put forward a theory that some ‘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** 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 to ‘push’ glucose into the cell for energy production.

It’s still not wholly clear that obesity – particularly truncal obesity – induces hyperinsulinaemia, or the other way round. 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***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 lean PCO females – BUT higher Free Testosterone levels – the effects of which can lead to thinning scalp hair and hirsutism.

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:
  • The taking of (synthetic) oestrogen found in contraceptives and hormone replacement therapy (HRT).
  • Pregnancy
  • Hyperthyroidism
  • Cirrhosis of the liver
  • Medication such as Phenytoin Sodium (Dilantin) that induce hepatic enzyme induction

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:
  • Age
  • 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 Dr. Peter Baratosy’s excellent text – ‘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 TT’ in females is not regulated by Follicle Stimulating Hormone (FSH) or Luteinizing Hormone (LH). FSH and LH stimulate ovarian TT production – but most is aromatased back to Oestrogen****

It’s important to note that in Insulin ‘sensitive’ females, FSH and ‘normal’ blood concentrations of Insulin (<10ng/ml) stimulate aromatase activity (i.e.: the conversion of TT back to Oestrogen); higher blood Insulin concentrations (100ng/ml) does NOT activate ‘aromatase’ – hyperinsulinaemia (found in PCOS) suppresses aromatase activity (Steroids: 2001).

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 with ‘androgenic’ follicle miniaturisation and (sometimes) an increased facial/body hair results when TT cannot be aromatased back to Oestrogen and up-converts to Dihydrotestosterone (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.
  • 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 colours 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*****
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 AND reduces efficacy of treatment therapies. I am (again) indebted to Dr. Peter Baratosy, Dr. Philip Van Zanden + Pharmacist Arthur Chan for their generous advice + encouragement.