Haemochromatosis is a hereditary disorder where the controlling hormone for iron absorption (hepcidin) is flawed. This causes excessive dietary iron absorption (which is not excreted) but continually deposited into the major organs: liver, spleen, heart and pancreas.
The adult body ordinarily stores approximately one gram (1G) of iron as a constant reserve but this is exceeded in haemochromatosis, as absorbed dietary iron is unrelentingly built up in organs and joints to ultimately cause overload.
There are different forms of haemochromatosis but the most common are hereditary or secondary, which arises from other disease processes such as certain anaemias or liver disease.
Hereditary haemochromatosis affects around 1:200 people; more common in northern Europeans than those of other ethnic backgrounds. The condition is equally represented in adults males and females; males tend to be diagnosed at an earlier age: 40 years vs. post-menopause or around 60 years in women.
Genetic expression: A mutation of the gene to exhibit haemochromatosis is passed from parents to their off-spring. The common mutations are:
- H63D: these people rarely develop significant long-term health problems with haemochromatosis (Cooke:2018).
- C282Y gene is the common cause for organ iron overload necessitating regular phlebotomy procedures in some for the removal of blood and excess iron.
Influence on follicle hair growth: haemochromatosis is often difficult to diagnose because early symptoms are also common to other nutrient-metabolic disturbance: joint or abdominal pain, lethargy, decreased libido, unstable insulin-blood glucose levels, ‘foggy’ thinking, heart palpitations or loss of body hair. One tell-tale clinical sign to an observant practitioner is a greyish hue or ‘bronzed’ tone to the skin of a patient with developing haemochromatosis.
In advanced haemochromatosis where organ damage results in diabetes or liver detoxification dysfunction, scalp hair growth would definitely be compromised.
Phlebotomy treatments to reduce iron overload habitually result in a Telogen Effluvium scalp hair shedding due to the sudden blood loss and fluctuation of body iron levels (1).
Essentially one’s own genetic expression determines the type of hair loss an individual will experience: a generalised scalp hair density thinning or alopecia areata. Frontal hairline margin fibrosing alopecia is reasonably common in post-menopausal women. Fibrosing alopecia progressively obliterates the underlying skin structures (2) leaving a scarred ‘barren’ appearance to the skin.
Whilst ‘sufficient’ iron is essential to body functioning, iron is also very metabolically reactive, oxidative and toxic in excess. For these same reasons I do not encourage my clients to undertake iron infusions unless they are experiencing a severe iron deficiency anaemia (3).
Even then any potential underlying causes such as malabsorption, parasitic or other pathogen infestation, menorrhagia or slow internal bleeding should first be thoroughly assessed by the appropriate qualified practitioner (4).
Testing for Haemochromatosis:
- Fasting full iron studies blood pathology test specifically assessing levels of Ferritin (iron stores) and Transferrin Saturation.
- Genetic testing for the HFE (haemochromatosis) gene for H63D or C282Y mutations (5,6).
Copyright Anthony Pearce 2021
- Refer to article at this website: Abrupt onset excessive hair loss – Telogen Effluvium.
- Hair follicles, sweat and sebaceous (oil) glands.
- Refer to article at this website: The downsides of iron supplementation …..
- Parasitic infestation which commonly results in low iron stores is Blastocystis Hominis; Helicobacter pylorri (HpSA) is a bacterium which infects the stomach and causes iron malabsorption. Menorrhagia is excessive, heavy menstruation in pre-menopausal women. Internal bleeding is usually assessed by testing for occult blood in the faeces, colonoscopy and/or endoscopy undertaken by a Gastroenterologist.
- If you are ‘heterozygous’ ie: one gene mutation found – you are unlikely to develop the serious symptoms of haemochromatosis but as a ‘carrier’ of the genetic mutation you may pass this SNiP (mutation) to your children.
- ‘Homozygous’ ie: two gene mutations found: you have the propensity to develop haemochromatosis to any degree of the condition’s severity.