Alopecia Areata & other autoimmune conditions
Autoimmune states are thought to be polygenic, i.e. there are multiple genetic factors to their susceptibility. These factors eventually interact with physiological &/or environmental issues to activate the condition. Some initiating triggers are:
- Decline in nutritional, metabolic or hormonal status creating disturbed homeostasis; e.g.: deficiency of Vitamin D or thyroid hormone issues.
- Sudden shock or protracted emotional/physiological stress. ‘Physiological stress’ may be an underlying disease that has begun to develop (e.g.: Haemochromatosis).
- Viral or bacterial infection, vaccinations, or chemical or other external substance not previously exposed to.
- Disordered gut function or liver detoxification pathways; 70% of the body’s immunity lies along the gut wall.
- Chronic infection (tooth abscess, chronic tonsillitis or sinusitis), or head trauma from accidents or contact sports such as rugby.
- Anaesthetised on an operating room table for extended periods of time for major surgery has caused ‘pressure lesions’ in predisposed people.
- Alopecia areata is frequently associated with other autoimmune problems such as autoimmune thyroiditis, Vitilligo, lupus, rheumatoid arthritis, Sjogren’s syndrome, & psoriasis.
Different autoimmune conditions are also regularly seen within related members of extended families. These families are referred to as ‘atopic’, meaning that they have a genetically inherited hypersensitivity to certain foods, chemicals, and/or their general environment. Atopy will reveal itself within the individual or family members as Alopecia, Psoriasis, Eczema, thyroid disease or other autoimmune condition.
Autoimmune problems can involve any system, organ or tissue of our body and the scalp is commonly affected. Conditions such as psoriasis may only involve the cells of the outer skin, leaving the hair relatively unscathed. Some may influence both, causing hair loss of a (sometimes) temporary nature – alopecia areata being one example. Still others ‘scar’ the skin destroying hair follicles and other underlying skin appendages as they progress. These are collectively termed ‘cicatricial’ alopecia and include Folliculitis Decalvans, Pseudopelade, Lichen Planus, and ‘lupus’ (discoid type). Permanent hair loss usually results from cicatricial alopecia.
Active Folliculitis Decalvans is accompanied by severe inflammatory reaction and (usually) pustular eruptions across the vertex (crown) area of the scalp. In susceptible people it’s thought their skin initiates an exaggerated immune response to the toxins of Staphylococcus Aureus bacteria. Medical practitioners will often prescribe topical and oral combinations of antibiotics to treat this form of scarring alopecia.
Scarring alopecia due to chemical damage can occur from any corrosive chemical contacting the scalp. This may be accidental contact; improperly prepared hair tints (usually bleaching) or the use of any topical treatment that may precipitate an irritant reaction to the skin.
Non-scarring inflammatory hair loss and scalp issues can occur in susceptible individuals. They are likely to be ‘early’ cicatricial alopecia of autoimmune origin – this would sometimes be confirmed by tissue biopsy.
The scalp may take on a red or perceptibly-inflamed, ‘boggy’ appearance – not unlike some fungal infections – with some scaling + pustular eruptions noted. Alternately the skin may be dry with a smooth, ’shiny’ appearance – akin to some Tinea conditions. Under image enhancement the general appearance of the affected area will differ from unaffected areas elsewhere on the scalp, with ‘miniaturised’ follicle openings and ‘stunted’ or vellus hair shafts.
Follicle hair shedding is either a direct result of this inflammatory ‘attack’ – or secondary to it. Any area of the scalp can be affected but the frontal hair line margin or crown is a common starting point.
Anti-inflammatory shampoos and topical treatments will often help relieve the immediate symptoms, but finding the underlying cause (low Cortisol, Vitamin D or other disturbance) is the key to arresting the problem.
Other hair loss conditions (or scalp problems) such as diffuse or ‘pattern’ scalp hair thinning may be observed concurrently with autoimmune issues of the skin & its appendages.*
NOTE: Generic Minoxidil or topicals containing Retinoic acid would be CONTRA-INDICATED for inflammatory hair or scalp conditions (in my opinion).
Most of the autoimmune problems that affect the hair and scalp can be treated and at least stabilised by a variety of therapies, which are often best used in combination.
Alopecia areata (AA):
Alopecia areata originates from the Greek word ‘Alopekia’ – a term used to describe the manner in which fur is shed from wild foxes with ‘mange’. AA typically presents as patchy, non-scarring* circular or oval ‘bald spots’ (lesions) that are well defined & appear suddenly. AA may involve the eyebrows/eyelashes, beard, or any other part of the body where hair grows. Nail involvement consisting of ‘pitting, splitting, or longitudinal ridging is a common feature.
There are three clinical variants of AA:
- Alopecia areata (also termed ‘partialis’ when incomplete hair loss from the lesions is observed)
- Totalis – total loss of scalp & body hair from the head. Includes eyebrows, eyelashes, facial hair/beard.
- Universalis – total loss of body hair from the entire body. A. Universalis is the most severe form of alopecia with potentially the poorest prognosis – and its spectre fills most AA-susceptible people with morbid dread. However it is also uncommon to progress to this extreme form of the condition, and is (in my opinion) strongly associated with undiagnosed or improperly managed Autoimmune Thyroiditis.
- AA sub-groups:
- ‘Ophiasis’ type “snakes” around the hairline margins at the bottom of the scalp.
- ‘Reticulate’ type most commonly starts at the back of the head, and leaves a patchwork of hair loss across the scalp. The surviving areas of hair resemble the “faun tails” of deer.
- ‘Diffuse’ alopecia areata is often difficult to diagnose as it mimics diffuse or androgenic hair loss in women.
- ‘Barbae’ is alopecia that commonly affects the beards of adult males.
- ‘Poliosis’ is a form of AA where lesions of unpigmented (white) hair are seen but the hair is NOT shed from the scalp.
Genetic & Autoimmune Factors:
- Ten-forty percent of patients seen report a family history of alopecia areata.
- >40% have associated atopic features in their personal &/or family history, and they or their extended family will frequently exhibit other autoimmune problems such as Vitilligo, Psoriasis/Eczema or Asthma, Gluten/Dairy or other food sensitivity etc.
- Diagnostic histology is lymphatic infiltration of activated CD+4 T lymphocytes in & around the hair follicles when the condition is active.
- Hair follicles are normally ‘immune response protected’ skin appendages. The consequences of AA result when the immune concessions against this tissue-specific autoimmune state are withdrawn.
- Pigmented hairs are most susceptible, whilst white (unpigmented) hairs are mostly unscathed. Exclamation point hairs (short, broken hairs) are a diagnostic feature of AA.
- >85% of patients will experience their first episode of alopecia before age 40. Males & females are affected equally** whilst there is an increased incidence of alopecia areata in dark haired and Asian people.
Current treatments for alopecia areata involve the use of ‘immunomodulators’ alone or in combination with biologic response modifiers such as Minoxidil topical solution. Anthony Pearce Trichology offers an exclusive Minoxidil Complex formulation for AA (Minoxidil + Betamethasone 0.025%).
An immunomodulator suppresses or increases the body’s immune response either locally or systemically. Corticosteroid injections, lotions or tablets, as well as contact sensitisers (Anthralin DCP) are the common immunomodulators. Topical or systemic (taken internally) immune-suppressors are used by some Dermatologists for the treatment of intractable alopecia and psoriasis.
Immunomodulators and immune-suppressors DO have their place in treatment regimens, but investigating and establishing any underlying cause/s for AA onset or relapse is always the best approach (in my opinion). Just providing Cortisone or other topical therapy WITHOUT prior pathology testing will often only ‘temporarily suppress’ the immune response – and lead to a continuance of the condition (or eventual relapse).
Whilst people who exhibit AA (or any other autoimmune condition) DO have the inherited genetic pre-disposition to exhibit it – it ALWAYS takes something to trigger it. Most often the condition’s appearance is telling us there is some deficiency or internal disturbance that’s unsettling the body. This may be as straightforward as a nutrient deficiency causing metabolic disturbance; inflammatory process or infection.
It’s also believed that a number of AA sufferers have a dysfunctional ‘iron regulating mechanism’ (Chan: 2013).
Increasing numbers of younger children appear to be presenting with Alopecia areata (readers might refer to ‘Alopecia areata ….in Children – a Practical Approach’ at). Anecdotal observations suggest the origins of this childhood onset are triggered – in part at least – by disturbances in the young gut. Listening to the child’s parents (+ the clinical history they provide) – as well as appropriate (+ minimally invasive) pathology testing – will help to clarify onset origins.
L-tyrosine amino acid is an immunomodulation therapy that Trichologists have used to successfully treat autoimmune diseases affecting the hair and scalp. Tyrosine helps raise the immunomodulation neuropeptides (IP) –produced by nerves in the skin – which modulate skin inflammation & are thought to provide the potential link between the brain & skin disease.
There is evidence that a deficiency of one IP – calcitonin gene-related peptide (CGRP) may influence the onset and course of AA. Calcitonin is the ‘active’ form of 25(OH)-D converted + stored in the liver. Blood levels of CGRP in patients with active AA are 50% less than that of the population unaffected by AA.
Tyrosine is considered a very safe & versatile oral supplement, but it must be used with caution – and under medical supervision – in persons with a history of epilepsy or schizophrenia – as it alters the balance of neurotransmitters in the brain. Migraine headache sufferers are advised to use caution as Tyrosine can induce headaches in some and relieve them in others. L-tyrosine therapy is essentially CONTRA-INDICATED in HYPER-thyroid states (i.e.: Graves Disease).
Tyrosine must also have added Betaine HCL (stomach acid) to prevent tyrosine converting to the toxic amine – ‘tyramine’ – a potential carcinogen. Adequate Vitamin C + B group levels should also be established as these Vitamins are essential to facilitate the tyrosine bio-pathways in the body. Tyrosine/Betaine PLUS Complex is available exclusively through Anthony Pearce Trichology.
‘Professional Series’ Activance Rhodanide – a more sophisticated formulation of the original European patent**** – is a natural/nutrient topical therapy that can be safely used on scalp, face and skin. Rhodanide’s anti-inflammatory and hypo-allergenic properties have demonstrated much promise in autoimmune, inflammatory and scaling skin disorders. Activance Rhodanide’s appeal is in it’s versatility of use; it has NO known adverse affects and can be safely used on young children, pregnant /nursing mothers or sensitive, atopic skin.
Photo-biotherapy such as ‘soft/cold’ low level laser light (LLLT) is a strong vasodilator & moderates skin immune response by inducing changes in T-cell reaction. To be therapeutically effective these laser appliances should be classified ‘3A/3B’ and be in the wavelength vicinity of 670nm & with a power output of at least 60mW. LLLT is a non-UV light source.
*Hair follicles, sweat + sebaceous (oil) glands
**In older or atopic females AA sometimes presents as a fibrosed (‘scarred’) appearance – particularly around the front hair line margins and temples. A scalp skin biopsy will usually provide the correct diagnosis.
***Research from the Mayo Clinic (Journal of Immunology, Nov.2004) illustrates that the male immune system is less reactive than the female, because testosterone slows & weakens T lymphocyte response. Though females are more susceptible to autoimmune disease (because of their lower levels of testosterone), a male’s immune response is blunted when faced with a similar threat because of their higher testosterone levels.
****Hair Care Foundation (Australia) acquired the world-wide rights to the original German patent to further R+D the original product.