Hair loss has baffled researchers for years, there are now dozens of theories. Plus many, many studies have been done, but as yet no one knows why it occurs.
Loss of hair can fall under several categories..
Loss of hair can be caused by, or associated with any one of the following...
In fact all of the above could be categorised under 'stress', as all the above increase stress in the body. Stress causes a cascade of inflammatory cytokines to be produced, which in turn increase oxidative stress. This leads to a drop in antioxidant levels, leading to inflammation.
During normal hair growth about 90% of the hair is growing. This is called the anagen phase and lasts between two to six years.
Next follows the catagen phase. It signals the end of the active growth of a hair and lasts for about 2-3 weeks.
The catagen phase is followed by the resting or telogen phase which lasts two to three months, at the end of which hair loss results. About 10% of the hair is in the telogen phase. Normal loss ranges from 50 to 100 hairs per day.
After a hair is shed the anagen phase begins again, with new hair growing from the same follicle. Hair on the scalp grows about 1 to 1.5 centimetres per month, ageing reduces this growth.
This usually occurs one to three months after a major stress to the body, such as surgery, an accident or illness. It can occur 1-3 months after childbirth in some women. This type of hair loss appears as a generalised thinning, rather than bald patches.
The stressful event stops the growth of some hairs, usually those near the end of their life. It takes 1-3 months for the hair to actually fall out.
Once the stress is past, the follicle initiates new hair growth.
Androgenic alopecia is the commonest cause of hair loss in both males and females. It's associated with increased androgen levels.
A proven association between AGA and cardiovascular disease indicates a common cause. Hypertension is strongly associated with androgenetic alopecia, so are glucose metabolism disorders, hypercholesterolemia, and benign prostate hyperplasia and/or carcinoma. Hypertension is also linked to hyperaldosteronism.
Spironolactone, the anti-hypertensive drug, is a mineralocorticoid receptor antagonist, and has been used in the treatment of AGA. Progesterone competes with the natural ligand aldosterone due to high binding affinity of progesterone to the human mineralocorticoid receptor. Progesterone would be the safer course to take.
An interesting comment in one study made a comparison of AGA in men, to women with polycystic ovaries. AGA is associated with significantly higher free testosterone in men, regardless of body mass index. Higher testosterone is also found in women with PCOS.
Hirsutism, acne, alopecia, and oligo-amenorrhea are signs of hyperandrogenism, one of the most frequent endocrine disorders in women of reproductive age.
There is an increased incidence of Insulin Resistance (IR) and it's associated disorders of high insulin, obesity, hypertension and dislipidaemia in men with early onset hair loss.
Oestrogen is one known cause of IR. Progesterone levels are dropping during peri-menopause, whereas oestrogen levels remain normal until menopause.
Testosterone is another cause of IR and therefor hair loss.
The enzyme 5 alpha-reductase converts testosterone into dihydrotestosterone (DHT). DHT is implicated in hair loss. Progesterone inhibits 5 alpha-reductase activity.
Both medoxyprogesterone acetate and ethinyl estradiol do not inhibit 5 alpha-reductase activity, oestradiol shows some inhibition.
Ironically androgen excess in women causes both hirsutism, including facial hair, and hair loss from the head. By reducing 5 alpha-reductase activity in the skin, progesterone assists in reversing this trend.
A few studies have found an application of 2% to 5% topical progesterone can help in some cases of hair loss.
Approximately 10% of pre-menopausal women show evidence of androgenetic alopecia. Age increases the incidence and 50-75 percent of women 65 years or older suffer from this condition.
Each month women secrete more testosterone than oestrogen, but normally most of it is converted to oestrogen. The enzyme aromatase effects the conversion, but as women get older this conversion slows. Plus the menopausal ovary is an androgen secreting organ. The adrenals also secrete androgens.
Weight loss undoubtedly reduces hair loss in hyperandrogenic women. Probably because of a decrease in androgen levels, testosterone is notorious for causing weight gain in women.
Low levels of sex hormone binding globulin (SHBG) increase free testosterone levels. It's essential to increase SHBG... avoid all sugars. Fructose reduces levels by 80%, sucrose by 50% and glucose by 40%. The increase in testosterone not only leads to hair loss, but to an increase in viseral fat, cancer, cysts and weight gain.
Oestradiol can detach dihydrotestosterone (DHT) from its binding sites on SHBG, thus making it more bioavailable. Avoid oestradiol, often used in HRT.
There is a theory that AGA may have evolved to protect men from prostate cancer, by increasing skin exposure to UVB radiation. High levels of vitamin D are found to be protective against many cancers.
Interestingly there's a greater incidence of AGA in cold climates. The link appears to be more one of higher latitude, rather than temperature. The higher the latitude, the less vitamin D is made in the skin.
The reason for female pattern hair loss in postmenopausal women with normal androgen levels is not known. But the condition does improve with the drug finasteride. This inhibits the enzyme 5 alpha-reductase, thus preventing DHT from forming. It's also used for treating androgenetic alopecia, which makes one suspect that FPHL is caused by excess androgens, although 'normal' levels are found. Often it's the total testosterone which is checked and not the free portion. This is the only active testosterone, the remainder being bound to SHBG, and therefore inactive. The total testosterone could fall into the normal range, but if free testosterone is higher than normal, this will not be found. Not unless it's checked for.
These are generally regarded as autoimmune diseases. But the precise etiology has not been discovered. Another theory is a genetic basis for the disease.
Adults with AA have experienced significantly more emotional and physical traumatic events, particularly in childhood.
Various triggers have been found, oxidative stress is high on the list, which leads to inflammation. So is emotional and physical stress. Nutritional deficiencies, and endocrine imbalances are others.
Hair loss during the anagen phase is usually caused by chemotherapy or radiation therapy.
Increased malondialdehyde (MDA) levels and lower superoxide dismutase (SOD) activity are found in people with AA compared with healthy controls. Malondialdehyde is a marker for peroxidation, SOD is a powerful antioxidant.
Mast cells, natural killer cells, substance P, IFN-gamma, interleukins, TNF-alpha, MIG, IP-10, BAFF, HLA antigens, MIG, as well as stress hormones are known to play a major role in the pathogenesis of the disease. Autoantibodies against thyroperoxidase and thyroglobulin are found more frequently.
AA is often associated with other autoimmune diseases.
One study acknowledges that the skin, endocrine, nervous and immune systems cannot be treated individually, but must now be considered together.
The triggers which stand out for all forms of alopecia are oxidative stress, emotional stress, excess testosterone, insulin resistance, and a lack of blood flow to the hair follicle, which prevents nutrients reaching the growing shaft thus causing hair loss.
Stress drops both progesterone levels and the B vitamins. Many B vitamins are essential for healthy hair...
This is often called the anti-alopecia vitamin. It increases the action of insulin and decreases insulin resistance, decreases serum androgen concentrations, blood pressure and helps reduce cholesterol levels.
thiamine (vitamin B1)
Is a coenzyme important in intracellular glucose metabolism. It's essential for glucose oxidation, improving glucose tolerance and insulin production by pancreatic cells.
Stabilises blood sugar and eliminates cravings for carbohydrates, in some instances better than chromium. It reduces high blood sugar, and is needed for healthy hair and skin.
Other nutrients which help hair growth are..
Essential for the anagen growth phase in hair. A lack is implicated in insulin resistance, cardiovascular disease, hypertension, glucose metabolism disorders, hypercholesterolemia, cancers, high insulin, obesity, autoimmune diseases and more.
N-acetyl cysteine (NAC)
Which is found in hair, skin and nails. It improves high-sucrose diet-induced obesity, glucose tolerance, lipid profile, in vivo LDL-oxidation and serum oxidative stress and enhances antioxidant defences. Oxidative stress can lead to abnormal changes in intracellular signalling, resulting in chronic inflammation and insulin resistance. Cysteine is also one of the precursors to glutathione, an essential antioxidant within cells.
Amounts to take of the above nutrients are..
There is also evidence that iron is needed. But a blood test is essential to see if there is a deficiency, excess iron is dangerous. There is some evidence the amino acid lysine is beneficial too.
Mentha spicata or spearmint and Mentha piperita or peppermint show anti-androgen properties. A cup of mint tea, drunk twice a day during the follicular phase of the menstrual cycle, showed a significant decrease in free testosterone, with an increase in luteinizing hormone, follicle-stimulating hormone and oestradiol in one study.
The common thread with all the alopecia's, ie those caused by excess testosterone, and the 'autoimmune' variety, is oxidative stress.
Recent studies have found oxidative stress behind most diseases and disorders..... high cholesterol, high CRP (a marker for Inflammation), high blood pressure, lipid peroxidation, Insulin Resistance, which leads to metabolic syndrome and heart disease, PCOS, Cancer, autoimmune diseases and more.
The common thread linking the above is a deficiency of vitamin D. A lack of this vitamin causes or is implicated in over 20 different cancers, in insulin resistance, high cholesterol, inflammation, heart disease, high blood pressure, PCOS, autoimmune diseases and more.
Vitamin D regulates gene expression, has a positive fundamental effect on cell differentiation and growth, with anti-oxidative and autoimmune anti-inflammatory mechanisms. It positively effects the nervous system by stimulating neurotrophic factors, quenching oxidative hyperactivity and regulating autoimmune responses.
Vitamin D comes in three forms
1,25-dihydroxyvitamin D modulates growth and differentiation of keratinocytes via binding to the vitamin D receptor.
The vitamin D receptor (VDR) appears to play a role independently of vitamin D. In mice who have had the VDR removed, it impairs Wnt signalling in keratinocytes, leading to alopecia, due to a defect in keratinocyte stem cells. The lack of VDR in keratinocytes leads to a defect in anagen initiation.
Alopecia is a feature of vitamin D receptor mutations. Mutations are generally caused by oxidative stress, ie free radical damage. This could quite possibly be due to lack of vitamin D, a potent antioxidant and hormone.
Keratinocyte growth is also inhibited by androgens, through the modification of Wnt signalling.
Interestingly, it's been found that alopecia is a frequent feature in hereditary resistance to 1,25-dihydroxyvitamin D, often diagnosed at a very early age. Unfortunately, as is often the case, giving 1,25-dihydroxyvitamin D showed no response. It's essential to give 25-hydroxyvitamin D too, as they work together. If 1,25-dihydroxyvitamin D is too high, vitamin D3 will be suppressed, the converse it also true.
It could well be that alopeica is what epigeneticists call 'the foetal origin of adult disease'. They've already found this is the case for type 1 diabetes, some types of tumours, and there's reason to believe autism is another. All due to a lack of vitamin D in utero.
Epigenetics is the study of altered gene expression without changes in DNA sequence. This is caused by an abnormal chemical environment in-utero, changing the gene expression.
A lack of vital nutrients, or insults by toxins during the first month of gestation, can produce abnormalities in gene expression that may persist when an adult. Gene expression errors can be transmitted to future generations by a process called transgenerational epigenetic inheritance.
This can explain why certain conditions run in families. Nothing to do with fundamental genetics, but a change in gene expression.
Epigenetic processes are far more vulnerable to toxic metals, viruses, lack of nutrients etc., when compared to genetic processes.
This is an excellent video on the subject...
There is a severe lack of safe and effective treatments for alopecia. Possibly because the drug route is not the answer.
This maybe lies in correcting an underlying nutritional imbalance. Or correcting an hormonal imbalance without drugs. Or it's an epigenetic cause, in which case there is probably no solution as the damage has already been done. But the body has an amazing capacity to heal and regenerate, it's certainly worth trying the natural route before giving up.
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