In 1975 a group of men were first studied because they had ambiguous genitalia when they were first born. They did not have what could be described as either a penis or vagina but something that resembled both. It was discovered that they did not have an enzyme called 5 Alpha Reductase or simply just 5AR that enables them to make DHT from testosterone. (An enzyme creates a chemical reaction without undergoing a change itself).
When these men reached puberty and their testosterone levels increased, a fully functioning penis developed. They continued to have small prostates (which is a benefit), sparse body hair and beard growth and they did not develop the traditional male pattern of receding temples. The significance of these studies is that they demonstrated that males from puberty onwards remain fully masculine in the absence of any DHT.
The conclusion drawn is that no DHT equals no hair loss and no prostate problems. Therefore a safe and effective avenue to treating hair loss was opened up from studying this group of men and the market moved to developing '5AR inhibitors'. These are a group of substances that stop the action of the 5AR enzyme and hence lower DHT levels, without effecting testosterone levels and sexual performance.
Over the last couple of years DHT inhibiting drugs have come onto the market and have shown good results in inhibiting hair loss and in many instances reversing it.
Environmental Factors?
It is interesting to note that countries that traditionally have little male pattern
baldness (referred to hereafter by the
initials M.P.B) like Japan, China, India and Africa, do see their males develop
M.P.B once they settle in the western world. As their genes do not change on such a
relocation it would be logical to conclude that other factors interplay with a
genetic predisposition. The incidence of MPB appears to increase in each successive
generation that remains in the western world.
One problem with MPB is that it is not considered strictly a medical problem and as such no reliable statistics are to hand. Fortunately there is another model we can switch to that is well documented, that gives us a clue as to the impact of environmental factors: Dihydrotestosterone (DHT), is the main hormone believed to be implicated in hair loss and is also implicated in prostatic enlargement and prostate cancer. By studying the figures on prostate cancer, more light is shed on the subject of DHT and hence hair loss: Native Japanese men have an incidence rate of prostate cancer of 4 per 100,000. The rate amongst Japanese living on the U.S. mainland increases to between 12 to 20 per 100,000 and a staggering 36 per 100,000 for those living in Hawaii.
Clearly environmental factors must affect DHT production or its cellular uptake.(Ref W. Martin, 'My Prostrate & Me' ISBN 1-56877-88-8).
Summary
There appears to be a genetic predisposition involved in hair loss which would seem to be affected by environmental factors. Scientists believe they have isolated the "bad guy" in hair loss which is an enzyme known as five alpha reductase (5AR). Studies of the inhibition of 5AR look promising in providing a solution to hair loss and appear to have limited risk of side effects.
5AR inhibitors have now been developed and are available in either drug form or as nutritional supplements. DHT is metabolised from testosterone, which is made by the testes. Castrates produce less DHT and do not suffer hair loss, it has often been suggested that higher levels of testosterone are the cause. No study has established a direct correlation between Testosterone, DHT and hair loss. In fact one study demonstrated that bald men have in fact lower testosterone levels than other men. Other studies show that the levels of testosterone are within normal ranges or are at the upper end of normal range.
What must also be understood is that total testosterone alone is not that important, as it is transported through the blood on a carrier molecule known as sex hormone binding globulin (SHBG). The free portion that is not bound in this manner is available to be converted through to DHT. There is a commonly held view that the genetic predisposition is the conversion rate from testosterone to DHT in the area of hair loss.
Little work has been done into what lowers sex hormone binding globulin but it is known that there is an inverse correlation between SHBG and insulin level. Insulin is touched upon in the dietary section but it is worth noting that its levels are raised by our dietary habits, stress and being over weight.
Females do produce some hormones that are predominant in males. These
hormones do appear to be implicated in some cases of female hair
loss. However, the reason why the male hormone is produced in all women, in the
first place, is still not fully understood. A number of studies have used drugs
which inhibit the production of the male hormone with improvement in the hair. This
is much more acceptable in females who generally produce a smaller amount of these
hormones than men. A complete blockade of male hormones may turn out to be
undesirable when we fully understand their function in women.
It is clear from the male studies that 5AR inhibitors seem to be the direction of dealing with male hair loss problems. This is because it does leave the male hormone testosterone fully functional and these inhibitors may prove to be useful in female hair loss in the future.
Females have two prime hormones: Progesterone and Oestrogen. Oestrogens are really a group name for three female hormones: Estrodoil, Estrial and Estrone. Progesterone refers to a single hormone and not a group. To understand female hair loss it helps to have an understanding of the female menstrual cycle as this is interrelated to her hormonal balance. In a normal menstrual cycle every 26 to 28 days the ovaries, which contain a woman'seggs, start to get some eggs ready to be fertilised. After 10 to 12 days , one egg is moved to the outer surface of the ovary and the follicle bursts which releases the egg into the fallopian tube for its journey to the uterus. The follicle then becomes known as the corpus luteum. When the egg is ripening in the ovary the uterus is preparing itself for the possibility of a growing foetus. Part of this preparation involves the uterine lining becoming thicker and engorged with blood that will nourish the growing embryo. If a fertilised egg is not implanted in the uterus, it sheds its lining resulting in menstruation. The cycle then begins again. Oestrogen is the dominant hormone during the first seven or so days of the cycle, with its level peaking at around day twelve. At this point progesterone which is being produced by the now empty follicle called the corpus luteum, becomes the dominant hormone. If pregnancy does not occur within 10 to 12 days both oestrogen and progesterone levels fall abruptly, triggering menstruation. After menopause, the eggs are no longer released and menstruation ceases, with a resultant reduction in oestrogen and progesterone levels. Female hormones are precursors to other hormones and the body therefore finds another route for production. This route results in the production of a hormone which is similar in structure to the male hormone testosterone and can, in fact, be converted into the male hormone. The hormonal shift put simply results in a slight masculinisation with hair loss in a male pattern (receding temples) and also a general thinning. Often younger women go through periods of time where they do not release an egg but still have menstrual periods. The hormones are therefore imbalanced in this set of circumstances and hair loss is common.
Males do produce a small amount of the female hormones and some work has been done on giving female hormones to men in an attempt to halt their hair loss. This route has not proved too popular to date as the hormones produce feminizing effects.
