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Harv Mens Health Watch 2002 Nov;7(4):6-7
Baldness: Does appearance matter?
It lacks the pain of a heart attack, the threat of prostate cancer, and the complications of hypertension. Still, despite the best efforts of Michael Jordan, millions of men are distressed by hair loss.
Normal hair growth
Whether straight or curly, hair grows in a cyclical pattern that has three phases: growth (called the anagen phase by biologists), involution (catagen), and rest (telogen). The growth phase lasts the longest; its duration determines how long a hair will grow. That's why eyebrow hairs stay short (growth phase, 13 months) while scalp hairs are long (5–8 years). After the growth phase, each follicle undergoes a brief period of involution, when some of its cells die off. Then comes a spell of inactivity. At the end of the rest phase, the hair falls out of its follicle and the cells get back to work, growing a new hair. In humans, each hair follicle cycles independently; that's why humans don't "shed" each season, as many animals do.
At birth, the human body is covered by about 5 million hair follicles, including about 100,000 on the scalp. This number remains constant throughout life, but the activity and productivity of each follicle varies according to a person's age.
In a healthy scalp, more than 90% of hair follicles are in the growth phase, less than 1% are undergoing involution, and 5%–10% are resting.
Fragile follicles
Hair follicles contain living cells. Like all cells, they can be damaged, which halts hair growth. If the problem is mild, the follicle recovers and resumes growing hair, but if it's severe, the damage may be permanent.
Any severe stress, physical or emotional, can damage hair follicles, halting hair growth. That's why patients often lose their hair two or three months after a major illness or traumatic life event. It's a temporary problem technically known as telogen effluvium. It's easy to recognize with a simple pull test: If you can extract more than five or six hairs with a single pull, you're likely to have telogen effluvium, and you'll most likely grow back all your hair within a few months, even without therapy.
Medication can damage hair follicles; chemotherapy drugs are the leading examples. Less often, toxic chemicals, radiation, thyroid disease, or infections can do the job. Skin diseases that produce scarring can also result in hair loss, which may be permanent. Fortunately, all these problems are uncommon. Contrary to popular belief, common woes like seborrhea and dandruff do not cause hair loss.
Normal hair loss
Men with male pattern baldness may not regard it as normal, but it is. Like it or not, losing scalp hair is part of the human condition. It may cause psychological distress that's important in its own right, but it's not a disease.
Virtually all people, male and female, lose scalp hair as they age. In a sense, male pattern baldness, known technically as androgenic alopecia, is just an exaggerated form of a normal event. It has two requirements: a genetic predisposition and the male hormone testosterone.
The genetics of male baldness are complex. Most experts believe that one gene is responsible, but several may play a role. In any case, the abnormal gene has variable penetrance, which means it is more likely to produce hair loss in some men than others. The abnormal gene can be passed down from a mother or a father, and boys or girls can inherit it. But men are much more likely to suffer from the gene's activity because they have the second requirement, testosterone.
Testosterone makes the man: It is responsible for the large muscles, strong bones, and deep voice that characterize the gender. It is also essential for male genital development in fetal life, for the sexual awakening of adolescence, and for libido and fertility in adulthood. Testosterone acts directly on tissues to produce all these effects, but it acts indirectly on the prostate and on hair follicles. In these areas, an enzyme called 5-alpha reductase converts testosterone to dihydrotestosterone (DHT), and DHT acts on the tissues.
DHT stimulates the growth of hair follicles in the beard and body, but it has the opposite effect on scalp hair. Hair loss usually starts between the age of 17 and 40; by 50, about half of all men display some degree of male pattern baldness. It usually begins with a receding hairline over the temples, followed by thinning of the hair at the vertex, or top of the scalp. The rate of hair loss varies considerably; some men go bald in less than 5 years, but most lose their hair gradually, over 15–25 years. On average, men with androgenic alopecia lose about 5% of their scalp hair each year, but the process can slow down or speed up without apparent reason.
Although it's small comfort to balding men, their hair follicles don't actually disappear. Instead, each successive growth phase gets shorter and each resting phase longer. With an abbreviated growth phase, the hair becomes shorter and finer; with an extended resting phase, the hairs are less tightly anchored to the scalp, so they fall out during washing or combing.
Adverse effects
Male pattern baldness is not a disease. Its only consequences are cosmetic, and its only implications are psychological.
Although baldness does not cause disease, it may be a marker for increased cardiac risk. The Harvard-sponsored U.S. Physicians' Health Study found that men with bald spots were more likely to develop coronary artery disease than men with full heads of hair; mild vertex baldness was linked to a 23% increase, moderate baldness to a 32% rise, and severe baldness to a 36% increase in risk. The effect was greatest in men with hypertension or high cholesterol levels. Frontal baldness, the receding hairline, was not associated with cardiac risk.
Treatment
Doctors may not think male pattern baldness is a problem, but many men disagree. That's why 33 million Americans spend about $1.5 billion a year to replace or restore lost hair.
Treatment takes many forms, ranging from wigs and toupees to scalp surgery and hair transplants. Many men prefer wigs to surgery. Some are worn on top of existing hair; others are interwoven with a man's own hair. Interwoven wigs have to be adjusted every few weeks as the natural hairs grow, adding to the expense and inconvenience.
For generations, a bewildering array of concoctions claiming to restore lost hair have been sold to gullible men. In 1989, the FDA issued guidelines that cleared the shelves of many expensive but worthless products. At present, only two drugs are approved for male pattern baldness.
When sold in tablet form, minoxidil is a prescription drug for hypertension. But for more than 10 years it has also been available as Rogaine, a nonprescription lotion for hair loss. Regular Rogaine solution or spray contains 2% minoxidil, extra strength Rogaine, 5%. The drug increases the duration of the hair follicles' growth phase, but it works only on follicles that are still active, and its benefits last only as long as it is used regularly. Rogaine is more effective for bald spots than receding hairlines, but it's only partially effective at that; in one study, 36% of men who had used the product for several years felt it was worth the time and money.
According to the manufacturer, Rogaine should be applied twice daily. Scalp irritation can occur; dizziness and low blood pressure are less common side effects. The drug is expensive.
Finasteride is an oral prescription medication that inhibits 5-alpha reductase, thereby blocking the conversion of testosterone to DHT. In a 5-mg tablet, finasteride is sold as Proscar, for benign prostatic hyperplasia (see Harvard Men's Health Watch, July 2000); in a 1-mg tablet, it's marketed as Propecia, for male baldness.
To date, only four studies of Propecia, all funded by the manufacturer, have been reported. Two of the trials involved a total of 1,553 men with mild to moderate male pattern baldness that was most prominent at the top of the scalp. Half the men were given Propecia, the other half a placebo. After three months, the men who took Propecia were more satisfied with the appearance of their hair: After a year, they had an average of 876 hairs in a 1-inch circle on the scalp, while those treated with the placebo had 769 hairs.
The third trial evaluated 326 men with mild to moderate frontal hair loss; after a year, 50% of the men taking Propecia and 30% of the men taking the placebo thought their appearance had improved. Finally, a small 2002 study (66 men) reported that finasteride increases hair thickness as well as hair counts, thus enhancing its cosmetic benefit.
The 1,879 men in the three large trials were between the ages of 18 and 41, and none was completely bald. Since Propecia will not revive hair follicles that are inactive, it cannot be expected to regrow hair in older men who are bald. As a result, it warrants consideration only by younger men with partial hair loss.
Because Propecia must be taken daily, years of therapy are required to maintain even modest improvements. Propecia is even more expensive than Rogaine. It is well tolerated, but 1%–2% of men experience diminished libido and potency on Propecia. Because finasteride can produce genital abnormalities in males exposed before birth, the drug should never be taken by women of childbearing age.
To treat or not?
From a medical point of view, there is no need to treat normal hair loss. At best, the treatments are only partially effective, and although they are generally safe, some men may experience side effects. Take a look in the mirror and think it over. And before you decide, try to imagine how Michael Jordan would look with a bit of hair.
Clin Exp Dermatol 2002 Jul;27(5):405-9
Epidemiology and genetics of alopecia areata.
The frequency of alopecia areata and observed patterns of heritability are in keeping with a polygenic inheritance model but the genetics of alopecia areata is still poorly understood. The role of environmental factors in triggering disease initiation or exacerbation remains almost entirely speculative. Using the candidate gene approach, three susceptibility/severity factors have been identified. HLA alleles were the first to show a strong association with alopecia areata and some DQB and DR alleles have been demonstrated to confer a high risk for disease by both case-control and family-based studies. Interleukin (IL)-1 cluster genes, mainly the IL-1 receptor antagonist, show a strong association with disease severity in alopecia areata and a number of other autoimmune and inflammatory diseases. Finally, the association of alopecia areata with Down's syndrome, the high frequency of alopecia areata in autoimmune polyglandular syndrome type I due to mutations of the autoimmune regulator (AIRE) gene on chromosome 21q22.3 and the finding of association with MX1, another gene in the Down's syndrome region of chromosome 21 indicate this area of the genome as a promising target for future-family based investigations. The role of individual genes of the MHC, IL-1 cluster or chromosome 21q22.3 is difficult to establish and further genetic and functional investigations are needed to confirm their involvement in the pathogenesis of alopecia areata.
J Dermatol 2002 Jul;29(7):414-8
Effect of two consecutive earthquakes on outbreaks of alopecia areata.
The pathogenesis of alopecia areata (AA) is still unknown. We investigated whether two consecutive earthquakes in Duzce, Turkey within a 3-month interval could precipitate AA. Patients who developed AA after the first earthquake in Duzce were included in this study. The admittance rate and demographic characteristics of AA patients admitted in the same period of the previous year (BE=before earthquake group) were compared to that of AA patients admitted after the earthquake (AE=after earthquake group). The admittance rate and onset of AA after the first earthquake were investigated retrospectively. In addition, possible relationships between the earthquake and age at the first attack, severity of the disease, and ophiasis were studied. The ratio of AA patients in the BE group was 12/1,121 (0.9%), while this value was 26/1,430 (1.8%) in the AE group (p=0.07). There were no significant differences with regard to sex, age of the first attack, severity of the disease, or ophiasis between the two groups. AA appeared between 18-28 weeks after the first earthquake in 14 (53.8%) of the patients. The earthquake did not increase the admittance rate of AA significantly. This finding suggests that a stressful event such a natural disaster is not a unique factor in AA outbreaks.
J Cutan Med Surg 2002 Jan-Feb;6(1):1-9
Effects of finasteride on apoptosis and regulation of the human hair cycle.
BACKGROUND: A number of studies have provided evidence that apoptosis is a central element in the regulation of hair follicle regression. In androgenetic alopecia (AGA), the exact location and control of key players in the apoptotic pathways remains obscure. OBJECTIVE: In the present study, we used a panel of antibodies and investigated the spatial and cellular pattern of expression of caspases and inhibitors of apoptosis (IAPs), such as XIAP and FLIP, in men with normal scalp and in men with AGA before and after 6 months of treatment with 1 mg oral finasteride treatment. METHODS AND RESULTS: Constitutive expression of caspases-1, -3, -8, and -9 and XIAP was detected predominantly within the isthmic and infundibular hair follicle area, basilar layer of the epidermis, and eccrine and sebaceous glands. AGA-affected tissues showed an increase in caspase (-1, -3, -6, -9) immunoreactivity with a concomitant decrease in XIAP staining. After 6 months of finasteride treatment, both caspases and XIAP were similar to levels exhibited by normal subjects. Immunoblot analysis was performed to determine antibody specificity and cellular expression of caspases. Purified populations of keratinocytes, melanocytes, dermal papilla, and dermal fibroblasts derived from human hair follicles were cultured in vitro and treated with 0.5 mm staurosporin. Time-course experiments revealed that processing of caspase-3 is a principal event during apoptosis of these hair cell types. CONCLUSION: These data suggest that alterations in levels of caspases and IAPs regulate hair follicle homeostasis. Moreover, finasteride appears to influence caspase and XIAP expression in hair follicle cells thus signaling anagen, active growth in the hair cycle.
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