As a Senior in college, I took a class on evolutionary medicine with Professor Paul Ewald. For my final project, I decided to explore male pattern baldness from an evolutionary perspective. This topic, to my knowledge, had never been previously addressed. I’ve included my entire (lengthy) paper below.
Why we go bald: an evolutionary hypothesis
Pattern baldness (PB), also called androgenetic alopecia, is characterized by a progressive patterned hair loss from the scalp, which begins usually during the twenties or thirties (Odom et al., 2000). PB was initially thought to occur as a result of shaving (Blaine, 1899). Because frequent use of the razor was believed to stimulate hair growth, researchers believed that the energetic drain to supply the rapid growth of the beard necessarily caused a weakness in other parts of the body and led to decreased hair growth on the scalp. Currently, it is believed that PB results from a combination of androgen levels and a genetic predisposition (Bertolino & Freedberg, 1987; Odom et al., 2000).
Pattern baldness has never been looked at from an evolutionary perspective. With the recent sequencing of the human genome, much research has focused its attention on finding genes that cause baldness, as well as other diseases such as Alzheimer’s, cancer, heart disease, and even infertility. However, most of those studies have ignored the role that the environment plays in the development of disease, and they overlook the importance of looking at the disease from an evolutionary approach. How can a gene for infertility possibly persist in our population at such a high rate? Why would a gene for cancer not be weeded out by natural selection? Some of these problems can be resolved if we consider the role of pathogens in these diseases. Pathogens are constantly evolving with their hosts: when a host discovers a way to fight the infection of a pathogen, the pathogen will be under great selective pressure to evolve and change its tactics. In a sense, we are involved in a never-ending arms race where neither the host nor the pathogen ever gets the upper hand for too long. This explains the persistence of infectious diseases in a population. However, because most chronic diseases take a long time to develop and do not have a clear pathogenic cause, we often overlook the possibility of infectious causation in the development of the disease. This paper will review the literature on pattern baldness and will attempt to understand it by looking at genetic, infectious, and non-infectious environmental causes using an evolutionary approach.
Hair plays no vital function in human physiology, as we can live perfectly well without having any hair (Bertolino & Freedberg, 1987). Hairs probably first evolved as a mechanoreceptor used to sense the outside environment. They are now used mainly for thermal insulation in other mammals. In humans, although hair is not essential, some hairs actually have specific functions. Pubic and auxiliary hairs help in disseminating odors, eyelash and eyebrow hairs protect the eyes, scalp hairs protect the head from the sun and are used for beauty, and beard hairs in men are used for sexual displays.
The human scalp normally contains 100,000 hairs that follow a specific growth cycle (Odom et al., 2000). The first phase is the anagen, or growing phase, which lasts about 3 years. During this period, hair grows about 0.37mm daily. Hairs then enter the catagen phase, which is a controlled regression of hair growth, a transitional phase between the growing and resting phase that lasts 1 or 2 weeks. Finally hairs enter the telogen phase, a resting state that lasts between 3 and 4 months until the hair falls out. A healthy human scalp contains 90% anagen hairs, and about 10% catagen or telogen hairs.
In PB, the hair loss is a result of an increase in the ratio of telogen to anagen hairs and the miniaturization of the hair follicle (Rushton et al., 1991; Sinclair, 1998). The anagen phase becomes progressively shorter and the telogen phase becomes longer. Since the length of the hair is a result of the duration of the anagen phase, each hair becomes progressively shorter than its precursor. Eventually, the hair becomes so short that it does not reach the skin surface. In addition, because telogen hairs are not as well attached to the follicle as are anagen hairs, the increase in telogen hair count results in an increase of hair shedding in individuals with PB. With every completion of the hair cycle the hair follicle becomes progressively smaller, and thus the hair they produce becomes smaller as well. The scalp is left with only vellus hairs, which are very fine and lack pigmentation (“peach fuzz”).
As suggested by the name, hair loss in PB follows a specific pattern, as described by Hamilton (1951, cited in Sinclair, 1998). In men, it generally begins with a bitemporal recession of the front hairline, followed by thinning over the vertex (Figure 1). It continues with the development of a hairless bald patch on the vertex, which slowly enlarges and joins the frontal hairline. In women, the hair loss pattern is different (Figure 2). There is little recession of the front hairline; instead there is a diffuse hair loss throughout the midscalp (Odom et al., 2000). PB affects about 30% of Caucasian men in their thirties, 40% in their forties, and so on until age 70 (Sinclair, 1998). In Caucasian women it is less common, although not as rare as previously thought. One study of over 500 women found that PB affected 13% of premenopausal women, and 37% of postmenopausal women (Venning & Dauber, 1988, cited in Keratin.com). The rates of PB are also different in other ethnic groups. Male African Americans are four times less likely to develop PB than are Caucasian males (Setty, 1970, Table 1).
Table 1. Age range and incidence of hair patterns of scalp of 300 Caucasian and 300 African American males. From Setty, 1970.
Androgens are hormones that play an essential role during adolescence in inducing and maintaining secondary sexual characteristics such as pubic and other body hairs. Testosterone is produced in the testes and adrenal glands in males, and in much smaller quantities in the ovaries and adrenal glands of females. Androgens are responsible for promoting the growth of pre-pubertal vellus hairs into pigmented terminal hairs (Sinclair, 1998). Paradoxically, the same androgens that promote adult body hair growth also seem to be involved in reducing scalp hair count and in the development of male pattern baldness. Hamilton (1942, cited in Hamilton, 1960) has shown that androgens are required in the development of PB, as men who have been castrated at an early age do not develop it. Furthermore, males who were castrated after they had begun balding experienced no further hair loss, and some of these even had increases in hair growth (Hamilton, 1960). In addition, castrated men given testosterone showed a continuation of hair loss.Although many bald men claim that their baldness is a sign of maleness and virility, no studies have found differences in hormone levels or other measures of masculinity between PB patients and controls (Phillipou & Kirk, 1981, cited in Herrera & Lynch, 1990). Instead, baldness seems to be a result of an increased ability to use testosterone and not an increase of testosterone per se. Researchers have found that the sebaceous glands of bald men have twice the number of testosterone receptors than those of controls, which makes their scalp more sensitive to androgen levels (Sawaya, 1986). In addition, the hair follicles in the scalps of individuals with PB have elevated levels of dihydrotestosterone (DHT) as compared to controls (Schweikert & Wilson, 1974, cited in Ellis et al., 2001). DHT is catalyzed from testosterone by a 5α-reductase enzyme present in hair follicle cells. DHT seems to be responsible for the miniaturization of hair follicles on the scalp, which turn the existing pigmented hairs into vellus hairs as they become thinner and smaller (Sinclair, 1998). This miniaturization results in the observed hair loss and consequent baldness.
Genetics also seem to play a role in the development of PB. Only two studies have been conducted to examine the prevalence of PB in twins. However, the results of twin studies must be looked at cautiously because they do not distinguish between genetic influences and the effects of sharing a common environment. The numbers must be read as the maximum possible genetic involvement in the development of the disease, not as its actual genetic contribution to because pathogens or other common environmental factors may contribute significantly to the disease.
The first twin study was conducted with 18 pairs of white American twins registered in the Twin Registry files (Lynfield, 1974). Of eight monozygotic twins that showed PB, all were concordant. Of five dizygotic twins that showed PB, four were concordant and one was discordant. The problem with this study, aside from the small sample size, is that subjects were selected on the basis of having a previous diagnosis of psoriasis or atopic dermatitis. It is likely that their results overestimated the actual number of twin concordance because a preexisting skin disease may have contributed to the development of PB. The second study examined 135 pairs of twins found in an Adult Twin Registry in Japan (Hayakawa et al., 1992). They observed that the degree of hair loss was identical in 92% of monozygotic twins, while it was identical in 67% of dizigotic twins. However, this study failed to distinguish between individuals with a full head of hair or those with PB, so they might have also overestimated the real figure.
Initially, the expression of PB was believed to be an autosomal dominant phenotype in men and an autosomal recesive phenotype in women, resulting in a classic mendelian pattern of inheritance (Osborn, 1916, cited in Küster & Happle, 1984). However, although careful family studies of the inheritance of MPB are lacking, new studies argue of a polygenic inheritance of the trait (Küster and Happle, 1984; Ellis et al. 2001).
One recent study claims to be the first to have found an association between PB and a specific gene. Ellis et al. (2001) have found a significant association between PB and a gene that codes for an androgen receptor. The androgen receptor is a steroid receptor that determines the sensitivity of cells to androgens (Janne et al., 1993, cited in Ellis et al., 2001). It has been shown in previous studies that the scalps of balding men exhibit higher levels of the androgen dihydrotestosterone (Schweikert & Wilson, 1974, cited in Ellis et al., 2001). Furthermore, expression of the androgen receptor is known to be higher in the scalps of balding subjects than in the scalps of controls (reviewed in Ellis et al., 2001). Ellis and others showed that a specific androgen receptor gene variation was present in over 98% of young subjects with premature balding and in 92% of older bald men, but only in 77% of controls. They concluded that the specific variation of the androgen receptor gene is necessary, but not sufficient for the development of PB.
From an evolutionary perspective, the presence of a baldness gene could be explained if baldness posed no negative effects on reproductive success. This is unlikely, since baldness has been shown to have negative effects on body image satisfaction (Cash, 1992). Individuals feel less satisfied about their overall physical appearance, they worry more about their current and future state of baldness, and show less adaptive psychosocial functioning. Most importantly, the most distressed balding men are those who are younger and are romantically unattached—men who are looking for a mate. If their social functioning is impaired because of their balding, as has been shown (Cash, 1992), then balding would certainly reduce their reproductive success and the gene for baldness would thus be weeded out of the population. In addition, because balding is too prevalent in our population, it cannot be sustained by mutation. Therefore, genetics cannot fully explain the cause of baldness.
Inflammation and Infection
New research has shown evidence that infectious causation may be partly responsible for PB. First, some types of baldness have already been shown to be a result of infectious diseases such as influenza, typhus, lyme meningitis, tick-borne encephalitis (Cimperman, 1999), HIV (Jan & Roudier-Pujol, 2000), scarlet fever, and pneumonia (Weigand, 1969). Second, there is growing evidence of the presence of inflammation in the scalp of balding individuals (Kligman, 1988; Young et al., 1991; Jaworsky et al., 1992; Piérard et al., 1996; Sueki et al., 1999; Mahé et al., 2000). Finally, PB has been associated with an increased risk of heart disease (Herrera & Lynch, 1990; Trevisan et al., 1993; Ford et al., 1996; Sasmaz et al., 1999). Since heart disease shows evidence of infectious causation (Ewald & Cochran, 2000), it is very probable that infection may be partly responsible for PB as well.
The presence of inflammation in the scalps of balding patients is now beginning to be recognized. Kligman (1988) was the first to notice the difference in the degree of inflammation in balding as opposed to control subjects. He observed the presence of substantial lymphohistiocytic infiltrate and abnormal inflamed streamers in the scalps of balding men, both of which were rare in non-bald controls. The inflammations in the scalp were localized around the infundibulum and sebaceous glands, and numerous lymphocytes, macrophages, and mast cells were found in those areas. The density of follicles was not noticeably diminished, although some were destroyed by the intense inflammatory infiltrate. Kligman explained that the chronic inflammation prevents the anagen follicles from being fully reconstructed during each new cycle, which explains the shortening of the anagen phase in PB. He concluded his paper by stating that PB is an “inflammatory disorder that should not be construed as premature aging.” He hypothesized that suppression of the inflammation could decelerate the process of PB. Furthermore, he noted that bald people often report scaling and itching during the early stages, presumably because of the inflammation. Finally, Kligman suggested studying PB in connection with seborrheic dermatitis and dandruff. Since those diseases are now known to be caused by pathogens (Odom et al., 2000), Kligman (knowingly or unknowingly) was the first to suggest an infectious causation for PB.
Subsequent studies have also reported the presence of inflammation on the scalp of individuals with PB. Young et al. (1991) found immunoglobulin M or C3 (or both) present on the basement membrane of 96% of individuals with PB and on 12% of controls. The presence of immunoglobulins on the scalp indicates that an antigen is present, perhaps a microbe. They also found porphyrins in 58% of PB subjects and in 12 % of controls. Porphyrins are water-soluble, nitrogenous biological pigments (Encyclopædia Britannica, 2001). Because Propionibacterium acnes has been shown to produce porphyrins (Cornelius & Ludwig, 1967, cited in Young et al., 1991), they suggested that P. acnes may be involved in the process of PB. The production of porphyrins by this organism may result in the observed inflammation when light-activated porphyrins oxydize squalene to produce a toxic inflammation. Since PB begins in areas that are most frequently exposed to the sun, Young and coworkers argued that light may excite porphyrin production by the resident flora, producing an inflammatory reaction. They concluded their paper by suggesting the use of antimicrobials to reduce the number of natural flora and a reduction in sun exposure to help control the extent of PB.
Other studies further support the presence of inflammation in PB. Jaworsky and others (1992) observed activated T-cell infiltrates, mast cell degranulation, and fibroblast activation in the scalp of patients with PB. They suggested that the inflammation might impair the normal hair cycle. Sueki and coworkers (1999) noticed a significantly greater number of lymphocytic inflammations around the hair follicle cells in PB patients than in controls. They concluded that the inflammation “may be, at least in part, responsible for the development” of PB.
With the growing evidence of the presence of inflammation in PB, one group decided to study the effects of an antimicrobial lotion on the progress of PB. Piérard and others (1996) supplied 20 men with PB with a lotion containing piroctone olamine and triclosan. Piroctone olamine is a powerful antifungal agent and triclosan is a common antibacterial. Patients were told to apply the lotion daily to the scalp. Long-term application of the cream resulted in decreased inflammation of the scalp as revealed by a decrease in the number of lymphosites, decreased number of skin flora, and decreased hair loss. The researchers suggested preventing PB by controlling the microorganisms that inhabit the scalp, which have been shown to be potent elicitors of the immune response (Piérard-Franchimont, 1995, cited in Piérard, 1996).
Further support for the role of infection in PB came from Dr. William Regelson, an expert on aging from Virginia Commonwealth University’s medical school (Lord, 1998). He observed that the common eyebrow mite, Demodex follicularum had infested the follicles of 50 balding men and women that he examined. Interestingly, D. follicularum has long been known to cause mange in animals, a disease characterized by inflammation, itching, thickening of the skin, and hair loss (Encyclopædia Britannica, 2001). Regelson speculated that the scalps of some individuals are sensitive to the mites, and thus become inflamed and interrupt the normal hair cycle.
Finally, a review article by Mahé and others (2000) suggested a way in which to incorporate inflammation with the previously proposed hypothesis of PB: androgens and genetics. It has been shown that the excess of DHT in the scalp enlarges the sebaceous glands (Lattanad & Johnson, 1975; Bergfeld, 1995, both cited in Mahé et al., 2000). As a result, the enlarged sebaceous glands may provide a more comfortable niche for pro-inflammatory microorganisms. Mahé and coworkers argue that for each individual, the causal agent may be different (androgens, microbial flora, stress, genetic imbalance). However, they stress the importance of inflammation in the development of PB, and suggest using an anti-inflammatory strategy to help prevent or control the progress of PB.
Pattern Baldness and Heart Disease
Well-known risk factors for the development of heart disease include age, hypertension, smoking, family history, and diabetes (Reviewed in Herrera & Lynch, 1990). However, new research has implicated PB as another risk factor for heart disease. This fact is interesting, because current research has also presented supporting evidence for infectious causation of heart disease (Ewald & Cochran, 2000). Heart disease has already been associated with other infectious diseases such as periodontitis (DeStefano et al., 1993). It has been proposed that the same bacteria that cause periodontitis are the causative agents of heart disease (Mattila et al., 1989, cited in DeStefano, 1993). Therefore, if PB is shown to correlate with heart disease, and if heart disease is shown to be caused by pathogens, then it is possible that pathogens are also responsible for the development of PB.
A paper by Herrera & Lynch (1990) reviewed the literature on baldness and heart disease, and concluded that the presence of PB does increase an individual’s risk of heart disease, but not as much as smoking or hypertension. Further studies have been conducted to assess exactly what the risks are with PB and heart disease. A longitudinal study conducted in Italy with 872 men set out to examine the relationship between PB and heart disease over a 15-year period (Trevisan et al., 1993). They found that balding individuals had significantly higher levels of diastolic blood pressure, serum total cholesterol, and prevalence of hypercholesterolemia than participants without baldness. Furthermore, within the bald populations, individuals with higher degrees of baldness had higher diastolic blood pressure than those with fewer degrees of baldness.
A study by Ford et al. (1996) also found a relationship between PB and heart disease. They followed 3,994 males for a period of 15 years. Researchers found evidence that men younger than 55 with severe PB had significant increases in rates of mortality and heart disease (Table 2). They suggested that PB was not a direct risk factor for heart disease, but instead it worked as a marker for some other underlying risk factor.
Table 2. Proportional hazards model examining male pattern baldness and ischemic heart disease incidence among all men and among men younger than age 55 years. All data were adjusted for age, race, education, systolic blood pressure, antihypersensitive medication, cholesterol, smoking, body mass index, and diabetes. From Ford et al., 1996.
Further support for the increased risk of heart disease with PB came from Sasmaz and coworkers (1999) who analyzed the difference of lipid parameters in 41 men with PB and 36 age-matched controls. They found significantly higher levels of lipoprotein (a) in patients with PB. This is important because other studies have found that high levels of lipoprotein (a) are by themselves a risk factor for heart disease (Ari & Yigitoglu, 1997, cited in Sasmaz et al., 1999). In addition, 47% of PB subjects had lipoprotein (a) levels higher than the level critical for atherosclerotic heart disease, as compared to 30% of controls. They also found higher levels of total cholesterol and LDL-cholesterol in PB subjects.
The above-mentioned articles suggest a link between heart disease and PB. This link is suspiciously similar to the link between heart disease and periodontitis (DeStefano et al., 1993). Periodontitis is an inflammation of the soft tissues around the teeth caused by bacteria (Encyclopædia Britannica, 2001). The bacteria that causes periodontitis has also been implicated in causing heart disease (Mattila et al., 1989, cited in DeStefano, 1993). If PB is an infectious disease, as has been suggested in the articles above, then perhaps the same pathogens that cause the inflammation of the scalp are also involved in causing inflammation of the arteries in heart disease.
There are four basic treatments available for individuals afflicted with PB to manage their baldness. The first is simply to do nothing. Because hair is not essential for survival, bald individuals are able to live healthy lives despite their lack of scalp hair. However, baldness has been shown to have negative psychosocial effects (Cash, 1992) so many individuals choose to do something about it. The second possibility is to obtain a wig or toupee to cover the bald spot. A third possibility is hair transplant surgery. This works by transferring hair follicles from one area of the scalp to another. Transferred hairs survive, grow, and retain the same characteristics they had in their original site (Norwood, 1973). It has been shown that occipital hairs that are transplanted onto the scalp maintain their resistance to PB, while scalp hairs transplanted to the forearm miniaturize in synchrony with their neighbors on the scalp (Norstrom, 1979, cited in Sinclair, 1998).
The fourth possibility is to take medication. Currently, there are two drugs in the market aimed at reducing hair loss and promoting hair growth. The first is minoxidil (Rogaine), which does not require a prescription. The product is applied directly to the scalp, and works by “revitalizing shrunken hair follicles and increasing their size,” although the exact mechanism is not known. The second drug is finasteride (Propecia), which is taken orally. It works by blocking the conversion of testosterone to DHT, and thus reduces scalp and serum DHT concentrations. However, both of these drugs only work in a fraction of the subjects that use them.
As I have shown, we are still far from determining with certainty the exact causes of pattern baldness. PB baldness is not simply a consequence of aging, as once thought; instead, it is an inflammatory disorder of the scalp. It is likely that genetic, infectious, and non-infectious environmental causes play a role in the development of the disease. Genetic instructions may code for the production of excess DHT, which enlarges the sebaceous glands and provides a more hospitable habitat for microbes. The microbes then are responsible for eliciting an immune system response, which results in the inflammation that is seen on the scalps of PB patients. Finally, light may further exacerbate the problem by acting on bacteria to produce porphyrins, which also excite the immune system and cause inflammation. It is only by considering all three possible causes for a disease that we are able to fully comprehend its etiology and find ways to treat it, or ultimately, prevent it from developing in the first place.
Further research should be conducted to determine the effects of antimicrobial creams on the progression of PB. As mentioned above, it appears that antibiotics may help in reducing hair loss by reducing the number of microbe flora and reducing inflammation (Piérard et al., 1996). In addition, studies should examine the effects of anti-inflammatory drugs such as aspirin on reducing inflammation of the scalp. Perhaps the combination of antimicrobial and anti-inflammatory lotions with minoxidil or finasteride will result in new drugs that will be more effective in attacking the many causes of baldness.
Bertolino, A. P., Freedberg, I. M. (1987) Disorders of epidermal appendages and related disorders: Hair. In Dermatology in General Medicine. In Fitzpatrick, T. B., Eisen, A. Z., Wolff, K., Freedberg, I. M., Austen, K. F. (Eds). Dermatology in General Medicine. New York: McGraw-Hill Book Company.
Blaine, J. M. (1899) Etiology of alopecia prematura. Journal of the American Medical Association 32: 524-525.
Cash, T. F. (1992) The psychological effects of androgenetic alopecia in men. Journal of the American Academy of Dermatology 26: 926-931.
Cimperman, J., Maraspin, V., Lotrič-Furlan, S., RužićSabljić, Avšič-Zupanc, T., Stre, F. (1999) Diffuse reversible alopecia in patients with Lyme meningitis and tick-borne encephalitis. Middle European Journal of Medicine 111: 976-977.
DeStefano, F., Anda, R. F., Kahn, H. S., Williamson, D. F., Russel, C. M. (1993) Dental disease and risk of coronary heart disease and mortality. British Medical Journal 306: 688-692.
Ellis, J. A., Stebbing, M., Harrap, S. B. (2001) Polymorphism of the androgen receptor gene is associated with male pattern baldness. The Journal of Investigative Dermatology 116: 452-455.
Encyclopædia Britannica (2001) “Mange.” Britannica.com.
Encyclopædia Britannica (2001) “Periodontitis.” Britannica.com.
Encyclopædia Britannica (2001) “Porphyrins.” Britannica.com.
Ewald, P. W., Cochran, G, M. (2000) Chlamidia pneumoniae and cardiovascular disease: an evolutionary perspective on infectious causation and antibiotic treatment. Journal of Infectious Diseases 181: 394-401.
Ford, E. S., Freedman, D. S., Byers, T. (1996) Baldness and ischemic heart disease in a national sample of men. American Journal of Epidemiology 143: 651-657.
Hamilton, J. B. (1958) Age, sex, and genetic factors in the regulation of hair growth in man: a comparison of Caucasian and Japanese populations. In Montagna, W., Ellis, R. A. (Eds) The Biology of Hair Growth. New York: Academic Press, Inc.
Hamilton, J. B. (1960) Effect of castration in adolescent and young adult males upon further changes in the proportions of bare and hairy scalp. The Journal of Clinical Endocrinology and Metabolism 20: 1309-1318.
Hayakawa, K., Shimizu, T., Ohba, Y., Tomioka, S., Takahasi, S., Amano, K., Yura, A., Yokoyama, Y., Hayakata, Y. (1992) Intrapair differences of physical aging and longetivity in identical twins. Acta Genet Med Gemellol 41: 177-185.
Herrera, C. R., Lynch, C. (1990) Is baldness a risk factor for coronary artery disease? A review of the literature. Journal of Clinical Epidemiology 43: 1255-1260.
Jan, V., Roudier-Pujol, C. (2000) Trichopathie associée à l’infection par le virus de l’immunodéficience humaine. Ann Dermatol Venereol 127:1534-1536.
Jaworsky, C., Kligman, A. M., Murphy, G. F. (1992) Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis. British Journal of Dermatology 127: 239-246.
Kligman, A. M. (1988) The comparative histopathology of male-pattern baldness and senescent baldness. Clinics in Dermatology 6: 108-118.
Küster, W., Happle, R. (1984) The inheritance of common baldness: Two B or not two B? Journal of the American Academy of Dermatology 11: 921-926.
Lord, M. (1998) Is a common bug cutting your rug? US News and World Report 124: 12.
Lynfield, Y. L. (1974) Skin diseases in twins. Archives of Dermatology 110: 722-724.
Mahé, Y. F., Michelet, J. F., Billoni, N., Jarrousse, F., Buan, B., Commo, S., Saint-Léger, D., Bernard, B. A. (2000) Androgenetic alopecia and microinflammation. International Journal of Dermatology 39: 576-584.
Norwood, O. T. (1973) Hair transplant surgery. Springfield: Charles C. Thomas Publisher.
Odom, R. B., James, W. D., Berger, T. G. (2000). Diseases of the Skin. New York: WB Saunders Company.
Piérard, G. E., Piérard-Franchimont, C., Nikkels-Tassoudji, N., Nikkels, A. F., Saint Léger, D. (1996) Improvement in the inflammatory aspect of androgenetic alopecia. A pilot study with an antimicrobial lotion. Journal of Dermatological Treatment 7: 153-157.
Sasmaz, S., Senol, M., Ozcan, A., Dogan, G., Tuncer, C., Akyol, O., Sener, S. (1999) Journal of the European Academy of Dermatology and Venereology 12: 123-125.
Sawaya, M. E. (1986) Blame it on your sebaceous glands. Science News 129: 318.
Setty, L. R. (1970) Hair patterns of the scalp of White and Negro males. American Journal of Physical Anthropology 33: 49-56.
Sinclair, R. (1998) Male pattern androgenetic alopecia. British Medical Journal 317: 865-869.
Sueki, H., Stoudemayer, T., Kligman, A. M., Murphy, G. F. (1999) Quantitative and ultrastructural analysis of inflammatory infiltrates in male pattern alopecia. Acta Derm Venereol 79: 347-350.
Trevisan, M., Farinaro, E., Krogh, V., Jossa, F., Giumetti, D., Fusco, G., Panico, S., Mellone, C., Frascatore, S., Scottoni, A., Mancini, M. (1993) Baldness and coronary heart disease risk factors. Journal of Clinical Epidemiology 46: 1213-1218.
Weigand, D. A. (1969) Alopecias—diagnostic and pathogenic considerations. In Nebraska, S. M. (Ed)
Young, J. W., Conte, E. T., Leavitt, M. L., Nafz, M. A. Schroeter, A. L. (1991) Cutaneous immunopathology of androgenetic alopecia. Journal of the American Ostheopathology Association 91: 765-771.