THE ACTIVITY OF THE HAIR FOLLICLE 453 clubs (15), though there is no conclusive evidence that they also prolong the period of anagen. This finding may contribute to an understanding of the phenomenon of post-partum hair shedding in women (21). Some- times there is an excessive loss of club hairs a few months after the end of pregnancy, even to the extent of producing a slight baldness. From a recent study (21) it seems that, during the latter half of pregnancy, the proportion of hairs in anagen can rise to 95% or more, i.e. less than 5% of the follicles are in the resting state as compared with a normal average of about 13%. Then after parturition the proportion of active follicles falls rapidly to a level of less than o/ 65/o, and club hairs are shed. It is reasonable to conclude that something produced during pregnancy pro- longs the active phase, but that after parturition such follicles are almost synchronously precipitated into catagen, so the anagen count falls. The experiments on the rat suggest that oestrogen could be responsible, and the large amounts of oestrogen produced by the placenta may well be implicated. At the time of labour, for example, the urinary oestriol may be a thousand times normal, but it falls rapidly within a month of delivery (22). Environmental factors There is substantial evidence that the photoperiodic affect of light has an important influence on the moult cycles in animals such as the mink (23), the weasel (24), the ox (25) and the ferret (8) and there is some evidence that temperature may be of importance in the mountain hare (9). In man there is little doubt that psychological states can affect the shedding of scalp hairs. Kligman (3) has described a spectacular case of psychogenic hair shedding, in which a prisoner, who had undergone a series of trials for murder over a period of three years, began to lose hairs at the rate of 1,000 per day about ten weeks after he was finally convicted. DEVELOPMENTAL AND AGEING CHANGES IN THE FOLLICLE During the life-time of the follicle, the type of hair produced may change. Everyone is familiar with the "puppy" fur of young animals, which is flufiler and finer than the adult coat. The maturation of the hair can be prevented by removal of the pituitary, and thus it appears to be brought about by a pituitary hormone. It is generally assumed that the growth hormone is responsible, but there is evidence to suggest that the lactogenic hormone may be the important factor (26). The succession of hairs in any particular follicle in man provides a rather more complex problem. In certain regions of the body the type of hair changes at puberty and long terminal hairs are produced instead of fine,

454 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS short, down hairs. The characteristic male facial, pubic, axillary and body hair develops i•x response to androgenic hormones. But women also develop axillary and the lower triangle of pubic hair, and this depends not on the presence of the ovaries but of the adrenals (27). Abnormally, but not perhaps infrequently, women tend to develop hirsutism of the male type. Sometimes this is associated with abnormally high excretion hence pro- duction-of low potency adrenal androgens (17-oxosteroids) sometimes it is not, but it seems that some of these cases of so called "idiopathic" hirsutism may be due to the production of the potent male hormone testosterone (28). There is no reason to suppose from these facts that different regions of the body respond to specific steroid hormones it is only necessary to postulate that they have different sensitivities to androgens. Follicles of the axillary and lower pubic regions are most sensitive, and will respond to the low potency androgens produced by the adrenal of the normal female. The upper pubic, body and facial hair need either the high potency testo- sterone, produced normally in the male and perhaps abnormally in the female, or high amounts of adrenal 17-oxosteroids. It is something of a paradox that the scalp follicles which require no hormonal stimulation to produce long hair, in some individuals change under the influence of androgens to produce only fine and cosmetically useless fluff. Follicles do not seem to be lost in the process of balding, they regress. Both the dermal papilla and the matrix become proportionally smaller (29) and the surrounding dermis appears to age with abnormal rapidity (30). It is now undisputed that the disposition to patterned bald- ness is hereditary but that, as first suggested by Hamilton (31), its mani- festation requires the presence of male hormone, as well as the ravages of time. Eunuchs do not go bald unless they are treated with testosterone but the follicular regression of baldness cannot, apparently, be reversed by castration even if one were prepared to make the sacrifice (32). Patchy baldness, or alopecia areata, like patterned baldness, does not involve complete cessation of follicular activity, but the hair bulbs remain in a phase of growth corresponding to that of early anagen and no clinically detectable hairs may be present (33). The whole follicle is very much smaller than normal. The papilla is reduced in size, but the matrix is proportionally smaller still and thus the proportions of the follicle are changed (29). A granular infiltrate has been observed in the dermis. The condition is reversible under treatment with adrenocortical steroids such as cortisone or prednisone. It may cure itself spontaneously, and it is claimed, on what seems rather inconclusive evidence, that cure can be aided by miscellaneous local treatments. (Received: $1st January 196•t.)