256 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS Estrogen can inhibit the growth promotion of PGH as well as inhibiting the gonadotropic secretion of the anterior pituitary. Estrogen also has the faculty of stimulating the output of adrenocorticotropic hormone (ACTH). ACTH is capable in turn of aggravating acne. Another estrogen effect is the hastening of skeletal maturation. Estrogen, used experimentally in ache therapy, can produce damage to the testicular tubules. The adrenocorticotropic hormones of the anterior pituitary elicit the adrenal cortical secretion of (1) DOCA, which regulates water metabolism, (2) the adrenal SFN hormones, which govern sugar, fat, and nitrogen metabolism--cortisone and corticosterone. The adrenal SFN hormones accelerate nitrogen catabolism, and so are antagonistic in effect to PGH. They have been demonstrated to have some bearing on the metabolism of compounds with SH groups--thus perhaps some bearing on skin meta- bolism. •6 Another adrenal cortical hormone is (3) adrenosterone, which may be a partial degradation product of the SFN hormones. The next area for consideration, and the particularly new aspect of the theory that is here presented, is the interplay between the sebaceous gland and the eccrine sweat gland. Because ache vulgaris is more severe in the tropics, where sweating is increased, the clinical effect of decreased sweating in patients with acne was assayed. •7 A complex form of aluminium hydroxychloride* was tested on skin in a 20 per cent aqueous solution. Thirty-three patients, treated for periods up to six monthsl between August 1954 and August 1956, showed accelerated initial clearing and easy maintenance of the end resultma less oily, acne-free skin. They were contrasted with 33 control patients. Laboratory investigators have observed that the rate of sebum spreading over a wet skin is of the order of at least 108 times the rate of flow and spread on a dry skin. •8 Conversely, variations in the level of ether-soluble substances (fats) in skin directly parallel the level of sweat delivery in the skin area. •9 Thus, an antiperspirant becomes a logical empirical sebaceous gland inhibitor. In the pathogenesis of acne, then, the substantial increase in sebum during puberty may be attributed to increased sweating. What are the causes of increased sweat production ? Normally, tempera- ture is an important conditioning factor. Hyperidrosis has two distinct mechanisms. One is an abnormal increase in nerve impulses to the sweat gland--such as may occur in central nervous system disorders and the other is emotional stimuli--such as fear, anger, etc. •ø Even straight mental problems--e.g., arithmetic---have been shown able to evoke sweat. The disturbance in all these cases produces the liberation of excessive amounts of acetylcholine, and subsequent excessive perspiration. * Astringen, supplied through the courtesy of Robinson, Wagner Co., New York City.

THE CHEMISTRY OF ACNE VULGARIS 257 \ The thought now occurs that the known emotional problems and emotional flux of puberty, the pubertal crisis, can evoke sweating which in turn can greatly increase the amount of sebum flow. As is generally accepted (and is the subject of a study by the author now with the New York City Board of Health and Board of Education), acne does not occur in all teenagers. Ache vulgaris is, then, not a universal response, or adaptation. At this date, only a suspicion can be recorded that it may have to do with unusually severe problems in adaptation. Now, the basic pattern of development of the comedone of ache vulgaris can be postulated as follows: A. The marked physical growth of puberty is accomplished largely via the Pituitary Growth Hormone. It, or a parallel hormone, causes simple increase in size of the sebaceous gland, with a directly propor- tional increase in sebum output. The PGH, which regulates protein armbolism, may relate again to the formation of the horny plug in the hair follicle, since this is a protein product. B. The stress or alarm reaction consists of increased nerve impulses to the hypothalamus, which in turn stimulates the anterior pituitary to put forth ACTH, which in turn again causes increased adreno- cortical hormone secretions. The adrenocortical SFN hormones--which cause nitrogen metabolism or breakdown--can foster the development of acne, apparently by an effect on the hair follicle hyperkeratotic or parakeratotic scale. Corticosterone and cortisone can induce the resting phase in the hair cycle--at which time the acne lesion appears. The increased 17 ketosteroid urinary output at puberty may reflect stimulation of the entire adrenal cortex rather than androgenic steroids only. C. Alarm or stress---the emotional stresses of puberty--produce increased nerve impulses (anatomically sympathetic pharmacologically parasympathetic) to the sweat glands, which in turn produce a tremendously increased amount of sebaceous gland secretion. Thus the great increase in sebaceous materiM behind the narrow plugged follicular orifice gives rise to the cornedone. (A whole series of secondary infections, and bacterial allergic pheno- mena must be considered in the evolution of acne pustule.) As the stresses of adolescence subside, the tendency for comedone formation abates spontaneously. The decisi9e reasons for acne vulgaris appear to be the adaptations unique to puberty. As these adaptations are inevitable, and culturally desirable, the treatment of acne vulgaris still remains in the exclusive sphere of derma- tology.