190 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS emptied to a significantly lesser extent than with the stronger solvents and therefore takes just about as long to refill. The other hypothesis is that the stronger lipid solvents also act as more powerful stimulants to lipid replacements so that each more drastic removal is at the same time a proportionately stronger stimulus to lipid production and delivery and consequently to accelerated rate of replacement of the somewhat larger amounts of lipids removed. This latter hypothesis is in agreement with the common clinical observation that in many instances the stronger and more effective the lipid solvent used to relieve "oily skin, .... greasy skin," "seborrhea," oily hair and scalp, etc., the greater the likelihood of producing a "compensatory" hypersecretion of grease, a "compensatory" seborrhea especially after long periods of repeated use. Clinical Implications and .4pplications of Modern Concepts of Sweat/Lipid Relationships and Interdependence Whenever the production, delivery and/or distribution of sweat and surface lipids are disturbed, whenever they are for any reason impaired in quantity, quality or ratio, whenever there are significant aberrations from the norm in the supracorneal surface film, in the contents of the intracorneal receptacle or in the quantity or quality, configuration or spacial arrangements, production or desquamation of the keratin of the horny receptacle itself--whenever any such changes occur, some abnor- mality of the skin's surface and of the skin's appendages (hairs, nails) can result. These abnormalities range from the mildest and most inapparent cosmetic deviations to the most severe and incapacitating cutaneous and generalized diseases. Unfortunately, I shall be able to present only a selected few of these to you today--and these only in fragmentary fashion- for their complete and detailed exposition would embrace a substantial segment of modern dermatology and cosmetology. Role of the Surface Film in Controlling Susceptibility to Infection The uninterrupted physical continuity and intactness of the skin's surface is, of course, an important mechanical barrier to the entry of infec- tions. Moreover, as emphasized by Pillsbury and collaborators, the dry- ing out of the surface and desquamation of dry horny substances (42a and b), (and also the dilution and washing off by sweat), are in and of themselves mechanical and physical destroyers and removers of myriads of potentially pathogenic microbrganisms and other potentially damaging agents and substances. There is, however, in addition to these simple physical mechanisms, a much more complex arid specific chemical device by means of which the healthy skin's surface destroys the constantly arriving, ever multiplying and menacing, obligatorily or facultatively pathogenic micro6rganisms.

CLINICAL DISTURBANCES IN SWEATING 191 As I have previously indicated, a number of fatty acids are normally pres- ent on the skin, and among these there are several wl•ich have been demonstrated to possess considerable antibacterial and antifungal potency. These acids are therefore a strong and ever-ready arm in the physiologic defense of the integument against microbial invasion. Among the numer- ous convincing experimental results supporting the preceding statements I shall be able to select for mention only a few, namely the early ones of Marchionini and collaborators (16), of Herrmann and Fuerst (17), the somewhat later ones of Peck and co-workers (18, 19, 43) and the more recent ones of Rothman et al. (44a and b) and of Miescher and the Ztirich school (45, 46). Although these protective fatty acids undoubtedly have their origins preponderantly from the sebum and "horn-wax," it now appears that their antimicrobial effectiveness requires their proper emulsification by the sweat. This fact is made obvious by the studies of Foley, Herrmann and Lee (47, 48) as well as by the more recent reports of Miescher and his group (45, 46). It has long been recognized that excessive wetness of the skin's surface (for example from excessive sweating and/or impeded evapo- ration of sweat), leads to maceration and impairment of fatty-acid protec- tion and thus to infections such as "intertrigo," moniliasis, folliculitis, dermatophytosis, etc. But the more recent concept outlined above for the first time makes comprehensible one way in which the opposite extreme, i.e., too little sweating and wetness, can lead to a water-deficiency in the sur- face film, to excessive dryness and to consequent impaired antimicrobial action of fatty acids and thus to infections. For many years the presenter has observed that while excessive wetness is inclined to diminish protection against certain types of infections (e.g., trichophyton gypseum, epider- mophyton, micrococcal and monilial infections) excessive dryness tends to reduce protection against others (e.g., trichophyton rubrum infec- tions). In support of this idea there are not only my own clinical observa- tions of the kinds of skin surface I have seen repeatedly associated with these various infections, but also numerous reports in the literature. Thus from our own school, Baer and Muskatblit (49) and lately Herrmann, Fried and Pascher (50) reported patients with extensive "idiopathic" hyperkeratosis or exfoliative erythrodermas associated with anhidrosis and affected by widespread, often chronic or recurrent and largely treat- ment-refractory superficial fungous infections--in most instances by trichophyton rubrum fungi. Similar reports have emanated from other places (51). Further investigations may well prove fruitful in bringing to light still other cases and still other kinds of skin infections in which absent or reduced sweating plays a role, as well as further facts concerning the mechanisms connecting faulty sweating and lack of resistance to infection.