Topical Linoleic Acid

Abstract: A preparation for the topical application of linoleic acid to treat male and female androgenetic alopecia, age-related alopecia, and keratosis pilaris contains between about 0.1% and about 10%, preferably between about 1% and about 5%, and specifically about 2% linoleic acid by volume in its carrier vehicle. This acts to correct the local linoleic acid deficiency that exists in the follicles in these conditions and provides linoleic acid to suppress growth of Propionibacterium acnes with resultant reduction in its porphyrin production which in turn reduces microinflammation and altered keratinization that damages follicles and eliminates functioning follicles in alopecia and causes follicle plugging in keratosis pilaris.

Microbiologic studies have shown that after puberty skin flora in hair follicles of oily skin areas such as the face and scalp is predominantly Propionibacterium acnes (P. acnes) with lesser presence of staphylococci and Malassezia species. P. acnes is 4 Young, J W et al., “Cutaneous Immunopathology of Androgenetic Alopecia”, Journal of the American Osteopathic Assn., Vol. 91 (#, p. 765, 1991. an anaerobic bacterium that is well adapted for life in the sebum-rich, oxygen-free environment inside face and scalp follicles. Metabolically, it produces a number of compounds that can cause inflammation inside and around hair follicles. Lipase enzymes result in breakdown of inert triglycerides into inflammatory free fatty acids which disrupt facial and upper trunk follicles and cause the papules, pustules, and cysts seen clinically as acne. Cyanocobalamin (vitamin B12) is also produced and is a known aggravator of acne when it is administered orally to acne-prone patients. Most pertinent to the present invention is the production of tetrapyrrole porphyrin compounds, especially coproporphyrin III, which are inflammatory by nature but are especially inflammatory when excited by their specific absorption of ultraviolet light in the 300-450 nanometer wavelength range which is abundantly available in natural sunlight. Such activated porphyrins have been shown to cause deposition of immunoglobulins and complement as described in AGA follicles. Scalp follicles in areas of alopecia are often seen to exhibit auto-fluorescence in UV light indicating the active production of porphyrins in these follicles. This has led some authors to even suggest that the normal location of AGA on the vertex of the scalp more than on the sides could make the process in part a photo-aggravated one. The end result of the follicular microinflammation, perifollicular fibrosis, and the miniaturization of normal follicles until they are non-functional could largely therefore be blamed on P. acnes, either through its production of inflammatory compounds or porphyrins or alternately due to antimicrobial peptides or other compounds produced locally as a5 Trueb, R M, “Is Androgenetic Alopecia a Photoaggravated Dermatosis”, Dermatology, Vol. 207, pp. 343-348, 2003. defense mechanism against it. In any event, reduction of the population of P. acnes in scalp follicles can prevent inflammation and slow or reverse the process of miniaturization that causes AGA and baldness.

Studies have shown that topically-applied linoleic acid can replenish even the depleted levels seen in systemic essential fatty acid deficiency states, so it is merely academic to state that topical linoleic acid compounds can supply adequate amounts to correct the localized deficiency in scalp follicles in AGA. The prior art presented by this inventor showed that only a 2% concentration of linoleic acid is required to completely inhibit growth of P. acnes in culture. The difference between the clinical outcome of localized linoleic acid deficiency in scalp and facial follicles in AGA and acne, respectively, is quite probably due to the difference in the normal patterns of keratinization in follicles of the two areas. In the scalp, the infundibular keratinization when pathologically altered becomes permeable to inflammatory compounds leading to microinflammation, perifollicular fibrosis, and miniaturized non-functional follicles. Clinical signs of acne in facial follicles results from action of P. acnes-produced lipases on the microcomedo, which is the product of altered follicular keratinization caused by linoleic acid-deficient sebum in sebaceous follicles that rarely produce full-sized hairs in the normal individual.