Essential fatty acids and their role in treatment of acne

Oily skin and hypersecretion of sebaceous glands is well known in acne subjects. However, composition of the secreted oil has been less studied. In this article we going to examine how different composition of oily secretions in acne patients are from those of normal subjects.

Considering essential fatty acids in acne treatments has not been standardized yet. However, there are many studies which bring up a possible role for essential fatty acids in treatment of acne. Acne is a multifactorial disease and pathologically characterized by increased sebum production which results in an oil forming skin, sebaceous gland hypertrophy, abnormal follicular keratinization and inflammation. Hyperactivity of sebaceous glands may be associated with change in lipid compostion of the sebum. There is evidence of association between sebum linoleate concentration and comedo formation. Essential fatty acids deficiency contributes to sebaceous gland hypertrophy and hyperkeratinization of the ducts. Linolenic acid level in the stratum corneum has been reported to be much higher in normal subjects than that in the comedones. There is no evidence of direct assocation betweeen acne and food intake, however, diet still viewed with skepticism. Processed food might contribute to acne exacerbations.

High sebum production and the resulting low level of linoleic acid leads to hyperkeratosis and comedo formation. Can providing the skin with essential linoleates prevent comedo formation and aid oil forming skin? An study reports that stratum corneum sphingolipids of adult acne patients is lower than that in control subjects. Decrease in sphingolipids content of cell walls contributes to diminished water barrier function which, in turn, suggests that impaired water barrier function maybe responsible in formation of initial acne lesion. One point that supports this hypothesis is that plasma phosopholipids are normal in patients with acne. Another study suggests role of a derivative of sphingomyelin, sphingosine 1-phosphate, in inhibiting keratinocytes proliferation and a possible role in wound re-epithelialization.

Increase in plasma androgen level induced by steroids cause an increase in cholesterol and free fatty acids in skin surface. Some essential fatty acids such as gamma linolenic acid are potent 5-alpha-reductase inhibitors and hypothetically by inhibition of androgen receptors can be effective in treatment of acne . In adult skin androgen action is dependent to conversion of testosterone to five-alpha-dihydrotestosterone. This conversion takes place under enzymatic act of five-alpha-reductase. Hypersensitivity of androgen receptors in pilosebaceous duct and the resulting increase in sebum production appears to be associated with an significant increase in free fatty acids rather than other surface skin lipids.

One hypothetical idea is that hypersensitive overworked sebaceous glands in an acne patient do not operate to produce their high-end products such as linoleates, rather, their overflow is associated with cheap secretions such as free fatty acids and cholesterol. There is an inverse relationship between secretion rates and the linoleate content of the surface wax esters. The question that whether local supply of essential fatty acids down regulate the overworked sebaceous glands is still a mystery. Thus, a practical role for lipid disregulation in acne treatment stays an area for research in treatments for acne and regulation of oil forming skin.

How control of sebaceous follicles can affect acne treatment? There are three types of follicles on the face. Beard follicels, Vellus follicles and sebaceous follicles. Among them the sebaceous follicle is more actively involved in development of adult acne and control of its secretions is one of the goals in acne treatment. The reason is that in beard and vellus follciles hair act as a strand facilitating drainage of the sebaceous galnd and protecting against obstruction. Sebaceous follicles consist of three parts. The short pilary portion hardly visible to the naked eye, a canal and sebaceous glands. Even though, sebaceous follicles have such large pores that they are often grossly visible, obstrucion-wise the dynamic of the whole canal must be considered. Sebum production control is one of the aims of most acne treatment regimens.

Lower amount of sphingolipids and ceramides in keratinocytes of acne subjects has been shown. this would be associated in decrease in ability of keratinocytes' walls to hold water, one possible mechanism that can explain how hyperkeratinization starts in comdeones since impaired water barrier function is concurrently seen in hyperkeratosis.

The localization of acne to the face and trunk is determined by the distribution of sebaceous follicles. Treatment of acne in face and trunk follows the same objective. The sebaceous glands, although larger in acne subjects, are similar in structure to those of normal subjects. The precise mechanism to the formation of the microcomedo ( the earliest lesion in formation of adult acne ) is not known, hyperproliferation of ductal keratinocytes in pilosebaceous ducts is suggested. Eventually the microcomedone evolves into a closed comedo and possibly into an open comedo. The sebaceous gland itself may undergo partial atrophy later on with or without acne treatments. Diffusion of inflammatory molecules through the duct wall into the dermis represents prodution of inflammation to the initial acne lesion. The level at which the inflammatory reaction develops into the dermis determines the type of adult acne lesion.

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Sebum changes during acne and one of the goals of any acne treatment is to contorl sebum. Let's look at the composition of sebum.

Skin surface lipids are derived from two major sources, sebaceous glands and epidermis. Distribution of sebaceous glands in different areas of the skin contribute to different composition of skin lipids in various areas. Rich areas of sebaceous glands such as forehead have a surface lipid composition very similar to sebum.

Sebum is formed in sebaceous glands by decompostion of lipid-containing cells. Three major elements of human sebum are triglycerides, wax esters and squalene. Synthesis of squalene and triglycerides is characteristic of sebaceous gland activity. The triglycerides make up about 60 percent of sebum while their presence in skin surface lipids reaches to about 40 percent.

Pore size is another variable that correlates with sebum secretions. The larger the pore size the more sebum production. Controling sebum hypersecretion is one way to manipulate skin's pores size .