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Pantothenic Acid in the Treatment of Acne Vulgaris
“A Medical Hypothesis”
by Lit-Hung Leung, M.D
This article originally appeared in the scientifically prestigious Journal of Orthromolecular Medicine Vol. 12 Number 2, 1997. Below is a condensed version of the study by Gunilla™ of Sweden to highlight the more pertinent factors related to Clearpoint® All Natural Clear Skin Supplement
Over the years the pathogenesis of acne vulgaris has been extensively studied including, the structure and function of the pilosebaceous follicle, the physiology of sebum, microflora in acne vulgaris, and abnormal follicular keratinization, considered to be one of the earliest events in acne formation. Despite the concerted effort of many scientists, internists, pathologists, and dermatologists, the pathogenesis of acne vulgaris remains mostly elusive.
In this paper, I would like to approach this problem from a different perspective. My clinical observations suggest that acne vulgaris may be closely related to the consumption of diets, which are rich in fat content. This impression is by no means novel. Textbooks do briefly mention this correlation though, more often than not, it is dismissed as irrelevant. However, my observations have led to quite the contrary conclusions. Not only is the fat content of food closely related to acne vulgaris but it forms some sort of linear relationship with the disease process. The more fat the patient consumes, the more severe will be the acne process. This observation is in line with the opinion of many dermatologists that chocolate, which is composed mainly of the creamy part of milk and has a high degree of fat content, is bad for acne. Significantly, in this group of patients, any deliberate attempt in trying to avoid a fatty diet over a period of weeks, if not days, will often result in an important compound, cholesterol, which in turn is primarily synthesized from units of acetyl-CoA. In the synthetic process, the body naturally is always trying not only to reach for a healthy level of androgens but an optimal level, to allow the body to function at its best.
However, this is not always possible, and the average level reached may not represent the optimal level. This is nature’s flexible way of dealing with a shortage of essential dietary elements in any form to achieve a level that is just enough to manage the present situation, leaving a variable degree of deficiency from the optimal level. In the current instance, in the two groups of boys, one group may have a reasonable level of androgens that is falling short of the optimum. One possible explanation for this is that there is a lack of basic building blocks, the acetyl-CoAs, which deter the body from operating at peak efficiency. If this is a viable possibility, it suggests that a plentiful supply or a deficiency of acetyl-CoA in the body may play a role in the acne process. This is certainly possible. Aside from its role in the synthesis of the sex hormones, acetyl-CoA, of which Coenzyme-A is the vital component, it is also essential in fatty acid metabolism as an acyl carrier in the lengthening and degradation of long chain fatty acids by adding or removing acyl groups in the metabolic process. Acne vulgaris is related to lipid metabolism as well as the sex hormones, both of which have a lot to do with Coenzyme A. This relationship provides a reasonable ground to link up the acne process to Coenzyme A and to investigate the pathogenesis of acne vulgaris along this line.
In trying to link acne vulgaris to Coenzyme-A, it is important to have a hypothesis supporting some basic facts. A closer look at Coenzyme-A may provide the evidence.
A Sharing scenario; as a coenzyme active in both fatty acid metabolism and sex hormone synthesis, Coenzyme-A is shared between two different metabolic processes. This is not uncommon in biochemical reactions in metabolism, where a coenzyme is often shared among a number of reactions. Coenzyme-A is arguably the most important coenzyme in the body, and when a coenzyme is involved in the metabolic process to such an extent as this, it becomes legitimate to ask if a shortage and deficiency is possible. To answer this, a brief look at the structure of Coenzyme-A is warranted.
Pantothenic Acid; Coenzyme-A is formed from adenosine triphosphate, cysteine, and pantothenic acid. Of these pantothenic acid is the only component that is a vitamin, and must be provided from our dietary intake. Could there be an insufficient intake of pantothenic acid resulting in a deficiency in Coenzyme-A, which would leave the body unable to cope with all the reactions, that it has to perform with that all-important coenzyme? Conventional wisdom does not think so. It is suggested that pantothenic acid, being ubiquitous, can be had from whatever kind of food that is taken in, and that there is no question as to its deficiency in our body. However, a deficiency is still possible. After all, when so many reactions are dependent on the same agent, its demand must be tremendous. Shortage under such circumstances is not entirely impossible.
If the question of deficiency of Coenzyme-A does come up, how does it affect acne, knowing its importance in fatty acid metabolism and sex hormone synthesis? This is the crucial question. This is where the new hypothesis on the pathogenesis of acne vulgaris is based, and this is where it diverges from conventional medical ideas. The author’s proposed hypothesis for the pathogenesis of acne vulgaris is that the disease process is not caused by androgens or any other sex hormones, but instead, the disease process results from a defect in lipid metabolism that is secondary to a deficiency in pantothenic acid, hence Coenzyme-A. Coenzyme-A, in carrying out its function efficiently both as an agent in fatty acid metabolism and an agent in androgen and sex hormone synthesis, has to be present in sufficient amounts, and anything less than sufficient will result in some compromise.
Faced with the dilemma of a shortage of Coenzyme-A the body will tend to make a choice that is to the best advantage of the individual. The body does so by mostly maintaining the functionally more important reaction, while at the same time slowing down the lesser important one. The choice here is a relatively simple one. Nature will seek to take care of the synthesis of hormones first because the continuation of the species depends on the development of the sex organs. Fatty acid metabolism is, for the time being, at least in part halted. Lipids start to accumulate in the sebaceous glands, sebum excretion is increased, and acne begins to appear. When there is enough Coenzyme-A in the body, however, both reactions will be well taken care of. There are enough sex hormones for the sex organs to develop. The lipids in the sebaceous glands are entirely metabolized by sufficient Coenzyme-A, and there will be no unwanted lipid in the glands, and little sebum will be excreted to cause acne vulgaris.
The mechanism proposed above may be the reason why two groups of adolescent boys both with a normal blood level of androgen may exhibit differences in the incidence of acne. The group with acne is the one that has not enough pantothenic acid in the body, whereas in the other group, pantothenic acid levels are not deficient.
This new theory seems to work well here, and can be tested in other metabolic situations. In the case in which endogenous androgen stimulates acne, whereas exogenous does not, the reasoning for the observation is the same. Any endogenous androgen synthesis will require the participation of extra amount of pantothenic acid. This will channel off some of those that are doing the work of fatty acid metabolism. Consequently, fatty acid metabolism becomes less efficient and the individual is more prone to have acne.
Today, the percentage of adult women that have acne is increasing. Some of these women may not have had acne as teenagers, and are surprised to find that they have to deal with this unpleasant problem during their adult years. Acne can have profound psychological and social effects on adults, just as it does in teenagers.
Microcomedo Acne vulgaris of adulthood is similar to teenage acne. The pilosebaceous units of the face, chest, and back can be involved. The primary lesion of acne is the “microcomedo.” A microscopic plug develops due to the presence of thickened and impacted keratin (dead cells) and excess oil production (sebum). More and more of the keratin and sebum back up behind this plug and form a distended follicular pore. This results in either an open comedo (blackhead) or a closed comedo (Whitehead). The enlarged pilosebaceous structure allows Propionibacterium acne’s, an anaerobic diphtheroid, to increase. Propionibacterium acne’s contributes to the breakdown of lipids to free fatty acids, which are highly inflammatory. The distended follicle can rupture, causing further inflammation and the development of papules, pustules, and nodules.