Pimple scar treatment

The document below is partly translated to text using a OCR program. Because the source (a JPEG file) wasn’t copied very cleary enough for my OCR program, OCR had some problems translating some parts correctly to text. So there might be type errors in it which are not in the original document. A Stone that Kills Two Birds: Pantothenic Acid in the Treatment of Acne Vulgaris and Obesity

Lit-Hung Leung, M.D. ‘

2. Abstract

Acne vulgaris is the most common disease of the skin. Obesity is arguably the commonest of a clinical entities in affluent societies. The pathogenesis of these disorders is far from clear cut and they appear to have little in common. In the present paper it is hypothesized that the pathogenesis of both acne vul garis and obesity is largely due to a relative deficiency of the same agent, pantothenic acid, a vitamin that is hitherto quite un known to cause any deficiency syndromes in man. Furthermore, the evidence suggests that surprisingly large doses of pantothenic acid are required to overcome deficiency states as illustrated in the treatment of acne vulgaris and obesity.

3. Introduction

In reviewing the numerous studies that deal with the pathogenesis of acne vulgaris, one gets the impression of reading a detective story. There is the victim; the facts are all there; there arc all the clues, as well as the suspects. But the culprit cannot be identified. The identification is made more difficult because the clues seem all tangled up. At times, they fit in with the suspects very well, other times however, the same clues arc contradictory, and appear to lead to a hopeless situation. In the same way, it is quite a mystery that an over-weight person, with an abundance of energy deposited as depot fat, cannot efficiently use this stored fat in times of need as during dieting when food intake does this precious stored energy unavailable, in some cases it is actually squandered.

In two previous articles1-2 the author reported that both of these conditions are related largely to a deficiency in dietary pantothenic acid. It is the aim or this present article to expand and to describe in greater detail the reason and logic be hind the hypothesis.

4. The Pathogenesis of Acne Vulgaris: a Hypothesis

Over the years, the pathogenesis of acne vulgaris has been extensively studied3,4,5 including, the structure and function of the pilosebaceous follicle,6 the physiology of sebum secretion,7,8,9 the composition of sebum,10-13 microflora in acne vulgaris,14 and abnormal follicular keratinization,15,16 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 largely 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 correlation17,18,19 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.20-23 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 improvement of the clinical condition. This observation forms the basis of my hypothesis that the disease process may be connected with fat metabolism-or a deficiency of it.

Other arguments also support this hypothesis. There is the composition of the sebum secretion which consists mainly of lipid material,10,11,13 When lipids are deposited in the sebaceous glands and excreted as sebum secretion, it does suggest some abnormality and hints that some form of fat metabolism may be at fault. These fatty materials, after all, are energy-rich compounds. Under normal circumstances, they should be stored away in far depots. To have them excreted with a concomitant wastage of energy is not nature’s way of handling excess energy. One possibility the body behaves in such a manner is that it is sim ply unable to cope effectively with all the fat that is being absorbed, resulting in some being dumped through some unusual venue. This perhaps helps to explain the observation that an increase in fat content of food appears to worsen acne.

Furthermore, there is the involvement of the sex hormones. The sex hormones, the androgens in particular, have long been recognized as important causative factors in the pathogenesis of acne vulgaris. A tremendous amount of very thorough work has been done in relation to this subject, and the conclusions of these studies are most intriguing. The findings, however, are often in conflict with one another, and no reasonable explanation can be provided for all the observations that are made. The sex hormones, aside from their established relationship with acne vulgaris, are of interest in another respect. This is their dose relationship with the important compound, cholesterol. It has long been established that the sex hormones are derivatives of cholesterol, whose synthesis has much to do with lipid metabolism. A hypothesis, therefore, which relates the acne process to lipid metabolism is worth looking into.

Before detailing such a hypothesis in any depth, it is relevant to recapitulate very briefly some of the main actions of the sex hormones relating to the acne process, and some of their apparent conflicting effects. Although the proposed hypothesis has little to do with the functional aspect of the hormones, it bears important association to these hormones as a whole. And remarkably enough, some of the conflicting hormonal effect lend strong support to the hypothesis.

5. The Effect of Sex Hormones on Acne Vulgaris 5.1. The androgens

Androgens have their effect on the acne process on several fronts. For a long time, it has been shown that androgens exert great influences on sebum secretion,24,25 which precedes acne formation. Equally significant is the observation that the severity of clinical acne is directly related to the rate of sebum excretion.26 Many studies have also revealed that the development of the sebaceous glands is influenced by androgens. Castrated men have smaller sebaceous glands and a much lower level of sebum secretion- as compared to a normal man.27,28 That the sebaceous gland is a target-organ of androgens can be shown by administration of testosterone co subjects that have very low levels of testosterone in their blood, like children and post- menopausal women, when there is prompt increase in sebaceous gland activity.29,30

5.2. The Estrogens

The consensus is that estrogens at physiological dosage have little effect on sebaceous activity. Doses in excess of this dosage will reduce sebaceous gland activity, hence sebum secretion.31

5.3. The Progestogens

It is generally agreed that progestogens have little effect on sebum production. It seems that things look quite straight forward with these observations and conclusions-androgen is to be the predominant factor in the pathogenesis of acne. Or is it? It is here that things start to look complicated and pose many problems.

6. The Controversies and Contradindications 6.1. Sex Distribution

Controversies abound in the realm of acne vulgaris and sex hormones. One of the fundamental questions to ask is if androgen is so closely related to sebaceous gland activity, why is the sex distribution of the disease process equal? With androgen level so much higher in males than in females, one would expect the disease process should largely occur in males. This is not true. This is something of a riddle that proves difficult to solve.

Some workers offer to explain this by saying that it is not the amount of androgens in the blood that matters, but the sensitivity of the target-organ, the sebaceous glands, towards androgens that counts.33With this explanation, a few questions inevitably follow. The question of sensitivity is an issue. Little is known about the nature of this sensitivity. With the incidence of the disease process divided between male and female it implies that the female sebaceous glands have to be much more sensitive towards androgens than the male glands. But apparently there is little supporting evidence for this.

Even more puzzling is the clinical condition of premenstrual flare, in which female patients have much more prominent acne eruptions premenstrually. For the explanation to hold true, the sebaceous glands have to be particularly sensitive to androgens premenstrually. Again, there is no evidence for this.

6.2. Exogenous and Endogenous Androgens

There is another observation concerning the relationship of acne and androgens that is difficult to explain. Administration of testosterone in prepubescent boys increases the size of the sebaceous glands, but not so in the adult.

Here, the glands would appear to be un der stimulation by endogenous androgens rather than exogenous androgens,28,29,32,34 This is an interesting phenomenon. The same compound, but with a different origin, will carry with it a different response in the adult body.

In trying to provide an answer to this observation, it is important to look beyond the relationship of androgens and acne, and perhaps look into other aspects relating to the androgens. The synthetic production of androgens, or the sex hormones as a whole, for example, may be worthwhile to examine, because the only difference between the two hormones is that one is synthesized in the body, whereas the other is not.

There is another reason for looking into the synthesis of hormones. It has been shown that pubescent boys with or without acne have about the same blood levels of testosterone.35,36 On the face of it, there is no basic difference between these two groups of boys. However, at this stage of their life, one particular feature stands out: They all need to start synthesizing androgens, probably a good amount of it, to cater to the development of the sex organs. One possible reason is that subsets within these two groups of boys may have some subtle differences in synthetic processes. Of course, the actual synthetic process will be the same, requiring the same enzymes, coenzymes and basic building blocks for the purpose. What constitutes the possible difference here is not so much as the nature, or quality, of these components, but rather some other factors. One possibility is the quantity of the dietary components may differ. One group may be provided with a good supply of all the components and the other with varied degrees of shortages. This difference could be significant and provide the logical basis for looking into the synthetic process.

The essential steps in the synthesis of androgens and the other sex hormones are well known. They are all derived from the important compound, cholesterol, which in turn is basically synthesized from units of aceryl-CoA. In the synthetic process, the body naturally is always trying not only to reach for a normal level of androgens, bur an optimal level, so as to allow the body to function at its best. However, this is not always possible, and the normal level reached may not represent the optimal level. This is nature’s flexible way of dealing with 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 shortage from the optimal level. In the present instance, in the two groups of boys, one group may have a normal 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. For, aside from its role in the synthesis of the sex hormones, acetyl-CoA, of which coenzyme A is the important component, is also important 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.

7. The Importance of Coenzyme A

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.

7.1. 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. But with Coenzyme A, it is somewhat different. With its involvement in more than one hundred reactions,37,38 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.

7.2. 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.

The Crucial Question and the New Theory 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 rather, the disease process results from a defects in lipid metabolism that is sec ondary to a deficiency in pantothenic acid, hence Coenzyme A. Coenzyme A, in car rying 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.

7.3. Mother Nature’s Choice

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 largely 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 lake care of the synthesis of hormones first, because 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 pantothenic acid 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 completely 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.

7.4. The Mystery Revealed

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. Exog-enous androgen, on the other hand, does not affect the pantothenic acid pool in any. manner, hence no effect on acne. This explains the seemingly mysterious nature of this observation.

What about premenstrual flare? In the luteal phase of the menstrual cycle, progesterone in is secreted abundantly by the corpus luteum. This naturally will take up a lot of pantothenic acid from the body’s pantothenic acid pool, leading to a re-distribution of the vitamin and putting enormous pressure on fatty acid metabolism. When this metabolic process is not performing satisfactorily, lipid begins to accumulate in the sebaceous glands, an in crease in sebum is excreted, and acne follows. That is why, even though progesterone has no effect on sebaceous gland activity, an increasing level of progesterone in the late stage of the luteal phase leaves the acne patient with a prominent flare.

Similarly, this may explain why eunuchs rarely exhibit acne.27,28Since so few sex hormones are secreted, the pantothenic acid pool can deploy a more significant portion of its reserve to metabolize fatty acids. When this is efficiently done, little sebum is excreted, and no acne is formed.

This theory also explains the paradoxical problem of equal sex distribution of acne incidence. It is not the male hormone androgen that is important but rather the absolute amount of sex hormones that counts. Both males and females need sex hormones for the development of sex or logical problem that may worry the patient will bring on new acne lesions.33 To understand this, one should recall that in combating stress, the body will secrete glucocorticoids from the adrenal glands as a means to adapt to stress, what is com monly known as the fight-or-flight reaction. The glucocorticoids, like the sex hormones, are derivatives of cholesterol, and increased demand for this hormone will draw on the pantothenic acid pool. Lipid metabolism may therefore be compromised, rendering the body more prone to acne.

If pantothenic acid deficiency is indeed the main causative agent in the pathogenesis of acne vulgaris, it is logical to ask how much pantothenic acid patients are lacking in absolute amounts.

8. Deficiency syndromes

Nutritional requirements can rarely be met through a well balanced diet, and dietary supplements, including vitamins, arc often required. It is the generally held belief of the medical profession that vitamins, though essential to life and not synthesized in the body, are not required in great amounts. This view was challenged, notably by Linus Pauling. In his book, How to Live Longer and Feel Better, Pauling provided vigorous proof, through comparative studies in animals and from an evolutionary point of view, that vitamin C supplements are needed if an optimal state of health is to be achieved. Not only is supplementation necessary, but the amount required is far greater than most people believe, as with the case of vitamin C where the optimal dose may be 10 or more grams a day.41

This issue was a point of heated debate in the 1970s and 1980s. Though Pauling has quite a large following, by and large, the issue was dismissed by the mainstream medical profession,** because of a lack theoretical support and a general bias against nutritional and vitamin therapy. But, in view of the new evidence suggested in this and many other papers, it seems appropriate that the issue be reconsidered.

9. How Much Pantothenic Acid?

In trying to determine the amount of pantothenic acid necessary to relieve acne patients of their symptoms, Pauling’s experience with vitamin C provides a good guideline. Pauling had for a long time recommended vitamin C in high dosages to achieve optimal health. Radically different from what is recommended by the Food and Nutrition Board of the National Research Council (who recommended 60 mg daily), Pauling’s recommended daily intake of vitamin C amounts to several grams a day. The recommendation was stepped up to 15- 20 grams a day in his later years. Using these recommendations as a background, it becomes somewhat easier to arrive at a proper dosage for pantothenic acid in the treatment of acne vulgaris.

Pantothenic acid, which acquires its name from the Greek word meaning ubiquitous, is present in all tissues. Its universal presence is an indication of its importance. This is further reflected by the many reactions that it catalyzes. If should not come as a surprise, then, if the amount of pantothenic acid required to for optimal health is of the same order of that of vitamin C. Based on this argument, the dose of pantothenic acid administered to the acne patients was up to 10 gm a day, and the result of these studies were first reported in Medical Hypotheses.1

10. The Effect of Pantothenic Acid on Acne Vulgaris

One hundred patients of Chinese descent were included in the study, 45 males and 55 females. The age ranged from 10-30, and with about 80% between 13 and 23. The severity of the disease process varied. They were given 10 g of pantothenic acid a day in four divided doses. To enhance the effect, the patients were also asked to apply a cream consisting of 20% by weight of pantothenic acid to the af-