Acne cure with B5

At one time or another, most of us have suffered from acne. Acne can be one of the most demoralizing conditions of all since it takes away a personssense of well being and self
confidence. Ever since I was 18, I have suffered from moderate acne until I came accross pantothenic acid (Vit B5). I know many of you will be skeptical (I was to), but it really
does work. Last year my acne cleared up totaly on a dose of 5 grams per day of pantothenic acid. I now take a maintenance dose of 2 grams per day and have not had one
single pimple in the last 6 months. Below is the research paper that prompted me to take pantothenic acid. The research was conducted in Singapore almost 3 years ago and the
results were staggering. Of the
100 patients in the study, all of them had a near 100% remission of their acne. I think that this study has not been publisized in the west because the drug companies would
loose so much money if people realized that acne could be cured by something a cheap and simple and pantothenic acid.
Even if you don?t regularly get acne, pantothenic acid is a great way to prevent post cycle flare-ups. Here is the research paper. If anyone has any questions, feel free to email
me.
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. The version below is from a reprint of the original
article and revisions were made in December 1998.
The Pathogenesis of Acne Vulgaris: A Medical Hypothesis
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 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 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 important compound,
cholesterol, which in turn is basically synthesized from
units of acetyl-CoA. In the synthetic process, the body naturally is always trying not only to reach for a normal level of androgens, but 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 natures 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. Aside from its role in the synthesis of the sex hormones, acetyl-CoA, of which coenzyme-A is the
important component, it 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.
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.
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.
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 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.
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
take 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 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 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.
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.
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.
Many women in their 30s and 40s experience high levels of life stress because they shoulder the multiple burdens of career, child rearing, and housework, and often the
responsibility of caring for their own aging parents. Perhaps this increasing level of stress has contributed to the rising incidence of acne in adult women.
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 proliferate. 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.
Acne Rosacea
Another skin disease that simulates and can coexist with acne vulgaris is acne rosacea. This skin problem is common in women, most often between the ages of 30 and 50. The
face, especially the middle third, is erythematous and flushed. Multiple telangiectasias are frequently present. Small papules and pustules, which may look similar to those seen in
acne vulgaris, are common, but the microcomedo component of acne vulgaris is absent in blepharitis.
Rosacea keratitis is less common, but potentially vision-threatening. Rosacea is another skin disorder that is frequently stress related.
What about premenstrual flare? In the luteal phase of the menstrual cycle, progesterone in is secreted abundantly by the corpus lutcum. This naturally will take up a lot of
pantothenic acid from the body?s pantothenic 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 sebaccous glands, an increase in sebum is excreted, and acne follows. That is why even thought
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. Since 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 hormones that counts. Both males and females need sex hormones for the development of sex organs and the
secondary sexual characteristics. The only difference is that in the male, the female sex hormones predominate. Apparently the synthesis of sex hormones uses a large portion of
the pantothenic acid pool, leaning a relative shortage of it to efficiently metabolize fatty acids. The result is that acne starts to erupt, at the same time the sex organs begin to
develop at puberty.
The reason acne first erupts at puberty is not, therefore, endocrinological, but rather secondary to the deployment of a substantial amount of pantothenic acid for the purposes
of synthesis of sex hormones, leaving a relative deficiency for fatty acid metabolism. The size of this pantothenic acid pool and the ability with which the individual can deploy
reserves from the pool varies and is likely to be influenced by genetic and dietary factors.
In conditions in which there is an increase in secretion of any hormone whose synthesis requires the participation of pantothenic acid, acne may erupt.
This is frequently seen with those hormone secreting tumours of the ovary, testis and the adrenals. The rapid decline in incidence of acne after adolescence can also be explained.
After the sex organs are fully developed, less sex hormones are required, leaving an adequate supply of pantothenic acid to serve the function of fatty acid metabolism. When
this function
Date: August 22, 2000 12:34 PM
Author: [email protected]