pantothenic acid and weight reduction

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Abstract Acne vulgaris is the most common disease

of the skin. Obesity is arguably the common-est of a clinical entities in the affluent soci-ety. T he pathogenesis of these disorders is far from clear cut and they appear to have little

in common. In the present paper it is hy- pothesized that the pathogenesis of both acnevulgaris and obesity is largely due to a rela-tive deficiency of the same agent, pantothenicacid, a vitamin that is hitherto quite un-known to cause any deficiency syndromes inman. Furthermore, the evidence suggests that surprisingly large doses of pantothenic acid are required to overcome deficiency states asillustrated in the treatment of acne vulgarisand weight reduction.

IntroductionIn reviewing the numerous studies

that deal with the pathogenesis of acnevulgaris, and one gets the impression of reading a detective story. There is the vic-tim. The facts are all there. There are allthe clues, as well as the suspects. But the

culprit cannot be identified. The identifi-cation is made the more difficult becausethe clues seem all tangled up. At times,they fit in with the suspects very well, othertimes however, the same clues are contra-dictory, and appear to lead to a hopelesssituation. In the same way, it is quite amystery that an over-weight person, withan abundance of energy deposited as fatdepot, cannot efficiently use this stored fat

in times of need as during dieting whenfood intake does not meet the energy de-mand. Not only is this precious storedunavailable,in some cases it is actuallysquandered.

In two previous articles1,2 the authorreported that both of these two conditionsare related largely to a deficiency in dietarypantothenic acid. It is the aim of thispresent article to expand and to describein greater detail the reason and logic be-

hind the hypothesis.

The Pathogenesis of Acne Vulgaris: aHypothesis

Over the years, the pathogenesis of acne vulgaris has been extensively stud-ied3,4,5 including, the structure and func-tion of the pilosebaceous follicle,6 thephysiology of sebum secretion7,8,9 the com-

position of sebum

10-13

microflora in acnevulgaris,14 and abnormal follicular kerati-nization15,16 considered to be one of theearliest events in acne formation. Despitethe concerted effort of many scientists,internists, pathologists and dermatologists,the pathogenesis of acne vulgaris remainslargely elusive.

In this paper, I would like to approachthis problem from a different perspective.

My clinical observations suggest that acnevulgaris may be closely related to the con-sumption of diets which are rich in fatcontent. This impression, however, is byno means novel. Textbooks do briefly men-tion this correlation17,18,19 though, moreoften than not, it is dismissed as irrelevant.However, my observations have led toquite the contrary conclusions. Not onlyis the fat content of food closely related to

acne vulgaris, but it forms some sort of linear relationship with the disease proc-ess. The more fat the patient consumes,the more severe will be the acne process.This observation is in line with the opin-ion of many dermatologists that chocolate,which is composed mainly of the creamy

A Stone that Kills two Birds: How PantothenicAcid Unveils the Mysteries of Acne

Vulgaris and Obesity

1. Department of Surgery. Hong Kong Central Hospital.Hong Kong

Lit-Hung Leung. M.D. 1

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Journal of Orthomolecular Medicine Vol. 12, No. 2, 1997

part of milk, and has a high degree of fatcontent, and is bad for acne.20-23 Signifi-cantly, in this group of patients, any de-

liberate attempt in trying to avoid a fattydiet over a period of weeks, if not days,will often result in an improvement of theclinical condition. This observation formsthe basis of my hypothesis that the diseaseprocess may be connected with fat metabo-lism–or a deficiency of it.

Other arguments also support thishypothesis. There is the composition of thesebum secretion which consists mainly of

lipid material.10,11,13 When lipids are depos-ited in the sebaceous glands and excretedas sebum secretion, it does suggest someabnormality is going on and hint that someform of fat metabolism may be at fault.These fatty materials, after all, are energy-rich compounds. Under normal circum-stances, they should be stored away in fatdepots. To have them excreted with a con-comitant wastage of energy is not nature’s

way of handling excess energy. One possi-bility the body behaves in such a manneris that it is simply unable to cope effectivelywith all the fat that is being absorbed, re-sulting in some being dumped throughsome unusual venue. This perhaps helps toexplain the observation that an increase infat content of food appears to worsen acne.

Furthermore, there is the involvementof the sex hormones. The sex hormones,the androgens in particular, have long beenrecognized as important causative factorsin the pathogenesis of acne vulgaris. A tre-mendous amount of very thorough work has been done in relation to this subject,and the conclusions of these studies aremost intriguing. The findings, however, areoften in conflict with one another, and noreasonable explanations can be provided

for all the observations that are made. Thesex hormones, aside from their establishedrelationship with acne vulgaris, are of in-terest in another respect. This is their closerelationship with the important com-pound cholesterol. It has long been estab-lished that the sex hormones are deriva-

tives of cholesterol, whose synthesis hasmuch to do with lipid metabolism. A hy-pothesis, therefore, which relates the acne

process to lipid metabolism becomessomething that is worthwhile looking into.Before detailing such a hypothesis in

any depth, it is relevant to recapitulate verybriefly some of the main actions of the sexhormones relating to the acne process, andsome of their apparent conflicting effects.Although the proposed hypothesis haslittle to do with the functional aspect of the hormones, it bears important associa-

tion to these hormones as a whole. Andremarkably enough, some of the conflict-ing hormonal effect lend strong supportto the hypothesis.

The effect of Sex Hormones on AcneVulgaris1.The androgens

Androgens have their effect onthe acne process on several fronts. For a

long time, it has been shown that an-drogens exert great influences on sebumsecretion,24,25 which preceeds acne forma-tion. Equally significant is the observa-tion that the severity of clinical acne isdirectly related to the rate of sebum ex-cretion.26 Many studies have also re-vealed that the development of the se-baceous glands is influenced by andro-gens. Castrated men have smaller seba-ceous glands and a much lower level of sebum secretion as compared to a nor-mal man.27,28 That the sebaceous glandis a target-organ of androgens can beshown by administration of testosteroneto subjects that have very low levels of testosterone in their blood, like childrenand post- menopausal women, whenthere is prompt increase in sebaceous

gland activity.29,30

2. The EstrogensThe consensus is that estrogens at

physiological dosage have little effect onsebaceous activity. Doses in excess of thisdosage will reduce sebaceous gland activ-ity, hence sebum secretion.31



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How Pantothenic Acid Unveils the Mysteries of Acne Vulgaris and Obesity

3.The ProgestogensIt is generally agreed that

progestogens have little effect on sebum

production. It seems that things look quite straight forward with these obser-vations and conclusions, androgen is tobe the predominant factor in thepathogenesis of acne. Or is it? It is herethat things start to look complicated andpose many problems.

The Controversies and Contradin-dications

1.Sex DistributionControversies abound in the realm

of acne vulgaris and sex hormones. Oneof the fundamental questions to ask isperhaps, if androgen is so closely relatedto sebaceous gland activity, why is the sexdistribution of the disease process equal?With androgen level so much higher inthe male than in the female, one wouldexpect the disease process should largely

occur m the males. This is not true. Thisis something of a riddle that proves diffi-culty to solve.

Some workers offer to explain this bysaying that it is not the amount of an-drogens in the blood that matters, but thesensitivity of the target-organ, the seba-ceous glands, towards androgens thatcounts.33 With this explanation, a fewquestions inevitably follow. The questionof sensitivity is an issue. Little is knownabout the nature of this sensitivity. Withthe incidence of the disease process di-vided between male and female. it car-ries with it the implication that the fe-male sebaceous glands have to be muchmore sensitive towards androgens thanthe male glands. But apparently there islittle supporting evidence for this.

Even more puzzling is the clinical con-dition of premenstrual flare, in which fe-male patients have much more prominentacne eruptions premenstrually. For the ex-planation to hold true. the sebaceous glandshave to be particularly sensitive to andro-gens premenstrually. Again. there is no evi-

dence for this. 2. Exogenous and Endogenous Androgens

There is another observation concern-

ing the relationship of acne and androgensthat is difficult to explain. Administrationof testosterone in prepubertal boys in-creases the size of the sebaceous glands, butnot so in the adult. Here, the glands wouldappear to be under stimulation by endog-enous androgens rather than exogenousandrogens.28,29,32,34 This is an interestingphenomenon. The same compound, butwith 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 beyondthe relationship of androgens and acne,and perhaps look into other aspects relat-ing to the androgens. The synthetic pro-duction of androgens, or the sex hormonesas a whole, for example, may beworthwhileto examine, because the onlydifference between the two hormones is

that one is synthesized in the body, whereasthe other is not.

There is another reason for lookinginto the synthesis of hormones. It has beenshown that pubertal boys with or withoutacne have about the same blood levels of testosterone.35,36 On the face of it, there isno basic difference between these twogroups of boys. However, at this stage of their life, one particular feature stands out:They all need to start synthesizing andro-gens, probably a good amount of it, tocater to the development of the sex organs.One possible reason that subsets withinthese two groups of boys may have somesubtle differences in synthetic processes.Of course, the actual synthetic process willbe the same, requiring the same enzymes,coenzymes and basic building blocks for

the purpose. What constitutes the possi-ble difference here is not so much as thenature, or quality, of these components,they should be the same, but rather someother factors. One possibility is the quan-tity of the dietary components may differ.One group may be provided with a good



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supply of all the components and the otherwith varied degrees of shortages. This dif-ference could be significant and provide

the logical basis for looking into the syn-thetic process.The essential steps in the synthesis of

androgens and the other sex hormones arewell known. They are all derived from theimportant compound cholesterol, whichin turn is basically synthesized from unitsof acetyl-CoA. That is to say, the basicconstituents or building blocks of the sexhormones are acetyl- CoA. In the synthetic

process, the body naturally is always try-ing not only to reach for a normal level of androgens, but an optimal level., so as toallow the body to function at its best.However, this does not always possible,and the normal level reached may not rep-resent the optimal level. This is nature’sflexible way of dealing with shortage of essential dietary elements in any form–toachieve a level that is just enough to man-

age the present situation, leaving a vari-able degree of shortage from the optimallevel. In the present instance, in the twogroups of boys, one group may have a nor-mal level of androgens that is falling shortof the optimum. One possible explanationfor this is that there is a lack of basic build-ing blocks, the acetyl-CoAs, which deterthe body from operating at peak efficiency.If this is a viable possibility, it suggests thata plentiful supply or a deficiency of acetyl-CoA in the body may play a role in theacne process. This is certainly possible. For,aside from its role in the synthesis of thesex hormones, acetyl-CoA, of whichcoenzyme A is the important component,is also important in fatty acid metabolism-as an acyl carrier in the lengthening anddegradation of long chain fatty acids by

adding or removing acyl groups in themetabolic process.To sum up the events, the situation

is such that acne vulgaris is related to lipidmetabolism as well as the sex hormones,both of which have a lot to do withCoenzyme A. This relationship provides a

reasonable ground to link up the acne proc-ess to Coenzyme A and to investigate thepathogenesis of acne vulgaris along this line.

The Importance of Coenzyme AIn trying to link up acne vulgaris to

Coenzyme A, it is important to have ahypothesis supporting some basic facts. Acloser look at Coenzyme A may providethe evidence.1.A Sharing Scenario

As a coenzyme active in both fatty acidmetabolism and sex hormone synthesis,

Coenzyme A is shared between two dif-ferent metabolic processes. This is notuncommon in biochemical reactions inmetabolism, where a coenzyme is oftenshared among a number of reactions. Butwith Coenzyme A, it is somewhat differ-ent. With its involvement in more thanone hundred reactions.37,38 Coenzyme A isarguably the most important coenzyme inthe body, and when a coenzyme is involved

in the metabolic process to such an extentas this, it becomes legitimate to ask if ashortage and deficiency is possible. To an-swer this, a brief look at the structure of Coenzyme A is warranted. 2. Pantothenic Acid

Coenzyme A is formed from adenos-ine triphosphate, cysteine, and pan-tothenic acid. Of these pantothenic acidis the only component that is a vitamin,and must be provided from our dietaryintake. Can there be an insufficient intakeof pantothenic acid resulting in a defi-ciency in Coenzyme A which would leavethe body unable to cope with all the reac-tions that it has to perform with that allimportant coenzyme? Conventional wis-dom does not think so. It is suggested thatpantothenic acid, being ubiquitous,

enough can be had from whatever kind of food that is taken in, and that there is noquestion as to its deficiency in our body.However, a deficiency is still possible. Af-ter all, when so many reactions are depend-ent on the same agent, its demand mustbe tremendous. Shortage under such cir-



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cumstances is not entirely impossible. 3.The Crucial Question and the NewTheory

If the question of deficiency of Coenzyme A does come up, how does itaffect acne, knowing its importance in fattyacid metabolism and sex hormone synthe-sis? This is the crucial question. This iswhere the new hypothesis on thepathogenesis of acne vulgaris is based, andthis is where it diverges from conventionalmedical ideas. The author’s proposed hy-pothesis for the pathogenesis of acne vul-

garis is that the disease process is not causedby androgens, or any other sex hormones.But rather, the disease process results froma 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 anagent in fatty acid metabolism and an agentin androgen and sex hormone synthesis, hasto be present in sufficient amounts, and

anything that is less than sufficient will re-sult in some compromise of the work. 4.Mother Nature’s Choice

Facing with the dilemma of a short-age of Coenzyme A, the body will tend tomake a choice that is to the best advan-tage of the individual. The body does bylargely maintaining the functionally moreimportant reaction, while at the same timeslowing down the lesser important one.The choice here is a relatively simple one.Nature will seek to take care of the syn-thesis of hormones first, because continu-ation of the species depends on the devel-opment of the sex organs. Fatty acid me-tabolism is for the time being at least inpart halted, Lipid in the sebaceous glandsstarts to accumulate, sebum excretion isincreased, and acne begins to appear.

When there is enough pantothenic acidin the body, however, both reactions willbe well taken care of. There is enough sexhormones for the sex organs to develop.The lipids in the sebaceous glands are com-pletely metabolized by sufficient CoezymeA, and there will be no unwanted lipid in

the glands and little sebum will be excretedto cause acne vulgaris.The Mystery Revealed

The mechanism proposed abovemay be the reason why two groups of ado-lescent boys–both with a normal bloodlevel of androgen–may exhibit differencesin the incidence of acne. The group withacne is the one that has not enough of pan-tothenic acid in the body, whereas in theother group, pantothenic acid levels are notdeficient.

This new theory seems to work well

here, and can be tested in other metabolicsituations. In the case in which endog-enous androgen stimulates acne, whereasexogenous does not, the reasoning for theobservation is the same. Any endogenousandrogen synthesis will require the partici-pation of extra amount of pantothenicacid. This will channel off some of thosethat are doing the work of fatty acid me-tabolism. Consequently, fatty acid metabo-

lism becomes less efficient and the indi-vidual is more prone to have acne. Exog-enous androgen, on the other hand, doesnot affect the pantothenic acid pool (whichis a term used to represent the total pan-tothenic acid in the body) in any manner,hence no effect on acne. This explains theseemingly mysterious nature of thisobservation.

What about premenstrual flare? In theluteal phase of the menstrual cycle, pro-gesterone in is secreted abundantly by thecorpus luteum. This naturally will take upa lot of pantothenic acid in the body’s pan-tothenic acid pool, leading to a re-distri-bution of the vitamin and putting enor-mous pressure on fatty acid metabolism.When this metabolic process is not per-forming satisfactorily, lipid begins to ac-

cumulate in the sebaceous glands, an in-crease in sebum is excreted, and acne fol-lows. That is why, even though progester-one has no effect on sebaceous gland ac-tivity, an increasing level of progesteronein the late stage of the luteal phase leavesthe acne patient with a prominent flare.



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A similar explanation may why eu-nuchs rarely exhibit acne.27,28 This may bebecause so few sex hormones are secreted,

the pantothenic acid pool can deploy amore significant portion of its reserve tometabolize fatty acids. When the job isefficiently done, little sebum is excreted,and no acne is formed.

This theory will also serve to explainthe paradoxical problem of equal sex dis-tribution of acne incidence. It is not themale hormone androgen that is important,but rather the absolute amount of sex hor-

mones that counts. Both males and femaleswill need sex hormones for the develop-ment of sex organs and the secondarysexual characteristics. The only differenceis that in the male, androgens predomi-nates, whereas in the females, the femalesex hormones. Apparently the synthesis of sex hormones, which probably ranks highup in the various reactions served by pan-tothenic acid, takes away a rather big por-

tion of the pantothenic acid pool, leavinga relative shortage of it to efficiently me-tabolize fatty acids. The result is that acnestarts to erupt, right at the time the sexorgans begin to develop—at puberty. Thereason acne first erupts at puberty is not,therefore, endocrinological, but rather sec-ondary to the deployment of a substantialamount of pantothenic acid for the pur-poses of synthesis of sex hormones, leav-ing a relative deficiency for fatty acid me-tabolism. The size of this pantothenic acidpool and the ability with which the indi-vidual can deploy any reserve from thecommon pool probably varies in differentindividuals and is likely to be influencedby genetic and dietary factors. That is why,in some individuals with little pantothenicacid in reserve, acne begins to appear early

on at puberty, whereas in some others,those with a large reserve, have their acneto appear relatively late, or not at all.

This hypothesis thus offers an expla-nation as to the relationship of the sexhormones and acne. It is suggested thatsex hormones and androgens are not im-

portant factors. What is important is theavailability of extra pantothenic acid todischarge the function of fatty acid me-

tabolism on top of the synthesis of the sexhormones. That is why, in conditions inwhich there is an increase in secretion of any hormone whose synthesis requires theparticipation of pantothenic acid, acnemay erupt This is frequently seen withthose hormone secreting tumour of theovary, testis and the adrenals. The rapiddecline in incidence of acne after adoles-cence, say in the late teens and early twen-

ties, can also be explained. After the sexorgans are fully developed, probably notas much sex hormones are required, leav-ing an adequate supply of pantothenic acidto serve the function of fatty acid metabo-lism. When this function is cleanly accom-plished, sebum secretion dries up, and acnestarts to fade.

Deficiency in Lipid Metabolism

In linking the pathogenesis of acnevulgaris to a deficiency in lipid metabo-lism and pantothenic acid, it is worthwhileto remember that fatty acid metabolism isnot the sole domain of pantothenic acid.There are some other essential dietary fac-tors that are also of importance in the sameprocess. Together they form a system thatwill make the whole metabolic process asefficient as possibly. Preliminary studies bythe author suggest that, together with pan-tothenic acid, biotin as well as nicotina-mide help to further improve the thera-peutic results. By themselves alone, theyare far less effective in helping acne pa-tients than pantothenic acid, and this, ina way, serves to support the suggestion thatpantothenic acid plays a central role in li-pid metabolism. Lipid metabolism is a

complicated process, and is often inter-twined with other metabolic processes,sharing with them common coenzymes inwidely different reactions. When there isan increase in level of some of thesecoenzymes, there may be a shift in the di-rections of some on-going reactions, and



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may affect lipid metabolism as a result.This can manifest clinically as acne vul-garis. To illustrate this, there are re-

ports39,40

saying that acne may be inducedby administration of large doses of vita-min B 12 alone or in combination withB6. Cessation of the administration of these vitamins will bring a halt to the acneeruptions. This may also be explained. If the body is in a relative deficiency statein B6 and B12, administration of the vi-tamins will enhance the reactions that in-volve the participation of these vitamins.

This will set up a chain of events, someof which will likely to entail the partici-pation of pantothenic acid. With the to-tal pantothenic acid pool fixed relative toan increase in other vitamins, emphasisof any reaction involving pantothenicacid will automatically mean a cuttingback on other reactions that require thesame vitamin as a coenzyme. This willoften include those involving lipid me-

tabolism, resulting in a certain degree of deficiency in that metabolic process,hence the increased incidence of acnevulgaris in these studies. It is probably thesame reason that in clinical practice, it isnot uncommon to find acne patients de-veloping a flare when given muti-vitamintablets.

Stress Related AcneIt is perhaps relevant here to con-

sider another common factor–stress–thatis known to affect acne adversely. Stressin many forms poses as an aggravatingfactor in acne lesions. Lack of sleep atnight, pre-examination tension, and anypsychological problem that may worrythe patient will bring on new acne le-sions.33 To explain this, one should re-

call that in combating stress, the body willsecrete glucocorticoids from the adrenalglands as a means to adapt to stress, whatis commonly known as the fight-or-flightreaction. The glucocorticoids, like the sexhormones, are derivatives of cholesterol,and increased demand for this hormone

will draw on the pantothenic acid pool.Lipid metabolism may therefore be com-promised, rendering the body more prone

to acne.If pantothenic acid deficiency is in-deed the main causative agent in thepathogenesis of acne vulgaris, it is logicalto ask how much pantothenic acid patientsare lacking in absolute amounts.

Deficiency syndromesFor decades, the medical profession

has tied their hands with a fiction of

their own device. They held, contrary tothe facts, that nutritional requirementscan be met through a well balanced diet,and that dietary supplements, includingvitamins, are not required. It is the be-lief of the medical profession that vita-mins, though essential to life and notsynthesized in the body, are not requiredin great amounts. To them, the impor-tance of vitamins lies mostly in ridding

patients of deficiency syndromes. Tokeep individuals in good health does isnot accepted as the major role of vita-mins. This view was challenged, nota-bly by Linus Pauling. In his book, Howto live longer and feel better, Paulingprovided vigorous proof, through com-parative studies in animals and from anevolutionary point of view, that vitaminC supplements are needed if an optimalstate of health is to be achieved. Not onlyis supplementation necessary, but theamount required is far greater than mostpeople believe, as with the case of vita-min C where the optimal dose is 10 ormore grams a day.41

This issue was a point of heateddebate in the 70s and 80s. ThoughPauling has quite a large following, by and

large, the issue was dismissed by the main-stream medical profession,42 because of alack of theoretical support and a generalbias against nutritional and vitamintherapy. But, in view of the new evidencesuggested in this paper, it seems appro-priate that the issue be raised again.



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How Much Pantothenic Acid?In trying to determine the actual

amount of pantothenic acid necessary to

relieve acne patients of their symptoms,Linus Pauling’s experience with vitamin Cprovides a good guideline. Pauling had fora long time recommended vitamin C inhigh dosages to achieve optimal health.Radically different from what is recom-mended by the Food and Nutrition Boardof the National Research Council (whorecommended 60 mg daily), Pauling’s rec-ommended daily intake of vitamin C

amounts to several grams a day. The rec-ommendation was stepped up to 15-20grams a day in his later years. Using theserecommendations as a background, it be-comes somewhat easier to arrive at a properdosage for pantothenic acid in the treat-ment of acne vulgaris.

Pantothenic acid, which acquires itsname from the Greek word meaning ubiq-uitous, is present in all tissues. Its univer-

sal presence is an indication of its impor-tance. This is further reflected by the manyreactions that it catalyzes. Given all these,it should not come as a surprise if theamoumt of pantothenic acid required tofor optimal health is of the same order of that of vitamin C. Based on this argument,the dose of pantothenic acid administeredto the acne patients was up to 10 gm aday, and the result of these studies werefirst reported in Medical Hypotheses.1

The Effect of Pantothenic Acid on AcneVulgaris

One hundred patients of Chinese de-scent were included in the study, 45 malesand 55 females. The age ranged from 10-30, and with about 80% between 13 and23. The severity of the disease process var-

ied. They were given 10 g of pantothenicacid a day in 4 divided doses. To enhancethe effect, the patients were also asked toapply a cream consisting of 20% byweight of pantothenic acid to the affectedarea, 4-6 times a day. With this treatmentregimen, the response is as prompt as it

is impressive. There is a noticeable de-crease in sebum secretion on the face usu-ally 2-3 days after initiation of therapy.

the face becomes less oily. After 2 weeks,existing lesions start to regress while therate of eruption of new acne lesions be-gins to slow down. In cases with moder-ate severity, the condition is normally incomplete control in about 8 weeks, withmost of the lesions gone and new lesionsonly to erupt occasionally. In those pa-tients with severe acne lesions, completecontrol may take months, sometimes up

to six months or longer. In some of thesecases, in order to get a more immediateresponse, it may even be necessary to stepup the dose to 15-20 grams a day. In anyevent, the improvement is normally agradual and steady process, with perhapsminor interruptions by premenstrualflare or excessive intakes of oily food.With this form of treatment, anotherstriking feature is the size of the facial skin

pore. The pore size becomes noticeablysmaller within 1-2 weeks, very oftenmuch sooner. Like sebum excretion, thepores will continue to shrink until theskin becomes much finer, giving the pa-tient a much more beautiful skin.

This decrease in skin pore size is pre-sumably related to sebum excretion.When an acne lesion is formed, there isin the epithelial cell of the hair follicle anaccumulation of lipids, leaving the epi-thelial cells bulky and the lumen of thegland narrowed. When there is a con-comitant increase in sebum flow, the fol-licle has no choice but to hypertrophy toaccommodate the changes, resulting in anenlarged skin pore and coarse skin. Withthe administration of pantothenic acid,the whole process is reversed Lipid me-

tabolism becomes normal and efficient.The epithelium is no longer laden withfat droplets, there is a decrease in sebumexcretion, the hypertrophy process is notrequired. The skin pore reverts to a muchsmaller size The skin becomes smooth andfine.



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Is a Maintenance Dose Necessary?Asacne lesions tend to subside spontaneouslyafter puberty, technically speaking, most

patients do not need a maintenance dose.But, if a patient is in his mid-teens, whenthe sexual characteristics are yet to fullydevelop, it becomes necessary that a re-placement therapy be implemented. Thismaintenance dose, though, can be lowered,or be titrated with the clinical symptoms.It is, however, a good idea to put all pa-tients on a maintenance dose. This will notonly act as a Preventive measure against

sporadic eruption, but the extra pan-tothenic acid will help to ease the relativedeficiency state, hopefully improving thegeneral heal th of the patient.

Pantothenic Acid and Weight ReductionWith pantothenic acid so closely re-

lated to lipid metabolism, it raises the ques-tion if it has anything to do with obesity,and hence weight reduction. In the rest of

this article, the author will try to explorethe problem of weight reduction which isequally, if not a more mysterious problem,than acne vulgaris.

Regarding negative calorie balanceand dieting, the only guiding principle be-hind weight reduction is that the calorieintake must be less than the calorie out-put, so that there is a negative calorie bal-ance. The body will try to make up forthis negative balance by burning the fatthat is stored in the fat cells, the so-calleddepot fat. With such a process, fat in thebody is consumed, and the individual losesweight. This sounds rather simple, and thegoal should therefore easily be achieved.In practice, however, this is quite a differ-ent story. By taking in less than what isactually needed, the dieter in fact faces two

hurdles that may prove too difficult toovercome. There is the problem of hun-ger. It takes enormous self- restraint anddetermination to keep the appetite incheck, and when hungry, there is the con-stant temptation to satiate this primitiveinstinct by grabbing whatever is available.

To keep this situation in check is difficult,but not insurmountable with a consciouseffort, conviction and perseverance. But

more troublsome and difficult to manageis the weakness, sweating, dizziness andfainting episodes that follow the sensationof hunger. Under such circumstances, thedieter will have little choice except to starteat ing again, gaining back the weight thathe has tried so hard to shed.

The ParadoxThe key question to the whole prob-

lem of weight reduction is why is one hun-gry and compelled to eat when one hasenough of stored fat in the body? In otherwords, why is one not able to convert,freely, one’s storage fat into energy? Stor-age fat, as the story of evolution will tell,is meant as an energy reserve in t me of need. Famine is a typical example of sucha needy time. So, why can’t one make useof the storage fat at a time when one needs

it most? Or can one do it? This is the keyquestion which needs to be examined verycarefully,

It is not strictly true to say that thebody is not able to utilize its stored fatwhen the situation warrants it. Not onlycan ti burn fat stores, but it can do it withgreat efficiency, initially at least. The trou-ble is that this ability does not last. Whenthe body is deprived of its food and en-ergy is not forthcoming from the externalsource, glycogen that is stored in the liveris first called on to furnish the energy defi-cit. Unfortunately, the glycogen store isvery limited, and very soon, even beforethe glycogen store is totally depleted, thebody will have to mobilize its stored fatfrom its fat depot to supplement its en-ergy requirement

For a short time, the body can freelyderive its energy from its stored fat All thefat that is mobilized will be completelyburnt with no wastage. But very soon, veryoccasionally within hours, for unknownreasons, the body can no longer maintainthis rate of functioning. It can still burn



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its mobilized fat, but no longer as effec-tively and as efficiently as before, with ke-tone bodies representing partially burnt

fatty acids appearing in the blood streamand urine. With time, if food is still notforthcoming, the accumulation of ketonebodies will significantly increase, an indi-cation that the power to metabolize storedfat is further being eroded. The individualbegins to feel hungry, with the concomi-tant symptoms of weakness, dizziness,sweating emerging.

It has been recognized that the time

taken from the start of fasting to the onsetof ketosis varies, sometimes to a consider-able extent among different individuals.While some may become weak within amatter of hours, others can get on very wellwithout food for more than one to twodays. In laboratory animals, it is not un-common for some to stay active and yetfree of ketosis for 2-5 days after the onsetof fasting.43,44

Ketosis and the Loss of EnergyHere, two most important points are

raised. Why is it that some people can tol-erate fasting better than the others in thesense that they can go on with their activ-ity without ketosis for a much longer pe-riod of time? And more important, why isthe body, with the development of keto-sis, losing precious stored energy at a timewhen the body needs it most? It appearsthat the body, resisting the onslaught of fasting, has installed a mechanism wherebyfat can readily be converted into energy.But this mechanism is far from perfect, andfails to keep engaged for very long in someindividuals, although in others the mecha-nism can maintain its function for severaldays. Still, the mechanism gets blunted

with time, and is unable to efficiently per-form its function-to completely burn off all the mobilized fat and provide the bodywith energy, with no ketogenic wasting of stored energy. This eventual blunting of the metabolic mechanism applies to everyindividual, without exception. In time, if

fasting is prolonged, this mechanism willbecome even more inefficient and moreketone bodies will build up as the body

loses more of its precious stored energythrough the urine and the breath.Judging from what actually happens

after the onset of fasting, there is littledoubt that the body is empowered with amechanism to metabolize mobilized fat.The only question is why this mechanismfails to last. If only one can identify theproblem, and prolong the mechanism of fat burning, then weight reduction will be

simple. One can just fast or semi-fast theindividual, and set the mechanism at work,then all the calorie deficit will be providedby energy converted from the body’s storedfat. The stored fat will be steadily depleted,and the individual will gradually andslowly lose weight.

The New Hypothesis of Ketone BodyFormation

It seems that the crux of the matterrests on the formation of ketone bodies.So long as mechanism is working effi-ciently, no ketone bodies will emerge, andthe first sign of failure of the mechanismis the appearance of ketone bodies in theblood stream. What then, is the reason forthe failure of the mechanism that leads tothe formation of ketone bodies? There isno conclusive answer, but there are someclues. It is known that ketone bodies onlyappear when the body is asked to catabolizea large amount of fat, as when the energyrequirement of the body is largely providedby its stored fat.45,46,47 At the point wherethe body can no longer cope with effi-ciently breaking down this large amountof fat, ketone bodies appear. To understandketone body formation, it seems pertinent

to have a good look at the catabolism of fat and fatty acids.48,49 Briefly, fat catabo-lism is a process in which the stored fat inthe form of triglycerides is first brokendown into glycerol and long-chain fattyacids. These long-chain fatty acids are thenserially broken down by a process called



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B-oxidation in which the long carbonchain is fragmented into units containingtwo carbon atoms each. Before this can

happen, the long-chain carbon has to beactivated into its high-energy CoenzymeA ester by reacting the acid with ATP andCoenzyme A. A subsequent cleavage at theB carbon atom of this long carbon chainby reacting with another molecule of Coenzyme A will spin off a molecule of acetyl-CoA, leaving the original long car-bon chain with 2 carbons less but still as aCoA ester. The whole process is then re-

peated again and again. with each processconsuming one molecule of Coenzyme A,until the whole long chain is totally brokendown into many fragments of acetyl CoA.

Take for example, palmitic acid, a l6-carbon saturated fatty acid, which is bro-ken down by this process of B oxidationinto 8 fragments of acetyl-CoA. It is to benoted that in converting palmitic acid into8 units of acetyl-CoA, a total of 8 mol-

ecules of Coenzyme A is taken up fromthe body’s pool of Coenzyme A molecules.All these units of acetyl-CoA will be me-tabolized via the citric acid cycle, releas-ing energy in the form of ATP, leaving car-bon dioxide and water as the final endproducts. This is how the body gets itsenergy from its stored depot fat. And thisis what is supposed to happen in an idealsituation, when all the mobilized fat ismetabolized completely, with no wastageof energy. For very obscured reasons, whenfat is broken down in large quantities, asin fasting, not all the units of acetyl-CoAwill go into the citric acid cycle. Some of these units will choose to combine witheach other. In the process, 2 molecules of acetyl-CoA will yield one molecule of ac-etoacetyl CoA and one molecule of

Coenzyme A. The acetoacetyl- CoA mol-ecule is very unstable, and will rapidly de-compose itself into one molecule of ac-etoacetic acid and another molecule of Coenzyme A Then, through a process of decarboxylation, which is an irreversibleprocess, acetoacetic acid is turned into ac-

etone, better known as a ketone body. Theaccumulation of any significant amountof ketone bodies in the body results in a

certain degree of acidosis. To off set suchacidosis, the body will try to eliminate theketone bodies in the urine as well as in thebreath. This is effectively a wastage of pre-cious stored energy that is originally in-tended for emergency use.

Coenzyme A DeficiencyIt is baffling that 2 molecules of

acetyl-CoA should start combining with

each other to form acetoacetyl-CoA, partof which is ultimately lost to the exteriorin the form of ketone bodies at a time of crisis. In an effort to understand the proc-ess, it is useful to remember the situationin the fasting state. In a bid to providesufficient energy, the body is scramblingto produce a large amount of long chainfatty acids from its fat depot that will meetthe calorie requirement. These long chain

fatty acids are then broken down, all atthe same time, into units of acetyl-CoA.The body sees it proper to do it this way.because, only by so doing, can it be in aposition to provide itself with enough en-ergy by burning these units of acetyl-CoAthrough the citric acid cycle. But, it has tobe remembered, for every 2-carbon unit,it is necessary to attach one molecule of Coenzyme A to it. Here, one must ask theall important and very practical question:Has the body, in its total pool of CoenzymeA, enough of such molecules to handle this?

The body may be able to do this for ashort period of time, but with an increas-ing portion of the body’s energy needsprovided for by fat, the call for extraCoenzyme A will sharply increase. Thepoint will be reached in which the body

will no longer be able to cope with thedemand, and under these conditions thebody will, within its scope of capability,try to generate more Coenzyme A to dealwith the situation. The easiest way to doit is for 2 molecules of acetyl-CoA to con-dense to form a molecule of acetoacetyl-



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CoA, generating one molecule of Coenzyme A along the way. This in factalso obeys the physical law of concentra-

tion of a chemical reaction. When theconcentrati on of acetyl-CoA is getting sohigh, the direction of the reaction will bedriven towards the formation of ac-etoacetyl-CoA and an molecule of Coenzyme A. To provide the body withmore Coenzyme A, which the body ur-gently needs in this state, the acetoacetyl-CoA molecule is quickly transformed intoacetoacetic acid, generating another mol-

ecule of Coenzyme A in the process. Thisis perhaps nature’s way of handling a diresituation in which generating energy tosustain life is of overriding importance.This serial event, the author would sus-pect, is the basis for the generation of ke-tone bodies. The subsequent event, whichis the loss of ketone bodies through theirexcretion from the kidneys and lungs, is adesperate attempt of the body to counter

the acidosis following the build up of ke-tone bodies, as well an attempt to main-tain a relatively normal pH of the bodyfluid. To maintain life, therefore, the bodyhas no choice but to compromise by sac-rificing some of its precious energy stores.

Overcoming CoA Deficiency withPantothenic acid

If this postulation is true, it wouldmean that, by providing the body with ahigh concentration of Coenzyme A, theacetyl-CoA molecules, instead of condens-ing with each other to form acetoacetyl-CoA, will stay as they are. They will alleventually go into the citric acid cycle andbe completely metabolized. The way toprovide the body with a high concentra-tion of Coenzyme A is rather simple. As

explained earlier, the only one componentof Coenzyme A that is an essential dietaryfactor is pantothenic acid. If the body beprovided with a large amount of pan-tothenic acid, an equivalent amount of Coenzyme A will be formed To ensure thatthe concentration of Coenzyme A is really

high, a huge dose of pantothenic acid canbe administered.

The New Concept of Weight ReductionThis is the author’s concept of a newway to achieve weight reduction, in awayin which one can overcome the tricky anddifficult part of weight reduction—to ridthe dieter of the sensation of hunger andat the same time allow them to have suf-ficient energy to see them through theirdaily activites. This is done with a dietthat is low in calorie, deliberately creat-

ing a situation in which there is an en-ergy deficit To make up for this, pan-tothenic acid is administered so that anymobilized fatty acids can be converted tofully utilized energy

A clinical study was carried out in 100individuals of Chinese descent, 40 malesand 60 females The age range was 15- 55,with even distribution. The participantswere given a carefully designed diet con-

taining about I000 calories a day, togetherwith all the essential nutrients. To go alongwith this diet, about 10 gm of pantothenicacid a day, in 4 divided doses with eachdose taken 4 hours apart, is administered.In practice, there are alternative ways of doing it The idea is to give pantothenicacid in between meals and when symptomsof hunger arise. The dieters have variedgoals which range from losing less than 5kg to more than 30 kg. Approximately half of them aimed at shedding 10-20 kg Theaverage weight loss was about 1.2 kg perweek. Ketone bodies in urine were moni-tored and were found absent in most in-stances. Occasionally, small amounts werepresent, indicating that in some individu-als, an amount of pantothenic acid largerthan 10 gm is required. The patients ex-

hibited no weakness. Often, there was thedesire to eat, but no actual hunger. Dailyactivites could be carried out normally.With determination and perseverence, thisprocess can be continued day after day,week after week, until the desired weightis achieved. The rate of weight loss can be



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regulated if the calorie deficit is made largerby eating very little, or it can be sloweddown by eating more, keeping the calorie

deficit to a very low level. However, it isnot a good idea to lose weight too quicklyfor health reasons.

The Salient FeaturesIn choosing to reduce body weight

with this method, there are 3 salient fea-tures to be noted. One is the unusuallyhigh successful rate, which is understand-able. To ensure success, the only prerequi-

site here is to maintain a calorie deficitthrough dieting. There is no hunger toworry about, and weakness will not be aproblem. With these 2 hurdles removed,extended dieting should not present amajor problem. The other feature, of course, is the significance of exercise, whichis the mainstay of most conventional meth-ods for weight reduction. What is neces-sary is the presence of a large amount of

pantothenic acid in a semi-fast state, sothat stored fat will be burnt slowly andsteadily. If the dieter does exercise, it cer-tainly will help to hasten the process.

The third feature, of course, is theabsence of side effects with such therapy.This is quite unlike the conventional drugtherapy with stimulants and appetitesuppressants in which unpleasant side ef-fects are common. Pantothenic acid, be-ing a food, and important component of the body, is non-toxic.50 No toxicity hasbeen observed by the author with anyonetaking pantothenic acid in doses of 10-20or more grams a day over a prolonged pe-riods, in some cases of more than a year.

Not only is there no toxicity, there isactually improvement of the general stateof health for those taking in large amount

of pantothenic acid every day. This too isnot difficult to understand since Pan-tothenic acid plays so many important anddiverified roles in the body as a coenzyme.Any supplement which will help the bodyto accomplish important reactions that itpreviously was unable to carry out, is evi-

dence of a prior deficiency state. Such re-actions are important to the optimal healthstate as well as the general well-being of

the individual When a relative deficiencystate is rectified, many of these importantreactions can go on, helping to improvethe general well being of the individual.

Pantothenic Acid and Weight ReductionIt seems that, aside from its other

functions, pantothenic acid is importantin keeping a stable body weight An indi-vidual has to have enough of it to stay away

from getting overweight if there is a defi-ciency, just missing a meal may bring on acertain degree of ketosis, reflecting clini-cally as hunger, weakness, and perhaps gid-diness. All these are signals that urge theindividual to have food immediately. Thiswill make any attempt to reduce bodyweight not only very difficult, but almostimpossible. It is not that the dieter is lack-ing in will power, but rather in pantothenic

acid, and it is unfair to label him as some-body who lacks perseverance and motiva-tion. He does not really have a choice un-der such circumstances other than to eat

And it is in these people that when-ever they overeat, all the extra energy deriv-ing from that meal will be put safely awayin the fat depot. It seems that, in the body,this primitive instinct of storing food awayin the fat cells for future needy times is re-tained, despite a deficiency in pantothenicacid. This leaves this group of people, whoalready have difficulty in reducing theirbody weight. particularly prone to put onweight. What a Herculean task it must befor those people without enough pan-tothenic acid in their bodies to achieveweight reduction! Failure to supplementdieters with pantothenic acid is perhaps the

main reason for the very high failure rate of diets which use conventional methods.

Further Supporting EvidenceWith the same principle, it is possi-

ble to explain many of the commonly ob-served phenomena that occur around us.



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For example, it can be explained why fe-males have a higher fat ratio in their bod-ies and that they are more prone to gain

weight than their male counterparts whenthey reach their middle age. It is not thedirect role of female hormones, as con-ventional wisdom postulates. One has toremember that the monthly menstrualcycle, which requires plenty of pantothenicacid to synthesize estrogens andprogestogens to support the cycle, is con-tinually drawing on the pantothenic acidpool that is very often quite deficient from

the start. This makes pantothenic aciddeficiency particularly common in the fe-males, especially at a time around theirmid-30s. This is the time when the cu-mulative effects of 20 years or so of repro-ductive cycles, with each cycle soaking upsome pantothenic acid from the body’stotal pool, begins to take shape. Added onto this is pregnancy. This requires evenmore female hormones to see it through,

allowing the deficiency to go even moresevere. With another pregnancy, and an-other, the situation gets from bad to worse.That is why, even though some womenwith I or 2 children may still be able toretain their slim figure with a carefullywatched diet, many more are gain a sig-nificant amount of weight. For those withmany children, few women can manageto stay slim, no matter how hard their di-eting attempt may be. Their pantothenicpool is dwindling.

There are probably more reasons forobesity than a deficiency in pantothenicacid alone, the most obvious of which isovereating. But judging from what has justbeen described, it appears that pantothenicacid must play a significant role in obesityas welll as weight loss. The body has a natu-

ral tendency to store away any excess calo-rie intake in its fat depot. Pantothenic acidis the key that unlocks this fat depot andis the agent that converts the mobilizedfat into energy. With plenty of pantothenicacid in the body, this conversion is alwayssimple and easy, allowing the body to re-

trieve as much energy from its depot as isnecessary. On a low calorie diet, theamount of pantothenic acid that is re-

quired to keep ketone bodies at a mini-mum level can actually be titrated with thecalorie intake. The lower the calorie in-take, the larger an amount of pantothenicacid is necessary. Within a certain range,the amount of pantothenic acid requiredforms almost a linear relati onship withthe calorie intake. In such cases, it can beseen that 10 gm a day, or even more, is infact, necessary. To maintain one’s body

weight after ones goal is reached can beachieved by supplying the body with a lib-eral amoumt of pantothenic acid, in theregion of 2-3 gm a day to enable the bodyto freely convert mobilized fat into energy,and the individual will appear active, ag-ile, and full of energy.

The More Important MessageThe relationship of pantothenic acid

with acne vulgaris and weight reductionis important and carries a message that isof greater significance regarding the use of megadoses of vitamins. The war of wordsbetween the Linus Pauling camp and themainstream medical profession serves toillustrate the opposing views of the twosides.41,42 This debate went on for morethan 2 decades, with the mainstream medi-cal profession maintaining their view thatvitamins in huge doses are not necessaryand until further proof is forthcoming,the idea of mega-dosage is quite wrong. Itis believed that this proof is now available,though not coming from ascorbic acid, butfrom another vitamin— pantothenic acid.

This conclusion leaves us ponderinganother important corollary: What is theposition of vitamins other than pan-

tothenic acid and ascorbic acid? Does oneneed huge doses of these vitamins as well?There are already hundreds of papers onvitamin C over the last 20 years that pro-vide evidence that large doses of the vita-min do help in various clinical conditions.With pantothenic acid, the situation is



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probably very much the same, Already.there is evidence that those who take inlarge doses of pantothenic acid, either for

acne vulgaris or for weight reduction, feela lot better, and do not tire as easily. Theirskin remains supple and taut, even afterlosing more than 20-30 kg of body weight.This is quite unlike other method of weight reduction in which excess loosenessof skin normally follows any significantweight reduction. In the future, other di-verse conditions, including conditionsthat are not very well defined clinically,

may be helped with large doses of pan-tothenic acidas will likely be true with mostother vitamins and nutrients.

ConclusionI would like to conclude this paper

with another question: Why is it that vi-tamins are needed in such a large dosage?Are they not supposed to work as catalystswhich can be recycled? To assume that

coenzymes work in the way that textbooksportray them—as a catalyst that will notperish—is perhaps unrealistic. Not onlyare they perishable, but the substrates inthe citric acid cycle, or for that matter,probably any substrate in biochemical cy-cles in the body, may share the same fate.The following observation helps to illus-trate this. In the course of weight reduc-tion, a few dieters chose to hasten theirprogress. They ate very little, sometimesnothing at all for more than 2 days, sur-viving only on water and a huge dose of pantothenic acid. Theoretically, these peo-ple have more than enough of fat storedin their body to see them through for manydays if not weeks. Since they have so muchpantothenic acid in their body, they shouldbe able to generate enough energy with-

out experiencing ketosis. But this is notthe case. Usually, in less than 2-3 days, theytoo develop ketosis regardless of how muchpantothenic acid is given. Under such cir-cumstances, the body’s many acetyl CoAunits cannot go into the citric acid cyclesto be burnt—not because of a lack in pan-

tothenic acid, but a lack in the substrates.This is evidenced by the fact that the situ-ation can readily be reversed by giving the

dieters a small amount of carbohydrates.Therefore we see how substrates of a bio-chemical cycle can be worn out, and needbe replaced constantly. The same probablyapplies to other coenzymes of the body.

Although this observation does notfully answer the question as to why largedoses of vitamins are needed, but doesthrow some new light on previous con-cepts about vitamins and coenzymes. With

the present clinical results of pantothenicacid on acne vulgaris and weight reduc-tion, it is perhaps time to focus more at-tention on how high doses of vitamins andnutrients can be used in the prevention andtreatment of diseases.

References1. Leung, L H: Pantothenic acid as a weight-re-

ducing agent: Fasting without hunger, weak-

ness and ketosis. Med Hypoth 1995; 44: 403-405.

2 Leung, L H: Pantothenic acid deficiency asthe pathogenesis of acne vulgaris. Med.Hypoth. 1995; 44: 490-492.

3. Eichenfield L F, Leyden J J: Acne: Currentconcepts of pathogensis and approach to ra-tional treatment Pediatrician, 1991; 18(3):218-223.

4. Leyden J J: New understandings of thepathogenesis of acne. J Am Acad Dermatol,

1995; 32S:15-25.5. Pochi P E: The pathogenesis and treatment of acne. Ann Rev Med 1990; 41: 187-98.

6. Montagna W: Structure and function of thepilosebaceous follicle, Dermatol Clin, 1983;1:331-333.

7. Dowmug D T, Strauss J S: On the mechanisismof sebsceous secretion Arch Dermatol. Res.1982; 272: 343-349.

8. Piemrd-Fmuchimont, C; Piemrd, G E;Kligman, A M, Rhythm of seburn exeretionduring the menstrual cycle. Dermatologica1991; 182(4): 211-3.

9. Yammamoto A, Ito M: Sebaceous glandacuivity and urinary androgen levels in chil-dren. J. Dermatol. Sci.1992; 4(2): 98 104.

10. Downing DT, Strauss JS, Synthesis and com-position of surface lipids of human skin,1974; 62: 228-244.




11.Mancuso S, et al: Changes in fatty acids in se-bum composition during human menstrual cy-cle: possible relationships with fertile period.1991; 22(1) 43-45.

12.Pochi PE, Downing DT, Strauss, JS: Sebaceousgland response in man to prolonged total caloriedeprivation. J. Invest Dermatol, 1970; 55: 303-309.

13.Stewart, ME: Sebaceous gland lipids. SeminDermatol, 1992; 11(2): lO0-105.

14. Leyden, JJ: Follicular microflora in acne vulgaris.Dermatol Clinic. 1983; 1: 345-351.

15.Plewig, G: Acne vulgaris: Proliferative cells in se-baceous glands. Br. J Dermatol, 1974; 90: 623.

16. Strauss, JS, Kligman, AM: The pathologic dy-

namics of acne vulgaris, Arch. Dematol. 1960;82: 779.

17.Canizares O: A manual of dermatology for de-veloping countries. Oxford University, Oxford.1982; 210.

18. Lewis GM, Wheeler Jr CE: Pracdcal Dermatol-ogy, 3rd ed, Philadelphia. W B Saunders, 1966;93-94.

19. Pillsbury DM, Shelley WB, Kligman AM: Der-matology. W B Saunders, Philadelphia. 1956;815.

20. Fulton Jr JE, Plewig G, Kligman AM: Effect of chocolate on acne vulgaris, JAMA, 1969;210(11): 2071-2074.

21.Mackie BS, Mackie LE: Chocolate and acne.Australian J, Dermatol. 1970;15(3):103-109.

22. Maslansky L, Wein G: Effect of chocolate onacne vulgaris. JAMA, 1970; 211(11): 1856.

23. Minkin W, Cohen HJ: Effect of chocolate onacne vulgaris. JAMA. 1970; 211(11): 1856.

24.Ebling FJ: Hormonal control and methods of measuring sebaceous gland activity J InvestDermatol. 1974; 62: 161-171.

25.Strauss JS, Kligman AM, Pochi PE: The effect of androgens and estrogens on human sebaceousglands. J Invest Dermatol, 1962; 39: 139-155.

26.Cunliffe WJ, Shuster S: Pathogenesis of acne.Lancet. 1969; 1: 685-687.

27. Emanuel S: Quantitative determinations of thesebaceceous glands’ function, with particularmention of the method employed. Acta Derm,Venereol, (Stockh) 1936; 17: 141-156. 28.Ham-ilton JB, Mestler GE: Low value for sebum ineunuchs and oophorectomized women. Proc Soc

Exp Biol Med. 1963; 112: 374- 378.29. Rony HR, Zakon SJ: Effect of androgen on the

sebaceous glands of human skin Arch Dermatol,1943; 48: 601-604.

30.Smith Jr JG, Brunot FR: Hormonal effects onaged human sebaceous glands. Acta DermVenereol, (Stockh). 1961; 41: 61-65.

31. Pochi PE; Strauss JS: Effect of cyclic administra-tion of conjugated equine estrogens on sebumproduction in women. J Invest Dermatol, 1966;47: 582-85.

32.Strauss JS, Kligman AM: The effect of progester-one and progesterone-like compounds on thehuman sebaceous glamd, J Invest Dermatol.1961; 36: 309-318.

33.Sneddon, IB; Church RE: Practical dermarology.London. Edward Arnold (Publisher), 1985.

34.Strauss IS, Pochi PE: The quantitative gravimet-ric determination of sebum production, 1961;36: 293-298.

35.Lee, PA: Acne and serum androgens during pu-berty, Arch Dermatol. 1976; 112: 482-484.

36.Zabel J: Serum testosterone concentration in boyswith acne. Przegl. Dermatol. 1981; 68: 189.

37.Abiko Y: Metabolism of coenzyme A. In: Ed.Greenberg, D M: Metabolism of Sulfur Com-pounds, Metabolic Pathways, 3rd ed. New York.Academic Press,1975; 7:1-25.

38. Robishaw JD, Neely JR: Coenzyme A metabo-lism. Am J Physiol, 1985; 248: El-E9.

39. Dupre A, Albarel N, Bonafe JL, Christol B,Lassere J: Vitamin B12 induced acnes, Cutis,1979; 24: 210-211.

40.Sherertz EF: Acneiform eruption due to“megadose” vitamin B6 and B12 Cutis, 1991;48(2): 119-20.

41.Pauling L: How to live longer and feel better.New York. Avon Books, 1986.

42. Moertel CG, Fleming TR, Creagan ET, RubinJ, O’Connell MJ. N. Engl J Med 1985; 312:137-141.

43. Fery F, Balasse EO: Ketone body turntover dur-ing and after exercise in overnight-fatigued andstarved humans. Am J Physiol, 1983; 245: E318-325.

44. Folin O, Denis W: On starvation and obesity,with special reference to acidosis. J Biol Chem1915; 21:183- 192.

45.Cahill Jr, GF: Starvation man. N Engl J Med.1970; 282: 668.

46. Krebs HA: The regulation of release of ketonebodies by the liver. Adv. Enzyme React 1966; 4:339-354.

47.Masoro, EJ: Lipids and lipid metabolism. AnnRev Physiol. 1977; 39: 301-21.

48. Greville GD, Tubbs PK: The catabolism of long-

chain fatty acids in mammaliam tissues. EssaysBiochem. 1968;4: 155-212.

49. Stumpf PK: Metabolism of fatty acids. Ann Rev.Biochem. 1969; 38:159- 212.

50. Ralli EP, Dumm ME: Relation of pantothenicacid load on adrenal cortical function. VitamHorm, 1953; 11: 133-158.

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