Pantothenic Acid in the Treatment of Obesity

Pantothenic Acid and Weight Reduction

With pantothenic acid so closely related to lipid metabolism, the question is raised if it has anything to do with obesity, and hence weight reduction. In the rest of this article, we will explore the problem of weight reduction which is an equally, if not more mysterious problem than acne vulgaris.

Regarding negative calorie balance and dieting, the only guiding principle behind weight reduction is that the calorie intake must be less than the calorie output, so that there is a negative calorie balance. The body will try to make up for this negative balance by burning the fat that is stored in the fat cells, the so-called depot fat. In this process, fat in the body is consumed, and the individual loses weight. This sounds rather simple and the goal should therefore easily be achieved. In practice, however, this is quite a different story. By taking in less than what is actually needed, the dieter in fact faces two hurdles that may prove too difficult to overcome. There is the problem of hunger. It takes enormous self-restraint and determination to keep the appetite in check and when hungry there is the constant temptation to satiate this primitive instinct by grabbing whatever is available. To keep this situation in check is difficult, but not insurmountable with a conscious effort, conviction and perseverance. But more troublesome and difficult to manage is the weakness, sweating, dizziness and fainting episodes that follow the sensation of hunger. Under such circumstances, the dieter will have little choice except to start eating again, gaining back the weight that he has tried so hard to shed.

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Pantothenic Acid in the Treatment of Acne Vulgaris “A Medical Hypothesis”

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,

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Pantethine Clinical Studies and Research

Pantethine: A review of its biochemistry and therapeutic applications

Pantethine is the stable disulfate form of pantetheine, the metabolic substrate which constitutes the active part of Coenzyme-A (CoA) molecules and acyl carrier proteins. Because pantethine is located nearer to Coenzyme-A than is pantothenic acid in the biosynthetic pathway of Coenzyme-A, it has been suggested it will have clinical benefits in conditions where pantothenic acid is not effective, and clinical trials with pantethine appear to prove this argument. Oral administration of pantethine has consistently shown an ability to favorably impact a variety of lipid risk factors in persons with hypercholesterolemia, arteriosclerosis, and diabetes. Pantethine administration positively affects parameters associated with platelet lipid composition and cell membrane fluidity. (Alt. Med. Rev. 1997;2(5):365-377)

Pantethine, which is known to be converted to Coenzyme-A, has been reported to have antiarrhythmic action on experimental cardiac arrhythmias

Using standard microelectrode techniques, the electrophysiological effects of pantethine under hypoxic (95% N2 + 5% CO2) perfusion were studied. Hypoxia decreased resting membrane potential, action potential amplitude and maximum velocity of phase 0 and shortened action potential duration and effective refractory period. Application of pantethine 5 X 10(-3) Gm/ml under hypoxic perfusion prolonged action potential duration and effective refractory period significantly. Prolongation of action potential duration by pantethine might be caused by an increase in intracellular ATP. The findings in this study could be an explanation of the possible antiarrhythmic effects of pantethine. Hayashi H, Kobayashi A, Terada H, Nagao B, Nishiyama T, Kamikawa T, Yamazaki N. Effects of pantethine on action potential of canine papillary muscle during hypoxic perfusion. In: Jpn Heart J (1985 Mar) 26(2):289-96.

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