Dietary fat intake, supplements, and weight loss.
Although there remains controversy regarding the role of macronutrient balance in the etiology of obesity, the consumption of high-fat diets appears to be strongly implicated in its development. Evidence that fat oxidation does not adjust rapidly to acute increases in dietary fat, as well as a decreased capacity to oxidize fat in the postprandial state in the obese, suggest that diets high in fat may lead to the accumulation of fat stores. Novel data is also presented suggesting that in rodents, high-fat diets may lead to the development of leptin resistance in skeletal muscle and subsequent accumulations of muscle triacylglycerol. Nevertheless, several current fad diets recommend drastically reduced carbohydrate intake, with a concurrent increase in fat content. Such recommendations are based on the underlying assumption that by reducing circulating insulin levels, lipolysis and lipid oxidation will be enhanced and fat storage reduced. Numerous supplements are purported to increase fat oxidation (carnitine, conjugated linoleic acid), increase metabolic rate (ephedrine, pyruvate), or inhibit hepatic lipogenesis (hydroxycitrate). All of these compounds are currently marketed in supplemental form to increase weight loss, but few have actually been shown to be effective in scientific studies. To date, there is little or no evidence supporting that carnitine or hydroxycitrate supplementation are of any value for weight loss in humans. Supplements such as pyruvate have been shown to be effective at high dosages, but there is little mechanistic information to explain its purported effect or data to indicate its effectiveness at lower dosages. Conjugated linoleic acid has been shown to stimulate fat utilization and decrease body fat content in mice but has not been tested in humans. The effects of ephedrine, in conjunction with methylxanthines and aspirin, in humans appears unequivocal but includes various cardiovascular side effects. None of these compounds have been tested for their effectiveness or safety over prolonged periods of time.
Dyck
D J
DJ
Department of Human Biology and Nutritional Sciences, University of Guelph, ON.
D000818:Animals; D019440:Anti-Obesity Agents / Q000009:adverse effects / Q000627:therapeutic use; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use; D002331:Carnitine / Q000627:therapeutic use; D002951:Citrates / Q000627:therapeutic use; D004041:Dietary Fats / Q000008:administration & dosage* / Q000009:adverse effects; D019587:Dietary Supplements / Q000009:adverse effects; D004809:Ephedrine / Q000627:therapeutic use; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000378:metabolism; D019787:Linoleic Acid / Q000627:therapeutic use; D050356:Lipid Metabolism; D008066:Lipolysis; D051379:Mice; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000209:etiology; D010084:Oxidation-Reduction; D011773:Pyruvates / Q000627:therapeutic use; D051381:Rats; D014280:Triglycerides / Q000378:metabolism; D015431:Weight Loss; D014970:Xanthines / Q000009:adverse effects / Q000627:therapeutic use
D019440:Anti-Obesity Agents; D002951:Citrates; D004041:Dietary Fats; D007328:Insulin; D020738:Leptin; D011773:Pyruvates; D014280:Triglycerides; D014970:Xanthines; C008514:methylxanthine; C007999:hydroxycitric acid; D019787:Linoleic Acid; D004809:Ephedrine; D001241:Aspirin; D002331:Carnitine