Losing bodyfat is easy: All you have to do is burn more calories than you eat, increasing your exercise and decreasing your total daily calorie intake. By reducing your current diet by 500 calories a day, you’ll lose one pound of fat each week, guaranteed. But as anyone who’s ever dieted knows, losing bodyfat just isn’t that simple.
Once you reach a certain bodyweight, your body establishes that as your norm and vigorously opposes any attempt to change your set point, resisting changes in composition by slowing your metabolism and increasing your hunger sensations. That’s why any attempt to lose a significant level of bodyfat turns into a matter of will’literally you against yourself. No wonder most diets fail. Another common scenario occurs when you diet and exercise steadfastly and lose weight, only to see the fat return with a vengeance when the diet ends.
So most people need help losing bodyfat’something to keep the fat-burning process at maximum capacity while diminishing the incessant food cravings that doom most diets. Several food supplements have been touted as meeting those goals. The most prominent and generally the most effective are so-called thermogenic agents. The word thermogenic refers to the activity of what scientists call ‘futile energy cycles,’ whereby calories convert into heat instead of being stored as fat.
Ephedrine and its native natural herbal source, mahuang, have been the thermogenic supplements of choice in recent years. Many published studies attest to the effectiveness of ephedrine-based food supplements for fat-loss purposes, but that’s also spelled their commercial doom. Reports of health problems related to ephedrine-based supplements are common these days, though such products have been used without problems for nearly a century. What really seems to be going on is that casting suspicion on ephedrine’s safety is in the best commercial interests of some industries’notably pharmaceuticals manufacturing.
Unfounded reports about the alleged dangers of ephedrine are often based on the experiences of people who either had no business using the supplements in the first place due to medical contraindications or had occult health problems that ephedrine aggravated. The fact is, untold numbers of people have used ephedrine daily, with no side effects besides the significant fat loss they experienced.
Nevertheless, ephedrine’s days appear to be numbered. Already, a few states have banned the sale of ephedrine and mahuang. Fearful of litigation, supplement companies have removed the substances from their thermogenic fat-loss formulas, replacing them with ingredients that are so ineffective that they perform little better than a placebo. The market for fat-loss supplements is so huge, however, that companies are loath to forgo the fat-loss cash cow.
Fat-loss supplements commonly contain two ingredients: hydroxycitrate (HCA) and chitosan. Now that ephedrine must relinquish its throne as king of the fat-loss supplements, the salient question becomes whether such ingredients as HCA and chitosan actually promote fat loss. Let’s take a look at the HCA evidence.
Hydroxycitrate Acid
HCA is extracted from the rind of a fruit common in Asia and India. It’s the principal acid found in the brindleberry, also known as Garcinia cambogia, making up 16 percent of the weight of the dried fruit. HCA works by inhibiting an enzyme called ATP citrate lyase, which controls the conversion of citrate and coenzyme A into oxaloacetate and acetyl coenzyme A, an ingredient in the synthesis of acetylcholine in the brain and in the synthesis of fatty acids, cholesterol and triglycerides elsewhere in the body. By suppressing the synthesis of acetyl coenzyme A, HCA may suppress fat synthesis.
Scientists also think that HCA prevents the conversion of carbohydrates into bodyfat, instead shifting excess carbs toward the metabolic pathway of glycogen formation in muscle and the liver. One theory of appetite suppression is that when liver glycogen stores are full, appetite is suppressed, which implies that HCA also functions as an appetite suppressant.
Particularly in the case of a carb-rich diet, acetyl coenzyme A may take another metabolic pathway that leads to production of a substance called malonyl coenzyme A (MCA). The problem with malonyl coenzyme A is that it blocks the activity of enzymes that work with carnitine in shuttling fat into the mitochondria of cells, where fat oxidation occurs. So inhibiting the activity of malonyl coenzyme A’as HCA supposedly does’would lead to greater fat oxidation during exercise.
It’s hard to overstate the fact that the primary enzyme HCA inhibits, ATP citrate lyase, is most active in high-carbohydrate diets. In fact, there’s some evidence that using HCA-based supplements during low-carbohydrate dieting is ineffective. High-carb diets always elevate the activity of ATP citrate lyase, making fat synthesis more likely. ALL A number of studies have examined HCA’s link to fat loss. Their findings have been equivocal at best. Some studies show that HCA extends definite beneficial effects, and others show few or no benefits. Many of the studies, however, have been influenced by such other factors as exercise and the nutrient composition of the diet.
In a study published two years ago, 24 overweight men and women took 900 milligrams of either a placebo or HCA for six weeks.1 After two weeks energy intake decreased by 15 to 30 percent in the HCA group, chiefly between meals. The authors suggest that HCA may be more effective at preventing weight regain due to its appetite-suppressing properties.
An earlier double-blind, placebo-controlled, randomized study, however, came to a different conclusion.2 For three days subjects took three grams of HCA or a placebo, and researchers examined the effects of exercise with and without HCA use. They found no differences in fat oxidation between the placebo and HCA. Nor did HCA affect energy expenditure, either at rest or during exercise.
The authors suggest that perhaps the HCA dose was too low and the three-day experiment too short for them to adequately gauge HCA activity. Another problem: The study subjects were on a typical American diet containing 35 percent fat, but the authors didn’t mention the diet’s carb content, even though HCA’s main function is to prevent conversion of excess carbs into fat.
A study presented at the 2002 Experimental Biology meeting that compared HCA to a placebo suggests that HCA may modulate obesity genes. The subjects took the HCA or a placebo 30 minutes before meals, and both groups took in the same number of daily calories’2,000. They also participated in a walking exercise program. At the end of eight weeks the HCA group showed a 4.8 percent loss in bodyweight and a 40 percent decline in plasma leptin levels.
In another study, scientists combined HCA with another popular supplement aimed at fat loss, medium-chain triglyceride, or MCT.3 For two weeks the subjects took either 500 milligrams of HCA alone or the same dose with three grams of MCT. Another group took nothing. All groups showed significant bodyweight loss, and there was no significant difference between the groups. Those in the supplement group showed no more evidence of increased energy expenditure, fat oxidation or satiety than the placebo group. Because the subjects were in a negative energy balance, however, no fat would be synthesized, and HCA wouldn’t be expected to do anything.
In analysis consistent with other research, the authors suggest that HCA would be more likely to prevent weight regain following a diet than to burn fat during one because it works by preventing excess calories from becoming fat. People who are dieting rarely get too many calories. As for those who do eat large amounts of carbs and then engage in endurance training, the question remains whether HCA intake would lead to greater fat oxidation.
In a study of endurance athletes subjects got either 250 milligrams of HCA or a placebo for five days, then did a cycling routine for an hour at 60 percent of maximum oxygen intake, followed by a routine that increased the pace to 80 percent of maximum oxygen intake, until exhaustion.4 The HCA group showed increased fat oxidation and lowered carb oxidation during exercise.
In another study that featured a two-hour cycling routine, however, HCA did nothing, even though the cyclist subjects got six to 30 times more HCA than the subjects of previous studies.5 No changes occurred in either fat or carb oxidation during exercise.
Evaluating HCA Research
HCA research shows equivocal results because of other factors that may affect how it works. In particular, HCA seems to do little or nothing for those on a low-calorie or low-carb diet, but it may be of some help in preventing weight regain after a diet, when you have a greater chance of taking in excess carbs or calories. HCA may also work on low-carb-diet ‘cheat days,’ when it would divert carbs away from storage and toward glycogen replenishment in muscle and the liver. Safety concerns about HCA aren’t a major problem. It doesn’t promote catecholamine release, as ephedrine does, so there are no cardiovascular complications to worry about. On the other hand, by limiting the synthesis of acetyl coenzyme A, HCA may also slightly inhibit the synthesis of acetylcholine, a brain neurotransmitter involved in learning and memory. Alzheimer’s disease is marked by a drop of acetylcholine levels in the brain, and people with memory problems should exercise caution before taking large doses of HCA.
By inhibiting acetyl coenzyme A, the starting point for cholesterol and steroid hormones, HCA could also, in theory, interfere with hormone synthesis. According to researchers, however, that should be of concern only to pregnant or breast-feeding women.6
Another substance HCA inhibits, malonyl coenzyme A, not only prevents fat-burning but also helps transmit the insulin signal to cells. So by inhibiting MCA production, HCA could foster insulin insensitivity. That’s never occurred with typical supplement doses, but diabetics should exercise caution with HCA all the same.
HCA works best when taken 30 to 60 minutes before meals and when taken in divided doses of 750 to 1,500 milligrams daily. Avoid HCA lactone supplements, which have zero activity in humans.
References
1 Westerterp, M.S., et al. (2002). The effect of hydroxycitrate on energy intake and satiety in overweight humans. Int J Obesity. 26:870-872.
2 Kriketos, A.D., et al. (1999). Hydroxycitric acid does not affect energy expenditure and substrate oxidation in adult males in a postabsorptive state. Int J Obesity. 23:867-873.
3 Kovacs, E.M.R., et al. (2001). The effects of two-week ingestion of hydroxycitrate and hydroxycitrate combined with medium-chain triglycerides on satiety, fat oxidation, energy expenditure and bodyweight. Int J Obesity. 25:1087-1094.
4 Lim, K., et al. (2002). Short-term hydroxycitrate ingestion increases fat oxidation during exercise in athletes. J Nutr Sci Vitaminol. 48:128-133.
5 Van Loon, J.C,. et al. (2000). Effects of acute hydroxycitrate supplementation on substrate metabolism at rest and during exercise in humans. Am J Clin Nutr. 72:1445-1450.
6 Jena, B.S., et al. (2002). Chemistry and biochemistry of hydroxycitrate acid from Garcinia. J Agric Food Chem. 50:10-22. IM
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