Losing bodyfat involves a simple mathematical formula: You have to burn more calories than you consume each day. That means you have to follow some type of diet that restricts calorie intake while increasing your use of calories through exercise. Other factors also enter into the fat-loss equation, however.
For example, diet without exercise leads to a loss of fat and muscle in equal proportions, with muscle loss dominating during some types of diets. Exercise, particularly weight training, preserves muscle during a diet, and that muscle, in turn, maintains the resting metabolic rate. The net effect is a greater likelihood that you will maintain the fat loss.
While the formula seems simple enough, the reality is quite different. The body attempts to maintain a set point of existing weight. It fights weight loss through mechanisms that include increased appetite, which occurs when calories are curtailed and makes the diet an exercise in willpower.
One way around that diet dilemma involves using drugs and other substances such as natural food fiber to reduce appetite by creating a feeling of satiety. That can involve either the physical effect promoted by increased fiber intake or by the manipulation of specific chemicals in the brain that control appetite sensations through the appetite center in the brain’s hypothalamus.
Most existing diet pills work by controlling the level of brain chemicals linked to appetite control’including the neurotransmitters serotonin and norepinephrine. Increasing levels of those substances in the brain leads to decreased appetite and even an increased feeling of satiety after eating. The net effect is that you eat less, which will result in weight loss.
The problem with pharmaceutical diet drugs is possible side effects. One example was the much publicized heart defects allegedly induced by a popular combination of prescription diet pills known as fen-phen.
Another approach to bodyfat control involves increasing thermogenesis; that is, increasing the activity of mechanisms in the body that ‘waste’ calories. Thermogenesis is what’s called a futile energy cycle, since no work is performed to burn energy. It involves the conversion of calories into heat. Most thermogenic activity occurs in a specialized fat tissue called brown adipose tissue (BAT), so named because of its red hue. (Fat is burned, or oxidized, in the mitochondria of cells, and the red color is due to increased mitochondrial content.)
The problem with BAT in humans is that it’s most active shortly after birth, which is thought to be a mechanism that maintains body temperature in newborns. As people age and their proportional levels of BAT dissipate, it becomes less of an influence on bodyfat accretion. Most BAT in adults is found around the armpits and between the shoulder blades’although that point is controversial. Some scientists believe that BAT may be more active in some people. If that’s true, those people would be able to eat more calories without getting fat, since the excess calories would be dissipated as heat due to the BAT activity.
The active ingredient in BAT is a specialized protein called uncoupling protein-1 (UCP1), which induces thermogenesis in BAT by uncoupling oxidative phosphorylation. Simply put, UCP1 interferes with the process by which ATP is synthesized in cells, forcing the body to use alternate energy pathways. UCP1 exists only in BAT, and because of that, most scientists dismiss the idea of UCP1 as a regulator of fat stores in humans because BAT activity is insignificant in adults. Emerging studies, however, show that in people who have excessive bodyfat levels, there may be defects in UCP1. The precise connection between UCP1 and bodyfat control is still being investigated.
In animals, however, UCP1 manipulation offers intriguing possibilities. An example is a recent study involving genetic manipulation of mice.1 As noted, UCP1 normally occurs only in BAT. In this study, though, mice were specially bred and genetically manipulated so that there was UCP1 in the rodents’ skeletal muscle tissue. Due to that change, the mice could eat as much as they wanted without any gain in bodyfat. They didn’t develop diabetes, since the flow of glucose into their muscles was enhanced by the change. They also had lower blood cholesterol levels. In contrast, a matching set of mice that were not genetically enhanced with the skeletal UCP1 also ate a high-fat diet, but those mice got fat, had increased blood cholesterol levels and all developed diabetes.
While UCP1 works by increased thermogenesis, none of the treated mice showed any type of overheating in their muscles. They were as physically fit as normal mice and showed the same levels of muscle ATP and creatine storage as the untreated mice. While the manipulation used on the mice remains a highly experimental procedure, it may one day be used in humans as a means of overcoming obesity and preventing diabetes.
Nutrients are known to increase the activity of UCP1 in animals. A recent study showed that retinoids, which are natural forms of vitamin A and its precursors, such as beta-carotene and lutein, can increase the gene expression reactions that lead to increased UCP1 in the BAT of animals.2 Eating a diet that’s higher in fat, especially saturated fat, also appears to increase UCP1 activity in animals.
The most familiar natural thermogenic combination consists of ephedrine and caffeine. Occasionally, aspirin is included in the stack. Studies show that about half the effect of the ephedrine-and-caffeine combo is due to thermogenic activity, while the other half results from appetite suppression. Much has been written about this combination, but other natural substances also have thermogenic properties and may be synergistic with ephedrine and caffeine as effective fat-loss aids.
The Other Natural Thermogenics
The popular ephedrine-and-caffeine combo works by promoting the release of substances such as norepinephrine and epinephrine, which are categorized as catecholamines and which interact with beta-adrenergic receptors in fat cells to promote the release of fatty acids into the blood.
Ephedrine also aids fat loss by promoting the conversion of the less active T4 thyroid hormone into the far more active T3 form. Thus, the ephedrine-and-caffeine stack has thermogenic, appetite-suppressing and metabolic-stimulating properties. Other natural substances, however, also possess some of the same properties.
One example is capsaicin, the active ingredient in hot red peppers. A recent 14-day study of rats that were given capsaicin and put on an exercise program found greater decreases in fat stores in the rats that got the capsaicin than what occured in control rats that were on the same exercise program but taking a placebo instead of the capsaicin.3 Previous studies showed that the fat-mobilizing effects of capsaicin are particularly effective during a high-fat diet.4 Other studies showed that capsaicin works equally well in promoting fat loss in rats that are on a high-carb diet.5
The mechanism of how capsaicin promotes fat mobilization involves increased release of catacholamines from the adrenal glands, followed by interaction with beta-adrenergic fat cell receptors. Note that it’s the same mechanism that’s associated with the ephedrine-and-caffeine combo. While most of the studies showing the fat-mobilizing effects of capsaicin have involved rats, a few human studies also found that effect. For example, a study of Japanese women who ate both high-carb and high-fat diets showed that adding red pepper to the diets led to increased energy expenditure and fat oxidation.6 Another study done with humans, however, showed that capsaicin taken before training increased the use of carbohydrates during exercise.
You can get capsaicin from eating hot red pepper (make sure you have something to drink with it!) or by taking certain supplements. Capsaicin supplements do exist, and lately a few makers of thermogenic supplements have begun to add capsaicin to their formulas.
Another pungent substance that may also provide thermogenic and fat-burning effects is garlic. One study showed that rats on a high-fat diet supplemented with eight grams per kilogram of bodyweight of garlic powder had enhanced triglyceride, or fat, breakdown coupled with increased growth of BAT.7 The active ingredients in garlic that lead to the reaction are various volatile sulfur compounds, which work by increasing the release of norepinephrine and fat through beta-adrenergic stimulation.8
A recent study also showed that garlic appears to increase the synthesis of UCP1 in BAT,9 the protein that controls thermogenic reactions in fat. While it’s true that BAT activity isn’t as significant in humans as it is in rats, the fact that garlic does promote the release of catecholamines makes it a possible fat-loss aid.
Garlic has many other health effects that would take an entire article to discuss. Briefly, it may help prevent the two primary causes of death in the United States: cardiovascular disease and cancer. Studies have shown that garlic appears to lower blood cholesterol an average of 9 to 12 percent. A recent analysis of published studies on garlic as a treatment for elevated cholesterol concluded that garlic is superior to a placebo in reducing total cholesterol levels but that the effect is modest.10
On the other hand, a four-year study of 280 adults published in the journal Atherosclerosis (144:237-249; 1999) found that those who took 900 milligrams of garlic powder each day had up to 18 percent less plaque in their arteries than those who took a placebo. The effect was thought to be due to a beneficial drop in platelet adhesion, meaning a drop in the formation of internal blood clots. Such clots can block a coronary artery that’s already narrowed due to atherosclerosis, leading to a heart attack or myocardial infarction.
One survey of published studies found that garlic may help prevent cancers of the stomach and colon,11 while still another controversial study found that although eating fruits and vegetables didn’t prevent colon cancer, garlic did show some activity in that area.
The reason for the paradoxical findings concerning the effectiveness of garlic in treating or preventing the onset of various medical conditions may be due to the quality of the garlic used in the studies. Unless the garlic’s volatile sulfur compounds are present in sufficient amounts, the garlic won’t be active; however, other ingredients in garlic, such as the mineral selenium, may also offer anticancer benefits. People who eat large amounts of tuna may also be interested to know that selenium blocks the bad effects of mercury, which is sometimes found in raw tuna, in the body.
A frequently overlooked thermogenic substance that, like garlic, also offers a host of valuable health benefits is green tea. In a study published last year, 10 men, average age 25, took either green tea extract with 50 milligrams of caffeine, 50 milligrams of caffeine or a placebo for six weeks.12
They ate a diet composed of 13 percent protein, 40 percent fat and 47 percent carbs’which is what you get in a typical Western diet’and they took two capsules with each meal. Measurements taken in a special metabolic chamber showed that the subjects getting the green tea extract had higher 24-hour energy expenditure than those getting just the caffeine or the placebo. Again, the mechanism was thought to involve increased promotion of norepinephrine, in this case by the green tea extract, due to inhibition of the main enzyme that degrades catacholamines in the body (COMT).
Another study found that green tea extract may help block fat digestion by inhibiting lipases, or fat-digesting enzymes.13 This study, however, involved isolated tissues, an in vitro protocol. If further studies confirm the activity, it may be that green tea mimics the effects of the obesity drug Xenical, which also reduces fat uptake in the body by inhibiting lipases.
The active ingredients in green tea are flavonoids, particularly one called epigallocatechin gallate (EGCG). A study presented at the 1999 meeting of the American College of Nutrition showed that green tea increased insulin secretion 20-fold in isolated fat cells. That can have both good and bad effects. Promoting insulin release increases bodyfat synthesis when combined with a high-calorie diet. On the other hand, insulin also promotes increased glycogen and muscle protein synthesis. That aspect of green tea requires more investigation, especially in humans, as opposed to tissue studies.
Also on the other hand, in a study in which rats were injected with EGCG, the rodents’ insulin levels dropped, and they also had lower levels of cholesterol, triglycerides, glucose, testosterone, estrogen, IGF-1 and luteinizing hormone.14 That apparently harmful effect of green tea on anabolic hormones like testosterone and IGF-1 appears problematic, unless you actually read the study. The effect only seemed to occur if the EGCG was injected. When taken orally, it had no such effect on hormones. Orally taken green tea, however, does seem to have the ability to lower blood cholesterol levels.
Another approach to manipulating metabolism to favor fat loss involves optimizing thyroid output. One often suggested method is to use a supplement containing an extract from an Indian tree called guggul. The active ingredients in the extract, called guggulsterones, appear to foster the conversion of relatively inactive T4 thyroid hormone into the more active T3 form. In doing that, guggul supplements also favorably modulate blood cholesterol levels, which are partially controlled by thyroid hormones.
A recent study from India found that combining guggul with two other herbal extracts, ashwagandha and bauhinia, led to a synergistic effect on thyroid function greater than when any of the extracts was given alone.15 They’re often found combined in certain herbal formulations.
Editor’s note: Two of the supplements included in this month’s installment of the IRONMAN Research Team contain fat-burning compounds mentioned in this feature. Pyroclen has the famous caffeine-ephedrine-and-aspirin combination and Nitro-Cuts contains guggulsetrones. See page 98 for more information.
1 Li, B., et al. (2000). Skeletal muscle respiratory uncoupling prevents diet-induced obesity and insulin resistance in mice. Nature Medicine.
2 Serra, F., et al. (1999). Stimulation of uncoupling protein 1 expression in brown adipocytes by naturally occurring carotenoids. Int J Obesity. 23:650-655.
3 Yoshioka, M., et al. (2000). Effects of capsaicin on abdominal fat and free fatty acids in exercise-trained rats. Nutrition Research. 20:1041-45. 4 Kawada, T., et al. (1986). Effects of capsaicin on lipid metabolism in rats fed a high-fat diet. J Nutrition. 116:1272-1278.
5 Matsuo, T., et al. (1996). Capsaicin in diet does not affect glycogen contents in the liver and muscle of rats before and after exercise. J Nutr Sci Vitaminol. 42:249-56.
6 Yoshioka, M., et al. (1998). Effect of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women. British J Nutrition. 80:503-510.
7 Oi, Y., et al. (1995). Garlic supplementation enhances norepinephrine secretion, growth of brown adipose tissue, and triglyceride metabolism in rats. J Nutr Biochem. 6:250-255.
8 Oi, Y., et al. (1998). Alliin and volatile sulfur-containing compounds in garlic enhance thermogenesis by increasing norepinephrine secretion in rats. J Nutr Biochem. 9:60-66.
9 Oi, Y., et al. (1999). Allyl-containing sulfides in garlic increase uncoupling protein content in brown adipose tissue and noradrenaline secretion in rats. J Nutrition. 129:336-342.
10 Stevinson, C., et al. (2000). Garlic for treating hypercholesterolemia. Ann Internal Med. 133:420-429.
11 Fleishauer, A.F., et al. (2000). Garlic consumption and cancer prevention: meta-analysis of colorectal and stomach cancers. American J Clinical Nutr. 72:1047-52.
12 Dulloo, A.G., et al. (1999). Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-hour energy expenditure and fat oxidation in humans. Am J Clin Nutr. 70:1040-5.
13 Julel, C., et al. (2000). Green tea extract inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro. J Nutr Biochem. 11:45-51.
14 Yung-hsi, K., et al. (2000). Modulation of endocrine systems and food intake by green tea epigallocatechin gallate. Endocrinology. 141:980-987.
15 Panda, S., et al. (2000). Combined effects of ashwagandha, guggulu and bauhinia extracts in the regulation of thyroid function and on lipid peroxidation in mice. Pharm Pharmcol Commun. 6:141-43. IM