Waist Size Reduction:
Three Easy Ways
espite the omnipresent emphasis in our culture on the value of physical activity and healthful, moderate eating habits, the American waistline continues to expand. Obesity and weight gain have reached epidemic proportions. Although the incidence of obesity in adults increased by only about 1% between 1960 and 1980, between 1988 and 1994, it had jumped by nearly 10% - from 15% to 25% in the general population.1
Concern about the growing problem of being overweight stems largely from the fact that too much body fat is a major risk factor for a large number of serious chronic diseases, including diabetes mellitus, cardiovascular disease, hyperinsulinemia, atherosclerosis, hypertension, and some types of cancer.2,3 After tobacco use, obesity is the second leading cause of preventable death.4
BODY MASS INDEX
Obesity has been defined as the excessive storage of body fat,5 but specifying exactly what is excessive has been somewhat problematic. The current standard for assessing obesity is the body mass index (BMI), which is defined as body weight (in kilograms) divided by the square of the height (in meters), or [body weight (kg)/m2].6 Although body weight may increase as a result of muscle and adipose tissue, BMI has been shown to correlate well with both adiposity and health risks.7
Too much body fat is a major risk factor for a
large number of serious chronic diseases,
including diabetes mellitus, cardiovascular
disease, hyperinsulinemia, atherosclerosis,
hypertension, and some types of cancer.
To determine your BMI, divide your weight in kilograms by the square of your height in meters. If you are among the many decimally challenged in the U.S., you can multiply your weight in pounds by 703; then divide by the square of your height in inches. For example, if you weigh 130 pounds and are 5'4" (64") tall, your BMI is (130x703)/(64x64) = 22.3. You can also approximate your BMI by finding your height and weight on Table 1.
Table 1. What Is Your BMI?*
Match your weight** with your height
* Weight is without shoes and clothes.
** If you have a large frame and/or a high muscle/fat ratio, this chart may place you mistakenly into a risk category.
According to current definitions, you are considered to be "overweight" if your BMI is greater than 25. You fall into the "obese" class if your BMI is greater than 30. Individuals with a BMI greater than 27 - which amounts to about 120% of desirable weight for your height - are considered to be at increased risk for morbidity and mortality.7-10
Recent studies have shown that even minimal increases in a person's BMI are associated with an increased risk of both fatal and nonfatal heart attacks, even if the person has no other risk factors for heart disease. At the same time, as little as a 5% weight loss has been shown to reduce or eliminate disorders associated with obesity.11
Although body weight may increase as a
result of muscle and adipose tissue gain,
BMI has been shown to correlate well
with both adiposity and health risks.
It's not only how much fat you're carrying around, but also how you carry it. Fat distribution, as measured by the waist-to-hip ratio (WHR) and waist circumference, for example, have been found to be good predictors of long-term complications.12 Ideally in women, the waist should be narrower than the hip - the classic "hourglass" figure. The familiar "spare-tire" fat distribution, in which the waist is wider than the hip, is an indication of potential health risks. This is true for men as well, although a man's risk ratio is different from a woman's.
To find out your waist-to-hip ratio, measure the waist at its narrowest point, then measure the hips at their widest point. Divide the waist measurement by the hip measurement. For a woman with a 35" waist and 46" hips, the WHR would be: 35/46 = 0.76. Women with a waist-to-hip ratio greater than 0.8 and men with a waist-to-hip ratio greater than 1.0 are at increased health risk because of their fat distribution.
Even if you don't gain body weight as
you age, you may still be increasing the
amount of fat relative to
lean muscle and bone mass.
GROWING OLDER, GROWING FATTER
Vladimir Dilman, M.D., Ph.D., one of the giants of antiaging medicine, observed that an increase in body weight is a "normal" accompaniment of advancing age.13 Even if you don't gain body weight as you age, you may still be increasing the amount of fat relative to lean muscle and bone mass for two primary reasons:
- Fat deposits typically increase with age, while bone and muscle mass decline
- Fat cells themselves grow larger with age
Dilman believed that age-associated obesity was caused by such factors as age-related hyperglycemia and hyperinsulinemia, decreased physical activity, and excessive food intake (particularly carbohydrates). He reasoned that people tend to overeat as they age because the hypothalamic brain centers that control satiety become less sensitive to the signals provided by blood glucose levels. "Consequently, with increasing age, those whose food consumption depends on their appetite are inevitably on a path to obesity," wrote Dilman.13
According to one British researcher,
of the many appetite suppressants found
to be "active" in laboratory animals, the most
promising candidates are those, like 5-HTP,
that increase central levels of serotonin.
REDUCING STORED FAT
Unfortunately, as Dilman demonstrated and as most people over age 40 eventually find out for themselves, the older one gets, the harder it is to keep the fat off. To most people - including most physicians and weight-loss "experts," caloric reduction is the key to weight (fat) loss. Caloric reduction is to be accomplished by drastically cutting fat intake in favor of a diet high in carbohydrates.
The only problem with this diet is that it doesn't work. In the long run, 95% of people who lose weight primarily by caloric/fat restriction gain the lost weight back, and they gain it back mostly as fat, rather than lean muscle or bone.
APPETITE SUPPRESSION + THERMOGENESIS: THE BETTER WAY TO LOSE FAT
Although it cannot be the whole answer, caloric restriction remains an important element in any weight-loss program. But, if Dilman is right, and appetite becomes a less and less reliable clue to the number of calories the body requires, then how can we best adjust appetite to a level more in keeping with our physiologic needs?
One means that has been used repeatedly over the last 30 or 40 years has been appetite-suppressing drugs. The best known of these have been the amphetamines, fen-phen (fenfluramine/phentermine), and dexfenfluramine (Redux), which work by a combination of adrenergic and serotonergic mechanisms. Although these drugs proved to be generally effective in reducing caloric intake, they have turned out to be dangerous, causing serious or even fatal side effects at a rate that led to their recent removal from the marketplace.
If you can "turn up the flame" on your
fat stores, you'll lose weight and fat.
A far safer avenue appears to be enhancing serotonergic function using metabolic precursors of serotonin, such as the amino acid tryptophan and the naturally derived 5-hydroxytryptophan (5-HTP). Studies have demonstrated that increasing serotonin levels can put a damper on appetite. According to one British researcher, of the many appetite suppressants found to be "active" in laboratory animals, very few have clinical potential. Among the most promising candidates, he argues, are those like 5-HTP that increase central levels of serotonin.14 A group of Italian researchers reporting on a small study found that 20 obese patients taking 5-HTP (900 mg/day) lost a significant amount of weight, had lower carbohydrate intake, and consistently became sated earlier than a similar group taking a placebo. They concluded that since 5-HTP was well-tolerated, it could be safely used to treat obesity.15
Too often ignored by conventional weight-loss programs is the value of enhanced thermogenesis. Thermogenesis is the process by which the body uses its fat stores to provide energy for its many functions. Fat is literally burned to generate heat (thermo = heat, genesis = generation). The more fat the body uses up in this way, the less it has to store in that "spare tire." If you can "turn up the flame" on your fat stores, you'll lose weight and fat, reduce your BMI and your WHR.
The ancient Chinese herb ephedra (ma huang) has long been recognized as a safe and effective way both to reduce appetite16 and stimulate thermogenesis.17-19 Furthermore, studies have shown that when ephedra is combined with substances such as caffeine, theophylline, and/or yohimbe and white willow, its thermogenic effects are amplified.20
Ingesting the amino acid arginine has
repeatedly been shown to result in a
natural release of GH from the pituitary
gland, which appears to provide the same
benefits of reduced fat mass and increased
lean tissue mass provided by GH injections.
The ephedra/caffeine combination simultaneously has been shown to help increase lean body tissue and preserve fat-free mass, while promoting fat loss. In a Danish study in obese women, the combination of ephedrine and caffeine was superior to placebo in preserving fat-free mass and enhancing fat loss. The effect was calculated to be due to appetite suppression (75%) and thermogenesis (25%).21
The addition of the active ingredient including white willow (which contains acetylsalicylic acid, generically known as aspirin) to ephedra/caffeine has also been found to be functionally effective in producing "modest, sustained weight loss even without prescribed caloric restriction." The authors speculated that restricting caloric intake might make this treatment even more effective. The combination was reported to be "well-tolerated in otherwise healthy obese subjects."22
GROWTH HORMONE RELEASE
Not to be overlooked in any weight-loss program is the importance of growth hormone (GH) release. Diminished secretion of growth hormone is responsible in part for the age-related decrease in lean body mass and the expansion of adipose-tissue mass.23 Administration of recombinant GH has been shown to produce dramatic changes in body composition, including increases in lean body mass and reductions in fat mass.24
Growth hormone injections are out of the question for most people because of cost, the need for a prescription (recombinant hGH has not been approved by the FDA for treating obesity), and medical concerns about various side effects. However, ingesting the amino acid arginine has repeatedly been shown to result in a natural release of GH from the pituitary gland,25 and appears to provide the same benefits of reducing fat mass and increasing lean tissue mass.
- Kuczmarski R, Flegal K, Campbell S, Johnson C. Increasing prevalence of overweight among US adults. The National Health and Nutrition Examination Surveys, 1960 to 1991. JAMA. 1994;272:205-211.
- Pi-Sunyer F. Medical hazards of obesity. Ann Intern Med. 1993;119:655-660.
- Stunkard A. Current views on obesity. Am J Med. 1996;100:230-236.
- McGinnis J, Foege W. Actual causes of death in the United States. JAMA. 1993;170:2207-2212.
- Colditz G, Wolf A. The public health impact of obesity. In: Angel A, Anderson C, Bouchard D, et al, eds. Progress in Obesity Research. London: John Libbey & Co.; 1996:517-523.
- NIH Technology Assessment Panel. Methods for voluntary weight loss and control. Ann Intern Med. 1993;119:764-770.
- Olefsky J. Obesity. New York: McGraw-Hill Inc; 1994:446-452.
- Doering P. Weight control products. Handbook of Nonprescription Drugs, 11th ed. Washington, DC: American Pharmaceutical Association; 1996:423-445.
- Dwyer J. Medical evaluation and classification of obesity. In: Blackburn G, Kanders B, eds. Obesity: Pathophysiology, Psychology, and Treatment. New York: Chapman & Hall; 1994:9-38.
- Wadden T. Obesity. In: Kaplan H, Saddock B, eds. Comprehensive Textbook of Psychiatry. Baltimore, MD: Williams and Wilkins; 1995:1481-1491.
- Blackburn G. Effect of degree of weight loss on health benefits. Obesity Research. 1995;3:211-216.
- Chan J, Rimm E, Colditz G, Stampfer M, Willett W. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care. 1994;17:961-969.
- Dilman V, Dean W. The Neuroendocrine Theory of Aging and Degeneration. Pensacola, FL: The Center for BioGerontology; 1992.
- Blundell J. Pharmacological approaches to appetite suppression. Trends Pharmacol. 1991;12:147-157.
- Cangiano C, Ceci F, Cascino A, et al. Eating behavior and adherence to dietary prescriptions in obese subjects treated with 5-hydroxytryptophan. Am J Clin Nutr. 1992;56:863-868.
- Zarrindast M, Hosseini-Nia T, Farnoodi F. Anorectic effect of ephedrine. Gen Pharmac. 1987;18:559-561.
- Pasquali R, Cesari M, Besteghi L, Melchionda N, Balestra V. Thermogenic agents in the treatment of human obesity: preliminary results. Int J Obesity:23-26.
- Pasquali R, Cesari M, Melchionda N, Steanini C, Raitano A, Labo G. Does ephedrine promote weight loss in low-energy-adapted obese women? Int J Obesity. 1987;11:163-168.
- Astrup A, Lundsgaard C, Madsen J, Christiensen N. Enhanced thermogenic responsiveness during chronic ephedrine treatment in man. J Clin Nutrition. 1985;42:83-94.
- Malchow-Møller A, Larsen S, Hey H, Stokholm K, Juhl E, Quaade F. Ephedrine as an anorectic: the story of the "Elsinore pill." Int J Obesity. 1981;5:183-187.
- Astrup A, Toubro S, Christensen N, Quaade F. Pharmacology of thermogenic drugs. Am J Clin Nutr. 1992;55 (1 Suppl ):246S-248S.
- Daly P, Krieger D, Dulloo A, Young J, Landsberg L. Ephedrine, caffeine and aspirin: safety and efficacy for treatment of human obesity. Int J Obes Relat Metab Disord. 1993;17 (Suppl 1):S73-S78.
- Rudman D, Feller A, Nagraj H, et al. Effects of human growth hormone in men over 60 years old. N Engl J Med. 1990;323:1-6.
- Carroll P, Littlewood R, Weissberger A, Bogalho P, McGauley G, Sonksen P. The effects of two doses of replacement growth hormone on the biochemical, body composition and psychological profiles of growth hormone-deficient adults. Eur J Endocrinol. 1997;137:146-153.
- Koppeschaar H, ten Horn C, Thijssen J, Page M, Dieguez C. Differential effects of arginine on growth hormone releasing hormone and insulin-induced growth hormone secretion. Clin Endocrinol. 1992;36:487-490.