The role of dietary intake in obesity remains controversial, although new data have shed more light on this subject. Obese patients often claim that they do not ingest excess food (399). These patients often seek medical evaluation for failure to lose weight despite a history of severe caloric restriction. They are fre quently thought to be hypometabolic and are often treated with thyroid or other hormones to facilitate weight loss. This is neither safe nor necessary; moreover, the observed minus the total predicted energy expenditure varies in relation to weight progression (368). Patients who gain weight increase their metabolic rate whereas those who are on diets and are losing weight may reduce their energy expenditure by 10% to 20%. Thus the results of dietary efforts can only be successful if the reduced intakes are accompanied by increased energy expenditures to overcome the metabolic adaptations that occur with dieting.
A number of studies have demonstrated that obese individuals tend to underreport food intake compared with normal-weight subjects (367,400,401). Indeed, careful metabolic balance studies in some obese adults have shown a failure to lose weight despite self-reported low caloric intakes. This may be due to substantial misreporting of food intake and physical activity and not to an abnormality in thermogenesis (366). However, the problem is often confounded in the clinical setting by the difficulties in assessing food intake and food efficiency.
A high susceptibility to obesity may also be the result of unlimited availability of palatable and high-calorie-density foods. Laboratory adult rats fed a ''supermarket diet'' consisting of high-carbohydrate/high-fat foods (i.e., chocolate chip cookies, marshmallows, peanut butter, etc.), gained 2.5 times more weight than normal controls (402). In some animals, the weight gain was not reversed after the rat was switched back to chow. It is believed that supermarket diets increase the number and size of fat cells. In children the portion size offered and the type of food given also play a role. Repeated exposure to a larger portion size of macaroni and cheese resulted in 25% more calorie intake when compared with feedings of an age-appropriate serving size, particularly in older children (403). Therefore, while younger children may be better at regulating the amount of food consumed they may lose this ability as they grow older if exposed to large portion sizes (404).
Dietary composition and different rates of nutrient utilization of ingested diets can influence body weight maintenance. Using indirect calorimetric technique in nonobese males, Flatt et al. (405) demonstrated that under sedentary conditions, ingested carbohydrates are quickly metabolized while the rate of fat oxidation remains unchanged. Moreover, it has been suggested that the body tightly regulates carbohydrate balance for up to 36 hours after ingestion and is not affected by alteration in the body's fat balance (405). On the other hand, fat balance is believed to be regulated over a varying long term and it may take several days before the fat balance adjusts to new levels of fat ingestion. Thus, it is believed that excessive fat consumption over a long period of time will result in a positive fat balance and weight gain (406,407).
Therefore, a number of medical organizations including the American Heart Association (408) and the American Diabetes Association (409) recommend consumption of low-fat diets in the prevention and treatment of obesity. However, the relationship between the dietary fat and obesity has recently been questioned (410-412), since both cross-sectional and longitudinal analyses have failed to show a consistent association between dietary fat and body fat (413,414). Furthermore, recent studies indicate that weight loss on low-fat diets is usually modest and transient (410,415). It is also noteworthy that the rate of obesity has continued to rise in the United States despite reported reduction in mean fat intake over the past 30 years, from 42% to about 34% of dietary calories (412,413,416-418).
Glycemic index (GI) is another dietary factor that may influence body weight. GI is a property of carbohydrate-containing food that describes the rise of blood-glucose after a meal (419). The GI of a meal is determined mainly by the amount of carbohydrate content and by other dietary factors affecting food digestibility, gastrointestinal motility, or insulin secretion (including carbohydrate type, food structure, fiber, protein, and fat) (419-422). The average American diet contains starchy foods that are primarily refined grain products, cereals, and potatoes and have a high GI. In contrast, vegetables, legumes, and fruits generally have a low GI (423). It has been suggested that a potential adverse consequence of the decrease observed in mean fat intake in recent years is a concomitant increase in dietary GI. A reduction of dietary fat tends to cause a compensatory increase in sugar and starch intake (424-426). In fact, a rise in total carbohydrate consumption and GI of American diets over the past two decades has been reported (413,424,426). Since fat slows gastric emptying (420), carbohydrate absorption from low-fat meals may be accelerated.
According to food supply data, U.S. consumption of added sugars increased 23% from 1970 to 1996 (427). Nine specific foods and beverages accounted for 73% of all the added sugars in the American diet. Soft drinks, carbonated sodas, and fruit drinks provided 43%, while candy, cakes, ice cream, ready-to-eat cereal, sugar and honey, cookies and brownies, and syrups and toppings each accounted for 4% to 5% of the added sugars. As the intake of soft drinks, carbonated sodas, and fruit-flavored drinks has increased, the consumption of milk and pure fruit juice has decreased and the quality of nutrient-rich foods containing Vitamins A, C, D, riboflavin and folate, and the minerals calcium, magnesium and phosphorous diminished (428). Diets high in added sugar have been associated with several health problems, including obesity, bone loss and fractures, dyslipidemia, cardiovascular disease, and dental caries. However, no single factor, including added sugar consumption, can be linked to their etiology. Indeed, the intake of non-nutritive sweeteners has increased significantly, while the prevalence of obesity continues to rise. Similarly, caries occurrence is compounded by frequency of meals and snacks, oral hygiene, fluoride supplementation and fluoride toothpaste. Although added sugar consumption has increased, the prevalence of caries has declined, probably due to fluoride supplementation and improved dental care. Similarly, the consequences of dyslipidemia (i.e., coronary artery disease and its complications) also have declined. Heart disease mortality has steadily declined for the past 30 years, and death rates were reduced independently of dietary intake. Although it is widely agreed that milk and soft drink intake are inversely related, it remains to be determined whether this is a cause and effect phenomenon. Ingestion of a variety of all foods in moderation is essential. Added sugars belong to the same biochemical class as other carbohydrates, and as such are processed in predictable metabolic pathways (428). Their intake, however, is best limited to the recommended modest amounts as part of a well-balanced diet over time (429).
High-carbohydrate diets have been demonstrated to increase basal plasma insulin levels in animals and humans (430,431). Dennison et al. suggested that consumption of ''fruit drinks'' equal to or greater than 12 fl oz/day by young children was associated with short stature and with obesity (432). Indeed, marked obesity has been associated with elevated basal plasma insulin secretory response to glucose and protein (433,434). The hyperinsulinemia of obesity has been regarded as a compensatory adaptation to the peripheral insulin resistance characteristics of the obese state (435). Since the diets of moderately obese individuals are excessive in both total calories and in the quantity of carbohydrate ingested, the hyperinsulinemia of obesity may also be a consequence of these dietary factors rather than merely a secondary response to insulin resistance. Indeed, it has recently been shown that voluntary intake after a high-GI meal was 53% greater than that after a medium-GI meal, and 81% greater than that after a low-GI meal. In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, plasma glucagon levels, postab-sorptive plasma glucose, and serum fatty acids levels, along with an elevation in plasma epinephrine (436). It is, therefore, likely that the slower absorption of glucose after ingestion of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese adolescents. Recently, Spieth et al. suggested that a low-GI diet in the treatment of childhood obesity resulted in greater weight loss than a standard reduced-fat diet (437).
Reduced meal frequency, or gorging (i.e., one to two meals daily), has been associated with an increased risk of obesity (438,439). This is also associated with high fasting serum lipid and insulin levels. Insulin stimulates hepatic synthesis of cholesterol and tissue lipogenesis (440,441). Increasing meal frequency or nibbling has been shown to significantly lower serum cholesterol and insulin levels (442). This is thought to have a beneficial effect in decreasing triglyceride synthesis in adipose tissue through a reduction in postprandial glucose and insulin levels. However, this effect may be significantly minimized by a parallel reduction in the postprandial thermogenesis stimulated by insulin and glucose (443).
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