Fat replacers: their use in foods and role in diabetes medical nutrition therapy.

The scientific literature demonstrates that fat replacers have a reasonable certainty of no harm. Whether they help produce desired health outcomes, i.e., decreased risk of coronary heart disease and certain types of cancer related to excess fat intake, weight reduction, changes in lipid profile, improved glycemic control, etc., depends on how individuals use these foods to change food choices and eating behaviors. As Miller and Rolls conclude, ...the use of fat-replaced foods alone should not be expected to produce spontaneous improvements in weight management. Such improvements will still be dependent on long-term behavioral changes that include not only modifications in fat, but also modifications in overall energy intake and increase in energy expenditure. (53) Though it has not been studied, one may conjecture that encouraging people with diabetes to use foods with fat replacers to achieve nutrition management goals requires sufficient education, continuous counseling, and an individual's conscientious commitment and readiness to change food habits.

Nutrition management for individuals with noninsulin-dependent diabetes mellitus in the 1990s: a review by the Diabetes Care and Education dietetic practice group.

Noninsulin-dependent diabetes mellitus (NIDDM), or Type II diabetes, is characterized by two primary defects: insulin resistance and insulin secretion. The two major goals of management of NIDDM are to achieve near normal metabolic control and to prevent/delay the microvascular and macrovascular complications of diabetes. Nutrition, exercise, and, if necessary, medication are the three primary treatment modalities used in NIDDM. Treatment regimens need to be individualized and developed with consideration for diabetes management goals and quality-of-life issues. Lean individuals with NIDDM should be encouraged to maintain their body weight and modify food composition and eating pattern to minimize glucose excursions. The primary treatment goal for an obese individual with NIDDM is weight loss. The process of teaching nutrition and meal planning involves developing a cooperative alliance, gathering information, setting realistic goals, intervention, and maintaining change. Nutrition intervention involves providing information in stages, beginning with "survival skill" information and progressing to in-depth information. The dietitian's responsibility is to promote continuity of learning by introducing new ideas and concepts and altering the learning environment. Dietitians can expand their role in the 1990s to that of a diabetes educator taking a leadership role to ensure that the individual with NIDDM receives comprehensive and individualized care.

Physiologic approaches to the control of obesity.

Morbid obesity is a major health problem in this country and throughout the world. In addition to its social stigma (in the western world), obesity exacerbates several disease states such as diabetes, hypertension, cardiac disease and restrictive lung disease. When effective medical treatment of obesity becomes available, it will depend in part upon understanding the physiologic factors that control satiety. This review summarizes the information available on brain and gut control mechanisms of satiety. Brain nuclei located in the lateral hypothalamus, ventromedial hypothalamus, and other paraventricular areas are the sites of action for potent neuropeptides, such as cholecystokinin (CCK) and neuropeptide Y, that appear to regulate feeding. Exogenous CCK has been used clinically to decrease meal size in obese patients. The sites of the satiety cascade that are most often manipulated are the gastric and intestinal phases. Physiologic gastric distension is a potent inhibitor of feeding, whereas the intermeal interval may be regulated by intestinal signals released by food in the gut. Jejunal-ileal bypass has fallen from favor and has been replaced by gastric restrictive procedures that create a small proximal gastric pouch that empties into the small bowel (gastric bypass) or the distal stomach (gastroplasty). These operations rely partially on their ability to produce gastric distension in the proximal gastric pouch at an early stage during a meal. Thus, failure results if the pouch compensates by distending or if the stoma widens with subsequent loss of slow emptying. Improved medical and surgical treatment will be designed to intervene at specific sites of the satiety cascade as knowledge of the physiologic control mechanisms of satiety increases.