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Diet and Exercise in Non-Insulin-Dependent 
Diabetes Mellitus

National Institutes of Health
Consensus Development Conference Statement
December 8-10, 1986

Conference artwork, a running figure from the waist down in front of figures of food plants (wheat, corn, etc.)

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus http://www.nlm.nih.gov/medlineplus/.

This statement was originally published as: Diet and Exercise in Non-Insulin-Dependent Diabetes Mellitus. NIH Consens Statement 1986 Dec 8-10;6(8):1-21.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Diet and Exercise in Noninsulin-Dependent Diabetes Mellitus. NIH Consens Statement Online 1986 Dec 8-10 [cited year month day];6(8):1-21.


Introduction

Diabetes mellitus is a major health problem. It is a leading cause of death. It is the chief reason for new blindness, kidney failure, and limb amputation. Dialysis for kidney failure from diabetes alone costs over $1 billion annually, and this is expected to double over the next few years. Moreover, diabetes is a major emotional burden for many families.

Non-insulin-dependent diabetes (NIDDM, also called adult-onset or Type II diabetes) affects about 10 million Americans, mid-age or older, or approximately 90 percent of all diabetic people. The cornerstone of therapy is a style of life centered around diet and supplemented, if needed, by insulin or oral agents. With the very high association of NIDDM with overnutrition and overweight (approximately 80 percent of patients), much dietary effort is directed to caloric reduction, with exercise as an auxiliary means to increase caloric loss and to assist in glucose regulation. The therapeutic aim is normalization of blood glucose and lipid levels with the hope of diminishing cardiovascular risk and preventing complications.

There has been much interest in recent years in clarifying the underlying relationships between NIDDM and obesity, heredity, nutrition, physical activity, and other factors. Much has been learned from clinical studies in individuals with and without NIDDM and from parallel studies in experimental animals. However, conflicting claims have emerged for the effectiveness of new dietary strategies and exercise programs. Many of these have been publicized in the professional and lay literature, and this has caused some concern and confusion. In an effort to resolve this problem, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the NIH Office of Medical Applications of Research, in collaboration with Institute National de la Sant� et de la R�cherche M�dicale (INSERM), France, sponsored a Consensus Development Conference on Diet and Exercise in Noninsulin-Dependent Diabetes Mellitus, December 8-10, 1986.

The conference brought together researchers, clinicians, other health professionals, and representatives of the public. Following 2 days of presentations and discussion by invited experts and the audience, a consensus panel, drawn from the health care and diabetes-interested communities, weighed the scientific evidence and formulated a draft statement in response to several questions:

  • What is the significance of excess body fat in the patient with non-insulin-dependent diabetes mellitus? How can weight reduction be achieved and maintained?
  • What are the appropriate components of the dietary prescription for patients with non-insulin-dependent diabetes mellitus?
  • What are the benefits and risks of exercise in patients with non-insulin-dependent diabetes mellitus? How should exercise be prescribed?
  • What is the evidence that weight control, diet, and/or exercise can prevent non-insulin-dependent diabetes mellitus?
  • What are the directions for future research?

 
 What Is the Significance of Excess Body Fat in the Patient With Noninsulin-Dependent Diabetes Mellitus? How Can Weight Reduction Be Achieved and Maintained?

There is strong evidence that NIDDM is genetically determined. Based on considerable epidemiologic data, it is apparent that obesity and aging promote the development of the disease in susceptible individuals. The prevalence of the disease increases steadily from the fourth decade. Individuals who are 20 to 30 percent overweight are clearly at an increased risk for NIDDM, and the risk accelerates with increased body weight. Data suggest that in addition to the degree of obesity, an increasing duration of obesity and the specific distribution of excess body fat are associated with the development of NIDDM. With regard to fat distribution, upper body or android obesity appears to be more strongly associated with diabetes than lower body or gynoid obesity. Individuals with a family history of NIDDM may develop the disease when they have only modest excess of body fat. These people should be assessed routinely for the presence of carbohydrate intolerance and encouraged to maintain desirable body weight.

Extensive studies demonstrate that obesity is characterized by insulin resistance. In the obese nondiabetic individual, the principal target tissues for insulin (liver, skeletal muscle, and adipose tissue) do not respond appropriately to those levels of the hormone found in nonobese individuals. The obese nondiabetic person can compensate for this impairment of hormone action by secreting increased amounts of insulin. Weight reduction in these nondiabetic individuals leads to reversal of insulin resistance and the return to a normal pattern of insulin secretion.

Pancreatic beta-cell dysfunction and insulin resistance are the cardinal pathophysiologic features of NIDDM. Both of these cellular alterations may be genetically determined. Although insulin resistance is present in the nonobese patient with NIDDM, associated obesity further aggravates the severity of impaired hormone action. Weight loss in the obese diabetic, as in the nondiabetic, ameliorates insulin resistance, and usually there is accompanying improvement in carbohydrate tolerance. Frequently, hyperglycemia is reduced when a low calorie diet is employed even before there is much weight loss. Furthermore, some studies have also shown modest improvement in beta-cell function when the blood glucose is lowered by diet or other means.

Some investigators are concerned that the hyperinsulinemia in NIDDM may contribute to the increased incidence of macrovascular disease. This possibility arises from the observation that the two most common conditions of hyperinsulinemia (obesity and NIDDM) are independently associated with increased cardiovascular risks. There are also data suggesting that the actions of insulin are not uniformly impaired in hyperinsulinemic states. Thus, it is possible that certain insulin-regulated, atherogenic processes may be accelerated in NIDDM with or without obesity. At present, the relationship between hyperinsulinemia and cardiovascular disease is largely speculative, and more definitive answers await additional investigation.

The cellular mechanisms of insulin action have been partially elucidated. There is universal agreement that insulin initiates its actions by interacting with specific receptors located on the surface of the target cell. The possibility that there is a receptor deficiency in human obesity and NIDDM has been extensively investigated. Most studies have examined the receptor status in readily available circulating monocytes or erythrocytes. The number of insulin receptors is often decreased in these cells, but the relevance of these findings to the major target tissues (liver, muscle, fat) for insulin action is not known. In fact, results of studies of insulin receptors in fat cells from individuals with NIDDM are conflicting, and studies are just emerging using human muscle and liver. The majority of investigators agree that cellular alterations, other than decreased receptor number, contribute to the insulin resistance of both obesity and NIDDM. Current areas of investigation include (1) functions of the insulin receptor subsequent to hormone binding, (2) the glucose transport process in muscle and adipose tissue, and (3) the status of those factors that may be the intracellular mediators of insulin action. Although the cellular alterations responsible for insulin resistance and beta-cell dysfunction in NIDDM are poorly understood, future studies of the beta cell and insulin action should provide new insights into the pathophysiology of this disease.

Blood glucose usually returns toward normal as weight loss occurs in the obese diabetic patient. Weight loss also improves hypertension, hypertriglyceridemia, and hypercholesterolemia. Achieving the goal of desirable weight is not easy. Twenty-five years ago, one-quarter of the patients who needed to lose 20 to 40 pounds were successful, and merely 5 percent lost more than 40 pounds. At that time, weight loss programs generally emphasized moderate caloric restriction and dietary counseling. Recently, several more successful strategies for weight loss have been developed. All these approaches continue to rely on reduced calorie ingestion. Although moderate caloric restriction (500 to 1,000 kcal below daily requirements) is preferred, fasts of several days duration and very low calorie diets (to 400-600 kcal intake per day) for several weeks have been successfully employed with careful medical supervision.

Other successful programs have utilized support groups, behavioral therapy, and/or exercise in combination with caloric restriction. In recent years, the public has become aware of the health hazards of obesity. Low calorie foods and beverages are readily available, and health clubs exist in many neighborhoods. While all of these benefit those who need or desire to lose weight, weight reduction continues to be difficult. Furthermore, most individuals who lose weight will regain some or all of the lost weight.

A greater understanding and resolution of the pathophysiology and behavioral determinants underlying altered eating behavior are needed. While acknowledging the poor prognosis for weight loss maintenance, the panel recommends that most obese patients with NIDDM be maintained on diets moderately restricted in calories. Ideally, this diet should be associated with behavior therapy, group support, and nutritional counseling. An intensive support program of considerable duration may improve the likelihood of maintaining a desirable weight. Increased physical activity and, if appropriate, structured exercise programs are also considered useful adjunctive therapy.
 

What Are the Appropriate Components of the Dietary Prescription for Patients With Noninsulin-Dependent Diabetes Mellitus?

In individuals with NIDDM, the primary goal for treatment is to reduce blood glucose levels to normal. The diet for all persons with NIDDM should be nutritionally sound, and it should satisfy the recommended dietary allowances (RDA) and follow the Dietary Guidelines for Americans (Home and Garden Bulletin #232, 2nd Edition, Washington, D.C.: USDA and HHS, 1985). Since most persons with NIDDM have excess body fat, the primary dietary treatment is reduction of weight through caloric restriction. Some people with NIDDM have additional medical problems (e.g., lipoprotein disorders and hypertension) that require additional dietary recommendations.

Calories

A weight-reducing diet should be nutritionally complete, using a variety of foods. Moderate caloric restriction of 500-1,000 kcal below daily requirements may be optimal in producing a gradual sustained weight loss. After the desired weight has been achieved, maintenance of that reduced weight may be sustained by adjusting the caloric intake. With low caloric intake, nutrient deficiencies should be avoided. For lean persons with NIDDM, caloric intake should be adequate to maintain body weight.

Fat and Carbohydrate

A diet reduced in total and saturated fat and cholesterol has been recommended for all Americans to decrease the risk of coronary heart disease (CHD). Patients with NIDDM are at increased risk for CHD by virtue of their diabetes. In addition, they frequently demonstrate blood lipid abnormalities, including reduced high density lipoprotein-cholesterol (HDL-C) and elevated triglyceride concentrations. The initial approach for normalizing serum lipids in the majority of patients with NIDDM is to reduce hyperglycemia because this will frequently increase HDL-C and reduce triglyceride concentrations. High carbohydrate diets (50-60 percent of total calories) may effect these changes in some patients by enhancing insulin sensitivity. When blood glucose is normalized, the panel recommends that patients with NIDDM should further attempt to reduce their risk of CHD by reducing low density lipoprotein-cholesterol. Present recommendations for the general population include a reduction of total fat intake to less than 30 percent of calories, with saturated fat comprising less than 10 percent of total calories. This may be suitable for some but not all NIDDM patients (as discussed below).

A reduction in calories from fat usually requires an increase in calories from carbohydrates. High carbohydrate diets may be harmful in some patients by reducing HDL-C and increasing triglycerides. These diets are less effective than weight loss in normalizing blood glucose and may represent a serious lifestyle alteration for many patients. Consequently, the panel suggests that patients' adherence to a regimen of caloric restriction for weight loss is more important than alterations in the macronutrient composition of the diet. Also, both serum lipid and glucose concentrations should be monitored to determine the effectiveness of any dietary changes.

Other Carbohydrate Issues

Sucrose (Table Sugar).

In the past, individuals with NIDDM have been advised to avoid sucrose. The use of sucrose as a taste additive in mixed meals is acceptable (up to 5 percent of carbohydrate calorie intake) in patients who are lean and do not have carbohydrate-aggravated hyperlipidemia. The advisability of added sucrose intake above 5 percent of carbohydrate calories requires further investigation.

Fiber.

Dietary fiber is plant material that is resistant to enzymes produced by humans. Most Americans consume 13 to 19 grams of dietary fiber per day. Some studies have suggested that dietary fiber is effective in controlling blood glucose and reducing plasma cholesterol, especially when used in very high carbohydrate diets (greater than 50 percent of calories); however, the results of these studies are inconclusive. Furthermore, high fiber diets may be less palatable, may require substantial changes in traditional eating patterns, may have effects on other nutrients, and may be contraindicated in patients with autonomic neuropathy.

Therefore, the panel reaffirms that the primary dietary intervention in NIDDM is weight reduction. However, if individuals desire to increase the fiber content of their diet, foods high in soluble fiber could replace some other carbohydrates. The use of purified fiber supplements is not recommended at this time for diabetes therapy.

Glycemic Index

Individual foods containing carbohydrate can have a high, medium, or low impact on postprandial blood glucose. This response can be quantified as "glycemic index." Several problems have been identified with the application of this methodology to the design of general guidelines of a dietary prescription for patients with NIDDM.

Many factors contribute to a different glycemic response from the same food. These include processing, cooking, and food storage time. Other considerations include the variable degree of mastication in the elderly with dental problems, the diurnal variation in absorption, and racial and ethnic differences. Some studies have shown diminution of glycemic effects when foods are combined in a mixed meal. For these reasons at this time the panel does not recommend the use of specific glycemic indices in the dietary therapy of patients with NIDDM.

Protein

There is no need to change the standard 12 to 20 percent protein content of the diet, providing RDA requirements are met, except in those who have specific problems in which protein intake should be reduced (i.e., in people with NIDDM who have renal disease).

Education

Different educational methods will be appropriate for individual patients and for varying ethnic diets. Whatever plan is used, intensive and frequent followup and support are needed until fasting euglycemia is achieved and maintained. Behavior modification and exercise may be combined with diet instruction to enhance weight loss efforts. Changes in diet need to be made gradually. No single educational tool can accommodate the needs of all individuals with NIDDM. When diet therapy alone is unsuccessful or unacceptable because of quality of life issues or failure to reduce hyperglycemia, then alternative euglycemic therapy is indicated.
 

What Are the Benefits and Risks of Exercise in Patients With Noninsulin-Dependent Diabetes Mellitus? How Should Exercise Be Prescribed?

The effect of regular physical exercise alone on metabolic control in NIDDM is quite variable and frequently of small magnitude. Greater improvement in glucose homeostasis can usually be obtained by weight loss. Despite the relatively small impact of exercise demonstrated to date, regular physical exercise may be a therapeutic component supplementing diet in selected patients.

There is epidemiologic and clinical evidence that physical activity may reduce the incidence of coronary heart disease (CHD) in the general population. The risk-benefit ratio of exercise in NIDDM remains to be defined. Because many of the complications of NIDDM are related to atherosclerotic cardiovascular disease, an increase in physical activity for NIDDM patients appears prudent. This recommendation is made despite the absence of conclusive studies and with recognition that improvements in CHD risk factors may not occur in those with NIDDM. Furthermore, the consensus panel seeks to emphasize that the possible benefits of body fat reduction outweigh putative exercise effects.

Vigorous exercise appears to blunt the rise in blood glucose that follows carbohydrate ingestion. In addition, exercise training may increase insulin sensitivity, but this change appears to be an acute effect associated with recent exercise and is reversed within 2 to 3 days by physical inactivity. Physical activity may assist in reducing body fat, but exercise without caloric restriction appears ineffective. Patients who exercise regularly may negate its weight-reducing effects by curtailing their usual activities and by increasing caloric intake.

Complications of exercise in NIDDM patients include cardiac events (infarction, arrhythmias, and sudden death), bone and soft tissue injuries, and retinal damage in patients--particularly with proliferative retinopathy. The incidence of these complications with exercise has not been defined.

NIDDM patients should undergo a thorough medical evaluation prior to increasing physical activity. The components of the evaluation will vary depending on the severity and duration of the diabetes, the presence of complications, the likelihood of asymptomatic CHD, and the intensity of the activity.

Because of the possible risks of retinal detachment and vitreous hemorrhage during exercise in patients with retinopathy, exercise that requires straining and breath holding (such as weight lifting) should be discouraged. Special attention should also be given to care of the feet during exercise.

In planning and recommending an exercise program for NIDDM patients, health professionals should be aware of several factors. The threshold of energy expenditure required to reduce postprandial hyperglycemia and to enhance insulin sensitivity has not been defined. The same holds true for the use of physical activity in lowering the incidence of CHD. The panel believes that NIDDM patients should tailor an increase in their overall physical activity to their physical capacity, preferences, age, and lifestyle. Also, because many of the metabolic effects of exercise are short-lived, it is extremely important that NIDDM patients choose exercises that they are likely to engage in frequently and continue over their lifetimes.
 

What Is the Evidence That Weight Control, Diet, and/or Exercise Can Prevent Noninsulin-Dependent Diabetes Mellitus?

Approximately 80 percent of persons with NIDDM have excess body fat. Cross-sectional population-based studies show that the prevalence of NIDDM increases with increasing body weight and that the risk of NIDDM is particularly high among obese persons with a family history of this disorder. These relationships suggest that avoidance or elimination of obesity in people whose relatives have NIDDM may delay or prevent the development of NIDDM. Weight reduction is best achieved through the use of hypocaloric diets. In normal weight people, there is no evidence that manipulation of dietary constituents (e.g., reducing refined carbohydrates or increasing complex carbohydrates or increasing dietary fiber) influences the risk of NIDDM. The possibility that exercise may prevent NIDDM is suggested by the observation that prolonged strenuous exercise in individuals with NIDDM may normalize fasting blood glucose and glucose tolerance.

However, there are as yet no irrefutable data to demonstrate that weight control, dietary modification, or exercise are effective in preventing or delaying NIDDM. Nevertheless, in the opinion of the panel, it is prudent to maintain or achieve normal body weight in an attempt to minimize the risk of NIDDM in susceptible persons.
 

What Are the Directions for Future Research?

Many of the issues discussed in this consensus conference need further research in laboratory, clinic, and community-based settings. The following major topics are suggested:

Questions Related to Obesity

  • What is the etiology of the insulin resistance in the obese state?
  • What is the etiologic basis of the obesity itself, from genetic, environmental, behavioral, and nutritional aspects?
  • What are effective strategies for therapy of the obese state, particularly as it relates to diabetes?

 

Questions Related to Diabetes and Its Prevention

  • What is the etiology of the beta-cell deficiency in NIDDM?
  • What is the pathophysiology of the insulin resistance in the diabetic state without obesity?
  • What is the nature of the inherited component in NIDDM?
  • What is the relative effectiveness of regular physical activity and/or weight control in the prevention and treatment of NIDDM and its complications?
  • What are predictors for the eventual development of NIDDM?

 

Questions Related to Nutrition

  • What is the relationship of particular diets such as high carbohydrate diets to glucose and lipid metabolism?
  • What are the roles of other dietary alterations such as changes in fiber content, various carbohydrates, and other foods on carbohydrate and lipid homeostasis?
  • What are the optimal strategies to improve acceptance of therapeutic regimens?

 

Questions Related to Exercise

  • What are the potential mediators of exercise effects?
  • Under what conditions and in which NIDDM patients is exercise likely to be effective in enhancing glucose homeostasis and reducing coronary heart disease?
  • Under what conditions is exercise likely to be counterproductive?

 

Questions Related to Complications

  • What are the contributions of hyperinsulinemia, obesity, and glucose control to the risk of complications in NIDDM?
  • What are the relationships of the carbohydrate and lipoprotein abnormalities and their treatments to the risk of macrovascular disease in NIDDM?

Conclusion

Non-insulin-dependent diabetes mellitus (NIDDM or Type II diabetes) is a major health problem. It is highly correlated with obesity and, thereby, with overeating. Normal weight maintenance continues as the cornerstone of therapy with oral agents or insulin added, if needed, to maintain blood glucose normal or near normal. For overweight individuals, reduced-calorie diets should be prescribed and attempts made to alter lifestyle within an acceptable degree for any given patient to encourage weight reduction. These alterations include increased physical activity, perhaps as prescribed exercise regimens, with the recognition that exercise alone is usually ineffective for weight loss unless accompanied by an appropriate diet.

Weight loss diminishes hyperglycemia to or toward normal. Exercise itself may have a small but transient direct effect in lowering blood glucose and insulin resistance. Various food combinations, and even different processing or cooking of the same foods, may produce different glucose responses. Incomplete information on these and other factors that affect this phenomenon in individual subjects minimizes the role of the glycemic index in overall diabetes management. Similarly, foods high in soluble fiber may diminish glucose elevation after meals and may be of use in individual patients, but high-fiber foods appear to be less important than adhering to a calorie-restricted diet and achieving weight loss in the obese diabetic person. Approximately four out of five patients with NIDDM are significantly overweight, and the panel's attention was focused on this group throughout their deliberations. Specific recommendations for diet and activity in the normal-weight NIDDM patient were not addressed except for endorsement of a lifestyle that avoids the development of obesity.

Finally, it appears prudent to prevent or reverse obesity, especially in individuals with a family history of diabetes, in the hope that the onset of diabetes may be prevented or postponed.
 

Consensus Development Panel

George F. Cahill, Jr., M.D.
Panel Chairman
Vice President
Howard Hughes Medical Institute
Bethesda, Maryland
Elsworth R. Buskirk, Ph.D.
Professor of Applied Physiology
Pennsylvania State University
University Park, Pennsylvania
Linda M. Delahanty, M.S., R.D.
Clinical Nutrition Specialist
Massachusetts General Hospital
Department of Dietetics
Boston, Massachusetts
Stefan S. Fajans, M.D.
Professor of Internal Medicine
Chief
Division of Endocrinology and Metabolism
University of Michigan
Medical Center
Ann Arbor, Michigan
James B. Field, M.D.
Rutherford Professor of Medicine
Baylor College of Medicine
Houston, Texas
Harmon E. Holverson, M.D.
Diplomate, ABFP
Private Practice
Emmett, Idaho
Joan Williams Hoover
Director
Consumer Health Information
United Seniors Consumer Cooperative
Washington, D.C.
Ralph I. Horwitz, M.D.
Associate Professor of Medicine and Epidemiology
Yale University School of Medicine
New Haven, Connecticut
Kathryn Iacocca Hentz
President
Iacocca Foundation
New York, New York
John M. Lachin, Sc.D.
Professor of Statistics
Codirector, Biostatistics Center
Department of Statistics, Computer and Information Systems
George Washington University
Rockville, Maryland
Dean H. Lockwood, M.D.
Professor of Medicine
Head
Endocrine Metabolism Unit
University of Rochester Medical Center
Rochester, New York
F. John Service, M.D., Ph.D.
Professor of Medicine
Mayo Medical School
Consultant in Endocrinology and Metabolism
Mayo Clinic
Rochester, Minnesota
Paul D. Thompson, M.D.
Associate Professor of Medicine
Brown University Program in Medicine
Miriam Hospital
Providence, Rhode Island
Madelyn L. Wheeler, M.S., R.D.
Coordinator
Research Dietetics
Diabetes Research and Training Center
Indiana University Medical Center
Indianapolis, Indiana

Speakers

James W. Anderson, M.D.
"Dietary Fiber and Noninsulin-Dependent Diabetes Mellitus"
Professor of Medicine and Clinical Nutrition
University of Kentucky
Chief
Metabolic-Endocrinology
Veterans Administration Medical Center
Lexington, Kentucky
John P. Bantle, M.D.
"The Glycemic Effects of Dietary Carbohydrate"
Assistant Professor in Medicine and Endocrinology
Division of Endocrinology and Metabolism
Department of Medicine
University of Minnesota
Minneapolis, Minnesota
Per A. Bj�rntorp, M.D., Ph.D.
"Weight Reduction: Clinical Studies"
Professor of Medicine
University of G�teborg
SWEDEN
Clifton Borgardus, M.D.
"Obesity and the Pathophysiology of Noninsulin-Dependent Diabetes Mellitus"
Chief
Clinical Diabetes and Nutrition Section
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Phoenix, Arizona
George A. Bray, M.D.
"Diabetes and Obesity"
Professor
University of Southern California
Section of Diabetes and Nutrition Los Angeles, California
John K. Davidson, M.D., Ph.D.
"The Practical Use of Dietary Techniques, Including a 1-Week Total Fast for Weight Reduction in Patients With NIDDM"
Professor of Medicine
Emory University School of Medicine
Atlanta, Georgia
Edward S. Horton, M.D.
"Benefits, Risks, and Practical Application of Exercise in the Treatment of NIDDM"
Professor of Medicine
University of Vermont College of Medicine
Burlington, Vermont
David J.A. Jenkins, M.D., Ph.D.
"The Glycemic Index and Starchy Foods"
Professor
Medicine and Nutritional Science
Faculty of Medicine
University of Toronto
Toronto, Ontario
CANADA
Errol B. Marliss, M.D. F.R.C.P.(C)
"Determinants of the Metabolic Response to Exercise"
Professor of Medicine
Director
McGill Nutrition and Food Science Centre
Royal Victoria Hospital
Montreal, Quebec
CANADA
F. Xavier Pi-Sunyer, M.D.
"Exercise: Effects on Appetite and Weight Loss"
Director
Division of Endocrinology and Diabetes
St. Luke's-Roosevelt Hospital
Associate Professor of Medicine
Columbia University
New York, New York
Daniel Porte, Jr., M.D.
"NIDDM as a Syndrome"
Professor of Medicine
Director
Diabetes Research Center
University of Washington
Salk Institute/PBL
San Diego, California
Gerald Reaven, M.D.
"Effect of Variations in Amount and Kinds of Dietary Carbohydrate on Carbohydrate and Lipid Metabolism in Patients With Noninsulin-Dependent Diabetes Mellitus"
Professor of Medicine
Stanford University School of Medicine
Stanford, California
Neil Ruderman, M.D., D.Phil.
"Exercise Benefits in NIDDM"
Professor of Medicine and Physiology
University Hospital
Boston University Medical Center
Boston, Massachusetts
Gustav Schonfeld, M.D.
"Effect of Diet and Exercise on Plasma Lipoproteins"
Professor of Preventive Medicine and Medicine Director
Lipid Research Center
Washington University School of Medicine
St. Louis, Missouri
G�rard Slama, M.D.
"Which Carbohydrates to Recommend to NIDDM Subjects?"
Professor
University Pierre et Marie Curie--Paris VI
Department of Diabetes
Hotel-Dieu Hospital
FRANCE
Aaron I. Vinik, M.D.
"Controversy on the Role of Dietary Fiber in the Management of Diabetes"
Professor of Internal Medicine and Surgery
University of Michigan Medical Center
Ann Arbor, Michigan
Rena R. Wing, Ph.D.
"Strategies for Weight Reduction in Noninsulin-Dependent Diabetes"
Associate Professor of Psychiatry
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania
Judith Wylie-Rosett, Ed.D.
"Dietary Content: An Overview of the Issues"
Assistant Professor
Epidemiology and Social Medicine
Albert Einstein College of Medicine
Bronx, New York
Bernard Zinman, M.D., F.R.C.P.(C), F.A.C.P.
"Acute Effects of Exercise in Noninsulin-Dependent Diabetes Mellitus"
Professor
Department of Medicine
University of Toronto
Toronto General Hospital
Toronto, Ontario
CANADA

Planning Committee

George F. Cahill, Jr., M.D.
Panel Chairman
Vice President
Howard Hughes Medical Institute
Bethesda, Maryland
Charlotte Armstrong
Public Affairs Specialist
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Michael J. Bernstein
Director of Communications
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Eveline Eschwege, M.D., M.P.H.
Directeur de l'Unite' de Recherches Statistiques
INSERM
Villejuif
FRANCE
Phillip Gorden, M.D.
Director
National Institute of Diabetes and Digestive and
Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Van S. Hubbard, M.D., Ph.D.
Director
Nutrient Metabolism
Obesity, Eating Disorders, and Energy Regulation
Programs
Division of Digestive Diseases and Nutrition
National Institute of Diabetes and Digestive and
Kidney Diseases
National Institutes of Health
Bethesda, Maryland
F. Xavier Pi-Sunyer, M.D.
Director
Division of Endocrinology and Diabetes
St. Luke's-Roosevelt Hospital Center
Associate Professor of Medicine
Columbia University
New York, New York
Martin Rose, M.D., J.D.
Chief Medical Officer
Office of the Director
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Robert Sherwin, M.D.
Associate Professor of Medicine
Yale University
School of Medicine
New Haven, Connecticut
Robert E. Silverman, M.D., Ph.D.
Chairperson
Chief
Diabetes Programs Branch
Division of Diabetes, Endocrinology, and Metabolic Diseases
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Simeon I. Taylor, M.D., Ph.D.
Senior Investigator
Diabetes Branch
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Georges Tchobroutsky, M.D.
Professor
University Pierre et Marie Curie
Head
Department of Diabetology
Hotel-Dieu Hospital
Paris, FRANCE
Judith Wylie-Rosett, Ed.D.
Assistant Professor
Epidemiology and Social Medicine
Albert Einstein College of Medicine
Bronx, New York

Conference Sponsors

National Institute of Diabetes and Digestive and Kidney Diseases
Phillip Gorden, M.D.
Director
NIH Office of Medical Applications of Research
Itzhak Jacoby, Ph.D.
Acting Director

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