Obesity and diabetes

David Stensel

CHAPTER CONTENTS

Learning objectives

Introduction

Aetiology of obesity and diabetes

Obesity

Diabetes

Prevalence of obesity and diabetes

Obesity

Diabetes

Evidence that physical activity reduces the risk of obesity and diabetes

Obesity

Diabetes

Role of physical activity in managing obesity and diabetes

Obesity

Diabetes

Exercise prescription for the prevention and management of obesity and diabetes

Obesity

Diabetes

Co-morbidities

Obesity

Diabetes

Gaps in the evidence and practical issues

Obesity

Diabetes

Key points

References

Further reading

LEARNING OBJECTIVES

After studying this chapter, you should be able to:

1. Explain the energy balance equation and describe how obesity develops.

2. Identify some of the hormones involved in appetite regulation and describe the significance of these for obesity.

3. Explain how obesity is defined in children and adults.

4. Distinguish between type 1 and type 2 diabetes.

5. Understand the underlying causes of type 1 and type 2 diabetes.

6. Explain the link between obesity and type 2 diabetes.

7. Highlight literature indicating that the prevalence of obesity and type 2 diabetes is increasing in children and adults.

8. Critically evaluate the strengths and limitations of the evidence linking physical activity with the prevention of obesity and type 2 diabetes.

9. Critically evaluate the strengths and limitations of the evidence suggesting that physical activity is beneficial in the management of obesity and type 2 diabetes.

10. Make recommendations regarding the prescription of exercise for preventing obesity and type 2 diabetes and explain the rationale for these recommendations.

11. Make recommendations regarding the prescription of exercise for managing obesity and type 2 diabetes and explain the rationale for these recommendations.

12. Explain the co-morbidities associated with obesity and diabetes.

13. Suggest avenues for future research in the areas of obesity and diabetes.

INTRODUCTION

The focus of this chapter is on the relationship between physical activity, obesity and type 2 diabetes. Type 1 diabetes is occasionally mentioned in this chapter but the predominant focus is on obesity and type 2 diabetes. There is currently great interest in these areas for several reasons: (1) the prevalence of obesity and type 2 diabetes has increased in many countries in recent years both in adults and in children, (2) there is evidence to suggest that these trends are related in part to a general decline in physical activity levels amongst the inhabitants of developed countries, (3) several hormones have been discovered recently which have enhanced understanding of the mechanisms underlying obesity and diabetes and (4) there is evidence that changes in lifestyle - including increased levels of physical activity - are effective in preventing and managing obesity and type 2 diabetes.

AETIOLOGY OF OBESITY AND DIABETES

Obesity

Obesity is a condition involving an excessive accumulation of body fat such that health is endangered. Obesity is often defined using the body mass index (BMI), which is calculated by dividing weight (in kilograms) by height (in metres) squared, i.e. kg/m2. A BMI =30 kg/m2 is usually used as a cut-off point to indicate obesity and a BMI =25 kg/m2 is usually used to indicate overweight. However, there are some issues with using the BMI as an indicator of obesity and these will be discussed later in the chapter.

It is generally accepted that obesity is caused by an imbalance between energy intake (food) and energy expenditure (physical activity). Thus, if energy consumption exceeds energy expenditure weight gain will occur and if this pattern continues over months and years then obesity will follow. Put simply, obesity is due to too much food and too little exercise. The validity of this 'model' has been questioned recently (see Gard & Wright 2005, pp. 37-67) but there does not seem to be a plausible alternative to this explanation. The situation is more complex than appears, however, since some of the energy consumed in food may be excreted instead of being absorbed into the body (Jacobsen et al 2005) and measurements of energy intake do not take this into account. Similarly, energy can be expended in 'non-purposeful' activities such as fidgeting (Levine et al 2000) and many of the methods used to estimate energy expenditure do not assess this.

A notable example of the influence of reduced food intake on bodyweight comes from a case report of a 27-year-old man who fasted under medical supervision for 382 days. The man initially weighed 207 kg and by the end of the fast his weight was reduced to 82 kg. Moreover, 5 years after undertaking the fast his weight was still relatively low at 89 kg (Stewart & Fleming 1973). Although this is an extreme example (which apparently made it into the Guinness Book of Records in 1971 as the longest recorded fast) it does illustrate clearly that weight loss occurs when food intake is reduced or absent. That the reverse is also true (i.e. weight gain occurs with overeating) has been demonstrated in an elegant experiment involving 12 pairs of monozygotic (identical) twins (Bouchard et al 1990). These twins were overfed by 4.2 MJ per day, 6 days per week for a total of 84 days during a 100-day period. This resulted in an excess energy intake of 353 MJ and an average weight gain of 8.1 kg (range 4.3 to 13.3 kg).

In addition to showing that overeating causes weight gain, the study of Bouchard and colleagues (1990) demonstrated that weight gain is dependent to some extent on genetic factors since there was about three times more variance in the amount of weight gain between twin pairs than within twin pairs. Other studies confirm that there is a genetic influence on weight gain. An interesting example is a study of 540 adult Danish adoptees. Despite the fact that 90% of these adoptees had been transferred to their adoptive homes within the first year of life there was a strong relationship between the weight class of the adoptees (thin, median weight, overweight and obese) and the BMI of their biological parents and no relationship between the weight class of the adoptees and the BMI of their adoptive parents (Stunkard et al 1986). These findings suggest that genetic influences are more important determinants of bodyweight (and presumably body fatness) than childhood family environment.

Although evidence consistently indicates obesity has a strong genetic component this does not rule out overeating and inactivity as major causes of obesity. What is suggested is that some individuals are more susceptible to overeating and inactivity than others. Precisely why this should be remains elusive. With respect to overeating one likely cause is a variation in hormonal regulation of appetite. A clear example of this is leptin deficiency. This is associated with extreme obesity due to hyperphagia (overeating) and leptin therapy is effective in treating this disorder (Box 2.1, Table 2.1, Fig. 2.1). Some other hormones involved in appetite regulation that may be involved in the development of obesity are included in Table 2.2.

Box 2.1   Leptin

Leptin is a hormone secreted from adipocytes. Leptin acts as a long-term regulator of appetite via the hypothalamus. Leptin secretion is positively associated with the fat content of adipocytes. Thus, when the fat content of adipocytes is high leptin secretion is increased and hunger is suppressed. Conversely, if the fat content of adipocytes is low then leptin secretion will be low and hunger will be enhanced.

The discovery of leptin (in the mid-1990s) brought hope of a cure for obesity. It was thought that injections of leptin would suppress appetite in obese individuals and prevent them from overeating. It was subsequently discovered, however, that most obese individuals are not deficient in leptin - rather they have elevated levels...