Chapter: Medicine and surgery: Nutritional and metabolic disorders

Obesity - Nutritional disorders

The World Health Organisation defines overweight and obesity in terms of the body mass index (weight in kilograms divided by the square of height in metres. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Nutritional disorders





The World Health Organisation defines overweight and obesity in terms of the body mass index (weight in kilograms divided by the square of height in metres (kg/m2)). A BMI over 25 kg/m2 is defined as overweight and a BMI of over 30 kg/m2 as obese. Although these definitions are useful, the risk of disease in populations increases progressively from lower BMI levels. A full consideration of obesity including prevention, identification, evaluation, treatment and weight maintenance of overweight and obesity in adults is being conducted by the National Institute for Clinical Excellence (NICE) with a proposed publication in 2006.




Worldwide more than 1 billion adults are overweight and 300 million of these are clinically obese. In England in 1998, 18–19% of individuals were clinically obese, a rate increasing dramatically. Prevalence increases by social class (15% in class I to 30% in class V).




Prevalence increases by age up to 60–65 years.




F > M




Most patients have simple obesity. Some conditions associated with obesity are as follows:


·        Druginduced weight gain: Antipsychotic drugs, anticonvulsant drugs, antidiabetic drugs and steroids.


·        Endocrine disorders may be associated with the development of obesity, such as Cushing’s syndrome, hypothyroidism and polycystic ovary syndrome.


·        Obesity is characteristic of some congenital disorders associated with hypogonadism, such as Prader– Willi syndrome and Laurence–Moon–Bardet–Biedl syndrome.


Simple obesity is likely to be a combination of genetic and enviromental factors:


·        Genetic factors: Studies of twins, adoption studies and family studies all suggest the existence of genetic factors in human obesity. Animal studies particularly in mice have identified several gene defects inherited in both dominant and recessive fashions that can cause obesity. Some correlates with human obesity have been identified, although the exact genetic basis remains unclear.


·        Prenatal influences and breast-feeding may influence obesity in childhood. Obesity in adolescence rather than earlier in childhood is a better predictor of adult obesity.


Several factors that are associated with a high risk of obesity have been identified:


·        Low metabolic rate, increased carbohydrate oxidation, insulin resistance and low sympathetic activity.


·        Lower socioeconomic class, lower education level and cessation of smoking.




The mechanisms of obesity are poorly understood. At a simplistic level weight gain results when the energy intake exceeds expenditure; however, both intake and expenditure are controlled in complex physiological systems. Women tend to gain excess weight after puberty, precipitated by events such as pregnancy, use of the oral contraceptive therapy and the menopause. Changes in lifestyle in men during the third and fourth decade lead to reduced physical activity and hence weight gain, which continues until the sixth decade. The quantity, type and pattern of food intake have all been implicated in the development of obesity. Both the appetite and the sensation of satiety (fullness) are implicated. Central adiposity (waist-to-hip ratio measurements >0.9 in men and >0.84 in women) increases the risk of many health problems such as diabetes and hyperinsulinaemia.


The control system is complex, it is regulated by a control centre thought to be located in the hypothalamus. Afferent signals to the control centre may include nerves, hormones and nutrients:


·        Leptin production correlates with body fat mass; a leptin receptor has been identified in the ventromedial region of the hypothalamus.


·        Gastric distention signals satiety.


·        Hormonal signals including cholecystokinin and glucagon-related peptides inhibit food intake; neu- ropeptide Y is a potent stimulus for appetite. Mono-amines, including noradrenaline and serotonin, also modulate the hypothalamic control centre.


The efferent of the control is energy expenditure. Approximately 70% of energy expenditure is for resting metabolic processes such as temperature control and physiological function. A further 10% of energy expenditure is related to the thermic responses to food. Catecholamine-stimulated lipolysis is mediated via β3 receptors, and low receptor activity decreases thermogenesis. The remaining 20% of energy expenditure is due to physical activity and exercise.


Clinical features


Evaluation of obese or overweight patients requires aetiological factors and comorbid conditions to be identified. Blood pressure, cardiovascular risk factors and diabetes should all be reviewed. Smoking cessation may lead to increase in weight; however, the health benefits of smoking cessation override the weight increase. The BMI should be calculated and the fat distribution documented by measurements of skin fold thickness, and waist and hip circumference ratio calculated.




It is important to use goal setting in the management of obesity. Initially the aim is to maintain weight prior to establishing a realistic weight loss (average of 0.5– 1 kg/week). Patients should be aware that weight loss induces a reduction in energy expenditure and there-fore makes further weight loss more difficult. Techniques used include the following:


·        Behaviour modification including examining the background of the individual, the eating behaviour and the consequences of the behaviour, usually conducted by psychologists.


·        Dietary manipulation: Reducing the calorie intake to below expenditure results in weight loss; however, food diaries are recognised to be inaccurate as all patients underestimate their intake. Diets include balanced low-calorie diets, low-fat diets and low-carbohydrate diets, which are ketogenic possibly inducing calcium loss and tend to be high in saturated fat.


·        Medications have a limited role in the treatment of obesity. Their use falls under guidelines issued by NICE.


1.     Sibutramine is a noradrenaline and serotonin re-uptake inhibitor and promotes a feeling of satiety. It should be prescribed only as part of an overall treatment plan for management of obesity in patients aged 18–65 years who have a BMI of 27.0 kg/m2 or more in the presence of significant comorbidities or a BMI of 30.0 kg/m2.


2.     Orlistat inhibits pancreatic lipases so that ingested fat is not completely hydrolysed or absorbed. NICE guidelines dictate that Orlistat should only be pre-scribed for patients aged 18–75 years who have lost at least 2.5 kg in weight by dietary control and increased physical activity in the month prior to the first prescription. They must have a BMI of 28 kg/m2 or more in the presence of significant co-morbidities or a BMI of 30 kg/m2. Treatment is reviewed at 4 and 6 months to confirm that weight continues to be lost and should stop at 12 months.


·        The use of surgery is also covered by guidelines issued by NICE. Its use is confined to patients with morbid obesity, i.e. BMI of 40 kg/m2 or more or between 35 and 40 kg/m2 in the presence of significant comorbid conditions. Surgery is considered only if a patient has been receiving intensive management in a specialised hospital or obesity clinic, is over 18 and all available non-surgical techniques have been tried and failed. Previously jejunoileal and gastric bypass procedures were performed, which despite being effective were associated with significant side effects. Vertical banded gastroplasty either by laparoscopic surgery or open procedure is the usual procedure of choice.




The greater the BMI, the higher the risk for morbidity and mortality from diabeticrelated illness and cardio-vascular, coronary artery and cerebrovascular diseases.

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