Obesity


The World Health Organization (WHO) has defined obesity as a BMI of 30 kg/m 2 or more. Individuals with a BMI between 25 and 29.9 are ‘overweight’.


Epidemiology


In most populations, the prevalence of overweight and obesity has steadily increased over the past 20 years. In the USA, the lifetime risks of becoming overweight or obese are about 50% and 25% respectively. In the United Kingdom, about 25% of adults are obese and about 50% are overweight.







Box 33.1 Causes of obesity

Lifestyle and social factors

Dietary factors

Genetic factors

Drugs

Neuroendocrine disorders

Prenatal factors

Psychological factors





Ethnicity influences the incidence of obesity. For example, black men tend to be less obese than white men. However, black women are more obese than white women. The prevalence of obesity in Hispanic men and women is higher than in white individuals.


Aetiology


Many factors may contribute to the development of obesity (Box 33.1).


Lifestyle and social factors


Sedentary lifestyle


A sedentary lifestyle reduces energy expenditure and promotes weight gain. In an affluent society, energy-sparing devices also reduce energy expenditure.


Sleep deprivation


Observational data suggest a possible association between sleep deprivation and obesity. Sleep restriction may be associated with a decrease in serum leptin (an anorexigenic hormone) and an increase in serum ghrelin (an orexigenic hormone).


Cessation of smoking


Weight gain is very common when people stop smoking. This may be mediated by nicotine withdrawal.


Social networks


A report of a social network constructed from the Framingham Offspring Study illustrated that an individual’s chance of becoming obese was increased if he or she had a friend, sibling or spouse who became obese.


Dietary factors


Energy intake and the composition of the diet play an important role in the pathogenesis of obesity. Overeating relative to energy expenditure causes obesity. Most obese subjects have lost control of their eating (disinhibition). Epidemiological data suggest that a diet high in fat is associated with obesity.


Night-eating syndrome is a well-known pattern of disturbed eating in the obese. It is characterized by the consumption of at least 25% of energy between the evening meal and the next morning.


Infant feeding practices may also contribute to weight gain. Breast-feeding, when compared with formula feeding, may be associated with a lower risk of overweight.


Genetic factors


Studies of twins, adoptees and families suggest the existence of genetic factors in obesity. Genetic factors influence obesity in two ways:



  • genes that are primary factors in the development of obesity, such as those relating to leptin deficiency
  • susceptibility genes on which environmental factors act to cause obesity.

Obesity is a feature of at least 24 genetic disorders such as Prader–Willi (caused by a deletion of paternal DNA on the long arm of chromosome 15) and Bardet–Biedl (an autosomal recessive disorder) syndromes.


A small proportion of obesity is due to monogenic causes. Heterozygous mutations in the gene encoding the melanocortin-4 receptor (MC4R) are the most common monogenic cause of obesity in childhood. MC4R is the receptor for α-MSH, which is a potent inhibitor of food intake. Obesity due to leptin deficiency has been reported in some consanguineous families. Obesity resulting from leptin receptor deficiency has also been described. However, most obese subjects do not have any abnormalities in the leptin gene and have intact leptin receptors and high serum leptin levels.


The genes that contribute to the more common forms of obesity have been difficult to identify. A variant in the FTO (fat mass and obesity associated) gene on chromosome 16 increases the risk of obesity in the general population. Mutations in the gene for peroxisome proliferator-activated receptor gamma 2 (a transcription factor involved in adipocyte differentiation) accelerate the differentiation of adipocytes and are associated with obesity in some subjects.


Drugs


A number of drugs can cause weight gain, including atypical antipsychotics (e.g. clozapine, olanzapine), tricyclic antidepressants, antiepileptic drugs (e.g. valproate, carbamazepine), insulin (possibly through hypoglycaemia), sulphonylureas, thiazolidinediones and glucocorticoids.


Neuroendocrine disorders


Several neuroendocrine disorders may be associated with the development of obesity:



  • Hypothalamic obesity is a rare syndrome in humans. Damage to certain hypothalamic nuclei, such as the ventromedial hypothalamus, by trauma, tumour, inflammatory disease or surgery may result in hyperphagia and obesity.
  • In patients with Cushing’s syndrome, a stimulation of food intake by excess glucocorticoids contributes to weight gain.
  • In patients with hypothyroidism, the slowing of metabolic activity leads to weight gain.
  • About half of patients with polycystic ovary syndrome are obese. The underlying aetiology is not fully understood.
  • GH deficiency results in increased abdominal and visceral fat.

Prenatal factors


Maternal smoking and diabetes increase the risk of obesity in the offspring. Infants who are small, short or have a small head circumference are at higher risk of abdominal fatness and other comor-bidities associated with obesity later in life.


Psychological factors


Seasonal affective disorder has been linked to weight gain.


Clinical evaluation


The clinical evaluation of overweight and obese individuals should include measurement of:



  • height and weight, and calculation of BMI
  • waist circumference in patients with a BMI less than 35 kg/m 2
  • blood pressure
  • lipid profile (serum triglyceride, high-density and low-density lipoprotein-cholesterol)
  • fasting blood glucose.

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Jun 4, 2016 | Posted by in ENDOCRINOLOGY | Comments Off on Obesity

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