Obesity: Causes, Complications Prevention and BMI Calculation by NJE


Obesity may be defined as an abnormal growth of the adipose tissue due to an enlargement of fat cell size (hypertrophic obesity) or an increase in fat cell number (hyperplastic obesity) or a combination of both. Obesity is often expressed in terms of body mass index (BMI). Overweight is usually due to obesity but can arise from other causes such as abnormal muscle development or fluid retention. 

However, obese individuals differ not only in the amount of excess fat that they store but also in the regional distribution of the fat within the body. The distribution of fat-induced by the weight gain affect the risk associated with obesity, and the kind of disease that results. It is useful, therefore, to be able to distinguish between those at increased risk as a result of “abdominal fat distribution” or “android obesity” from those with the less serious “gynoid” fat distribution, in which fat is more evenly and peripherally distributed around the body.


Obesity is perhaps the most prevalent form of malnutrition. As a chronic disease, prevalent in both developed and developing countries, and affecting children as well as adults, it is now so common that it is replacing the more traditional public health concerns including undernutrition. It is one of the most significant contributors to ill health. For industrialized countries, it has been suggested that such increase in body weight have been caused primarily by reduced levels of physical activity, rather than by changes in food intake or by other factors. It is extremely difficult to assess the size of the problem and compare the prevalence rates in different countries as no exact figures are available and also because the definitions of obesity are not standardized.

 Overweight and obesity are the fifth leading risk of global deaths. Worldwide, obesity has more than doubled since 1980. In 2008, more than 1.4 billion adults, 20 years and older, were overweight. Of these over 200 million men and nearly 300 million women were obese.

 In 2012, more than 40 million children under 5 years of age were overweight. Once considered a high-income country problem, overweight and obesity are now rising in low-and middle-income countries, particularly in urban settings. Close to 30 million overweight children are living in developing and 10 million in developed countries. Childhood obesity is associated with a higher chance of obesity, premature death and disability in adulthood. In addition, it is associated with future risk of increased breathing difficulties, increased risk of fractures, hypertension, early markers of cardiovascular disease, insulin resistance and psychological effects. 

At least 3.4 million adults die each year as a result of being overweight or obese. In addition, 44 per cent of the diabetes burden, 23 per cent of ischaemic heart disease burden and between 7 to 41 per cent of certain cancer burdens are attributable to overweight and obesity. Overweight and obesity are linked to more deaths worldwide than underweight.

Epidemiological determinants

The aetiology of obesity is complex, and is one of multiple causation: 

(a) AGE: Obesity can occur at any age, and generally increases with age. Infants with excessive weight gain have an increased incidence of obesity in later life. About one-third of obese adults have been so since childhood. It has been well established that most adipose cells are formed early in life and the obese infant lays down more of thes cells (hyperplastic obesity) than the normal infant. Hyperplastic obesity in adults is extremely difficult to treat with conventional methods. 

(b) SEX: Women generally have higher rate of obesity than men, although men may have higher rates of overweight. In the Framingham, USA study, men were found to gain most weight between the ages of 29 and 35 years, while women gain most between 45 and 49 years of age, i.e. at menopausal age. It has been claimed that woman’s BMI increases with successive pregnancies. The recent evidence suggested that this increase is likely to be, on an average, about 1 kg per pregnancy. On the other hand in many developing countries, consecutive pregnancies at short intervals are often associated with weight loss rather than weight gain. 

(c) GENETIC FACTORS: There is a genetic component in the aetiology of obesity. Twin studies have shown a close correlation between the weights of identical twins even when they are reared in dissimilar environments. The profile of fat distribution is also characterized by a significant heritability level of the order of about 50 per cent of the total human variation. Recent studies have shown that the amount of abdominal fat was influenced by a genetic component accounting for 50-60 per cent of the individual differences. 

(d) PHYSICAL INACTNITY: There is convincing evidence that regular physical activity is protective against unhealthy weight gain. Whereas sedentary lifestyle particularly sedentary occupation and inactive recreation such as watching television promote it, physical activity and physical fitness are important modifiers of mortality and morbidity related to overweight and obesity. In some individuals, a major reduction in activity without the compensatory decrease in habitual energy intake may be the major cause of increased obesity, e.g. in athletes when they retire and in young people who sustain injuries etc. Physical inactivity may cause obesity, which in turn restricts activity. This is a vicious circle. It is the reduced energy output that is probably more important in the aetiology of obesity than used to be thought. 

(e) SOCIO-ECONOMIC STATUS: The relationship of obesity to social class has been studied in some detail. There is a clear inverse relationship between socio-economic status and obesity. Within some affluent countries, however, obesity has been found to be more prevalent in the lower socio-economic groups. 

(f) EATING HABITS: Eating habits (e.g., eating in between meals, preference to sweets, refined foods and fats) are established very early in life. The composition of the diet, the periodicity with which it is eaten and the amount of energy derived from it are all relevant to the aetiology of obesity. A diet containing more energy than needed may lead to prolonged post-prandial hyperlipidaemia and to deposition of triglycerides in the adipose tissue resulting in obesity. Nowadays television and print media is playing an important role in producing obesity by heavy advertisement of fast food outlets of energy-dense, micronutrient poor food and beverages (usually classified under the “eat least” category in diet guidelines) of multinational corporations, which influence the daily eating habits. The consumer demand by itself may be influenced by advertising, marketing, culture, fashion and convenience. It has been calculated that a child whose energy requirement is 2000 kcal/day and who consumes 100 kcal/day extra will gain about 5 kg a year (10). The accumulation of one kilo of fat corresponds to 7, 700 kcal of energy. 

(g) PSYCHOSOCIAL FACTORS: Psychosocial factors (e.g., emotional disturbances) are deeply involved in the aetiology of obesity. Overeating may be a symptom of depression, anxiety, frustration and loneliness in childhood as it is in adult life. Excessively obese individuals are usually withdrawn, self-conscious, lonely and secret eaters. An insight into the circumstances in which obesity has developed is essential for planning the most suitable management. 

(h) FAMILIAL TENDENCY: Obesity frequently runs in families (obese parents frequently having obese children), but this is not necessarily explained solely by the influence of genes. 

(i) ENDOCRINE FACTORS: These may be involved in occasional cases, e.g., Cushing’s syndrome, growth hormone deficiency. · 

(j) ALCOHOL: A recent review of studies concluded that the relationship between alcohol consumption and adiposity was generally positive for men and negative for women (6). 

(k) EDUCATION: In most affluent societies, there is an inverse relationship between educational level and prevalence of overweight (6). 

(I) SMOKING: Reports that the use of tobacco lowers body weight began to appear more than 100 years ago, but detailed studies have been reported only during the past 10 years or so. In most populations, smokers weigh somewhat less than ex-smokers; individuals who have never smoked fall somewhat between the two. 

(m) ETHNICITY: Ethnic groups in many industrialized countries appear to be especially susceptible to the development of obesity and its complications. Evidence suggests that this may be due to a genetic predisposition to obesity that only becomes apparent when such groups are exposed to a more affluent lifestyle. 

(n) DRUGS: Use of certain drugs, e.g., corticosteroids, contraceptives, insulin, ~-adrenergic blockers, etc. can promote weight gain.

Use of BMI to classify obesity 

Body mass index (BMI) is a simple index of weight-for-height that is commonly used to classify underweight, overweight and obesity in adults. It is defined as the weight in kilograms divided by the square of the height in metres (kg/m2). 

For example, an adult who weighs 70 kg and whose height is 1. 75 m will have a BMI of 22.9: 

BMI = 70 (kg)/ 1.752 (m2 ) = 22.9 

The classification of overweight and obesity, according to BMI, is shown in Table 2. Obesity is classified as a BMI 2 30.0. The classification shown is in agreement with that recommended by WHO (12) but includes an additional subdivision at BMI 35.0-39.9 in recognition of the fact that management options for dealing with obesity differ above a BMI of 35. The WHO classification is based primarily on the association between BMI and mortality. 

 Classification of adults according to BMI

ClassificationBMIRisk comorbidities 
Underweight< 18.50Low (but risk of other
clinical problems increased)
Normal range18.50-24.99Average
Overweight :
Obese Class.I
Obese class II
Obese class III
≥ 40.00
 Very severe 

These BMI values are age-independent and the same for both sexes. The table shows a simplistic relationship between BMI and the risk of comorbidity, which can be affected by a range of factors, including the nature of the diet, ethnic group and activity level. The risks associated with increasing BMI are continuous and graded and begin at a BMI above 25. 

Although it can generally be assumed that individuals with a BMI of 30 or above have an excess fat mass in their body, BMI does not distinguish between weight associated with muscle and weight associated with fat. As a result, the relationship between BMI and body fat content varies according to body build and proportion, and it has been shown repeatedly that a given BMI may. does not correspond to the same degree of fatness across populations. Polynesians, for example, tend to have a lower fat percentage than Caucasian Australians at an identical BMI. In addition, the percentage of body fat mass increases with age up to 60-65years in both sexes, and is higher in women than in men of equivalent BM!. In cross-sectional comparisons, therefore, BMI values should be interpreted with caution if estimates of body fat are required. 



Compared with subcutaneous adipose tissue, intraabdominal adipose tissue has more cells per unit mass, higher blood flow, more glucocorticoid (cortisol) receptors, probably more androgen (testosterone) receptors, and greater catecholamine-induced lipolysis. These differences make intra-abdominal adipose tissue more susceptible to both normal stimulation and changes in lipid accumulation and metabolism. Furthermore, intra-abdominal adipocytes are located upstream from liver in the portal circulation. This means that there is a marked increase in the flux of nonesterified fatty acid to the liver via the portal blood in patients with abdominal obesity. 

There is good evidence that abdominal obesity is important in the development of insulin resistance, and in the metabolic syndrome (hyperinsulinaemia, dyslipidaemia, glucose intolerance, and hypertension) that link obesity with CHO. Premenopausal women have quantitatively more lipoprotein lipase (LPL) and higher LPL activity in the gluteal and femoral subcutaneous regions, which contain fat cells larger than those in men, but these differences disappear after menopause.

Assessment of obesity 

Before we consider the assessment of obesity, it will be useful to first look at body composition as under; 

a. the active mass (muscle, liver, heart etc.) 

b. the fatty mass (fat) 

c. the extracellular fluid (blood, lymph, etc.) 

d. the connective tissue (skin, bones, connective tissue) 

Structurally speaking, the state of obesity is characterized by an increase in fatty mass at the expense of the other parts of the body. The water content of the body is never increased in case of obesity. 

Although obesity can easily be identified at first sight, a precise assessment requires measurements and reference standards. The most widely used criteria are : 


Bodyweight, though not an accurate measure of excess fat, is a widely used index. In epidemiological studies, it is conventional to accept + 2 SD (standard deviations) from the median weight for height as a cut-off point for obesity. 

For adults, some people calculate various other indicators such as: 

The body mass index (BMI) and the Brocca index are widely used. A FAO//WHO/UNU Report gives the much-needed reference tables for body mass index which can be used internationally as reference standards for assessing the prevalence of obesity in a community. 


A large proportion of total body fat is located just under the skin. Since it is most accessible, the method most used is the measurement of skinfold thickness. It is a rapid and “non-invasive” method for assessing body fat. Several varieties of callipers (e.g., Harpenden skin callipers) are available for this purpose. The measurement may be taken at all four sites mid-triceps, biceps, subscapular and suprailiac regions. The sum of the measurements should. be less than 40 mm in boys and 50 mm in girls. 

Unfortunately, standards for subcutaneous fat do not exist for comparison. Further, in extreme obesity, measurements may be impossible. The main drawback of skinfold measurements is their poor repeatability. 


Waist circumference is measured at the midpoint between the lower border of the rib cage and the iliac crest. It is a convenient and simple measurement that is unrelated to height, correlates closely with BMI and WHR and is an approximate index of intra-abdominal fat mass and total body fat. Changes in waist circumference reflect changes in risk factors for cardiovascular disease and other forms of chronic diseases. There is an increased risk of metabolic complications for men with a waist circumference ≥102 cm, and women with a waist circumference of ≥ 88 cm. 

Over the past 10 years or so, it has become accepted that a high WHR (> 1.0 in men and> 0.85 in women) indicates abdominal fat accumulation. 


In addition to the above, three well-established and more accurate measurements are used for the estimation of body fat. They are measurements of total body water, of total body potassium and of body density. The techniques involved are relatively complex and cannot be used for routine clinical purposes or for epidemiological studies. The introduction of measuring fat cells has opened up a new field in obesity research. 

Hazards of obesity

Obesity is a health hazard and a detriment to well-being which is reflected in the increased morbidity and mortality: 

a) INCREASED MORBIDITY: Obesity is a positive risk factor in the development of hypertension, diabetes, gall bladder disease and coronary heart disease and certain types of cancers, especially the hormonally related and large bowel cancers. There are in addition, several associated diseases, which, although not usually fatal, cause a great deal of morbidity in the community, e.g., varicose veins, abdominal hernia, osteoarthritis of the knees, hips and lumbar spine, flat feet and psychological stresses, particularly during adolescence. Obese persons are exposed to increased risk from surgery. Obesity may lead to lowered fertility.

(b) INCREASED MORTALITY: The Framingham Heart Study in the United States showed a dramatic increase in sudden death among men more than 20 per cent overweight as compared with those with normal weight. The increased mortality is brought about mainly by the increased incidence of hypertension and coronary heart disease. There is also an excess number of deaths from renal diseases. Obesity lowers life expectancy. More information is needed about the relationship between different degrees of obesity and morbidity and mortality. 

Prevention and control 

Weight control is widely defined as approach to maintaining weight within the ‘healthy’ (i.e. ‘normal’ or ‘acceptable’) range of body mass index of 18.5 to 24. 9 kg/m2 throughout adulthood (WHO Expert Committee, 1995). It should also include the prevention of weight gain of more than 5 kg in all people. In those who are already overweight, a reduction of 5-10 per cent of body weight is recommended as an initial goal. 

Prevention of obesity should begin in early childhood. Obesity is harder to treat in adults than it is in children. The control of obesity centres around weight reduction. This can be achieved by dietary changes, increased physical activity and a combination of both. 

(a) DIETARY CHANGES: The following dietary principles apply both to prevention and treatment : the proportion of energy-dense foods such as simple carbohydrates and fats should be reduced; the fibre content in the diet should be increased through the consumption of common un-refined foods; adequate levels of essential nutrients in the low energy diets (most conventional diets for weight reduction are based on 1000 kcal daily model for an adult) should be ensured, and reducing diets should be as close as possible to existing nutritional patterns. The most basic consideration is that the food energy intake should not be greater than what is necessary for energy expenditure. It requires modification of the patient’s behaviour and strong motivation to lose weight and maintain ideal weight. Unfortunately, most attempts to reduce weight in obese persons by dietary advice remain unsuccessful. 

(b) INCREASED PHYSICAL ACTIVITY: This is an important part of weight reducing programme. Regular physical exercise is the key to increased energy expenditure. 

(c) OTHERS: Appetite suppressing drugs have been tried in the control of obesity. They are generally inadequate to produce massive weight loss in severely obese patients. Surgical treatment (e.g., gastric bypass, gastroplasty, jaw-wiring, to eliminate the eating of solid food have all been tried with limited success. In short, one should not expect quick or even tangible results in all cases from obesity prevention programmes. 

Health education has an important role to play in teaching people how to reduce overweight and prevent obesity. A fruitful approach will be to identify those children who are at risk of becoming obese and find way of preventing it. 


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