Once regarded as a single disease entity, diabetes is now seen as a heterogeneous group of diseases, characterized by a state of chronic hyperglycemia, resulting from a diversity of aetiologies, environmental and genetic, acting jointly (1). The underlying cause of diabetes is the defective production or action of insulin, a hormone that controls glucose, fat and amino acid metabolism. Characteristically, diabetes is a long-term disease with variable clinical manifestations and progression. Chronic hyperglycaemia, from whatever cause, leads to a number of complications — cardiovascular, renal, neurological, ocular and others such as_ intercurrent infections. Classification The classification adopted by WHO (2) is given in Table 1. TABLE 1 Clinical classification of diabetes mellitus 1. Diabetes mellitus (DM) i) Typel or Insulin-dependent diabetes mellitus ii) Type2 or Non-insulin dependent diabetes mellitus iii) Malnutrition-related diabetes mellitus (MRDM) iv) Other types (secondary to pancreatic, hormonal, drug-induced, genetic and other abnormalities) 2. Impaired glucose tolerance (IGT) 3. Gestational diabetes mellitus (GDM) Source (2) Type 1 diabetes (Insulin-dependent diabetes mellitus) is the most severe form of the disease. Its onset is typically abrupt and is usually seen in individuals less than 30 years of age. It is lethal unless promptly diagnosed and treated. This form of diabetes is immune-mediated in over 90 per cent of cases and idiopathic in less than 10 per cent cases. The rate of destruction of pancreatic f cell is quite variable. Rapid in some individuals and slow in others. Type 1 diabetes is usually associated with ketosis in its untreated state. It occurs mostly in children, the incidence is highest among 10-14 year old group, but occasionally occur in adults. It is catabolic disorder in which circulating insulin is virtually absent, plasma glucagon is elevated, and the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonaemia, and reduce blood glucose (3). Type 2 diabetes is much more common than type 1 diabetes. It is often discovered by chance. It is typically gradual in onset and occurs mainly in the middle-aged and elderly, frequently mild, slow to ketosis and is compatible with long survival if given adequate treatment. Its clinical picture is usually complicated by the presence of other disease processes. Gastational diabetes is hyperglycaemia with blood glucose values above normal but below those diagnostic of diabetes, occurring during pregnancy. Women with gastational diabetes are at an increased risk of complications during pregnancy and at delivery. They and their children are also at increased risk of type 2 diabetes in the future. Impaired glucose tolerance (IGT) describes a state intermediate— “at-risk” group — between diabetes mellitus and normality. It can only be defined by the oral glucose tolerance test (see Table 3).Insulin resistance syndrome (Syndrome X) In cuese patients with type 2 diabetes, the ussociation. of hyperglycaemia, hyperinsulinaemia, dyslipidaemia and hypertension, which leads to coronary artery disease and stroke, may result from a genetic defect producing insulin resistance, with the latter being exaggerated by obesity. It has been proposed that insulin resistance predisposes to hyperglycaemia, which results in hyperinsulinaemia (which may or may not be of sufficient magnitude to correct the hyperglycaemia) and this excessive insulin level then contributes to high levels of triglycerides and increased sodium retention by renal tubules, thus inducing hypertension. High levels of insulin can stimulate endothelial proliferation to initiate atherosclerosis (3). Problem statement WORLD Diabetes is an “iceberg” disease. Although increase in both the prevalence and incidence of type 2 diabetes have occurred gloablly, they have been especially dramatic in societies in economic transition, in newly industrialized countries and in developing countries. During year 2014, the number of cases of diabetes worlwide is estimated to be around 422 million, of these more than 90 per cent are type 2 diabetes. In 2015, an estimated 1.6 million people died from consequences of high blood sugar (4). More than 80 per cent diabetes deaths occur in low and middle income countries. The apparent prevalence of hyperglycaemia depends on the diagnostic criteria used in epidemiological surveys. The global prevalence of diabetes in 2014 was estimated to be 8.5% in adults aged 18+ years (4). The prevalence of diabetes was highest in the Eastern Mediterranean Region and the Region of the Americas (11% for both sexes) and lowest in the WHO European and Western Pacific Regions (9% for both sexes). The magnitude of diabetes and other abnormalities of glucose tolerance are considerably higher than the above estimates if the categories of ‘impaired fasting’ and ‘impaired glucose tolerance’ are also included. The estimated prevalence of diabetes was relatively consistent across the income groupings of countries. Low- income countries showed the lowest prevalence (8% for both sexes), and the upper-middle-income countries showed the highest (10% for both sexes) (5). Unfavourable modification of lifestyle and dietary habits that are associated with urbanization are believed to be the most important factors for the development of diabetes. The prevalence of diabetes is approximately twice in urban areas than in rural population. A bulk of evidence from studies on migrants indicates that the ethnic, presumably genetic, vulnerability of Asians manifests into diabetes when subjected to unfavourable life- styles. Population-based surveys completed recently in Bangladesh, India and Indonesia have shown considerable increase in the prevalence rate of the disease in both urban and rural dwellers when compared to results obtained earlier. Diabetic patients, if undiagnosed or inadequately treated, develop multiple chronic complications leading to irreversible disability and death. Coronary heart disease and stroke are more common in diabetics than in the general population. Microvascular complications like diabetic renal disease and diabetic retinopathy and neuropathy are serious health problems resulting in deterioration of the quality oflife and premature death. In fact, diabetes is listed among 2 ke nost important determinants of the cardisvas ular disease epidemic in Asia. Lower limb amputation are at least 10 times more common in diabetic than in non-diabetic individuals in developed countries, more than half of all non-traumatic lower limb amputations are due to diabetes (5). Metabolic disorders in pregnant diabetic women as well as those caused by gestational diabetes (diabetes diagnosed for the first time during pregnancy) pose a high health risk, to both the mother and foetus. Unfortunately, there is still inadequate awareness about the real dimension of the problem among the general public. There is also a lack of awareness about the existing interventions for preventing diabetes and the management of complications. Inadequacies in primary health care systems, which are not designed to cope with the additional challenges posed by the chronic non-communicable diseases, result in poor detection of cases, suboptimal treatment and insufficient follow-up leading to unnecessary disabilities and severe complications, often resulting in early death. The age-adjusted mortality rates among the people with diabetes are 1.5 to 2.5 times higher than in the general population (6). In Caucassian population, much of the excess mortality is attributable to cardiovascular disease, especially coronary heart disease; amongst Asian and American Indian population, renal disease is a major contributor (6); whereas in some developing societies, infections are an important cause of death. It is conceivable that the decline in mortality due to coronary heart disease which has occurred in many affluent countries may be halted or even reversed if rates of type 2 diabetes continue to rise. This may occur if the coronary risk factors associated with diabetes increase to the extent that the risk they mediate outweighs the benefit accrued from improvements in conventional cardiovascular risk factors, and the improved care of patients with established cardiovascular disease (6). In addition to non-insulin dependent diabetes, which is rather silent, chronic, often unidentified killer mostly among the adult population, the insulin dependent form of the disease (type 1) makes an even more dramatic appearance in affected children. They develop symptoms of ketoacidosis and often die, since the majority do not have access to adequate medical care, and since insulin is not available or too expensive. It is estimated that the prevalence of type 1 diabetes in Asia is relatively low, accounting for about 9.7 per cent of all diabetes mellitus cases in the Region. The insulin dependent diabetes registry at Chennai (India) reported an incidence of 10.5 per 100,000 children in the age group of 10-12 years (7). INDIA The population in India has an increased susceptibility to diabetes mellitus. This propensity was demonstrated by multiple surveys of migrant Indians residing in Fiji, Singapore, South Africa, U.K. and USA. The rates of diabetes in migrants from the Indian subcontinent have consistently shown to exceed those of the local population. During the year 2012 in India, the proportional mortality (% of total death, all ages) due to diabetes was about 2 per cent. The number of deaths due to diabetes in age group 30-69 was 75,900 in males and 51,700 in females and in age 70+ years about 46,800 in males and 45,600 in females. The mortality rate was about 30.2 per 100,000 population for men and 22.7 per 100,000 population for women. The number of deaths attributable to high bloodglucose in age group 30-69 was 251,300 for men and 145,7() 40: women, and for age group 70+ years, 13%, /0( for men and 139,900 for women (8). National programme for prevention and control of noncommunicable diseases are operational in India and it includes diabetes and diabetes registry. For details please refer to chapter 7. Natural history Epidemiological determinants 1. AGENT The underlying cause of diabetes is insulin deficiency which is absolute in type 1 diabetes and partial in type 2 diabetes. This may be due to a wide variety of mechanisms: (a) pancreatic disorders — inflammatory, neoplastic and other disorders such as cystic fibrosis, (b) defects in the formation of insulin, e.g., synthesis of an abnormal, biologically less active insulin molecule; (c) destruction of beta cells, e.g., viral infections and chemical agents, (d) decreased insulin sensitivity, due to decreased numbers of adipocyte and monocyte insulin receptors. (e) genetic defects, e.g., mutation of insulin gene; and (f) auto- immunity. Evidence is accumulating that the insulin response to glucose is genetically controlled. The overall effect of these mechanisms is reduced utilization of glucose which leads to hyperglycaemia accompanied by glycosuria. 2. HOST FACTORS (a) AGE : Although diabetes may occur at any age, surveys indicate that prevalence rises steeply with age. Type 2 diabetes usually comes to light in the middle years of life and thereafter begins to rise in frequency. Malnutrition related diabetes affects large number of young people. The prognosis is worse in younger diabetics who tend to develop complications earlier than older diabetics. (b) SEX : In some countries (e.g., UK) the overall male-female ratio is about equal (9). In south-east Asia, an excess of male diabetics has been observed (1), but this is open to question. (c) GENETIC FACTORS: The genetic nature of diabetes is undisputed. Twin studies showed that in identical twins who developed type 2 diabetes, concordance was approximately 90 per cent (2), thus demonstrating a strong genetic component. In type 1 diabetes, the concordance was only about 50 per cent indicating that type 1 diabetes is not totally a genetic entity. (d) GENETIC MARKERS : Type 1 diabetes is associated with HLA-B8 and B15, and more powerfully with HLA-DR3 and DR4. The highest risk of type 1 diabetes is carried by individuals with both DR3 and DR4. On the other hand type 2 diabetes is not HLA~associated (2). (e) IMMUNE MECHANISMS : There is some evidence of both cell- mediated and of humoral activity against islet cells. Some people appear to have defective immunological mechanisms, and under the influence of some environmental “trigger”, attack their own insulin producing cells. (f) OBESITY : Obesity particularly central adiposity has long been accepted as a risk factor for type 2 diabetes and the risk is related to both the duration and degree of obesity. The association has been repeatedly demonstrated in longitudinal studies in different populations, with a striking gradient of risk apparent with increasing level of BMI, adult weight gain, waist circumference or waist to hip ratio. Indeed waist circumference or waist to hip ratio (reflecting abdominal or visceral adiposity) are more powerful determinants of subsequent risk of type 2 diabetes than BMI (6). Central obesity is also an important determinant ofinsulin resistance, the underlying abnormality in most cases of tyze © diabetes. In some instances obesity reduces 1¢ number of insulin receptors on target cells. Voluntary weight loss improves insulin sensitivity and in several randomized controlled trials has shown to reduce the risk of progression from impaired glucose tolerence to type 2 diabetes (10, 11). However, many obese subjects are not diabetic. Thus obesity by itself is inadequate to account for all, or even most, cases of type 2 diabetes; physical inactivity and/or deficiencies of specific nutrients may also be involved (2). Obesity appears to play no role in type 1 diabetes pathogenesis (12). (g) MATERNAL DIABETES : Offsprings of diabetic pregnancies including gestational diabetes are often large and heavy at birth, tend to develop obesity in childhood and are at high risk of developing type 2 diabetes at an early age. Those born to mothers after they have developed diabetes have a three-fold higher risk of developing diabetes than those born before. Maternal diabetes associated with intrauterine growth retardation and low birth weight, when associated with rapid growth catch-up later on, appears to increase the risk of subsequent diabetes in the child (6). 3. ENVIRONMENTAL RISK FACTORS Susceptibility to diabetes appears to be unmasked by a number of environmental factors acting on genetically susceptible individuals. They include : (a) SEDENTARY LIFESTYLE : Sedentary life style appears to be an important risk factor for the development of type 2 diabetes. Lack of exercise may alter the interaction between insulin and its receptors and subsequently lead to type 2 diabetes (2). (b) DIET : A high saturated fat intake has been associated with a higher risk of impaired glucose tolerance, and higher fasting glucose and insulin levels (6). Higher proportions of saturated fatty acids in serum lipid or muscle phospholipid have been associated with higher fasting insulin, lower insulin sensitivity and a higher risk of type 2 diabetes. Higher unsaturated fatty acids from vegetable sources and polyunsaturated fatty acids have been associated with reduced risk of type 2 diabetes and lower fasting and 2-hour glucose concentrations. Higher proportions of long-chain polyunsaturated fatty acids in skeletal muscle phospholipids have been associated with increased insulin sensitivity (6). In human intervention studies, replacement of saturated by unsaturated fatty acids leads to improved glucose tolerence and enhanced insulin sensitivity. However, long chain polyunsaturated fatty acids do not appear to confer additional benefit over monounsaturated fatty acids. When total fat intake is high (greater than 37 per cent of total energy), altering the quality of dietary fat appears to have little effect (13). (c) DIETARY FIBRE : In many controlled experimental studies, high intakes of dietary fibre have been shown to result in reduced blood glucose and insulin levels in people with type 2 diabetes and impaired glucose tolerance (14). Moreover an increased intake of wholegrain cereals, vegetables and fruits (all rich in NSP) was a feature of diets in randomized controlled trials. Thus the evidence for a potential protective effect of dietary fibre appears strong. A minimum daily intake of 20 grams of dietary fibre is recommended (6). Table 2 shows a summary of lifestyle and dietary factors associated with diabetes.(d) MALNUTRITION : Malnutrition (PEM) in early infancy and childhood may result in partial failure of B-cell function. Damage to beta cells may well explain the associated impaired carbohydrate tolerance in kwashiorkor (2). (e) ALCOHOL : Excessive intake of alcohol can increase the risk of diabetes by damaging the pancreasTABLE 2 Suminary of strength of evidence on lifestyie factors and risk of developing type 2 diabetes Convincing Voluntary weight loss Overweight and in overweight and obesity obese people Abdominal obesity Physical activity Physical inactivity Maternal diabetes* Probable NSP? Saturated fats Intrauterine growth retardation Possible 1-3 fatty acids Total fat intake Low glycaemic Trans-fatty acids index foods Exclusive breast-feeding? Insufficient Vitamin E Excess alcohol Chromium Magnesium Moderate alcohol 1 NSP = Non-starch Polysaccharides. a_ Includes gestational diabetes. b As a global public health recommendation, infants should be exclusively breast-fed for the first six months of life to achieve optimal growth, development and health. Source : (6) and liver and by promoting obesity (2). (f) VIRAL INFECTIONS: Among the viruses that have been implicated are rubella, mumps, and human coxsackie virus B4. Viral infections may trigger in immunogenetically susceptible people a sequence of events resulting in B-cell destruction. (g) CHEMICAL AGENTS : A number of chemical agents are known to be toxic to beta cells, e.g., alloxan, streptozotocin, the rodenticide VALCOR, etc (15). A high intake of cyanide producing foods (e.g., cassava and certain beans) may also have toxic effects on B-cells. (h) STRESS : Surgery, trauma, and stress of situations, internal or external, may “bring out” the disease. (i) OTHER FACTORS : High and low rates of diabetes have been linked to a number of social factors such as occupation, marital status, religion, economic status, education, urbanization and changes in life style which are elements of what is broadly known as social class. One of the most important epidemiological features of diabetes is that it is now common in the lower social classes whereas 50 years ago, the gradient was the reverse. One reason could be rapid changes in lifestyle in lower classes. SCREENING FOR DIABETES In the past, the commonest approach to diabetes screening was a preliminary, semi—quantitative test for glucose in a urine sample, followed by an oral glucose tolerance test for those found to have glycosuria. The underlying assumption is that early detection and effective control of hyperglycaemia in asymptomatic diabetics reduces morbidity. 1. Urine examination Urine test for glucose, 2 hours after a meal, is commonly used in medical practice for detecting cases of diabetes. All those with glycosuria are considered diabetic unless otherwise proved by a standard oral glucose tolerance test.Most studies now confirm that although glucose is found in uriie it, the most severe cases of diabetes, it .s often avsent in milder forms of the disease, and such cases are likely to be missed by urine test. This is known as lack of “sensitivity”. To be more precise, the sensitivity of the test (i.e., proportion of people with disease who have a positive test) varies between 10-50 per cent. The lack of sensitivity means that many diabetics would have been missed if this had been the only test. That is, the test yields too many “false-negatives”. Further, glycosuria may be found in perfectly normal people; this gives rise to “false-positives”. Since the specificity of the test is over 90 per cent, the yield of false-positives is not very high. For these reasons, urine testing is not considered an appropriate tool for case-finding or epidemiological surveys of the population (2). 2. Blood sugar testing Because of the inadequacies of urine examination, “standard oral glucose test” remains the cornerstone of diagnosis of diabetes. Mass screening programmes have used glucose measurements of fasting, postprandial or random blood sample. The measurement of glucose levels in random blood samples is considered unsatisfactory _ for epidemiological use; at the most, it can give only a crude estimate of the frequency of diabetes in a population (2). The fasting value alone is considered less reliable since true fasting cannot be assured and spurious diagnosis of diabetes may more readily occur. Therefore, for epidemiological purposes, the 2—hour value after 75 g oral glucose may be used either alone or with the fasting value (2). Automated biochemistry has now made it possible to screen thousands of samples for glucose estimation. The criteria for the diagnosis of diabetes, proposed by WHO, are given in Table 3. Target population Screening of the whole population for diabetes is not considered a rewarding exercise (17, 18). However, screening of “high-risk” groups is considered more appropriate. These groups are: (i) those in the age group 40 and over; (ii) those with a family history of diabetes; (iii) the obese; (iv) women who have had a baby weighing more TABLE 3 The WHO recommendations for the diagnostic criteria for diabetes and intermediate hyperglycaemia Diabetes | Fasting plasma glucose 2 7.0 mmol/l (126 mg/dl) or 2-h plasma glucose* > 11.1 mmol/l (200 mg/dl) Impaired Glucose Tolerance (IGT) Fasting plasma glucose < 7.0 mmol/l (126 mg/dl) and 2-h plasma glucose* 27.8 and < 11.1 mmol/ mg/dl to 200 mg/dl) p Impaired Fasting Glucose (IFG) Fasting plasma glucose 6.1 to 6.9 mmol/l 110 mg/dl to 125 mg/dl) and (if measured) 2-h plasma glucose*# < 78 mmol/l (140 mg/dl) * Venous plasma glucose 2-h after ingestion of 75g oral glucose load. # If 2-h plasma glucose is not measured, status is uncertain as diabetes or IGT cannot be excluded. Source : (16)thar, 45 kq ‘or 3.5 kg in constitutionally small populations): (v) women who show excess weight gain during pregnanicy, and (vi) patients with premature atherosclerosis. PREVENTION AND CARE 1. Primary prevention Two strategies for primary prevention have been suggested: (a) population strategy, and (b) high-risk strategy (2). a. POPULATION STRATEGY The scope for primary prevention of type 1 diabetes is limited on the basis of current knowledge and is probably not appropriate (2). However, the development of prevention programmes for type 2 diabetes based on elimination of environmental risk factors is possible. There is pressing need for primordial prevention — that is, prevention of the emergence of risk factors in countries in which they have not yet appeared. The preventive measures comprise maintenance of normal body weight through adoption of healthy nutritional habits and physical exercise. The nutritional habits include an adequate protein intake, a high intake of dietary fibre and avoidance of sweet foods. Elimination of other less well defined factors such as protein deficiency and food toxins may be considered in some populations. These measures should be fully integrated into other community-based programmes for the prevention of non-communicable diseases (e.g., coronary heart disease). b. HIGH-RISK STRATEGY There is no special high-risk strategy for type 1 diabetes. At present, there is no practical justification for genetic counselling as a method of prevention (2). Since NIDDM appears to be linked with sedentary life— style, over-nutrition and obesity, correction of these may reduce the risk of diabetes and its complications. Since alcohol can indirectly increase the risk of diabetes, it should be avoided. Subjects at risk should avoid diabetogenic drugs like oral contraceptives. It is wise to reduce factors that promote atherosclerosis, e.g., smoking, high blood pressure, elevated cholesterol and high triglyceride levels. These programmes may most effectively be directed at target population groups. 2. Secondary prevention When diabetes is detected, it must be adequately treated. The aims of treatment are : (a) to maintain blood glucose levels as close within the normal limits as is practicable (see Table 3), and (b) to maintain ideal body weight. Treatment is based on (a) diet alone — small balanced meals more frequently, (b) diet and oral antidiabetic drugs, or (c) diet and insulin. Good control of blood glucose protects against the development of complications. Please see in chapter 10 “Nutrition and health” under title “Nutritional factors in selected diseases” for details. Proper management of the diabetic is most important to prevent complications. Routine checking of blood sugar, of urine for proteins and ketones, of blood pressure, visual acuity and weight should be done periodically. The feet should be examined for any defective blood circulation (Doppler ultrasound probes are advised), loss of sensation and the health of the skin. Primary health care is of great importance to diabetic patients since most care is obtained at this level.Glycosvlated haemoglobin There should be an estin:acior. of glycated (glycosylated) haemogl>in at Aa i yearly intervals. This test provides a long-term index of glucose control. This test is based on the following rationale: glucose in the blood is complexed to a certain fraction of haemoglobin to an extent proportional to the blood glucose concentration. The percentage of such glycosylated haemoglobin reflects the mean blood glucose levels during the red cell life-time (i.e., about the previous 2-3 months) (19). Self-care : A crucial element in secondary prevention is self care. That is, the diabetic should take a major responsibility for his own care with medical guidance — e.g., adherence to diet and drug regimens, examination of his own urine and where possible blood glucose monitoring; self administration of insulin, abstinence from alcohol, maintenance of optimum weight, attending periodic check-ups, recognition of symptoms associated with glycosuria and hypoglycaemia, etc. Table 4 shows some of the individual interventions in diabetes with evidence of efficacy. Home blood glucose monitoring : Assessment of control has been greatly aided by the recent facility of immediate, reasonably accurate, capillary blood glucose measurements either by one of the many meters now available or the direct reading Haemoglukotest strips (20). The patient should carry an identification card showing his name, address, telephone number (if any) and the details of treatment he is receiving. In short, he must have a working knowledge of diabetes. All these mean education of patients and their families to optimize the effectiveness of primary health care services. 3. Tertiary prevention Diabetes is major cause of disability through its complications, e.g., blindness, kidney failure, coronary thrombosis, gangrene of the lower extremities, etc. The main TABLE 4 Individual interventions in diabetes with evidence of efficacy Interventions with evidence Benefit of efficacy Lifestyle interventions for Reduction of 35-58% in preventing type 2 diabetes in incidence people of high risk Metformin for preventing type 2 Reduction of 25-31% in diabetes for people at high risk incidence Glycaemic control in people Reduction of 30% in with HbA 1c greater than 9% microvascular disease per 1 Blood pressure control in people whose pressure is higher than 130/80 mmHg Annual eye examinations Foot care in people with high risk of ulcers Angiotensin converting enzyme inhibitor use in all people with diabetes percent drop in HbAlc Reduction of 35% in macrovascular and microvascular disease per .10 mmHg drop in blood pressure Reduction of 60 to 70% in serious vision loss Reduction of 50 to 60% in serious foot disease Reduction of 42% in nephropathy; 22% drop in cardiovascular disease Source : (5)NON-COMMUNICABLE DISEASES objec iv at the tertiary level is to organize speci lizec\ clit «cs (Diabetic clinics) and units capable of providing diagnostic and management skills of a high order. There is a great need to establish such clinics in large towns and cities (21). The tertiary level should also be involved in basic, clinical and epidemiological research. It has also been recommended that local and national registries for diabetics should be established (2). References 1. WHO (1980). Techn. Rep. Ser., No. 646. 2. WHO (1985). Techn, Rep. Ser., No. 727. 3. Lawrence M. Tierney, Jr. Stephen J. McPhee Maxine A. Papadakis (2002), Current Medical Diagnosis and Treatment, 41st ed., Lange Publication. 4. WHO (2018), Diabetes Fact Sheet No. 312, Oct. 2018. 5. Shits (2011), Global Status Report on Non-communicable Diseases, 1010. 6. WHO (2003), Tech. Rep. Ser., N 916. 7. WHO (2002), Health Situation in the South-East Asia Region 1998- 2000, New Delhi. 8. WHO (2016), Diabetic Country Profile, India, 2016. 9. Drury, M.I. (1979). Diabetes Mellitus, Blackwell, Oxford. 10. Tuomilento J. et al. (2002), Prevention of type 2 diabetes Mellitus by changes in lifestyle among subjects with impaired glucose tolerance, New England Journal of Medicine, 2002, 344 : 1343-1350. 11. Knowler WC et al. (2002), Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin, New England Journal of Medicine, 2002, 346 : 393-403. 12. Keen, H. (1985). In: Oxford Textbook of Public Health, Vol.4, p.268. 13. Vessby B. et al. (2001), Substituting dietary saturated for monounsaturated fat impairs insuline sensitivity in healthy men and women : the KANWU study. Diabetologia, 2001, 44 : 312-319. 14. Marshal JA etal. (1994), Dietary fat predicts conversion from impaired glucose tolerance to NIDDM, The San Luis Valley Diabetes Study, Diabetes Care, 1994, 17 : 50-56. 15. Arky, R.A. (1983). Nutrition Reviews, 41 (6) 165. 16. WHO (2012), Prevention and Control of Non-communicable Diseases : Guidelines for Primary Health Care in Low-resource Settings. 17. Melins, J.M. (1974). Lancet, 2 : 1367. 18. Redhead, I.H. (1975). In: Screening in General Practice, C.R. Hart (ed), Churchill Livingstone. 19. Anonymous (1978). Glycosylated Haemoglobin and Diabetic Control, Brit, Med. J., 1: 1373-4. 20. Sonksen, PH. et al (1978). Home Monitoring of Blood Glucose. Lancet, 1 : 729-32. 21. Diabetic Clinics Today and Tomorrow : Brit. Med. J. (1973) 2 :534 and Brit. Med. J. (1971) 4: 161. 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 (1). Obesity is often expressed in terms of body mass index (BMI) (see Table 1). Overweight is usually due to obesity but can arise from other causes such as abnormal muscle development or fluid retention (2). 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 affects 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.