Type II Diabetes Epidemic in India
We all probably know at least one person who has diabetes, but arguably we never worry about it to the same extent as cancer or cardiovascular disease. Perhaps this is because diabetes rarely causes death directly, or because we assume it is curable since most dia- betics seem fairly healthy (incidentally, it is treatable, not curable). Maybe we do not realise that nearly one sixth of the world’s population today has diabetes, with an annual global treatment cost of $250 billion, a figure expected to rise to $400 billion by 2030. [1] Yet, the brunt of that disease burden and cost is in the developing world, in countries such as India, which we usually associate with outbreaks of exotic diseases like cholera and typhoid. So, why is it that India, where 80% of the population lives on less than $2 a day, is the capital of this so-called ‘disease of affluence’? In India, and the rest of the world, it is really Type II diabetes that is the main problem. Although Type I has risen in prevalence over the last 20 years, this pales in comparison to the growth of Type II diabetes, which is really starting to take effect in developing nations such as India and China.
Firstly, it is important to realise that Type II diabetes can be caused by two different processes. [2] There can be dysfunction of the beta cells that produce insulin due to a reduced ability of the cells to pump out the insulin even when glucose levels are high. Alternatively, direct resistance to insulin can occur, for example, via defects in the receptors that mediate its actions, or via obesity- mediated effects. McKeigue et al. report that Indians are more directly insulin-resistant than other ethnic groups, [3] suggesting a particular pathogenic mechanism by which diabetes develops in the Indian ethnic groups. For example, insulin resistance is often linked to obesity and high levels of fats – so clearly, diet is a factor that could explain this predilection for insulin resistance in Indians. The typical Indian meal is carbohydrate rich with heavy emphasis on rice-based foods; sweet desserts are lavishly consumed and are considered obligatory at social events. Much of the food is cooked in ‘ghee’, a butter-like substance that is almost entirely composed of saturated fats, which worsen cholesterol levels and increase risk of obesity and cardiovascular disease. Added to this, classical Indian snacks, such as pakoras and samosas are highly calori? c, with one samosa estimated to contain up to 25g of fat [4] (more than one third of the entire daily recommended amount!)
Another related factor is an increasing trend in eating fast foods and processed goods, particularly in the young, urban population. Although only 30% of the Indian population is urban, [5] there is significant rural-urban migration occurring as people move to the big cities to find jobs in a growing economy. These jobs are often in the booming software and IT industries, where workers sit in front of computers, typically for the whole day with little exercise. This rising trend towards a ‘Westernised’ lifestyle is placing them at greater risk for diabetes, a fact con? rmed by studies showing that the longer an Indian immigrant spends in a well-developed country, such as the United States or the United Kingdom, the greater the risk of diabetes becomes. [6] Indeed, as people become richer, the shift from the more traditional diet to Western foods diabetes, but arguably we never worry about it to the same extent as cancer or cardiovascular disease.
Nevertheless, food and diet alone cannot explain the Type II diabetic epidemic in India – India is expected to see twice the increase in diabetes as the USA over the next 20 years, despite two thirds of the US population being obese or overweight – so, as with any disease, there is a gene-environment interaction that underlies disease pathogenesis.
There is interesting evidence that Indian migrants to the US or UK do not have higher obesity rates than their Caucasian counterparts. Yet, Indians have a greater risk for abdominal obesity, which has been correlated with insulin resistance. [8] This points to a hypothesis that the Indian body constitution is geared towards storing excess calories in the abdomen – compared to the hips for example – putting Indians at higher risk of diabetes. Even without direct links to obesity, another finding points to some unidentified genetic susceptibility to insulin resistance present in many Indians; so many will develop diabetes even though they are classified as normal or only slightly overweight by the body mass index (BMI). [9] For example, the typical American type II diabetic is usually ‘obese’ or ‘morbidly obese’ (BMI of ≥30 or ≥35 respectively); in contrast, a significant number of Indians who seem lean and thin develop diabetes even when their BMI is within the normal range – indeed, these findings are leading to calls to reclassify BMI categories depending on ethnic groups. [10] Even though Indian diabetics may be thinner than their Western counterparts, they have more body fat for the same BMI, as well as higher amounts of abdominal fat, suggesting a peculiar thin- fat body composition that could explain insulin resistance. [11] Yet, even when controlling for total body fat and abdominal skinfold thickness, Indians have higher insulin resistance than Caucasians. [12] This indicates that there is a genetic component to the picture that predisposes Indian people to becoming insulin resistant and developing Type II diabetes. There is also evidence of a further genetic contribution to the Indian diabetes problem, and it relates to the fetal origin hypothesis, [9] which proposes that undernutrition at critical periods in fetal development leads to permanent changes in developing organ systems. In the case of Type II diabetes, the argument is that Asians, as a race, have smaller body sizes, and mothers, particularly in the rural parts of India, are small and chronically undernourished, leading to various nutritional de? ciencies. Consequently, Indian babies are amongst the smallest in the world, with a third classified as ‘low birth weight’. But, being small as a fetus leads to acquisition and expression of so-called thrifty genes that enable a growing fetus to procure as many nutrients as possible in the face of scarcity. This is transmitted through life, such that even though Indians may be relatively normal in size, they absorb more calories than their Caucasian counterparts, leading to the thin-fat body composition that triggers insulin resistance. This hypothesis has been borne out in some studies [13] that have found associations between a low birth weight and insulin resistance, and it is commonly found that Indians, on average, develop Type II diabetes around 10 years before their Western counterparts suggesting the process is somehow accelerated. [9]
So, it seems apparent that India needs to start its “War on Diabetes”, in a similar way to how President Nixon launched the “War on Cancer” in the US nearly 40 years ago. [14] Unfortunately, whilst the diabetes epidemic has been gaining strength, healthcare policy in India has largely ignored the problem, preferring to concentrate on communicable diseases, which arguably represent the more immediate threat. Nevertheless, there are signs that the country is waking up to this silent scourge; in January 2008, the Indian Government rolled out a $1.3 million pilot National Programme for Prevention and Control of Diabetes, Cardiovascular Disease and Stroke (NPCDS), [15] recognising that diabetes forms a nodal point to a myriad of associated diseases. The strategy is simple – educate the population on healthy eating and physical activity, raise standards of care for those who either already have Type II diabetes or are on the verge of it, and devote more resources towards specialised diabetic clinics that aim to catch the disease early to reduce its morbid complications. Whilst India may have entered into this war too late, it may still be able to contain the advances of this seemingly innocuous but highly devastating disease.
Praful Ravi is a fourth year Medicine student at Christ’s College.