Despite a lower average BMI compared to Western populations, Indian adults accumulate disproportionate amounts of visceral and upper-body fat.
Published Jan 13, 2026 | 7:00 AM ⚊ Updated Jan 13, 2026 | 7:00 AM
The pathway from obesity to cardiovascular disease in India is not inevitable, but is accelerated and more severe than in the West. (iStock)
Summary: Obesity, diabetes and hyperlipidaemia are interlinked and can lead to cardiovascular events. Propensity for visceral fat puts individuals, particularly Indians, at risk. Monitoring and early interventions are critical.
Imagine a cascading set of dominoes, each piece striking the next in an inevitably accelerating sequence. This is the metabolic story of obesity, a disease that operates silently, damaging the body’s control systems long before obvious symptoms appear.
Understanding this chain — from fat accumulation to insulin dysregulation to diabetes to cardiovascular catastrophe — is essential for recognising why early intervention matters.
The journey does not begin with high blood sugar or heart attacks, but with fat cells doing what they were designed to do: expanding. When excessive calories accumulate, white adipose tissue (fat) expands, but in obesity, something more sinister occurs. The tissue undergoes pathological remodelling characterised by chronic inflammation, fibrosis (thickening or hardening of tissue), and abnormal hormone secretion, leading to metabolic liability.
Visceral fat, the intra-abdominal fat surrounding organs, emerges as the primary villain in this story. Unlike subcutaneous fat (the pinchable fat under skin), visceral fat actively secretes inflammatory molecules, called cytokines. These cytokines act like smoke alarms, triggering inflammation throughout the body. The liver responds by increasing production of C-reactive protein (CRP), amplifying systemic inflammation. Simultaneously, visceral fat releases excessive free fatty acids (FFAs) into circulation.
In India, this pathway unfolds with particular aggression. Despite a lower average Body Mass Index (BMI) compared to Western populations, Indian adults accumulate disproportionate amounts of visceral and upper-body (android) fat. Indians show cardiometabolic abnormalities at BMI levels that would be considered normal in Caucasian populations. This visceral obesity phenotype appears to be driven by genetic predisposition, dietary patterns high in refined carbohydrates and low in fibre, and lifestyle changes following economic liberalisation.
Here is where the dominoes begin to fall. The circulating FFAs (Free Fatty Acids) impair the insulin-signalling pathway in muscle cells and the liver. Normally, when glucose enters the bloodstream after a meal, insulin binds to receptors on muscle cells, allowing glucose uptake. But high FFA levels interfere with this process, a phenomenon called insulin resistance.
The pancreatic beta cells, sensing rising blood glucose, respond by secreting more insulin in a compensatory attempt to overcome the resistance. This hyperinsulinemia, or elevated circulating insulin, temporarily maintains normal blood glucose but represents metabolic dysfunction.
Approximately 136 million Indians currently live in a prediabetic state (fasting glucose levels of 100-125 mg/gL, or 140-199 mg/dL two hours after food). Even at the prediabetic stage, when no symptoms exist, and blood sugar remains technically “borderline,” the risk of a cardiovascular event increases 1.5-fold compared to people with normal glucose. Most individuals with prediabetes will progress to overt diabetes within 3-10 years without intensive lifestyle intervention.
The progression to type-2 diabetes involves accelerating beta-cell failure.
In India, this progression carries particular speed and severity. The ICMR-INDIAB study estimates that 101 million Indians have diabetes. Tamil Nadu, Goa, and Karnataka report among the highest age-standardised prevalence rates, while rural areas show lower but rapidly increasing rates. The clustering of diabetes with hypertension (35.5% prevalence nationally), obesity, and dyslipidemia creates a “toxic quartet” of cardiometabolic risk.
An illustrative clinical vignette: a 38-year-old executive in Hyderabad presents with fatigue and occasional shortness of breath with exertion. His BMI is 26 kg/m², only slightly elevated, yet his waist circumference is 92 cm, within the abdominal obesity threshold. His fasting glucose is 112 mg/dL (prediabetic range), his HDL is 35 mg/dL (low), his triglycerides are 240 mg/dL (elevated), and his blood pressure is 138/88 mmHg. His inflammatory markers (CRP, fibrinogen) are elevated. A stress test reveals mild ischemia (i.e., a part of the body not getting enough blood supply). Without intervention, he represents the statistic: the Indian adult developing premature cardiovascular disease driven by obesity-induced metabolic derangement. Yet his BMI alone would not have flagged him as high-risk in Western guidelines.
The pathway from obesity to cardiovascular disease in India is not inevitable, but is accelerated and more severe than in the West. Understanding this chain of causation underscores why obesity in India represents not merely a cosmetic concern but a public health emergency requiring urgent, intensive intervention at every stage from primary prevention through management of established complications.
(Edited by Majnu Babu).
