Skip to main content
NCBI home page
Diabetes Care logoLink to Diabetes Care
. 2025 Jan 22;48(2):153–163. doi: 10.2337/dci24-0046

Lessons Learned From Epidemiology of Type 2 Diabetes in South Asians: Kelly West Award Lecture 2024

Viswanathan Mohan 1,✉
PMCID: PMC11770170  PMID: 39841965

Abstract

South Asia has high prevalence rates of type 2 diabetes (T2D). Until the 1990s, the prevalence of T2D within South Asia was low but much higher in the South Asian diaspora living abroad. Today, high prevalence rates of T2D are reported among those living in South Asia. T2D in South Asians presents with unique clinical features described as the “South Asian phenotype” that include younger age at onset of diabetes than in White Europeans, much lower BMI, hyperinsulinemia and greater insulin resistance, rapid decline in β-cell function resulting in low insulin reserve, low muscle mass, and greater ectopic fat deposition, especially in the liver. Also, prevalence of impaired fasting glucose is higher among South Asians than prevalence of impaired glucose tolerance. Genetic predisposition combined with intrauterine fetal programming (low vitamin B12 intake and high folate intake) increases susceptibility to T2D, from birth. In later life, overnutrition, especially a high carbohydrate intake with refined grains of higher glycemic index, coupled with low physical activity likely triggers the T2D epidemic in South Asians. Additionally, there are emerging risk factors like air pollution. Preventing T2D in South Asians requires a multifactorial approach, including improvements in maternal and fetal nutrition with special reference to vitamin B12 and folate intake, decreasing refined carbohydrate and increasing protein and fiber intake in the diet, increasing physical activity, and control of air pollution. Lessons learned from epidemiology of T2D in South Asians could be useful to other developing countries that are in earlier stages of epidemiological transition.

Graphical Abstract

graphic file with name dci240046F0GA.jpg

Open in a new tab

Introduction

Type 2 diabetes (T2D) is now a global public health problem affecting more than 537 million people worldwide, of whom an estimated 70%–80% live in low- and middle-income countries (1). South Asia, also referred to as the “Indian subcontinent,” includes eight countries—Afghanistan, Bangladesh, Bhutan, India, Maldives, Nepal, Pakistan, and Sri Lanka—and is home to 2.04 billion people representing approximately 25% of the total world population. South Asians share common genetic, environmental, sociocultural, and lifestyle factors that contribute to similar disease patterns; however, there are differences in dietary, alcohol, and tobacco intake based on religious affiliations between Bangladeshi, Pakistani, and Indian immigrants and even within regions of their native countries. India currently has the largest population in the world with 1.44 billion people, which represents 70% of all South Asians (2). India thus serves as a microcosm of South Asia for understanding the health trends in this region, with particular reference to T2D. In this article, the terms South Asia and India are used interchangeably.

Epidemiology of T2D in Migrant South Asians

The first epidemiological studies of diabetes in India were conducted in the 1970s, among adults aged ≥20 years, and the investigators reported a prevalence of ∼2% in urban areas and 1% in rural regions (3). Around this period, South Asians (especially from India) started migrating to different parts of the world like the U.S., the U.K., Canada, Malaysia, Singapore, South Africa and other countries, in search of better jobs. Reports of epidemiological studies performed in the 1980s and 1990s, i.e., 10–20 years later, showed very high prevalence rates of diabetes in migrant South Asians in these diasporas as compared with native Indians (4–10). This led to the widely held view at the time, that T2D was mainly a “migrant South Asian phenomenon.” This was understandable as those who migrated were usually affluent and more exposed to the obesogenic and diabetogenic factors than native South Asians. However, the surprising finding was that the prevalence rates of T2D in the diaspora of South Asian ancestry were also higher than those reported among people of the local ancestries of these countries or other migrant groups (4–8) (Table 1).

Table 1.

Prevalence of T2D among migrant South Asians and other ethnic groups

Authors (reference nos.) City/country Year South Asians White Europeans Chinese Malays Creole Melanesian
Zimmet et al. (4) Fiji 1983 M 12.9, F 11.0 M 3.5, F 7.1
Dowse et al. (5) Mauritius 1990 12.4 11.5 10.4
McKeigue et al. (6) U.K. 1992 26.0 7.0
Lee et al. (7) Singapore 1998 M 16.7, F 14.9 M 7.7, F 8.4 M 8.2, F 14.3
Anand et al. (8) Canada 2000 11.0 5.0 2.0
Open in a new tab

Data are percentages. F, female; M, male.

Oza-Frank and Narayan (9) compared the age-adjusted prevalence of overweight and T2D among migrants to the U.S. from nine regions of birth, covering 100 countries, with categorization by BMI, which revealed interesting findings. Firstly, prevalence of diabetes was highest for individuals originating from the Indian subcontinent across all BMI categories in comparisons with other ethnic groups. Strikingly, the prevalence of T2D among individuals with obesity of White European ancestry was lower than that of normal weight individuals from the Indian subcontinent (10,11). Furthermore, while the prevalence rates of T2D increased significantly among individuals with obesity of all ethnicities, the increase was most marked among those from the Indian subcontinent (9–11). These findings raised the possibility of different pathophysiological defects operating in T2D among individuals of different ethnicities.

Rapid Rise of Diabetes Within the Subcontinent

Meanwhile, rapid socioeconomic changes were taking place in India. In the 1960s, for its food, India was largely dependent on imports, chiefly wheat under the U.S. Public Law 480 (PL-480) agreement (12). Paradoxically, two significant turning points in India’s progress turned out to be the very ones that increased T2D and obesity rates in India. Firstly, India’s journey from a country of starvation to a nation self-sufficient in food is a remarkable success story. This was largely due to the “green revolution” in India. The “green revolution,” with increased agricultural output, was achieved through use of high yielding seed varieties; use of chemical fertilizers, insecticides, and pesticides; and a lot of technological assistance (13). From its “ship to mouth” existence, India not only within a couple of decades became a nation that was self-sufficient in food but today is a food surplus nation. Secondly, in 1991, India, which was on the brink of bankruptcy, opened up its economy and allowed foreign investments to flow into the country. Liberalization, privatization, and globalization quickly followed. The influx of foreign investments, coupled with the disbanding of archaic regulatory laws, led to a booming economy. Wages rose substantially, and the country moved from undernutrition to a state of overnutrition, coupled with physical inactivity as people could now afford motorized transport. This resulted in a steady increase in prevalence rates of T2D, rising rapidly from the single-digit figures prior to 1991 to double digits (3,14–20). Later, in larger cities like Chennai and Delhi, the prevalence rates rose to 22%–25% of adults aged ≥20 years (21).

At this point, our team wanted to revisit the earlier hypothesis that T2D was a “migrant South Asian phenomenon.” In 2015, we compared the prevalence of T2D among those >40 years of age in the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study, which included Indians living in the San Francisco Bay area in California and the greater Chicago area, with that among participants in the Centre for cArdio-metabolic Risk Reduction in South Asia (CARRS) study in Chennai in southern India (22). As seen in Fig. 1, age-adjusted prevalence rates of T2D were higher among Indians in Chennai (38%) than among their counterparts in the U.S. (24%) (22). Although these differences disappeared after adjustment for socioeconomic status, this was nevertheless the first report of T2D prevalence rates in South Asia equalling or exceeding that of its migrants to other countries. However, as this study was done in a single large city in India, the question arose as to whether this finding could be applied to the whole country, particularly in the more impoverished rural areas, given the huge heterogeneity in socioeconomic status between various states and regions of the country. The need for a nationally representative diabetes epidemiology study in India was thus clear (14,23).

Figure 1.

Figure 1

Open in a new tab

Comparison of diabetes prevalence among migrant Indians in the U.S. and urban Indians in India (data are from Gujral et al. [22]).

The ICMR-INDIAB Study

Most epidemiological studies on prevalence of diabetes in India up to 2010 were confined to selected urban or rural areas. No diabetes study had been conducted that covered the whole country or, indeed, even a whole state of the country. As health is a state subject in India, data on each state were needed. To address this gap, our team led the Indian Council of Medical Research–India Diabetes (ICMR-INDIAB) study, which was funded by the Indian Council of Medical Research and Ministry of Health, Government of India (23). This was the largest epidemiological survey on diabetes in India, based on a sample size of 124,000 individuals representative of India’s 1.44 billion people and covering all its 31 states and union territories, and was carried out in phases over a 12-year period from 2008 to 2020 (23,24). The study showed that in 2021 there were an estimated 101 million people with diabetes (11.4%) in India and, additionally, an estimated 136 million people with prediabetes (15.3%) (25). While the magnitude of diabetes itself was daunting, the study threw up additional worries. A significant finding from the study was a sharp increase in the prevalence of T2D between the ages of 25 and 34 years (Fig. 2A). The trend was consistent across urban and rural populations and among both sexes. Data from the U.K. published by Wright et al. (26) for people of different ancestries puts this finding into better perspective. Figure 2B shows that while the peak prevalence of T2D in people of White European ancestry occurred between the ages of 64 and 68 years, in South Asians it occurred a decade earlier, between ages 52 and 56 years, similar to the distribution in individuals of Black European ancestry of Afro-Caribbean and African descent (26). Adjustment is needed, however, for the life expectancy of the different groups studied.

Figure 2.

Figure 2

Open in a new tab

A: Age-wise prevalence of diabetes in ICMR-INDIAB study. *P for trend <0.001. B: Age at diagnosis of South Asians, White Europeans, and Black Europeans of Afro-Caribbean and African descent. Adapted from Wright et al. (26).

We next stratified diabetes prevalence on the basis of BMI. Figure 3A shows that in the ICMR-INDIAB study, starting from a BMI of 18 kg/m2, there was a steady rise in prevalence of T2D but a substantial proportion of individuals with T2D had BMI <25 kg/m2. This trend was corroborated by data from a U.K. population-based study (Fig. 3B) that showed that the rise in prevalence of diabetes in both Pakistanis and Indians of both sexes occurred at much lower BMI in comparison with individuals of White European ancestry (27).

Figure 3.

Figure 3

Open in a new tab

A: Prevalence of diabetes stratified by BMI in the ICMR-INDIAB study. B: Prevalence of T2D in South Asians and White Europeans stratified by BMI in a U.K. population-based study. Left panel, women; right panel, men. Adapted from Sattar and Gill (27).

The “South Asian Phenotype” of T2D

The distinct characteristics of T2D in South Asians described above, including the lower age at diagnosis of T2D and its occurrence at a lower BMI, are well supported in the literature (28–36), and were referred to as the South Asian phenotype; features are summarized in Fig. 4. There appears to be a phase of hyperinsulinemia and greater insulin resistance as well as a rapid decline in β-cell function, leading to T2D characterized by severe insulin deficiency. Other notable features of the South Asian phenotype include excess ectopic fat, particularly in the abdominal region (visceral and deep subcutaneous fat and the liver). There is also a characteristic dyslipidemia with very low HDL cholesterol levels and elevated serum triglyceride levels (36,37)—which, however, has not been corroborated by some studies (38). Other biochemical markers of the South Asian phenotype include lower levels of adiponectin, elevated hs-CRP, and lower levels of vitamin B12 and vitamin D (28–36).

Figure 4.

Figure 4

Open in a new tab

“South Asian phenotype” (28–36). NAFLD, nonalcoholic fatty liver disease; Vit, vitamin.

Hyperinsulinemia in South Asians: Role of Intergenerational Cycle of Insulin Resistance

While working in the U.K. in 1984–1985, I had the opportunity to study plasma glucose and insulin levels in South Asian and White European adults who had undergone oral glucose tolerance tests (28). We reported, for the first time, that even among those with normal glucose tolerance, South Asians in the U.K. had much higher insulin levels compared with White Europeans (28). This finding suggested that the pancreas had to put out more insulin to maintain normal glucose tolerance, implying greater insulin resistance. The same phenomenon of higher plasma insulin levels was observed among South Asian individuals with newly diagnosed T2D (28). We next conducted euglycemic clamp studies that confirmed greater insulin resistance in South Asians with normal glucose tolerance, who were matched for glucose, age, and BMI with White Europeans (29). Several groups from different countries later confirmed that hyperinsulinemia and increased insulin resistance were features of South Asian adults (6,32,39–46).

Further insights came from the studies of Yajnik et al. (47), who compared newborn children in Pune, India, with White European children born in Whittington Hospital, London, U.K. The studies showed that despite lower birth weights, the Indian newborns had higher insulin and leptin levels, indicating higher body fat. This was referred to as the “thin-fat Indian,” another feature of the South Asian phenotype (48). Various explanations have been offered for this unique phenotype including low vitamin B12 levels and high folate levels leading to intrauterine programming making South Asians more susceptible to diabetes (49). Yajnik (50) has proposed that there is a “double malnutrition” with intrauterine undernutrition leading to a small, thin, and fat, but insulin-resistant, baby. After birth, if this baby is overnourished, it comes to have obesity and hyperglycemia. A hyperglycemic mother with obesity produces a “macrosomic” baby, who is also at higher risk of obesity and hyperglycemia. Thus, the intergenerational insulin resistance–diabetes cycle is propagated through a girl child (50).

Ectopic Fat

Meanwhile, a series of studies comparing body composition of South Asians with those of other ancestries, especially White Europeans, were published. While reports of most studies showed excess abdominal fat deposition, some showed excess visceral, while others reported excess deep subcutaneous, fat (34,51–57). Gujral et al. (53), using computed tomography scans, showed that the prevalence of the phenotype of metabolic abnormalities but normal weight (MAN) was highest among South Asians, pointing to the limitations of using BMI to define overweight. Modi et al. (55) conducted whole-body MRI of healthy newborn infants and demonstrated increased adiposity in the three abdominal compartments, i.e., internal (visceral), deep subcutaneous, and superficial subcutaneous, in Asian Indian neonates compared with White European babies, despite similar whole-body adipose tissue content. These observations were further confirmed by MRI studies in adults, which demonstrated both increased subcutaneous, as well as visceral, fat accumulation in South Asians (56). A fat overflow, or “nutrient overflow,” hypothesis was proposed according to which the fat initially accumulates in the subcutaneous and visceral abdominal compartments but later it “overflows” leading to excess fat deposition in the liver, leading to hepatic insulin resistance (57,58). This hypothesis remains to be proven as most studies are cross-sectional in nature and there are no longitudinal studies with serial measurement of ectopic fat. In a meta-analysis comparing visceral and subcutaneous fat and liver fat in South Asians and White Europeans, investigators concluded that South Asians have significantly higher levels of ectopic fat, predominantly in the liver, which was likely the driver of the insulin resistance (59). However, there were no differences between subcutaneous and visceral fat (59). It is possible that the “personal fat threshold,” as proposed by Taylor and Holman (60) is different in South Asians, predisposing them to development of T2D. A recent study by McLaren et al. (61) sheds new light on this. In response to overfeeding and 5%–7% gain in body weight, South Asians had a smaller increase in lean mass than Europeans. Moreover, the South Asians had fewer small adipocytes, which led to decreased “metabolic buffering” of the fat, resulting in increased ectopic fat, especially in the liver. The expression of SREBF1 also differed between South Asians and White Europeans. Longitudinal studies are needed to throw further light on the evolution of ectopic fat in South Asians and its relationship with other features of the South Asian phenotype.

Rapid Loss of β-Cell Function and Severe Insulin Deficiency

Although longitudinal data are currently unavailable, an important phase in the development of T2D in South Asians appears to be a rapid loss of β-cell function leading to severe insulin deficiency. The evidence for this comes from several cross-sectional studies. Kanaya (62) studied insulin secretion in adults aged 40–80 years of different ancestries and showed that South Asians had the lowest insulin secretion even with stratification by BMI and waist circumference. This was further corroborated by a large cross-sectional study in Chennai, which demonstrated markedly lower β-cell function and insulin secretion as measured with the insulin disposition index, even at the stage of prediabetes (63).

This phenotype seems to be distinctly different from those of other ancestries where hyperinsulinemia associated with obesity seems to be a prominent feature of T2D. This is exemplified by the evidence propounded by Narayan and colleagues (10,64), who compared Pima Indians and Asian Indians, two ethnic groups known to have very high prevalence rates of T2D, reaching almost 50%, by 50 years of age. However, T2D in the Pima Indians is characterized by severe insulin resistance and marked obesity (mean BMI 33.7 kg/m2), whereas the Asian Indians with T2D were thinner (BMI 25.7 kg/m2) with insulin deficiency as the predominant defect (64). This stark difference in pathophysiology points to the need for considering different therapeutic approaches for managing T2D in different ethnicities where obesity rates differ markedly.

Subtypes of T2D in South Asians

It is well-known that T2D is a heterogenous condition with respect to age at onset, obesity, insulin resistance, insulin secretory defects, and proneness to complications. However, it was the pioneering work of Ahlqvist et al. (65) that first subclassified T2D into different subtypes. They performed data-driven cluster analysis (k-means and hierarchical clustering) for patients with newly diagnosed diabetes. Clusters were based on six variables (GAD antibodies, age at diagnosis, BMI, HbA1c, HOMA of β-cell function, and HOMA of insulin resistance). They described four subclusters of T2D: severe insulin-deficient diabetes (SIDD), severe insulin resistance diabetes (SIRD), mild obesity-related diabetes (MOD), and mild age-related diabetes (MARD). Given the unique features of the South Asian phenotype of T2D pointed out above, we wanted to see whether the same subtypes of T2D exist in our population (66). When using the same variables as used in the Swedish study, we did not have clinically meaningful clusters in our populations. However, when HDL cholesterol and triglycerides were added in the model, the results became more clear. We identified four distinct subgroups of T2D, two of which, SIDD and MARD, were similar to those seen in the Scandinavian cohort, except that they occurred at a lower age and at a lower BMI. However, we identified two novel subtypes of T2D, insulin-resistant obese diabetes (IROD) and a unique combined insulin-resistant and -deficient diabetes (CIRDD) (67). Notably, ∼40% of South Asian patients with T2D belonged to the two insulin-deficient subtypes (SIDD and CIRDD)—in contrast to the Scandinavian study, where 17.5% had SIDD (66). Those with the CIRDD subtype also had the lowest HDL cholesterol and highest triglycerides, and they were more prone to both retinopathy and diabetic kidney disease (66,67) These subtypes of T2D were also replicated in South Asians living in the U.K. (Pakistanis and Bangladeshis), indicating similar T2D phenotypes in people belonging to this ancestry (68). When individuals with T2D <45 years of age were studied by another group in India, the majority were classified as belonging to SIDD and MOD categories, while SIRD and MARD were rare (69). These authors also applied polygenic risk scores of diabetes-related traits with their subtypes of T2D (70). They showed that the European genetic risk score for diabetes could be applied to the T2D subgroups in India, although they did see some distinct Indian genetic signatures compared with those seen in White Europeans.

Is Prediabetes Also Different in South Asians?

Rooney et al. (71) recently published one of the largest reports to date on the prevalence of prediabetes, i.e., impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), in different regions of the world. Of interest, North America and Europe had the highest, and Southeast Asia the lowest, prevalence of IGT. Conversely, Southeast Asia had the highest prevalence of IFG, while its prevalence was much lower among those of White European ancestry (71). In India, also, we reported that the prevalence of IFG was much higher (10.1%) than that of IGT (3.3%) (72).

Do these findings have any clinical relevance, particularly in terms of prevention of diabetes? The early prevention trials like the Diabetes Prevention Program (DPP) (73), the Finnish Diabetes Prevention Study (74), the Da Qing study in China (75), and the Indian Diabetes Prevention Programme (IDPP) (76) all primarily included individuals with IGT or with both IGT and IFG, and in most of these studies individuals with isolated IFG, the predominant prediabetes type in South Asians, were excluded (72–76). We therefore took up the Diabetes Community Lifestyle Improvement Program (D-CLIP) studying the effect of lifestyle modification (with/without metformin) in individuals with isolated IFG, isolated IGT, and combined IFG and IGT (77). We found that the incidence of new-onset T2D could be reduced by 31% in those with IGT and by 36% in those with combined IFG and IGT, whereas only 12% of those with isolated IFG could be prevented from developing T2D (77). Three other studies have confirmed these findings (78–80). A meta-analysis of these four studies was done, which showed a 35%–49% reduction in progression to diabetes in the groups that included IGT but only a 3% reduction in progression to diabetes in the isolated IFG group, highlighting the greater challenges in preventing diabetes in individuals with isolated IFG (81).

Role of Genetic and Environmental Factors in the South Asian Phenotype

The obvious question that arises is whether the various features of the South Asian phenotype of T2D and prediabetes described above are due to genetic factors or whether they are driven primarily by environmental influences. Previous genome-wide association studies identified several novel gene variants, including 1) growth factor receptor–bound protein 14 (GRB14), 2) β-galactoside α-2,6-sialyltransferase 1 (ST6GAL1), 3) vacuolar protein sorting–associated protein 26A (VPS26A), 4) high-mobility group protein 20A (HMG20A), 5) Adaptor Related Protein Complex 3 Subunit Sigma 2 (AP3S2), 6) hepatocyte nuclear factor 4 α (HNF4A), and 7) transmembrane protein (TMEM), to be associated with T2D in South Asians (82–84). However, these genes had very small effect sizes in relation to causation of T2D. Further genetic investigations were conducted to look at partitioned polygenic scores, which revealed a greater genetic risk for initial insulin oversecretion, likely driven by dietary (carbohydrate) excess, ultimately leading to severe insulin secretory defects (85). Specific studies looking at partitioned polygenic risk scores for β-cell dysfunction showed different patterns for South Asians compared with Europeans (86,87) (Fig. 5).

Figure 5.

Figure 5

Open in a new tab

Genetic risk of β-cell dysfunction in South Asians (partitioned polygenic scores [pPS]) (87).

Despite the possible genetic contribution to the South Asian phenotype, the rapid increase in diabetes rates within a relatively short period of time points to a larger role of environmental factors as a cause in the epidemic of T2D in South Asians. The rapid economic progress in South Asia led to increased calorie intake, primarily from carbohydrates, which is the staple food in South Asia. Is there evidence for an association between excess carbohydrate intake and prevalence of T2D? In a cross-sectional study performed in Chennai, we showed a strong association of total carbohydrate intake, glycemic load, and glycemic index with the prevalence of T2D, even after adjusting for possible confounders, while dietary fiber showed a protective effect (88). Subsequently, in the Prospective Urban Rural Epidemiology (PURE) study involving 132,000 participants across 21 countries followed longitudinally for 15 years, we showed that higher white rice consumption significantly increased the risk of developing incident T2D, particularly in South Asia, where white rice intake was the highest (89).

Independently, the association of physical inactivity with T2D prevalence was also shown in the Chennai Urban Population Study (CUPS) (90). Based on a follow-up of the Chennai Urban Rural Epidemiology Study (CURES) cohort, using partial population attributable risk we looked at the preventable factors for T2D (91). The model predicted that with adoption of a healthy diet and increase in physical activity up to 50% of new-onset T2D could be prevented. Our real-world randomized controlled trial on prevention of diabetes (using lifestyle modification and metformin) achieved 36% prevention in those with IFG and IGT and 12% prevention in those with isolated IFG (77).

The next question was by how much the carbohydrate intake had to be decreased to postpone T2D. We used nationwide dietary data in India from the ICMR-INDIAB study to answer this question and carried out mathematical modeling studies, which suggested that even a 10% reduction in carbohydrate intake, if replaced with protein (preferably plant based), along with increased fiber and healthy fats (mostly monounsaturated and polyunsaturated fat), could potentially postpone T2D (92). However, randomized clinical trials are needed to confirm these findings.

Meanwhile, newer risk factors for T2D in South Asians are also emerging. Air pollution, both outdoor and indoor, has now been identified as a risk factor for diabetes. In the CARRS study carried out in New Delhi and Chennai, a strong association between PM2.5 exposure and new-onset T2D was shown (93). This indicates that reducing air pollution could be another avenue for prevention of T2D in South Asians (94).

Potential Solutions

Figure 6 summarizes the current understanding of pathogenesis of T2D in South Asians based on various epidemiological studies presented above. Clearly there is a unique South Asian T2D phenotype, which may be influenced by genetic, intrauterine, and lifestyle factors. Of interest, even from birth, South Asians exhibit hyperinsulinemia and insulin resistance with excess fat accumulation in the intraabdominal region, particularly in the liver. Early β-cell exhaustion and severe insulin deficiency appear to be important characteristics of the South Asian T2D phenotype. Addressing T2D in South Asians therefore requires a multifaceted, multisectoral approach, including improvement of maternal nutrition during pregnancy, with increased vitamin B12 and lower folate. After birth, modification of both childhood and adult lifestyles is important, with a focus on preventing overnutrition. It is particularly important to reduce consumption of high–glycemic index refined-carbohydrate foods like white rice; increase the protein and fiber intake; and include healthy (mono- and polyunsaturated) fats in the diet (95). In addition, promoting physical activity, especially improving muscle strength, preferably with resistance training (96), and reducing exposure to both outdoor and indoor pollution appear to be important (94). These interventions could potentially lower the incidence of T2D in the South Asian population. However, there is also a need for future studies looking at both the prevention and management of diabetes in this ethnic group, as treating lean T2D may require strategies different from those used in treating obese T2DM. More research is needed on T2D in South Asians, not only on its pathophysiology but also on the response to various antidiabetes drugs. There is evidence, for example, that South Asians respond better to dipeptidyl peptidase 4 inhibitors and sodium–glucose cotransporter 2 inhibitors (97–99). The lessons learned from such studies may be applicable to other developing countries in similar or earlier stages of epidemiological transition. Indeed, studies may also contribute to better understanding of the pathogenesis and heterogeneity of T2D itself, which would be an essential step in applying precision medicine in the prevention and management of T2D, especially in low- and middle-income countries (100,101).

Figure 6.

Figure 6

Open in a new tab

Lessons learned from epidemiology of T2D in South Asians.

Article Information

Acknowledgments. V.M. thanks the Indian Council of Medical Research (ICMR) and the Department of Health Research, Ministry of Health, Government of India, for supporting the ICMR-INDIAB study. He also thanks all the principal investigators of the ICMR-INDIAB study as well as participants involved in this study. The author gives special thanks to the National Institutes of Health (including the National Heart, Lung, and Blood Institute and National Institute on Aging) and the National Institute for Health and Care Research of the U.K. He acknowledges the support of all collaborators in India and abroad, particularly the Emory Global Diabetes Research Center, Atlanta, GA; University of California, San Francisco; McMaster University, Hamilton, Canada; Harvard T.H. Chan School of Public Health; Imperial College London, London, U.K.; University of Dundee, Dundee, U.K.; and Queen Mary University of London, London, U.K. Finally, the author gratefully thanks the staff of Madras Diabetes Research Foundation and Dr. Mohan’s Diabetes Specialities Centre and his family for their unstinted support.

Funding. The ICMR and Ministry of Health, Government of India, funded the ICMR-INDIAB study.

Duality of Interest. No potential conflicts of interest relevant to this article were reported.

Handling Editors. The journal editor responsible for overseeing the review of the manuscript was Steven E. Kahn.

Funding Statement

The ICMR and Ministry of Health, Government of India, funded the ICMR-INDIAB study.

Footnotes

The 2024 Kelly West Award Lecture was presented at the American Diabetes Association’s 84th Scientific Sessions, Orlando, FL, 23 June 2024.

This article is featured in a podcast available at diabetesjournals.org/care/pages/diabetes_care_on_air.

References

  • 1. International Diabetes Federation . IDF Diabetes Atlas, 10th edition, 2021. Accessed 15 July 2024. Available from https://diabetesatlas.org/atlas/tenth-edition/
  • 2. UN-Library. India Overtakes China as the World’s Most Populous Country . Accessed 15 July 2024. Available from https://www.un-ilibrary.org/content/papers/10.18356/27081990-153#:∼:text=The%20latest%20estimates%20and%20projections,the%20population%20of%20mainland%20China
  • 3. Gupta OP, Joshi MH, Dave SK. Prevalence of diabetes in India. Adv Metab Dis 1978;9:147–165 [DOI] [PubMed] [Google Scholar]
  • 4. Zimmet P, Taylor R, Ram P, et al. Prevalence of diabetes and impaired glucose tolerance in the biracial (Melanesian and Indian) population of Fiji: a rural-urban comparison. Am J Epidemiol 1983;118:673–688 [DOI] [PubMed] [Google Scholar]
  • 5. Dowse GK, Gareeboo H, Zimmet PZ, et al.; Mauritius Noncommunicable Disease Study Group . High prevalence of NIDDM and impaired glucose tolerance in Indian, Creole, and Chinese Mauritians. Diabetes 1990;39:390–396 [DOI] [PubMed] [Google Scholar]
  • 6. McKeigue PM, Shah B, Marmot MG. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991;337:382–386 [DOI] [PubMed] [Google Scholar]
  • 7. Lee WR, Lim HS, Thai AC, et al.; Diabcare Singapore Local Working Group & Diabetic Society of Singapore . A window on the current status of diabetes mellitus in Singapore--the Diabcare-Singapore 1998 study. Singapore Med J 2001;42:501–507 [PubMed] [Google Scholar]
  • 8. Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: the Study of Health Assessment and Risk in Ethnic groups (SHARE). Lancet 2000;356:279–284 [DOI] [PubMed] [Google Scholar]
  • 9. Oza-Frank R, Narayan KMV. Overweight and diabetes prevalence among US immigrants. Am J Public Health 2010;100:661–668 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Narayan KMV. Type 2 diabetes: why we are winning the battle but losing the war? 2015 Kelly West award lecture. Diabetes Care 2016;39:653–663 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Oza-Frank R, Ali MK, Vaccarino V, Narayan KMV. Asian Americans: diabetes prevalence across U.S. and World Health Organization weight classifications. Diabetes Care 2009;32:1644–1646 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12. Rath N, Patvardhan VS. Impact of assistance under P. L. 480 on Indian economy. Asia Publishing House, 1967. Accessed 15 July 2024. Available from https://pdf.usaid.gov/pdf_docs/Pcaac181.pdf
  • 13. Stepha GEJ. Impact of green revolution in India. Int J Health Sci 2022;6:5291–5297 [Google Scholar]
  • 14. Anjana RM, Ali MK, Pradeepa R, et al. The need for obtaining accurate nationwide estimates of diabetes prevalence in India - rationale for a national study on diabetes. Indian J Med Res 2011;133:369–380 [PMC free article] [PubMed] [Google Scholar]
  • 15. Ramachandran A, Jali MV, Mohan V, Snehalatha C, Viswanathan M. High prevalence of diabetes in an urban population in south India. BMJ 1988;297:587–590 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16. Kutty VR, Soman CR, Joseph A, Pisharody R, Vijayakumar K. Type 2 diabetes in southern Kerala: variation in prevalence among geographic divisions within a region. Natl Med J India 2000;13:287–292 [PubMed] [Google Scholar]
  • 17. Ramachandran A, Snehalatha C, Kapur A, et al.; Diabetes Epidemiology Study Group in India (DESI) . High prevalence of diabetes and impaired glucose tolerance in India: National Urban Diabetes Survey. Diabetologia 2001;44:1094–1101 [DOI] [PubMed] [Google Scholar]
  • 18. Mohan V, Shanthirani S, Deepa R, Premalatha G, Sastry NG, Saroja R; Chennai Urban Population Study (CUPS No. 4) . Intra-urban differences in the prevalence of the metabolic syndrome in southern India - the Chennai Urban Population Study (CUPS No. 4). Diabet Med 2001;18:280–287 [DOI] [PubMed] [Google Scholar]
  • 19. Mohan V, Deepa M, Deepa R, et al. Secular trends in the prevalence of diabetes and impaired glucose tolerance in urban South India-the Chennai Urban Rural Epidemiology Study (CURES-17). Diabetologia 2006;49:1175–1178 [DOI] [PubMed] [Google Scholar]
  • 20. Vijayakumar G, Arun R, Kutty VR. High prevalence of type 2 diabetes mellitus and other metabolic disorders in rural Central Kerala. J Assoc Physicians India 2009;57:563–567 [PubMed] [Google Scholar]
  • 21. Deepa M, Grace M, Binukumar B, et al.; CARRS Surveillance Research Group . High burden of prediabetes and diabetes in three large cities in South Asia: the Center for cArdio-metabolic Risk Reduction in South Asia (CARRS) Study. Diabetes Res Clin Pract 2015;110:172–182 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22. Gujral UP, Narayan KMV, Pradeepa RG, et al. Comparing type 2 diabetes, prediabetes, and their associated risk factors in Asian Indians in India and in the U.S.: the CARRS and MASALA studies. Diabetes Care 2015;38:1312–1318 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23. Anjana RM, Pradeepa R, Deepa M, et al. The Indian Council of Medical Research-India Diabetes (ICMR-INDIAB) study: methodological details. J Diabetes Sci Technol 2011;5:906–914 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Anjana RM, Deepa M, Pradeepa R, et al.; ICMR–INDIAB Collaborative Study Group . Prevalence of diabetes and prediabetes in 15 states of India: results from the ICMR-INDIAB population-based cross-sectional study. Lancet Diabetes Endocrinol 2017;5:585–596 [DOI] [PubMed] [Google Scholar]
  • 25. Anjana RM, Unnikrishnan R, Deepa M, et al.; ICMR-INDIAB Collaborative Study Group . Metabolic non-communicable disease health report of India: the ICMR-INDIAB national cross-sectional study (ICMR-INDIAB-17). Lancet Diabetes Endocrinol 2023;11:474–489 [DOI] [PubMed] [Google Scholar]
  • 26. Wright AK, Welsh P, Gill JMR, et al. Age-, sex- and ethnicity-related differences in body weight, blood pressure, HbA1c and lipid levels at the diagnosis of type 2 diabetes relative to people without diabetes. Diabetologia 2020;63:1542–1553 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27. Sattar N, Gill JMR. Type 2 diabetes in migrant south Asians: mechanisms, mitigation, and management. Lancet Diabetes Endocrinol 2015;3:1004–1016 [DOI] [PubMed] [Google Scholar]
  • 28. Mohan V, Sharp PS, Cloke HR, Burrin JM, Schumer B, Kohner EM. Serum immunoreactive insulin responses to a glucose load in Asian Indian and European type 2 (non-insulin-dependent) diabetic patients and control subjects. Diabetologia 1986;29:235–237 [DOI] [PubMed] [Google Scholar]
  • 29. Sharp PS, Mohan V, Levy JC, Mather HM, Kohner EM. Insulin resistance in patients of Asian Indian and European origin with non-insulin dependent diabetes. Horm Metab Res 1987;19:84–85 [DOI] [PubMed] [Google Scholar]
  • 30. Yajnik CS. Early life origins of insulin resistance and type 2 diabetes in India and other Asian countries. J Nutr 2004;134:205–210 [DOI] [PubMed] [Google Scholar]
  • 31. Banerji MA, Faridi N, Atluri R, Chaiken RL, Lebovitz HE. Body composition, visceral fat, leptin, and insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999;84:137–144 [DOI] [PubMed] [Google Scholar]
  • 32. Chandalia M, Abate N, Garg A, Stray-Gunderson J, Grundy GM. Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men. J Clin Endocrinol Metab 1999;84:2329–2335 [DOI] [PubMed] [Google Scholar]
  • 33. Chambers JC, Eda S, Bassett P, et al. C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European whites. Circulation 2001;104:145–150 [DOI] [PubMed] [Google Scholar]
  • 34. Misra A, Vikram NK. Clinical and pathophysiological consequences of abdominal adiposity and abdominal adipose tissue depots. Nutrition 2003;19:457–466 [DOI] [PubMed] [Google Scholar]
  • 35. Abate N, Chandalia M, Snell PG, Grundy SM. Adipose tissue metabolites and insulin resistance in nondiabetic Asian Indian men. J Clin Endocrinol Metab 2004;89:2750–2755 [DOI] [PubMed] [Google Scholar]
  • 36. Unnikrishnan R, Anjana RM, Mohan V. Diabetes in South Asians: is the phenotype different? Diabetes 2014;63:53–55 [DOI] [PubMed] [Google Scholar]
  • 37. Frank ATH, Zhao B, Jose PO, Azar KMJ, Fortmann SP, Palaniappan LP. Racial/ethnic differences in dyslipidemia patterns. Circulation 2014;129:570–579 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38. Kanaya AM, Kandula NR, Ewing SK, et al. Comparing coronary artery calcium among U.S. South Asians with four racial/ethnic groups: the MASALA and MESA studies. Atherosclerosis 2014. May;234:102–107 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39. McKeigue PM, Pierpoint T, Ferrie JE, Marmot MG. Relationship of glucose intolerance and hyperinsulinaemia to body fat pattern in south Asians and Europeans. Diabetologia 1992;35:785–791 [DOI] [PubMed] [Google Scholar]
  • 40. Simmons D, Powell MJ. Metabolic and clinical characteristics of south Asians and Europeans in Coventry. Diabet Med 1993;10:751–758 [DOI] [PubMed] [Google Scholar]
  • 41. Dhawan J, Bray CL, Warburton R, Ghambhir DS, Morris J. Insulin resistance, high prevalence of diabetes, and cardiovascular risk in immigrant Asians. Genetic or environmental effect? Br Heart J 1994;72:413–421 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42. Hughes K, Aw TC, Kuperan P, Choo M. Central obesity, insulin resistance, syndrome X, lipoprotein(a), and cardiovascular risk in Indians, Malays, and Chinese in Singapore. J Epidemiol Community Health 1997;51:394–399 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43. Forouhi NG, Jenkinson G, Thomas EL, et al. Relation of triglyceride stores in skeletal muscle cells to central obesity and insulin sensitivity in European and South Asian men. Diabetologia 1999;42:932–935 [DOI] [PubMed] [Google Scholar]
  • 44. Liew C-F, Seah E-S, Yeo K-P, Lee K-O, Wise SD. Lean, nondiabetic Asian Indians have decreased insulin sensitivity and insulin clearance, and raised leptin compared to Caucasians and Chinese subjects. Int J Obes Relat Metab Disord 2003;27:784–789 [DOI] [PubMed] [Google Scholar]
  • 45. Suraamornkul S, Kwancharoen R, Ovartlarnporn M, Rawdaree P, Bajaj M. Insulin clamp-derived measurements of insulin sensitivity and insulin secretion in lean and obese asian type 2 diabetic patients. Metab Syndr Relat Disord 2010;8:113–118 [DOI] [PubMed] [Google Scholar]
  • 46. Tan HC, Yew TW, Chacko S, et al. Comprehensive assessment of insulin resistance in non-obese Asian Indian and Chinese men. J Diabetes Investig 2018;9:1296–1303 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47. Yajnik CS, Lubree HG, Rege SS, et al. Adiposity and hyperinsulinemia in Indians are present at birth. J Clin Endocrinol Metab 2002;87:5575–5580 [DOI] [PubMed] [Google Scholar]
  • 48. Yajnik CS, Fall CHD, Coyaji KJ, et al. Neonatal anthropometry: the thin-fat Indian baby. The Pune Maternal Nutrition Study. Int J Obes Relat Metab Disord 2003;27:173–180 [DOI] [PubMed] [Google Scholar]
  • 49. Yajnik CS, Deshpande SS, Jackson AA, et al. Vitamin B12 and folate concentrations during pregnancy and insulin resistance in the offspring: the Pune Maternal Nutrition Study. Diabetologia 2008;51:29–38 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 50. Yajnik CS. Nutrient-mediated teratogenesis and fuel-mediated teratogenesis: two pathways of intrauterine programming of diabetes. Int J Gynaecol Obstet 2009;104(Suppl. 1):S27–S31 [DOI] [PubMed] [Google Scholar]
  • 51. Deurenberg P, Deurenberg-Yap M, Guricci S. Asians are different from Caucasians and from each other in their body mass index/body fat per cent relationship. Obes Rev 2002;3:141–146 [DOI] [PubMed] [Google Scholar]
  • 52. Klein S. The case of visceral fat: argument for the defense. J Clin Invest 2004;113:1530–1532 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 53. Gujral UP, Vittinghoff E, Mongraw-Chaffin M, et al. Cardiometabolic abnormalities among normal-weight persons from five racial/ethnic groups in the United States: a cross-sectional analysis of two cohort studies. Ann Intern Med 2017;166:628–636 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54. Garg UK, Mathur N, Sahlot R, et al. Abdominal fat depots and their association with insulin resistance in patients with type 2 diabetes. PLoS One 2023;18:e0295492. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55. Modi N, Thomas EL, Uthaya SN, Umranikar S, Bell JD, Yajnik C. Whole body magnetic resonance imaging of healthy newborn infants demonstrates increased central adiposity in Asian Indians. Pediatr Res 2009;65:584–587 [DOI] [PubMed] [Google Scholar]
  • 56. Kumar A, Tiwari P, Saxena A, et al. The transcriptomic evidence on the role of abdominal visceral vs. subcutaneous adipose tissue in the pathophysiology of diabetes in Asian Indians indicates the involvement of both. Biomolecules 2020;10:1230. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57. Sniderman AD, Bhopal R, Prabhakaran D, Sarrafzadegan N, Tchernof A. Why might South Asians be so susceptible to central obesity and its atherogenic consequences? The adipose tissue overflow hypothesis. Int J Epidemiol 2007;36:220–225 [DOI] [PubMed] [Google Scholar]
  • 58. Sattar N, Gill JMR. Type 2 diabetes as a disease of ectopic fat? BMC Med 2014;12:123. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 59. Iliodromiti S, McLaren J, Ghouri N, et al. Liver, visceral and subcutaneous fat in men and women of South Asian and white European descent: a systematic review and meta-analysis of new and published data. Diabetologia 2023;66:44–56 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60. Taylor R, Holman RR. Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond) 2015;128:405–410 [DOI] [PubMed] [Google Scholar]
  • 61. McLaren J, Gao X, Ghouri N, et al. Weight gain leads to greater adverse metabolic responses in South Asian compared with white European men: the GlasVEGAS study. Nat Metab 2024;6:1632–1645 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62. Kanaya AM. Diabetes in South Asians: Uncovering novel risk factors with longitudinal epidemiologic data: Kelly West award lecture 2023. Diabetes Care 2024;47:7–16 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 63. Staimez LR, Weber MB, Ranjani H, et al. Evidence of reduced β-cell function in Asian Indians with mild dysglycemia. Diabetes Care 2013;36:2772–2778 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 64. Staimez LR, Deepa M, Ali MK, Mohan V, Hanson RL, Narayan KMV. Tale of two Indians: heterogeneity in type 2 diabetes pathophysiology. Diabetes Metab Res Rev 2019;35:e3192. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65. Ahlqvist E, Storm P, Käräjämäki A, et al. Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables. Lancet Diabetes Endocrinol 2018;6:361–369 [DOI] [PubMed] [Google Scholar]
  • 66. Anjana RM, Baskar V, Nair ATN, et al. Novel subgroups of type 2 diabetes and their association with microvascular outcomes in an Asian Indian population: a data-driven cluster analysis: the INSPIRED study. BMJ Open Diabetes Res Care 2020;8:e001506. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 67. Anjana RM, Pradeepa R, Unnikrishnan R, et al. New and unique clusters of type 2 diabetes identified in Indians. J Assoc Physicians India 2021;69:58–61 [PubMed] [Google Scholar]
  • 68. Hodgson S, Huang QQ, Sallah N, et al.; Genes & Health Research Team . Integrating polygenic risk scores in the prediction of type 2 diabetes risk and subtypes in British Pakistanis and Bangladeshis: a population-based cohort study. PLoS Med 2022;19:e1003981. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 69. Prasad RB, Asplund O, Shukla SR, et al. Subgroups of patients with young-onset type 2 diabetes in India reveal insulin deficiency as a major driver. Diabetologia 2022;65:65–78 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 70. Yajnik CS, Wagh R, Kunte P, et al. Polygenic scores of diabetes-related traits in subgroups of type 2 diabetes in India: a cohort study. Lancet Reg Health Southeast Asia 2023;14:100182. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71. Rooney MR, Fang M, Ogurtsova K, et al. Global prevalence of prediabetes. Diabetes Care 2023;46:1388–139437196350 [Google Scholar]
  • 72. Mohan V, Unnikrishnan R, Anjana RM. Comment on Rooney et al. Global prevalence of prediabetes. Diabetes Care 2023;46:1388–1394 (Letter). Diabetes Care 2023;46:e220. [DOI] [PubMed] [Google Scholar]
  • 73. Knowler WC, Barrett-Connor E, Fowler SE, et al.; Diabetes Prevention Program Research Group . Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393–403 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 74. Lindström J, Louheranta A, Mannelin M, et al.; Finnish Diabetes Prevention Study Group . The Finnish Diabetes Prevention Study (DPS): lifestyle intervention and 3-year results on diet and physical activity. Diabetes Care 2003;26:3230–3236 [DOI] [PubMed] [Google Scholar]
  • 75. Pan X-R, Li G-W, Hu Y-H, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: the Da Qing IGT and diabetes study. Diabetes Care 1997;20:537–544 [DOI] [PubMed] [Google Scholar]
  • 76. Ramachandran A, Snehalatha C, Mary S, Mukesh B, Bhaskar AD, Vijay V; Indian Diabetes Prevention Programme (IDPP) . The Indian Diabetes Prevention Programme shows that lifestyle modification and metformin prevent type 2 diabetes in Asian Indian subjects with impaired glucose tolerance (IDPP-1). Diabetologia 2006;49:289–297 [DOI] [PubMed] [Google Scholar]
  • 77. Weber MB, Ranjani H, Staimez LR, et al. The stepwise approach to diabetes prevention: results from the D-CLIP randomized controlled trial. Diabetes Care 2016;39:1760–1767 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 78. Thankappan KR, Sathish T, Tapp RJ, et al. A peer-support lifestyle intervention for preventing type 2 diabetes in India: a cluster-randomized controlled trial of the Kerala Diabetes Prevention Program. PLoS Med 2018;15:e1002575. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 79. Davies MJ, Gray LJ, Troughton J, et al.; Let’s Prevent Diabetes Team . A community based primary prevention programme for type 2 diabetes integrating identification and lifestyle intervention for prevention: the Let's Prevent Diabetes cluster randomised controlled trial. Prev Med 2016;84:48–56 [DOI] [PubMed] [Google Scholar]
  • 80. Saito T, Watanabe M, Nishida J, et al.; Zensharen Study for Prevention of Lifestyle Diseases Group . Lifestyle modification and prevention of type 2 diabetes in overweight Japanese with impaired fasting glucose levels: a randomized controlled trial. Arch Intern Med 2011;171:1352–1360 [DOI] [PubMed] [Google Scholar]
  • 81. Sathish T, Khunti K, Narayan KMV, et al. Effect of conventional lifestyle interventions on type 2 diabetes incidence by glucose-defined prediabetes phenotype: an individual participant data meta-analysis of randomized controlled trials. Diabetes Care 2023;46:1903–1907 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 82. Kooner JS, Saleheen D, Sim X, et al.; DIAGRAM ; MuTHER. Genome-wide association study in individuals of South Asian ancestry identifies six new type 2 diabetes susceptibility loci. Nat Genet 2011;43:984–989 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 83. Tabassum R, Chauhan G, Dwivedi OP, et al.; DIAGRAM ; INDICO. Genome-wide association study for type 2 diabetes in Indians identifies a new susceptibility locus at 2q21. Diabetes 2013;62:977–986 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 84. Saxena R, Saleheen D, Been LF, et al.; DIAGRAM ; MuTHER; AGEN. Genome-wide association study identifies a novel locus contributing to type 2 diabetes susceptibility in Sikhs of Punjabi origin from India. Diabetes 2013;62:1746–1755 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 85. Kim H, Westerman KE, Smith K, et al. High-throughput genetic clustering of type 2 diabetes loci reveals heterogeneous mechanistic pathways of metabolic disease. Diabetologia 2023;66:495–507 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 86. Siddiqui M, Hodgson S, Williamson A, et al. Partitioned polygenic scores highlight role of beta-cell function and unfavourable fat distribution patterns in young onset type 2 diabetes in south Asians. 11 March 2024 [preprint]. Research Square. Accessed 15 July 2024. Available from 10.21203/rs.3.rs-4027509/v1 [DOI]
  • 87. Siddiqui MK, Anjana RM, Dawed AY, et al. Young-onset diabetes in Asian Indians is associated with lower measured and genetically determined beta cell function. Diabetologia 2022;65:973–983 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 88. Mohan V, Radhika G, Sathya RM, Tamil SR, Ganesan A, Sudha V. Dietary carbohydrates, glycaemic load, food groups and newly detected type 2 diabetes among urban Asian Indian population in Chennai, India (Chennai Urban Rural Epidemiology Study 59). Br J Nutr 2009;102:1498–1506 [DOI] [PubMed] [Google Scholar]
  • 89. Bhavadharini B, Mohan V, Dehghan M, et al. White rice intake and incident diabetes: a study of 132,373 participants in 21 countries. Diabetes Care 2020;43:2643–2650 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 90. Mohan V, Gokulakrishnan K, Deepa R, Shanthirani CS, Datta M. Association of physical inactivity with components of metabolic syndrome and coronary artery disease--the Chennai Urban Population Study (CUPS no. 15). Diabet Med 2005;22:1206–1211 [DOI] [PubMed] [Google Scholar]
  • 91. Anjana RM, Sudha V, Nair DH, et al. Diabetes in Asian Indians-how much is preventable? Ten-year follow-up of the Chennai Urban Rural Epidemiology Study (CURES-142). Diabetes Res Clin Pract 2015;109:253–261 [DOI] [PubMed] [Google Scholar]
  • 92. Anjana RM, Srinivasan S, Sudha V, et al.; ICMR-INDIAB Collaborative Study Group . Macronutrient recommendations for remission and prevention of diabetes in Asian Indians based on a data-driven optimization model: the ICMR-INDIAB national study. Diabetes Care 2022;45:2883–2891 [DOI] [PubMed] [Google Scholar]
  • 93. Mandal S, Jaganathan S, Kondal D, et al. PM2.5 exposure, glycemic markers and incidence of type 2 diabetes in two large Indian cities. BMJ Open Diabetes Res Care 2023;11:e003333. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 94. Mohan V, Tiwaskar M, Unnikrishnan R. Air pollution: a new cause of type 2 diabetes? J Assoc Physicians India 2024;72:11–12 [DOI] [PubMed] [Google Scholar]
  • 95. Forouhi NG, Misra A, Mohan V, Taylor R, Yancy W. Dietary and nutritional approaches for prevention and management of type 2 diabetes. BMJ 2018;361:k2234. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 96. Misra A, Alappan NK, Vikram NK, et al. Effect of supervised progressive resistance-exercise training protocol on insulin sensitivity, glycemia, lipids, and body composition in Asian Indians with type 2 diabetes. Diabetes Care 2008;31:1282–1287 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 97. Mohan V, Yang W, Son H-Y, et al. Efficacy and safety of sitagliptin in the treatment of patients with type 2 diabetes in China, India, and Korea. Diabetes Res Clin Pract 2009;83:106–116 [DOI] [PubMed] [Google Scholar]
  • 98. Gan S, Dawed AY, Donnelly LA, et al. Efficacy of modern diabetes treatments DPP-4i, SGLT-2i, and GLP-1RA in White and Asian patients with diabetes: a systematic review and meta-analysis of randomized controlled trials. Diabetes Care 2020;43:1948–1957 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 99. Sivadas A, Sahana S, Jolly B, et al. Landscape of pharmacogenetic variants associated with non-insulin antidiabetic drugs in the Indian population. BMJ Open Diabetes Res Care 2024;12:e003769. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 100. Misra S, Aguilar-Salinas CA, Chikowore T, et al. The case for precision medicine in the prevention, diagnosis, and treatment of cardiometabolic diseases in low-income and middle-income countries. Lancet Diabetes Endocrinol 2023;11:836–847 [DOI] [PubMed] [Google Scholar]
  • 101. Bodhini D, Morton RW, Santhakumar V, et al.; ADA/EASD PMDI . Impact of individual and environmental factors on dietary or lifestyle interventions to prevent type 2 diabetes development: a systematic review. Commun Med (Lond) 2023;3:133. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Diabetes Care are provided here courtesy of American Diabetes Association

RESOURCES