Getting to the Heart of it: 

While administrative and documented accounts are able to provide some insight into the evolution of foodways, it is argued that oral histories serve as equally important accounts of sociocultural transitions2. In interviews with women farmers that form the basis of the cited article1, the researchers found that ragi was typical in local diets even in the 1960s and 1970s. Only in the last three decades has rice, and wheat, made substantial inroads among traditionally millet-eating households. This development is owed in part to economic policies introduced by the Indian government to curb malnutrition through the implementation of a system called the Public Distribution System (PDS), involving the distribution of rice, sugar, milk, oil, amongst other food resources as rations. The women interviewed in this study also described how they would prepare delicious, fragrant millet-based “rice” dishes from millets such as arka (kodo millet), saame (little millet) and navne (foxtail millet). A reduction in the cultivation of several whole grain crops and diverse varieties of rice has largely been attributed to a series of predominantly technological changes to the agriculture sector beginning in the 1960s termed the Green Revolution, which will be explored further in the next article of this series.

The consequences of dietary shifts, old and new, and evolving foodways

Dietary shifts in food consumption in South Asia, especially the more recent shifts (in the last 50 years) to highly processed and calorie-heavy diets3 (Figure 2), are likely to have had significant physiological consequences, the most obvious one being perhaps the effect of carbohydrate-heavy diets on blood sugar levels. The glycemic index (GI) of a food, or its ability to affect blood sugar levels, has been shown to impact blood glucose, serum cholesterol and triglyceride levels, all risk factors that are typically preconditions for CVD. Studies investigating the role of diet in cardiovascular risk have extensively shown that high-GI food consumption is associated with CVD4. Millets and other unpolished whole grain foods are known to have lower glycemic scores than the varieties of polished rice and wheat that are widely consumed. It is possible that the increased consumption of sugar, rice and wheat compared to traditional, largely seasonal grains and staple foods, along with high fat diets, has impacted the risk of developing CVD. It is of note that rice, wheat flour, sugar and oil are amongst the most important foods distributed as a part of government food-based social safety net programs to support poor households and aid nutrition in different parts of South Asia. In the previous article of this series, it was mentioned that CVD disproportionately affects low- and middle-income countries. Appallingly, half the population of South Asia is unable to afford a healthy diet that meets the needs for health and well-being5. While there is likely an association between poor trends in nutrition and a predisposition to CVD, it is difficult to pinpoint precise causative factors due to the complex nature of this problem. Instead, a general picture of the problem can be formed taking into consideration the region’s history and cultural evolution. 

The Barker hypothesis and the history underlying the biology of CVD

In the final section of this article, the focus is shifted to a biological basis for predisposition to CVD. In a study focused on understanding disease susceptibility developed in the 1980s, researchers David Barker and C. Osmond postulated that maternal nutritional status during gestation is a predictor of heart disease risk later in life6. The central tenet of the Barker hypothesis is that environmental exposures encountered during stages of fetal development and early infancy can induce permanent physiological changes. In biology, epigenetics is the study of how environmental factors can alter and modulate genetics. A more modern interpretation of the Barker hypothesis deals with the concept of “metabolic memory”, suggesting that adverse early life events like maternal obesity could in theory modify the fetal epigenome and form metabolic memories that propagate through generations. The rationale for Barker’s work on this topic was the peculiar observation that though CVD rates increase with increasing economic prosperity in most countries, CVD disproportionately affects the poorer residents of these countries7. 

Building on later studies, Barker developed the hypothesis that low birth weight was linked to cardiovascular risk in adulthood8. It is known that South Asian countries bear a disproportionately high burden of low birth weight and estimates suggest that approximately one in four newborns in South Asia weighs less than 2.5 kg (5.5 lbs) at birth, with India alone accounting for over 30 percent of the global total9. The “thrifty phenotype hypothesis” raises the possibility that a fetus, when facing poor nutritional conditions, makes adaptations to conserve energy and maximize survival in conditions perceived to be nutrient-deficient. These adaptations could include changes in insulin sensitivity, altered fat deposition and hormonal changes. While these adaptations could be advantageous in nutritionally scarce environments, they become maladaptive if individuals subsequently encounter nutritional abundance10. This mismatch is thought to increase the risk of developing metabolic disorders like type 2 diabetes, obesity, and consequently, CVD, and quite strongly resonates with the recent history of many South Asian nations. As mentioned before, these countries have had rapid socioeconomic development and nutritional transition, shifting away from traditional diets towards increased consumption of refined carbohydrates, fats, and processed foods. This rapid shift creates the precise conditions predicted by the thrifty phenotype hypothesis to increase the risk of developing CVD.

To fully recognize the potential impacts of changes in nutrition on South Asian populations, it is essential to consider the period of British colonial rule and expansion into South Asia, spanning roughly two centuries. This period was riddled with severe and widespread famine, as mentioned in the previous article. Historical accounts point to an increase in the frequency and scale of devastating famines during the 18th, 19th, and early 20th centuries under the British empire11. These historical accounts implicate colonial administrative policies in the severity of disease and mortalities linked to these famines12. The colonial regime emphasized the cultivation of cash crops for export over seasonal and sustainable food grains, high land revenue demands that impoverished peasants, and demanded the continued export of grain from regions experiencing famine. These policies prioritized imperial economic concerns and wartime logistics over saving lives and there was undeniably repeated exposure of vast sections of the South Asian population to extreme nutritional deprivation during the colonial era.

The historical context of large-scale famines under colonial rule provides a plausible scenario for environmental exposures capable of inducing potentially heritable epigenetic modifications relevant to metabolic and cardiovascular health in South Asian populations. This perspective shifts the focus from factors like low birth weight, or other cardiovascular risk factors, in isolation, to consider the possibility of a deeper, historically imprinted biological vulnerability within the population. The epigenetic legacy of the thrifty phenotype could make South Asians particularly vulnerable to CVD when faced with modern nutritional environments and lifestyles. In the next article of this series, South Asian predisposition to CVD will be explored from the lens of economics and the implementation of social and welfare programs, which influenced nutrition and cultural shifts.

1acaste – a term that has a deep-rooted meaning within Indian society, broadly referring to the division of society into distinct groups each with their own roles or exclusive privileges, which has historically been used to facilitate the systemic and oftentimes violent exploitation of large sections of society by the perceived “upper caste” groups.

References

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2. In their own words. Nat. Cell Biol. 7, 533 (2005).

3. IFPRI. South Asia. Global Food Policy Report 2024: Food Systems for Healthy Diets and Nutrition https://gfpr.ifpri.info/2024/05/28/regional-developments-south-asia-4/ (2024).

4. Jenkins, D. J. A. et al. Association of glycaemic index and glycaemic load with type 2 diabetes, cardiovascular disease, cancer, and all-cause mortality: a meta-analysis of mega cohorts of more than 100 000 participants. Lancet Diabetes Endocrinol. 12, 107–118 (2024).

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6. Faa, G. et al. The fascinating theory of fetal programming of adult diseases: A review of the fundamentals of the Barker hypothesis. J. Public Health Res. 13, 22799036241226817 (2024).

7. Schulz, L. C. The Dutch Hunger Winter and the developmental origins of health and disease. Proc. Natl. Acad. Sci. U. S. A. 107, 16757–16758 (2010).

8. de Boo, H. A. & Harding, J. E. The developmental origins of adult disease (Barker) hypothesis. Aust. N. Z. J. Obstet. Gynaecol. 46, 4–14 (2006).

9. Kumaran, K., Osmond, C. & Fall, C. H. D. Early origins of cardiometabolic disease. in Disease Control Priorities, Third Edition (Volume 5): Cardiovascular, Respiratory, and Related Disorders 37–55 (The World Bank, 2017).

10. Fall, C. H. D. & Sachdev, H. S. Developmental origins of health and disease: implications for developing countries. in Developmental Origins of Health and Disease (eds. Gluckman, P. & Hanson, M.) 456–471 (Cambridge University Press, Cambridge, 2006).

11. Satish, S. Famines in Colonial India. ClearIAS https://www.clearias.com/famines-in-colonial-india/ (2023).

12. Sharma, J. & Lambert-Hurley, S. Introduction: Forgotten food histories of south Asia. Glob. Food Hist. 9, 95–106 (2023).