Starvation Sickness: How Famine Fuels Type II Diabetes Onset

By: Meena Seshadri

In the United States, the health of the global south is often treated as a one-dimensional issue. We look down upon countries with high rates of non-communicable diseases, seeing it as a personal failure of those in the population.

We often fail to recognize all the factors which determine health, repeatedly pointing to poor lifestyle choices while completely overlooking social determinants of health.

The historical presence of violence, colonization, famine, among other forms of subjugation, have lasting impacts that must be considered when addressing the health of certain populations.

Type II diabetes mellitus, or T2D, is the most common form of diabetes mellitus and is responsible for over 90% of worldwide diabetes. Type II diabetes is a chronic illness where those afflicted are unable to process sugar correctly due to improper insulin function. The onset of T2D is caused by a combination of both genetic and environmental factors and can lead to numerous adverse health effects, including cardiovascular disease, neuropathy, and nephropathy, among other complications (Wu et. al., 2014).

Famine is a prolonged shortage of food that leads to mass starvation and can be caused by a multitude of factors including environmental, social, and political (Devereux 2000). While famines can lead to mass mortality, they can also affect the health of populations by leading to a decrease in fertility, an increase in exposure to new disease vectors, and an increase in predisposition to metabolic diseases, such as type II diabetes (Devereux 2000; van Abeelen et. al. 2012).

Beyond momentarily increasing health risks, long-term famine can cause lifelong and even generational health detriments in populations.

Subjection to prolonged starvation, specifically prenatal exposure to famine, is shown to increase the risk of adult obesity and type II diabetes onset, as improper fetal nutrition can lead to ongoing epigenetic changes in body composition as well as endocrine and metabolic responses (Fernandez-Twinn et. al. 2019; Fall et. al. 2019; Vaiserman 2017). Such alterations in tissue structure and metabolism can lead to an increased risk of cardio-metabolic diseases, such as T2D (Fall et. al. 2019). Beyond lifelong implications, exposure to famine has also been proven to lead to metabolic alterations and chronic hyperglycemia in successive generations (Li 2016). Such genetic predisposition to T2D due to personal or familial exposure to famine continues to have lasting effects on many populations worldwide, including in India and Ukraine.

With its ever-increasing rate of type II diabetes, India has become a world “diabetes capital”, with over 100 million in the population estimated to be afflicted (Anjana et. al. 2023; Wells 2016). Many research articles have attributed this to the high type II diabetes prevalence on the “thrifty genotype” hypothesis, in which ancestral exposure to famine has influenced differences in metabolism, which has then caused differing risk of diabetes in varying populations (Wells 2016). Ancestral exposure to famine in the Asian Indian population has led to the evolution of increased fat storage as a survival mechanism against starvation (Ramachandran 2004). While increased fat storage served as a beneficial protective mechanism during famine periods, the evolved trait is no longer critical for survival and can lead to increased proneness to obesity and type II diabetes in the current environment, where food is plentiful (Ramachandran 2004). Also current is the ongoing genetic predisposition to low birth weight in the Indian population (Wells 2016). Proneness to low birth weight can lead to a low metabolic capacity, which can cause increased blood sugar and a higher risk of developing type II diabetes (Qi 2019; Wells 2016). Low birth weight can also result in low lean mass, meaning the Indian population has a greater fat mass to lean mass ratio than their European counterparts (Narayan et. al. 2020; Wells 2016).  Additionally, Indians have a greater metabolic sensitivity to adipose tissue, meaning for a set level of insulin resistance, Indians require a smaller amount of fat and a lower BMI (Wells 2016). Such hereditary predispositions combined with the lifestyle changes stemming from urbanization, including overeating and lack of physical activity, have influenced the continually rising prevalence of diabetes in the Indian population (Ramachandran 2004). To address the T2D crisis in India, a number of social programs have been implemented to improve education and resources on the subject, including the National Diabetes Control Program and the National Program for Prevention and Control of Diabetes, Cardiovascular Disease, and Stroke (Kumar et. al. 2013).

Figure 1: Heat map of mean birth weight globally using data collected by the World Health Organization (Wells et. al. 2016).

Figure 2: Schematic diagram demonstrating diabetes risk between European phenotype and Indian phenotype. Shaded cylinder represents metabolic capacity while unshaded cylinder represents metabolic load. Despite Europeans and Indians having similar metabolic loads, Indians have a much smaller metabolic capacity, leading to an increased risk of type II diabetes (Wells et. al., 2016).

A lesser known world diabetes center is Ukraine, with two million people in the population being afflicted. The high presence of T2D in Ukraine is largely blamed on the Great Ukranian Famine of 1933–a years-long, man-made famine enforced by the Soviet Union. The effects of the famine were brutal, with over 5 million deaths as well as life-long, and in some cases, generational metabolic damage (Vaiserman 2013). Such shifts in population-wide metabolic damage are evidenced by the Ukrainian type II diabetes trends, which are consistent with the famine patterns (Vaiserman 2013). The Ukrainian famine was most drastic during April to July of 1933, and was part of a more widespread Soviet famine that spanned from 1931 to 1934 (Vaiserman 2013). The trend in famine severity is reflected by the prevalence rate of T2D in the Ukrainian population, as those born in the first half of 1934 were most likely to develop type II diabetes, which aligns with the poor pre-natal nutrition that would have been the case during the worst of the famine (Vaiserman 2013). The role of famine in determining type II diabetes prevalence in the Ukrainian population has been verified, as the rate of type II diabetes is much lower in non-afflicted placed during this time frame (Vaiserman 2013). Similar findings have been proven for various other famine-affected countries. .

Figure 3: Type II diabetes prevalence in various Eastern Ukrainian regions exposed to 1933 famine by birth month (Vaiserman 2013).

Type II diabetes is a complex chronic illness whose onset is dependent on a complicated combination of heritable and environmental factors, with no one component being completely responsible for one’s affliction. Many people, including healthcare providers, are quick to characterize groups as unhealthy without first understanding the historical and medical contexts which influence populations’ afflictions. Rather than making broad generalizations about groups of people, we should instead work to understand the risk factors and predispositions in certain populations so that we can better prevent, diagnose, and treat type II diabetes.

References

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Images:

Vaiserman, Alexander M., Khalangot, M. D., Strele, I., & Lumey, L. H. (2013). Early-Life Exposure to the Ukraine Famine of 1933 and Type 2 Diabetes in Adulthood. In Early life nutrition, and Adult Health, and development: Lessons from changing dietary patterns, famines, and experimental studies (pp. 145–160). essay, Nova Biomedical. 

Wells, J. C., Pomeroy, E., Walimbe, S. R., Popkin, B. M., & Yajnik, C. S. (2016). The Elevated Susceptibility to Diabetes in India: An Evolutionary Perspective. Frontiers in Public Health, 4. https://doi.org/10.3389/fpubh.2016.00145