Diabetes UK, a leading charity in the UK, recently announced that by 2030, 1 in 10 people in the United Kingdom (UK) would have type 2 diabetes if the government didn’t invest in prevention services. 

Sadly, this isn’t just a UK problem. Type 2 diabetes is spiralling out of control worldwide, affecting low- and middle-income countries more frequently than high-income countries. This finding is reflected in the UK as Africans, Caribbeans, and South Asians, are more affected with type 2 diabetes than Caucasians. 

The question is, why? 

There is no clear-cut answer just yet. But the reason Africans, Caribbeans, and South Asians are more affected with type 2 diabetes may be due to genetic, environmental, social and lifestyle factors.

This article explores the genetic and social factors contributing to the higher incidence of type 2 diabetes in Africans, Caribbeans and South Asians. 

Genetic Factors

In the 1970s, Anders Forsdahl, a Norwegian epidemiologist, found a link between socioeconomic status and a child’s risk of developing various metabolic diseases later in life (Forsdahl, 1977). His work suggested that poverty increased the risk of metabolic disease. But while intriguing, his discovery wasn’t comprehensive enough to convince all scientists.  

Another epidemiologist, David Barker, proposed in 1990 that stunted growth in the womb, low birth weight and premature birth were related to hypertension, type 2 diabetes, and cardiovascular disease (CVD) in adulthood (Barker, 1990). Later in the early 1990s, Barker and another scientist, Hales, conducted more research that put Forsdahl’s finding into context and found direct evidence for Barker’s theory. 

Hales and Barker found that children born with low birth weights in the UK were more likely to develop diabetes, hypertension, elevated lipids, and insulin resistance later in life (Hales and Barker, 1992; Barker et al., 1993). Shortly after, similar findings were observed in Pima Indians, Swedes and many other populations globally (Lithell et al., 1996; McCance et al., 1994). More recent studies have also confirmed these findings (Donghua et al., 2017).

After further analysis, experts reached a consensus. They theorised that a foetus’s nutrition while in its mother’s womb might predetermine its risk of several metabolic diseases, including type 2 diabetes and CVD risk in adulthood (Lakshmy, 2013). 

That said, not all children with low birth weights are destined for metabolic dysfunction in adulthood. Studies show that children who gain weight at an appropriate rate relative to their birth weight don’t have a raised risk. 

Conversely, children who experience catch-up growth – small at birth but have an average or above-average body weight from age seven – have a high risk of CVD, insulin resistance and obesity (Levy-Marchal and Czernichow, 2006).

One explanation for this increased risk is the ‘thrifty gene hypothesis’ (Vaag et al., 2012). The theory suggests that undernourishment during pregnancy alters gene expression in children, making them insulin resistant at birth.

In a famine-like environment, insulin resistance is useful because it increases survival chances by encouraging their bodies to absorb and store energy faster. In an environment of excess, such as the Western world, this trait is detrimental because these children are likely to become obese. 

Many children in low and middle-income countries are born to mothers with low socioeconomic status who cannot eat nutritious diets while pregnant (Sing et al., 2019; Desyibelew and Dadi, 2019). During pregnancy, these children become undernourished and potentially programmed for insulin resistance, obesity, and type 2 diabetes (Yajnik, 2014). This might partly explain why South Asians, Black Africans and African-Caribbeans are disproportionately affected by type 2 diabetes.  

While this article has focused on undernutrition, please note that overnutrition, especially excess sugar intake during critical periods of pregnancy, is also detrimental to the developing baby; it may promote obesity due to the direct effect of sugar on fat tissue or disrupt signalling between the brain and fat tissues (Goran et al., 2013). 

Social Factors

The incidence and prevalence of type 2 diabetes seem to depend on social factors; a Canadian study showed that individuals with lower income are four-fold more likely to develop diabetes than more advantaged individuals (Dinca-Panaitescu et al., 2011).  

People with lower education in higher-income countries are also up to two-fold more likely to develop diabetes than those with higher education (Hill et al., 2013). However, this association doesn’t seem to be true for Black people (Borrell et al., 2006) and those in low-income countries. In fact, people with high education in low-income countries are more likely than those with low education to develop type 2 diabetes (Seiglie et al., 2020).

Why are individuals with low socioeconomic status in high-income countries more prone to type 2 diabetes?

Individuals with poor socioeconomic status in high-income countries are constantly under pressure to survive, putting them under chronic stress. Stress causes disturbances in the body’s functioning, leading to depression, anxiety, low self-esteem, demotivation, and a lack of energy. 

Altogether, these factors increase the likelihood of self-destructive behaviours and choices such as smoking, heavy drinking, unhealthy eating habits and a lack of exercise. These behaviours can eventually lead to high blood pressure, high cortisol levels, high blood sugar, high blood lipids, obesity, and eventually type 2 diabetes. 

It is no secret that South Asians and people of Black descent in the UK and other high-income countries are more likely to be in poverty than white British people (Institute of Race Relations, 2020; Kyrou et al., 2020), and thus more prone to metabolic disease (Nagar et al., 2021). 

A review of the lifestyle factors that contribute to type 2 diabetes is beyond the scope of this article, but it is crucial to emphasise that unhealthy eating habits and inadequate physical activity are strongly linked to a higher risk of type 2 diabetes. This is because they both promote overweight and obesity and increase the risk of other metabolic disorders such as high blood pressure and blood lipids that increase the risk of type 2 diabetes. 

Now you know some of the genetic and social factors that contribute to the higher rates of type 2 diabetes in African, Caribbean, and South Asian communities. 

While you can’t change your genetics, you can make diet and lifestyle changes within your budget to lower your risk of type 2 diabetes. Start by reducing your intake of processed foods, and increasing your intake of whole, unprocessed foods in appropriate amounts.

No universal approach to improving diet and lifestyle exists; that is why it is crucial to work with a certified professional to improve your eating habits, especially if you’ve found it difficult to change on your own.  

Need help? You can download my free guide with ten tips for improving your eating habits HERE. 

REFERENCES

1. Forsdahl, A. (1977) Are poor living conditions in childhood and adolescence an important risk factor for arteriosclerotic heart disease? British Journal of Preventive and Social Medicine, 31(2): 91–95.
2. Barker, D.J. (1990) The foetal and infant origins of adult disease. BMJ, 301(6761): 111
3. Hales, C.N., Barker, D.J. (1992) Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologica, 35: 595–601.
4. Barker, D.J., Hales, C.N., Fall, C.H., Osmond, C., Phipps, K., Clark, P.M. (1993) Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologica, 20: 87–93.
5. Lithell, H.O., McKeigue, P.M., Berglund, L., Mohsen, R., Lithell, U.B., Leon, D.A. (1996) Relation of size at birth to non-insulin-dependent diabetes and insulin concentrations in men aged 50–60 years. BMJ, 312(7028): 406–10.
6. McCance, D.R., Pettitt, D.J., Hanson, R.L., Jacobsson, L.T., Knowler, W.C., Bennett, P.H. (1994) Birth weight and non-insulin-dependent diabetes: thrifty genotype, thrifty phenotype, or surviving small baby genotype? BMJ, 308(6934): 942–5. 
7. Donghua, M.I., Fang, H., Zhao, Y., Zhong, L. (2017) Birthweight and type 2 diabetes: a meta-analysis. Experimental and Therapeutic Medicine, 14)6): 5313-5320.
8. Lakshmy, R. (2013) Metabolic syndrome: role of maternal undernutrition and fetal programming. Reviews in Endocrine and Metabolic Disorders, 14(3); 229–40.
9. Levy-Marchal, C., Czernichow, P. (2006) Small for gestational age and the metabolic syndrome: Which mechanism is suggested by epidemiological and clinical studies? Hormone Research, 65 (suppl 3): 123–130.
10. Vaag, A.A., Grunnet, L.G., Arora, G.P., Brons, C. (2012) The thrifty phenotype hypothesis revisited. Diabetologia, 55: 2085–2088.
11. Singh, S., Srivastava, S., Upadhyay, A.K. (2019) Socioeconomic inequality in malnutrition among children in India: an analysis of 640 districts from National Family Health Survey (2015–16). International Journal for Equity in Health, 18; 
12. Desyibelew, H.D., Dadi, A.F. (2019) Burden and determinants of malnutrition among pregnant women in Africa: a systematic review and meta-analysis. PLoS One, 14(9): e0221712. 
13. Yajnik, C.S. (2014) Transmission of obesity-adiposity and related disorders from the mother to the baby. Annals of Nutrition and Metabolism, 64(Supp 1): 8–17.
14. Goran, M.I., Dumke, K., Bouret, S.G., Kayser, B., Walker, R.W., Blumberg, B. (2013) The obesogenic effect of high fructose exposure during early development. Nature Reviews Endocrinology, doi:10.1038/nrendo.2013.108.
15. Desai, D., Kandasamy, S., Limbachia, J., Zulyniak, M.A., Ritvo, P., Sherifali, D., Wahi, G., Anand, S.S., and de Souza, R.J. (2021) Studies to improve perinatal health through diet and lifestyle among South Asian women living in Canda: A brief history and future research directions. Nutrients, 13(9): 2932.
16. Dinica-Panaitescu, S., Dinca-Panaitescu, M., Bryant, T., Daiski, I., Pilkington, B., Raphael, D. (2011) Diabetes prevalence and income: results of the Canadian community health survey. Health Policy, 99(2): 116–23.
17. Hill, J., Nielsen, M., Fox, M. (2013) Understanding the social factors that contribute to diabetes: a means to informing health care and social policies for the chronically ill. The Permanente Journal, 17(2): 67–72.
18. Borrell, L.N., Dallo, F.J., White, K. (2006) Education and diabetes in a racially and ethnically diverse population. American Journal of Public Health, 96(9): 1637–1642.
19. Seiglie, J.A., Macrus, M-E., Ebert, C., Prodromidis, N., Geldsetzer, P., Theilmann, M., Agoudavi, K., Andall-Brereton, G., Aryal, K.K., Bicaba, B.W., Bovet, P., Brian, G. et al. (2020) Diabetes prevalence and its relationship with education, wealth and BMI in 20 low-and middle-income countries. Diabetes Care, 43(4): 767–775.
20. Institute of Race Relations. (2020) BME statistics on poverty and housing and employment. Available: https://irr.org.uk/research/statistics/poverty/. Accessed: 14 November 2021.
21. Kyrou, I., Tsigos, C., Mavrogianni, C., Cardon, G., Stappen, V.V., Latomme, J.K. et al. (2020) Sociodemographic and lifestyle-related risk factors for identifying vulnerable groups for type 2 diabetes: a narrative review with emphasis on data from Europe. BMC Endocrine Disorders, 20(1): 134
22. Nagar, S.D., Napoles, A.M., Jordan, I.K., Marino-Ramirez, L. (2021) Socioeconomic deprivation and genetic ancestry interact to modify type 2 diabetes ethnic disparities in the United Kingdom. EClinicalMedicine, 37; https://doi.org/10.1016/jj.eclinm.202.100960.