Diabetes Risk Factors

• Diabetes is rare where traditional lifestyles have persisted but where communities have undergone westernization and urbanization the prevalence of diabetes ranges from 14 to 20%.¹ Lifestyle change has been demonstrated to improve all cardiovascular risk factors.

• Excessive caloric intake is the major driving force behind the escalating obesity and diabetes epidemics worldwide. The combination of excess energy intake and reduced energy output leads to increased obesity and insulin resistance, which results in diabetes.²

• Quality of the diet, particularly the quality of the fats and carbohydrates play an important role in the development of diabetes, independent of body mass index (BMI) and other risk factors.^{2, 3}

• Greater consumption of fiber and polyunsaturated fats are associated with a decreased risk of diabetes, whereas soft drinks, glycemic load, and trans fats are associated with an increased risk of diabetes.^{4, 5}

• Sedentary lifestyle increases the risk of diabetes and conversely increased physical activity decreases the risk of diabetes. Each two hour per day increment of time spent watching television is associated with a 14% increased risk of diabetes, whereas, each two hour increment of standing or walking around at home is associated with a 12% reduced risk.⁶ Brisk walking, one hour per day, is associated with a 34% decreased risk in diabetes.⁶ Thus, the greater the physical activity, the lower the risk of developing diabetes.

• Tobacco use is an underappreciated but important risk factor for diabetes. Compared with non-smokers, cigarette smoking is associated with a 45% increased risk of diabetes independent of other risk factors.⁷ Although smokers are leaner than non-smokers, smoking is associated with abdominal obesity, an established risk factor for metabolic syndrome (MS) and diabetes.^{8, 9}

• Because of a high prevalence, smoking is an important contributor to diabetes in men in India, China, and other Asian countries. An estimated 50-60% of adult males in India are regular smokers and is expected to increase rather than decrease as multinational tobacco companies shift their focus to developing countries.

• One in three cigarettes manufactured is consumed in China, who currently holds the official world record for the number of diabetic subjects.¹⁰ India is the second largest producer and consumer of tobacco worldwide and may indeed be the country with the highest number of diabetics if the 20% prevalence in urban South India is confirmed in other parts of urban India.^{11, 12}

• In India many use smokeless tobacco products such as betel quid, and 40% smoke bidis which is less than half the size of cigarettes but may contain more nicotine and other harmful products. The consumption of bidis is likely to remain high because it is non-taxable and provides employment for a large number of the urban poor.

• Reducing high consumption of high smoking rates in developing countries should be a key public objective to prevent and control the global diabetes epidemic and its complications.^{2, 13}

• Light to moderate alcohol consumption (1-2 drinks per day) is associated with a 30-40% reduced risk of diabetes in a meta-analysis of 370,000 subjects with a 12 year follow-up.¹⁴  Heavy consumption is associated with harm rather than benefit. However, no benefit of alcohol consumption has been shown among studies in Indians.

• Both fetal undernutrition (low birth weight) and overnutrition (baby of a diabetic mother) are associated with a future risk of diabetes.¹⁵

• Although many experts have blamed the thrifty genotype, (mismatch between ancestral genes and modern environments), such a gene has so far remained elusive.¹⁶ However, a thrifty phenotype offers a better explanation for the epidemic of diabetes in developing countries. This hypothesis postulates a mismatch between intrauterine and adult life environments. According to this hypothesis, adaptations in response to fetal undernutrition lead to metabolic and structural changes (e.g. decreased beta cell mass and function and increased insulin resistance) that are beneficial for early survival, but may increase the risk of chronic diseases, such as diabetes, in adulthood.

• The risks of adverse long term consequences are likely to be exacerbated in a nutrition rich environment later in life. This might explain early life origins of insulin resistance and diabetes in India.^{2, 17, 18} For example, fetal undernutrition was associated with a 2-fold risk of diabetes which increased to an 8-fold risk among those who are exposed to overnutrition in adult life.¹⁹

• Like coronary artery disease (CAD), diabetes is a product of interplay of genetics and environmental factors. Although 40 genetic loci has been associated with diabetes, these loci confer only a modest effect size and do not add to the clinical prediction of diabetes beyond traditional risk factors such as obesity, physical inactivity, unhealthy diet, tobacco use, and family history of diabetes.²

• It appears that adverse effects of fast foods and western diets are enhanced in people with greater genetic susceptibility.  Conversely, those who are genetically predisposed to diabetes by virtue of family history may prevent or delay the development of diabetes by appropriate diet and lifestyle measures.²

• Accumulating evidence strongly indicates that a vast majority of diabetes can be prevented through diet and lifestyle modifications.² Eating a heart healthy diet of appropriate caloric content, and initiating and maintaining a regular program of physical activity, remain as a cornerstone approach to maintaining optimal weight in healthy individuals, lose weight in overweight persons, and prevent the development of diabetes in the later years of life. ²⁰

Sources

1. International Diabetes Federation. Diabetes Atlas, Fourth  Edition  Brussels  2009.

2. Hu FB. Globalization of Diabetes: The role of diet, lifestyle, and genes. Diabetes Care. Jun 2011;34(6):1249-1257.

3. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med. 2001;345(11):790-797.

4. de Munter JS, Hu FB, Spiegelman D, Franz M, van Dam RM. Whole grain, bran, and germ intake and risk of type 2 diabetes: a prospective cohort study and systematic review. PLoS Med. Aug 2007;4(8):e261.

5. Malik VS, Popkin BM, Bray GA, Despres JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care. Nov 2010;33(11):2477-2483.

6. Hu FB, Li TY, Colditz GA, Willett WC, Manson JE. Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women. Jama. Apr 9 2003;289(14):1785-1791.

7. Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz J. Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis. Jama. Dec 12 2007;298(22):2654-2664.

8. Barrett-Connor E, Khaw KT. Cigarette smoking and increased central adiposity. Annals of internal medicine. Nov 15 1989;111(10):783-787.

9. Shimokata H, Muller DC, Andres R. Studies in the distribution of body fat. III. Effects of cigarette smoking. JAMA. Feb 24 1989;261(8):1169-1173.

10. Chan JC, Malik V, Jia W, et al. Diabetes in Asia: epidemiology, risk factors, and pathophysiology. JAMA. May 27 2009;301(20):2129-2140.

11. Ramachandran A, Ma RC, Snehalatha C. Diabetes in Asia. Lancet. Jan 30 2010;375(9712):408-418.

12. Ramachandran A, Mary S, Yamuna A, Murugesan N, Snehalatha C. High prevalence of diabetes and cardiovascular risk factors associated with urbanization in India. Diabetes Care. May 2008;31(5):893-898.

13. Kabir Z, Clancy L, Connolly GN. Tobacco control efforts: where is India now? Lancet. Jul 14 2007;370(9582):134.

14. Koppes LL, Dekker JM, Hendriks HF, Bouter LM, Heine RJ. Meta-analysis of the relationship between alcohol consumption and coronary heart disease and mortality in type 2 diabetic patients. Diabetologia. Apr 2006;49(4):648-652.

15. Yajnik CS. Nutrient-mediated teratogenesis and fuel-mediated teratogenesis: two pathways of intrauterine programming of diabetes. Int J Gynaecol Obstet. Mar 2009;104 Suppl 1:S27-31.

16. Neel JV. Diabetes mellitus:  a “thrifty genotype rendered detrimental by “progress”  1962. Am Hum Genet. 1962;14:353 – 362.

17. Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5-20.

18. Gluckman PD, Hanson MA, Bateson P, et al. Towards a new developmental synthesis: adaptive developmental plasticity and human disease. Lancet. May 9 2009;373(9675):1654-1657.

19. Li Y, He Y, Qi L, et al. Exposure to the Chinese famine in early life and the risk of hyperglycemia and type 2 diabetes in adulthood. Diabetes. Oct 2010;59(10):2400-2406.

20. Balducci S, Zanuso S, Nicolucci A, et al. Effect of an intensive exercise intervention strategy on modifiable cardiovascular risk factors in subjects with type 2 diabetes mellitus: a randomized controlled trial: the Italian Diabetes and Exercise Study (IDES). Arch Intern Med. Nov 8 2010;170(20):1794-1803.