The role of diet as a risk factor for T2DM

In the past 30 years, six trials investigated the effects of lifestyle interventions on the development of type 2 diabetes in people with impaired glucose tolerance (IGT), which is a pre-stage of diabetes (see ‘Criteria for diagnosis of DM, IFG, IGT’). A total of 5,496 people were included in these trials and initially followed up for 3 to 6 years. In all trials the effects of a lifestyle intervention, that included a combination of healthy eating and increased physical exercise, were compared with no intervention or usual care.

The dietary interventions in all studies were similar and overall contained the following recommendations: decreased intake of total energy (kcal), total fat, saturated fat, refined sugar and simple carbohydrates and increased intake of unsaturated fat and fiber. In addition, increased intakes of vegetables, fruits and moderate intake of alcohol were recommended. Conclusively all trials showed that, compared to no intervention or usual care, intensive lifestyle interventions reduced the development of diabetes. The Malmö Study[1] and Da Qing IGT and Diabetes Study[2] both showed that compared to no intervention, healthy eating and increased physical exercise lowered the risk of developing diabetes after 6 years with 63% and 42% respectively. Besides the combined lifestyle intervention the Da Qing study also included a group that received only dietary intervention. Within this group the diabetes risk was also lowered with 31%. Three other studies (Diabetes Prevention Programme[3]; Finnish Diabetes Prevention Study[4] and SLIM study[5]) with a follow up of approximately 3 years all showed a reduced diabetes risk of 58% in the lifestyle intervention group compared to usual care. Besides, the lifestyle intervention in the DPP showed to be more effective than intervention with metformin (39%)3. Similarly, after a follow up of 3 years the intervention group in the Indian Diabetes Prevention Programme had a reduced diabetes risk of 29%, which was also higher than the metformin group (26%)[6]. Extended follow-up of the Da Qing Study[7], Diabetes Prevention Programme[8] and Finnish Diabetes Prevention Study[9] was performed. The conclusion of these trials was that after 10 to 14 years (from the start of the intervention) the diabetes risk was reduced by 34 to 43% compared to the control group.

It is not entirely clear yet what exactly causes the observed reduction in diabetes risk. Several investigators suggest it is caused by the weight loss, which in its turn is caused by the lifestyle interventions. For instance, in the Diabetes Prevention Programme each kg of body weight loss was associated with a 16% lower diabetes risk after 3 years of follow up. However, the average reported weight loss in all trials ranged from 1 to 6 kg and the reduction only sustained for a short period of time. After one year body weight increased and after 10 to 14 years average body weight in the intervention groups was practically back to the initial weight, whereas the reduced diabetes risk remained. This suggests that other factors than body weight loss may also be responsible for the reduced risk after lifestyle interventions, such as change in body composition, blood pressure or increased insulin sensitivity. But this warrants further investigation. Besides ambiguity about the underlying mechanisms, it is unclear how independent the role of diet is in the development of diabetes type 2. All dietary interventions contained recommendations on macronutrient compositions rather than specific foods, which leads to the question which foods may affect the development of type 2 diabetes. Many observational studies have investigated the associations between specific foods and diabetes occurrence. Although well conducted trials give best evidence on causes of disease, observational studies can generate new hypotheses for potential dietary factors that are important in the risk development of diabetes.

Processed (and red meat) is one of the foods that is associated with a higher diabetes type 2 risk in observational studies. A meta-analysis of 21 prospective cohort studies showed that each additional intake of 50 grams of processed meat increased the type 2 diabetes risk with 32%[10]. The same article showed based on 14 cohort studies that total red meat intake was associated with a 13% higher risk. Another type of food that may be associated with an increased risk of type 2 diabetes is sugar-sweetened beverages (SSB). A meta-analysis of 11 studies of 310,819 people showed that consumption of 1 to 2 servings of SSB per day was related to a 26% higher risk of diabetes compared to less than 1 serving a month[11]. A large European study confirmed a 22% higher diabetes risk for each additional SSB intake of 336 grams[12]. Besides foods of which higher consumption may increase the risk of diabetes, several foods were associated with a lower risk in observational studies, including coffee, dairy, whole grains, and green leafy vegetables. To illustrate, each additional intake of 2 cups of coffee per day was associated with a lower diabetes risk of 12% in a meta-analysis of 22 studies[13]. Similar risk reductions were observed in another meta-analysis of 32 studies[14], which additionally found a lower diabetes risk for higher intake of decaffeinated coffee. A meta-analysis in 457,893 people showed that dairy intake of 200 grams a day reduced the type 2 diabetes risk with 6%[15] and with regard to whole grains a meta-analysis of 10 studies showed a 32% decreased risk for an intake of three servings a day[16]. Also, a recent meta-analysis, that found no association between total intake of fruits or vegetables and diabetes, showed that 1.35 servings/ day of green leafy vegetables, compared to 0.2 servings/ day was associated with a 14% lower risk of diabetes[17]. A modest alcohol consumption (22 to 26 g/day for women and men respectively) was related to a lower diabetes risk compared to no alcohol consumption[18]. However, high intake of alcohol was related to an increased risk and caution should be taken with recommendations for alcohol consumption, because of other known adverse health effects. A nutrient which has been associated with diabetes risk is vitamin D. A meta-analysis of 18 prospective studies in 210,107 subjects showed that compared to lower intakes, high intake of vitamin D was associated to a 19% lower diabetes type 2 risk[19].

Even though the consumption of individual foods has been associated with diabetes occurrence, foods are always consumed in combination and therefore it may be more important to identify which specific dietary pattern is most beneficial in diabetes prevention. Dietary patterns that were found to be related to a lower diabetes type 2 risk are high in fruits, vegetables, whole grains, fish and poultry and low in red meat, processed foods, sugar-sweetened beverages, starchy foods and high-fat dairy[20][21]. Particularly the role of the Mediterranean diet in diabetes development is evaluated. A recent meta-analysis in 136,846 subjects from 10 observational cohort studies showed that the risk of developing diabetes was 23% lower in subjects with the highest adherence to the Mediterranean diet, as compared to subjects with the lowest adherence. Also, the PREDIMED trial showed that compared to subjects in a low-fat control group, the subjects in two Mediterranean diet groups had an 18 to 40% lower risk of diabetes type 2 after a median of 4.1 years of follow up[22]. Other dietary patterns that showed associations with lower diabetes risk, are the Prudent diet and the DASH diet, whereas the Western diet most likely increases the diabetes risk[23].

Click to see PDF of Table - Characteristics of trials that investigated the effect of lifestyle interventions on the occurrence of type 2 diabetes in people with impaired glucose tolerance.


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  2. ^ Pan XR, Li GW, Hu YH, Wang JX, Yang WY, et al. (1997) Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 20: 537-544.

  3. ^ Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, et al. (2002) Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 346: 393-403.

  4. ^ Lindstrom J, Eriksson JG, Valle TT, Aunola S, Cepaitis Z, et al. (2003) Prevention of diabetes mellitus in subjects with impaired glucose tolerance in the Finnish Diabetes Prevention Study: results from a randomized clinical trial. J Am Soc Nephrol 14: S108-113.

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  6. ^ Ramachandran A, Snehalatha C, Mary S, Mukesh B, Bhaskar AD, et al. (2006) 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 49: 289-297.

  7. ^ Li G, Zhang P, Wang J, Gregg EW, Yang W, et al. (2008) The long-term effect of lifestyle interventions to prevent diabetes in the China Da Qing Diabetes Prevention Study: a 20-year follow-up study. Lancet 371: 1783-1789.

  8. ^ Hamman RF, Wing RR, Edelstein SL, Lachin JM, Bray GA, et al. (2006) Effect of weight loss with lifestyle intervention on risk of diabetes. Diabetes Care 29: 2102-2107.

  9. ^ Lindstrom J, Peltonen M, Eriksson JG, Ilanne-Parikka P, Aunola S, et al. (2013) Improved lifestyle and decreased diabetes risk over 13 years: long-term follow-up of the randomised Finnish Diabetes Prevention Study (DPS). Diabetologia 56: 284-293.

  10. ^ Feskens EJ, Sluik D, van Woudenbergh GJ (2013) Meat consumption, diabetes, and its complications. Curr Diab Rep 13: 298-306.

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

  12. ^ The Interact Consortium (2013) Consumption of sweet beverages and type 2 diabetes incidence in European adults: results from EPIC-InterAct. Diabetologia 56: 1520-1530.

  13. ^ Jiang X, Zhang D, Jiang W (2014) Coffee and caffeine intake and incidence of type 2 diabetes mellitus: a meta-analysis of prospective studies. Eur J Nutr 53: 25-38.

  14. ^ Ding M, Bhupathiraju SN, Chen M, van Dam RM, Hu FB (2014) Caffeinated and decaffeinated coffee consumption and risk of type 2 diabetes: a systematic review and a dose-response meta-analysis. Diabetes Care 37: 569-586.

  15. ^ Gao D, Ning N, Wang C, Wang Y, Li Q, et al. (2013) Dairy products consumption and risk of type 2 diabetes: systematic review and dose-response meta-analysis. PLoS One 8: e73965.

  16. ^ Aune D, Norat T, Romundstad P, Vatten LJ (2013) Whole grain and refined grain consumption and the risk of type 2 diabetes: a systematic review and dose-response meta-analysis of cohort studies. Eur J Epidemiol 28: 845-858.

  17. ^ Carter P, Gray LJ, Troughton J, Khunti K, Davies MJ (2010) Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis. BMJ 341: c4229.

  18. ^ Baliunas DO, Taylor BJ, Irving H, Roerecke M, Patra J, et al. (2009) Alcohol as a risk factor for type 2 diabetes: A systematic review and meta-analysis. Diabetes Care 32: 2123-2132.

  19. ^ Khan H, Kunutsor S, Franco OH, Chowdhury R (2013) Vitamin D, type 2 diabetes and other metabolic outcomes: a systematic review and meta-analysis of prospective studies. Proc Nutr Soc 72: 89-97.

  20. ^ Alhazmi A, Stojanovski E, McEvoy M, Garg ML (2014) The association between dietary patterns and type 2 diabetes: a systematic review and meta-analysis of cohort studies. J Hum Nutr Diet 27: 251-260.

  21. ^ Esposito K, Kastorini CM, Panagiotakos DB, Giugliano D (2010) Prevention of type 2 diabetes by dietary patterns: a systematic review of prospective studies and meta-analysis. Metab Syndr Relat Disord 8: 471-476.

  22. ^ Salas-Salvado J, Bullo M, Estruch R, Ros E, Covas MI, et al. (2014) Prevention of diabetes with Mediterranean diets: a subgroup analysis of a randomized trial. Ann Intern Med 160: 1-10.

  23. ^ Maghsoudi Z, Azadbakht L (2012) How dietary patterns could have a role in prevention, progression, or management of diabetes mellitus? Review on the current evidence. J Res Med Sci 17: 694-709.


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