Physicians' Academy for Cardiovascular Education

Inflammatory potential of diet affects glucose metabolism

Literature - van Woudenbergh et al., Am J Clin Nutr. 2013 - Am J Clin Nutr. 2013 Oct 23


Adapted dietary inflammatory index and its association with a summary score for low-grade inflammation and markers of glucose metabolism: the Cohort study on Diabetes and Atherosclerosis Maastricht (CODAM) and the Hoorn study.

 
van Woudenbergh GJ, Theofylaktopoulou D, Kuijsten A
Am J Clin Nutr. 2013 Oct 23. [Epub ahead of print]
 

Background

Chronic mildly elevated concentrations of circulating proinflammatory markers such as C-reactive protein (CRP), IL-6 and TNF-α have been associated with higher risk of type 2 diabetes [1,2]. Levels of these markers may be negatively influenced by risk factors for diabetes such as being overweight [3], physical inactivity [4] and diet [3]. Certain nutrients assumed to have an anti-inflammatory effect may be associated with a lower risk of diabetes [3,5,6], while proinflammatory markers may be associated with a higher risk [7].
Thus, it is proposed that nutrients may influence markers of glucose metabolism through their effect on chronic low-grade inflammation. Because nutrients are rarely consumed alone, it is important to study effects of overall diet on markers of glucose metabolism. An index has been developed to reflect the inflammatory potential of a diet; the Dietary Inflammatory Index (DII) is obtained by multiplying the weight assigned to both anti- and pro-inflammatory nutrients by their daily intake[8].
This study investigated whether a DII is associated with a low-grade inflammation score and with markers of glucose metabolism. This was studied in two Dutch cohorts: the Cohort study on Diabetes and Atherosclerosis Maastricht (CODAM) and the Hoorn study. An adapted DII (ADII) was obtained by multiplying the dietary inflammatory weight of multiple nutrients by the standardised energy-adjusted intake, to correct for variation in intake due to differences in physical activity, body size and metabolic efficiency. ADII can therefore be seen as a measure for diet quality.
 

Main results

  • An increase of 1 SD in the ADII (i.e. 2.88 units) was associated with a 0.04-unit (95%CI: 0.001-0.07) higher summary score for low-grade inflammation (P=0.01), while the original DII was not associated with the low-grade inflammation score (β=-0.002, 95%CI: -0.03, 0.03).
  • An increment of 1 unit of in the low-grade inflammation summary score was associated with an average 4% (95%CI: 2-6) higher fasting glucose concentration, 9% (95%CI: 4-14) higher postload glucose concentration, 16% (95%CI: 11-22) higher HOMA-IR, and 0.21% (95%CI: 0.13-0.29) higher HbA1c concentration.
  • An increase of 1 SD in the ADII was also associated with 0.9% (95%CI: 0.1-1.7) higher fasting glucose concentration, 2.3% (95%CI: 0.0-4.) higher postload glucose concentration, and 3.5% (95%CI: 0.6-6.3) higher HOMA-IR. ADII was not associated with HbA1c concentration. Associations were attenuated after correction for the low-grade inflammation score, and further adjustment for BMI. The low-grade inflammation score explained a significant proportion of the association between ADII and HOMA-IR and postload glucose.
  • Out of 592 participants who did not have type 2 diabetes at baseline and who had done an oral glucose tolerance test after on average 7.2 years, 99 had developed type 2 diabetes. ADII was not associated with the incidence of type 2 diabetes.
 

Conclusion

An adverse association was seen between the ADII score and the low-grade inflammation summary score, suggesting that the inflammatory potential of a diet indeed affects markers of inflammation. The inflammatory potential of a diet also seems to affect insulin resistance.
Thus, low-grade inflammation appears to be one of the pathways through which diet affects insulin resistance. Further research should shed light on whether low-grade inflammation mediates the association between diet and the development of type 2 diabetes.
 

References

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2. Kolb H, Mandrup-Poulsen T. An immune origin of type 2 diabetes? Diabetologia 2005;48:1038–50.
3. Calder PC, Ahluwalia N, Brouns F, et al. Dietary factors and low-grade inflammation in relation to overweight and obesity. Br J Nutr 2011;106(suppl 3):S5–78.
4. Petersen AM, Pedersen BK. The anti-inflammatory effect of exercise. J Appl Physiol 2005;98:1154–62.
5. Schulze MB, Schulz M, Heidemann C et al. Fiber and magnesium intake and incidence of type 2 diabetes: a prospective study and meta-analysis. Arch Intern Med 2007; 167:956–65.
6. Baliunas DO, Taylor BJ, Irving H, et al. Alcohol as a risk factor for type 2 diabetes: a systematic review and meta-analysis. Diabetes Care 2009;32:2123–32.
7. Kolb H, Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade  inflammation. Diabetologia 2010;53:10–20.
8. Cavicchia PP, Steck SE, Hurley TG, Hussey et al. A new dietary inflammatory index predicts interval changes in serum high-sensitivity C-reactive protein. J Nutr 2009;139:2365–72.
 

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