PROGRESSION from prediabetes to diabetes could be influenced by the inflammatory index of an individual’s diet, according to novel research evaluating the association between Type 2 diabetes (T2D) risk and low-inflammatory diets.
The study included a total of 142,271 individuals who were not diabetic from the UK Biobank, of whom 126,203 were classified as normoglycaemic (baseline haemoglobin A1c: <5.7%), and 16,068 were classified as prediabetic (baseline haemoglobin A1c: 5.7–6.4%). The Oxford WebQ questionnaire was used to assess 24-hour food and drink intake and an inflammatory diet index (IDI) was calculated by estimating the weighted sum of intake for 16 anti-inflammatory and 18 pro-inflammatory food groups. The effect of genetic risk on T2D was evaluated through use of a computed weighted genetic risk score.
During the follow-up period (median 8.4 years), 3,348 and 2,496 individuals with normoglycaemia and prediabetes, respectively, subsequently developed T2D. Those with moderate or high T2D genetic risk were more likely to develop T2D than those with a low genetic risk.
Further findings revealed that a higher IDI was associated with increased risk for T2D in participants with normoglycaemia. Conversely, a moderate or low IDI was associated with a reduced T2D risk. For those with prediabetes, a dose-dependent association was seen between IDI and T2D risk, with a 5% increased T2D risk for each standard deviation increment in IDI. Additionally, lower T2D risk and a delay in T2D onset by 0.71 and 1.11 years were seen with moderate and low IDI scores, respectively.
In those with normoglycaemia and a low genetic risk, low and moderate IDIs were associated with significantly reduced risk of developing T2D (74% and 71%, respectively). The contrary was true for those with a high IDI and high genetic risk. Furthermore, for those with normoglycaemia and a high genetic risk, moderate or low IDIs were associated with reductions in T2D risk of 34% and 17%, respectively. Similarly, in those with prediabetes and a low genetic risk, low IDI was found to be associated with significantly reduced T2D risk (51%) compared to those with a high IDI and high genetic risk.
The authors noted generalisability as a limitation of the study, as participants were of White British ancestry. They concluded that the study highlights a dose-dependent association between low IDI and reduced T2D risk. Diets with a low IDI may delay onset of T2D in individuals with normoglycaemia and prediabetes, and low IDI diets could lessen the impact of genetic risk.
