In a recent study published in BMC Medicine, researchers examined associations between a low-inflammatory diet and type 2 diabetes (T2D) risk.
Study: A low-inflammatory diet is associated with a lower incidence of diabetes: role of diabetes-related genetic risk. Image Credit: Chiociolla/Shutterstock.com
Background
Over 7% of the world’s population had diabetes in 2021, and it caused 6.7 million deaths. There is no cure for diabetes; however, lifestyle modifications and a healthy diet can reduce the relative risk of diabetes by 40% to 70%.
Evidence suggests a causal role for low-grade systemic inflammation in chronic conditions, including T2D, and a few studies have reported significant associations between high-inflammatory diets and elevated T2D risk.
However, no study has examined the effect of anti-inflammatory diets on prediabetes-to-diabetes progression. Lifestyle and genetic factors may contribute to T2D. Exploring the gene-diet interactions in T2D development could identify susceptible individuals.
This may also help to determine whether personalized nutrition recommendations could prevent T2D. Moreover, whether adherence to a low-inflammatory diet could reduce the genetic predisposition to T2D remains unknown.
About the study
The present study examined associations between low-inflammatory diets and T2D risk. Participants from the United Kingdom (UK) Biobank were included, and data on their age, sex, socioeconomic status, and education were obtained through questionnaires and interviews.
Glycated hemoglobin (HbA1c) and high-sensitivity C-reactive protein (hsCRP) levels were measured at initial screening.
The Oxford WebQ questionnaire assessed the 24-hour intake of foods and beverages. Individuals were considered prediabetic if the baseline HbA1c ranged between 5.7% and 6.4% and normoglycemic if it was < 5.7%.
The researchers computed a weighted genetic risk score (GRS) to evaluate the effect of genetic risk on T2D. More than 400 T2D-associated risk variants identified in a previous study on Europeans were used to build the GRS.
An inflammatory diet index (IDI) was estimated from the weighted sum of intake of 18 pro-inflammatory and 16 anti-inflammatory food groups. Cox proportional hazards regression was used to calculate hazard ratios and corresponding 95% confidence intervals for T2D incidence by IDI tertiles.
The cumulative effect of genetic background and low-inflammatory diet on T2D risk was assessed, and additive and multiplicative interactions were also examined.
Findings
The study included 142,271 non-diabetic individuals. Of these, 16,068 were prediabetic, and 126,203 were normoglycemic. During a median follow-up of 8.4 years, 3,348 normoglycemic and 2,496 prediabetic individuals developed T2D.
Higher IDI scores were associated with an increased T2D risk in the normoglycemia group, whereas moderate or low IDI was associated with a reduced risk.
In addition, diets with a moderate IDI delayed the onset of T2D by 2.2 years compared to those with a high IDI. In the prediabetes group, IDI was dose-dependently associated with T2D. Each one standard deviation (SD) increment in the IDI was associated with a 5% higher T2D risk.
Consistently, moderate and low IDI scores were associated with a lower T2D risk, delaying T2D onset by 0.71 and 1.11 years, respectively.
Further, there was a higher incidence of T2D among participants with a moderate or high genetic risk for T2D relative to those with a low genetic risk.
Among normoglycemic individuals with low genetic risk, low or moderate IDI was significantly associated with a 74% or 71% reduced T2D risk, respectively, compared to those with high IDI and genetic risk. Besides, moderate or low IDI was associated with 34% or 17% lower T2D risk among those with high genetic risk.
Significant additive and multiplicative interactions existed between IDI and GRS on T2D risk. Among prediabetic individuals with low genetic risk, low IDI was significantly associated with a 51% decrease in T2D risk compared to those with high IDI and genetic risk.
However, additive and multiplicative interactions between IDI and GRS on T2D risk were insignificant. Further, the team found that hsCRP mediated 7.1% of the association between IDI and T2D.
Conclusions
In sum, the findings illustrate that a low IDI was associated with a reduced T2D risk in a dose-dependent manner. Low-inflammatory diets may also delay T2D onset by two years among people with normoglycemia and 1.2 years among those with prediabetes.
Further, low-inflammatory diets may alleviate the risk of genetic factors for T2D development. Notably, participants belonged to white British ancestry, which may limit the generalizability of the findings. The study highlighted that adherence to low-inflammatory diets may contribute to T2D prevention.
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