Scientists have linked protection from diabetes to epigenetic changes

The benefits of a healthy diet for the prevention of type 2 diabetes may vary depending on a person's epigenetic profile, whereas hereditary predisposition, according to the new study, did not change the relationship between diet quality and disease risk. About how epigenetics differs from genetics, how scientists evaluated nutrition and why the results cannot yet be turned into personal diets, see the "Izvestia" material.

Why Nutrition is important for Diabetes prevention

However, the same diet is not always associated with the same reduction in risk in different people. The likelihood of the disease is influenced by age, body weight, physical activity, metabolism, family history, and many genetic variants. The authors of the new study decided to test whether the relationship between diet and diabetes depends separately on hereditary and epigenetic risk.

How does epigenetics differ from genetics?

The genetic risk is related to the DNA sequence that a person receives from their parents. To assess it, the scientists used polygenic scales: they combine the contribution of many common DNA variants, each of which by itself affects the likelihood of the disease only slightly. In addition to the general indicator, the researchers used scales related to individual mechanisms of diabetes, such as the functioning of pancreatic beta cells and liver metabolism.

Epigenetics does not change the DNA text itself. We are talking about chemical tags that help the cell regulate the activity of genes. One of the most studied mechanisms is methylation: methyl groups attach to certain sections of DNA, which can influence how actively a cell uses a nearby genetic instruction. If you compare DNA with a book, the genetic sequence will be its text, and the epigenetic marks will be marks that tell the cell which fragments are more active to read and which are less frequent.

According to the US National Institute for Human Genome Research, the epigenome can change over the course of a lifetime. It can be affected by age, diet, smoking, infections, and other environmental factors. At the same time, the epigenetic label is not necessarily the cause of the disease: it may be a trace of previous effects or metabolic disorders that have already begun.

The authors of the study combined data on methylation in 144 DNA regions into a single indicator, the methylation risk index, or MRS. These areas have previously been associated with the likelihood of type 2 diabetes. The higher the MRS, the higher the subsequent risk of the disease.

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What scientists have found out about the genetic risk

Researchers have not found convincing evidence that hereditary predisposition changes the relationship between nutritional quality and the likelihood of diabetes. In other words, healthier dietary patterns in general were associated with a favorable direction of risk in both people with relatively low and high polygenic indices.

This result does not mean that heredity does not play a role in the development of diabetes. In the study, higher polygenic indices were expected to be associated with a higher likelihood of disease. However, genetic risk did not determine whether a higher-quality diet would be associated with a lower risk. The practical meaning of the conclusion is that unfavorable heredity cannot be considered a reason to abandon general preventive measures.

When comparing participants with the highest and lowest AHEI-2010 scores, the first group had a 27% lower risk of diabetes. This is a relative difference: the risk score was 0.73 with a 95% confidence interval of 0.54 to 0.98. However, with another method of analysis, when all four indexes were considered as continuous scales, there was no statistically significant overall relationship after taking into account the accompanying factors. Therefore, a single figure cannot be perceived as a guaranteed effect for a particular person.

How was epigenetic risk associated with nutrition?

The picture was different for the epigenetic index. Statistical analysis indicated that MRS may change the relationship between diet quality and diabetes risk. Such a signal appeared for the AHEI-2010, Mediterranean and inflammatory indices, however, only the interaction of MRS with AHEI-2010 remained in all additional checks of the stability of the result.

The association of a healthy diet with a lower likelihood of disease looked stronger in participants with low or medium MRS. In the group with a high score, the same clear benefit was not observed. But the authors themselves emphasize that when the three groups were analyzed separately, the differences did not reach statistical significance, and there was no clear sequence of results for the Mediterranean and inflammatory indices.

Therefore, the correct conclusion is not that a healthy diet "does not help" people with high epigenetic risk. The work only suggests that accumulated biological changes can influence the strength of the link between diet and future diabetes. This hypothesis has yet to be tested on larger and more independent samples.

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Which diet was considered healthy

The study did not evaluate a single "healthy" product, but the general pattern of nutrition. A diet with lots of vegetables, fruits, whole grains, legumes, nuts, fish, and vegetable fats received higher scores. Lower scores were associated with frequent consumption of red and processed meat, as well as drinks with added sugar.

The authors note that such a diet structure can support tissue sensitivity to insulin and normal glucose metabolism, affect the intestinal microbiota, and reduce inflammation and oxidative stress. However, the study was observational: participants were not assigned a specific menu or randomly assigned to groups. Therefore, it shows statistical relationships, but by itself it does not prove that it was nutrition that caused the identified differences.

Why Epigenetic Changes can Matter

MRS may reflect the accumulated metabolic load over the years. DNA methylation can be influenced by previous diet, obesity, low physical activity, age and conditions of intrauterine development. Some of the labels studied are associated with inflammation, fat metabolism, insulin secretion and the work of tissues that must respond to this hormone.

According to the authors, pronounced epigenetic and related metabolic disorders may affect how the body adapts to the intake of nutrients. For example, they can potentially be accompanied by a decrease in insulin production by beta cells, less glucose uptake by muscles, and increased glucose production in the liver. This is a possible biological explanation, not a proven mechanism.

There is also a reverse version: high MRS may not weaken the effect of the diet, but reflect already accumulated health problems. The indicator includes signals related to glycated hemoglobin, body mass index, triglyceride levels and high-density lipoprotein cholesterol. After taking these parameters into account, the association of MRS with diabetes became weaker, although it did not disappear. The exclusion of participants with initially high levels of glycated hemoglobin also did not reverse the main statistical signal. Nevertheless, the researchers admit that they have not been able to completely rule out reverse causation.