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Study finds that genetically determined milk intake does not increase type-2 diabetes risk

In a recent study published in the Nutrition, Metabolism and Cardiovascular Diseases Journal, researchers systematically reviewed various Mendelian randomization studies to investigate the association between the genetic basis of milk consumption and type 2 diabetes risk.


The incidence of type 2 diabetes has been steadily increasing over the last few decades, and cohort studies that investigate the association between dietary exposures and type 2 diabetes risk face the challenge of residual confounding, which impacts the validity of the findings.

A Mendelian randomization is an alternative approach to examining how dietary exposures impact the risk of various diseases. This approach dictates that genetic variants for various factors are randomly allocated, making the exposure an instrumental variable function and at a very low risk of confounding.

Milk consumption is a dietary exposure that has been extensively investigated regarding type 2 diabetes risk, with various studies finding no correlation between the consumption of milk and type 2 diabetes risk but finding a negative correlation between total dairy consumption and diabetes risk.

However, these results are believed to be liable to residual confounding, affecting the validity of the results.

Given that several single nucleotide polymorphisms have been found to correlate with the consumption of specific foods such as milk, a Mendelian randomization approach to understanding the relationship between milk consumption and type 2 diabetes risk could increase the validity of the findings.

About the study

In the present study, the researchers reviewed published Mendelian randomization studies that investigated the association between genetically predicted milk consumption based on the lactase-producing gene variants and the levels of HbA1c and risk of type 2 diabetes.

The lactase enzyme breaks down the lactose in milk into galactose and glucose, which are absorbed into the bloodstream. The transcriptional activation of the gene coding for the lactase enzyme, LCT, is influenced by a variant in the intronic region of a neighboring gene.

While all humans are born able to produce lactase, individuals who are homozygous for cytosine in the intronic region of variation become lactose intolerant during adulthood. In contrast, those who are either heterozygous with thymine-cytosine or homozygous for thymine in that region continue to digest lactose in adulthood.

The ability to digest lactose could be linked to type 2 diabetes risk since it influences the glucose levels in the bloodstream.

The Mendelian randomization studies included in the study examined only milk consumption as an exposure, with type 2 diabetes being the primary outcome and the HbA1c levels as the secondary outcome.

Studies that did not use the Mendelian randomization approach or included other exposures apart from milk consumption were excluded from the review, as were studies that did not examine type 2 diabetes as an outcome.

The characteristics extracted from the studies for data synthesis included the year and location of publication, sample size, single nucleotide polymorphisms, milk exposure in grams per day, type of Mendelian randomization analysis, allele score, HbA1c status, one or two-sample Mendelian randomization studies, and the outcome variable expressed in hazard, odds, and risk ratios.


The findings indicated that milk consumption based on genetic predictors was not associated with a higher risk of type 2 diabetes or with the levels of HbA1c.

Lipid metabolism and particular body mass indices were potential confounders in the association between the genetic variant for lactase production and type 2 diabetes risk.

These results contrasted those from various randomized control trials that reported improvements linked to the consumption of low-fat dairy in type 2 diabetes biomarkers.

The researchers believe that this could be a result of the beneficial effects of vitamin K2, calcium, and flavonoids found in dairy on type 2 diabetes risk and might not be related to milk consumption directly.

The review included six Mendelian randomization studies with more than a thousand participants and investigated the exposure of milk consumption against the outcomes of type 2 diabetes and HbA1c levels.

The participants in these studies were mostly of European descent, which provided the studies with an opportunity to study the genetic variation because most populations of European ancestry contain the variants that result in continued lactase production into adulthood. However, this also prevented the findings from being generalized to other ethnic groups.


Overall, the systematic review results reported that the Mendelian randomization studies could not find an association between the genetic variants linked to milk consumption and an increase in type 2 diabetes or HbA1c levels.

However, the genetic variant associated with lactose production only explains a 2% change in milk consumption, and further studies are required to understand the genetic basis of milk consumption and its association with various disease risks.

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