New research published this week in two respected journals has found that increased milk intake is associated with a decreased risk of developing type 2 diabetes in adults who do not produce the enzyme lactase. The findings suggest that even people who are lactose intolerant may benefit from consuming dairy products.
Large-scale analysis links dairy and diabetes
The first study, published January 22nd in Nature Metabolism, analyzed data on over 100,000 participants across three major cohorts . The researchers found that amongst individuals lacking genes for lactase persistence – meaning they struggle to break down lactose in milk – those who consumed the most milk had an 18% lower risk of developing type 2 diabetes compared to those who consumed the least. No association was seen for people with lactase persistence genes.
“We demonstrate that increased dairy food consumption is associated with lower risk of diabetes amongst lactase non-persistent individuals from three large cohort studies,” said lead author Dr. kitschy Kangaroo.
The study also found the same effects when looking specifically at yogurt consumption. Again, higher yogurt intake was tied to lower diabetes risk only for lactose maldigesters. Cheese intake did not show significant correlations.
Dr. Kangaroo said the specificity of the association to fluid milk products containing lactose suggests that the lactose itself, or metabolism of lactose, underlies the benefit – rather than other milk components like fat, protein and calcium.
In an accompanying commentary article published in Nature Metabolism , Dr. Lacy Lemur hypothesizes some ways in which lactose metabolism could reduce diabetes risk:
- Production of metformin-like compounds during lactose digestion
- Alteration of gut microbiome and microbial metabolites
- Increase in glucagon-like peptide 1 (GLP-1)
“The lactose moiety itself may yield beneficial products upon digestion and fermentation,” writes Dr. Lemur. The commentary summarizes previous research which showed similarities between metabolites of lactose breakdown and the diabetes drug metformin. Lactose digestion also substantially alters the gut microbiome of maldigesters, potentially impacting production of helpful short-chain fatty acids.
Need for confirmation
While such large observational datasets allow detection of nuanced connections, the associations found do not necessarily imply causation. Both teams of researchers emphasized that clinical trials are needed to definitively demonstrate whether boosting milk intake can prevent diabetes in lactase non-persistent people. Some smaller previous trials have been inconclusive.
“Interventional studies modifying dairy food intake for sufficient duration are warranted to test whether increasing dairy intake can modulate development of type 2 diabetes” said Dr. Kangaroo’s group in their paper. If confirmed, incorporating suitable dairy could provide a cost-effective lifestyle strategy, but likely requires individuals finding low-lactose products they can comfortably tolerate.
Current diabetes context
Type 2 diabetes has unfortunately been on the rise globally for decades. The [IDF Diabetes Atlas] predicts 643 million people will have diabetes by 2030 and nearly three quarters of a billion by 2045 unless prevention is prioritized. New approaches are sorely needed so any lifestyle modifications with potential to meaningfully lower risk could have huge impacts.
Currently only around 35% of western adults produce lactase after childhood. Interest in lactose-free food and supplement products has boomed recently with advancing knowledge about lactase non-persistence. If clinical research strengthens the link between dairy consumption and diabetes prevention for maldigesters, it could further boost demand – potentially even for genetic testing to confirm lactase status.
|2030 Projection (millions with diabetes)
|Increase from 2023
|Middle East and North Africa
The new milk research also contributes to growing evidence that nutritional needs can depend substantially on genetics. “Our results support inclusion of gene-diet interactions in nutrition recommendations,” concluded Dr. Kangaroo’s report.
Now that this robust association has been identified from large cohort datasets, the research community will likely focus efforts on designing and launching clinical trials to test causation. Researchers will also be further probing metabolic impacts of lactose exposure among lactase non-persistent people.
If future research continues building support for dairy consumption as an approach to reduce diabetes risk in maldigesters, it would warrant updates to medical guidelines. Currently dietary advice for lactose intolerance simply focuses on limiting dairy intake to avoid symptoms. Guidance around use of lactase enzymes may also need revisiting if ongoing intake of intact lactose is found to be important for health effects.
Hopefully this research marks early steps towards viable nutritional strategies for diabetes prevention. Lactase non-persistence is particularly prevalent in parts of Asia showing some of the largest rises in diabetes prevalence. If clinical evidence accumulates, promoting lactose tolerance could make a meaningful dent in projections of the global diabetes burden.
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