GeneBites

Guest Article by Hridya Rao

Ever hated that you experience an upset stomach after drinking milk or eating a cheesy pizza while your friend or sibling doesn’t? Even though lactose intolerance seems more like a bane than a boon, the authors of a recent paper found that high milk intake is associated with lower type 2 diabetes risk in lactose intolerant individuals. This could be because of gut bacteria and metabolites that have created solutions to co-metabolize milk in lactose intolerant individuals with particular genetic variations. We all know the benefits of probiotics – imagine having genes that make probiotics in your gut to protect against diabetes even if you are lactose intolerant!

Around 68% of the world’s population is lactose intolerant, with symptoms ranging from general gassiness to severe abdominal pain. Genetically, it is the LCT gene that is responsible for the adequate production of the enzyme lactase that helps digest lactose-containing dairy, like milk. Many individuals have the protective version of this gene that helps them code for proteins that digest milk. Generally, researchers associate milk intolerance with poor nutrition that could cause potential metabolic disorders, but the truth could be more complex. In fact, our bodies have developed mechanisms to combat the inflammation that arises due to lactose intolerance with the help of beneficial gut bacteria, as confirmed by Luo et al. in their paper published in Nature Metabolism.

The authors also found that higher milk consumption is associated with higher risk of T2D in those who can efficiently digest milk. Not being able to consume milk due to lactose intolerance could actually mean that one is protected against T2D. Study authors used data from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), representing roughly 12,000 individuals with complete genetic and demographic data. Though lactose intolerance and health effects have been studied in Non-Hispanic white populations before, extending it to this Hispanic/Latino dataset helps us better understand these effects in groups where lactose intolerance is more or less prevalent.

Multiple studies have found different emergence patterns of lactose intolerance across the world over the last several thousand years – e.g., in Saudi Arabia, India, and Europe. The appearance of these genetic variations in different contexts over time is a testament to the importance of studying diverse populations to identify mechanisms that affect human health.

Switching gears back to the complex relationship between milk consumption and Diabetes – some studies say it is beneficial while others have found contradictory evidence. In the current literature, it is now widely accepted that it isn’t milk inherently that determines adiposity and metabolic disorders, but its fat content. Low-fat milk and milk products have been found to be beneficial. This is also found to be true in lactose intolerant individuals which was a surprising finding made by Luo et al. in their paper. For lactose intolerant individuals, high milk intake is associated with lower T2D risk, and this could be due to a protective mechanism driven by both the gut bacteria and metabolites. The authors observed that the Bifidobacterium species of bacteria plays a role in the lactose degradation pathway. This and other Bifidobacterium species such as, B.longum, B.breve, B.reuteri, and Bacteroides fragilis were found to participate in metabolic pathways that reduce adiposity and fasting glucose, as well. Bifidobacterium may also be working in conjunction with metabolites such as BCAA (α-hydroxyisocaproate and β-hydroxyisovalerate), GAA (γ-glutamylvaline) and tryptophan
(indolepropionate) to digest milk. These gut microbiota and metabolites coming together to digest lactose in those who consume a lot of milk may be one possible explanation of the reduced diabetes risk in lactose intolerant individuals.

As fascinating as this finding is (and a relief to many lactose intolerant people), the researchers state that additional research should be conducted in African, Middle Eastern, and Asian populations to find out if a similar protective mechanism against T2D exists in these populations where lactose intolerance evolved independently.

Edited by Jayati Sharma