If milk makes you poo, it might protect you from diabetes type 2

Embargoed until: Publicly released:

Ironically, for those who cannot produce lactase – a condition often referred to as lactose intolerance – drinking milk is associated with a decreased risk of type 2 diabetes (T2D), say US researchers. Lactase-deficient people are often in extreme discomfort if they even look at milk products funny, but the team says an increase in consuming milk was actually found to alter the levels of specific bacterial species in their guts and metabolic molecules, which in turn are linked to a lowered risk of developing T2D. The team found this out by looking at the diets, belly-bugs and prevalence of T2D in close to 200,000 people, adding that those people who were lactose intolerant lowered their risk by close to 30% by drinking cow juice.

Journal/conference: Nature Metabolism

Link to research (DOI): 10.1038/s42255-023-00961-1

Organisation/s: Albert Einstein College of Medicine, USA

Funder: The present work is supported by R01-DK119268 (to Q.Q.) and
R01-DK126698 (to Q.Q.) from the National Institute of Diabetes
and Digestive and Kidney Diseases (NIDDK), and R01-MD011389
(to R.K., R.D.B. and R.C.K.) from the National Institute on Minority
Health and Health Disparities. B.Y. is supported by R01-HL141824 and
R01-HL142003 from the National Heart, Lung and Blood Institute
(NHLBI). J.-Y.M. is supported by BioData Catalyst Fellowship.
J.L. is supported by R00-DK122128 from the NIDDK. G.H. is partially
supported by R01-DK132011 from the NIDDK and U54GM104940 from
the National Institute of General Medical Sciences. K.L. is supported
by an AHA postdoctoral fellowship award (23POST1020455).
Other funding sources for this study include UM1-HG008898 from
the National Human Genome Research Institute; R01-HL060712,
R01-HL140976 and R01-HL136266 from the NHLBI; and R01-DK120870
and the New York Regional Center for Diabetes Translation Research
(P30-DK111022) from the NIDDK. Support for metabolomics data was
graciously provided by the JLH Foundation (Houston, Texas, to B.Y.).
The HCHS/SOL is a collaborative study supported by contracts from
the NHLBI to the University of North Carolina (HHSN268201300001I/
N01-HC-65233), University of Miami (HHSN268201300004I/
N01-HC-65234), Albert Einstein College of Medicine
(HHSN268201300002I/N01-HC-65235), University of Illinois at
Chicago (HHSN268201300003I/N01-HC-65236 Northwestern
University) and San Diego State University (HHSN268201300005I/
N01-HC-65237). The following institutes/centres/offices have
contributed to the HCHS/SOL through a transfer of funds to the
NHLBI: National Institute on Minority Health and Health Disparities,
National Institute on Deafness and Other Communication Disorders,
National Institute of Dental and Craniofacial Research, NIDDK, National
Institute of Neurological Disorders and Stroke and National Institutes
of Health (NIH) Institution-Office of Dietary Supplements. We thank the
staff and participants of HCHS/SOL for their important contributions.
A complete list of staff and investigators is available on the study
website at http://www.cscc.unc.edu/hchs/.
The ARIC study has been funded in whole or in part with
Federal funds from the NHLBI, NIH, Department of Health and
Human Services (contract numbers HHSN268201700001I,
HHSN268201700002I, HHSN268201700003I, HHSN268201700004I
and HHSN268201700005I), R01-HL087641, R01-HL059367 and
R01-HL086694; National Human Genome Research Institute
contract number U01HG004402; and NIH contract number
HHSN268200625226C. We thank the staff and participants of the
ARIC study for their important contributions. Infrastructure was
partly supported by grant number UL1RR025005, a component
of the NIH and NIH Roadmap for Medical Research. Metabolomics
measurements were sponsored by the National Human Genome Research Institute (3U01HG004402-02S1). This research is part of our
Diet and Cardiometabolic Health Collection. The funding agencies
have no role in the data analyses and results interpretation.

Media release

From: Springer Nature

Increased milk intake associated with reduced risk of type 2 diabetes for some

Increased milk intake is associated with a decreased risk of type 2 diabetes (T2D) in adults who do not produce lactase (are lactase non-persistent), according to a study in Nature Metabolism. Exclusively in lactase-deficient individuals, increased milk intake was found to alter the levels of specific bacterial species in the gut microbiome and of circulating metabolites, which was linked to a lowered risk of developing T2D.

The genotype of the single nucleotide polymorphism rs4988235 at the LCT (lactase) gene determines whether individuals retain lactase expression in adulthood. Individuals with lactase persistence (AA/AG genotypes) can easily digest high-lactose dairy products (e.g. milk) in adulthood, whereas lactase non-persistence (GG) leads to lactase deficiency and in many cases to lactose intolerance.

Qibin Qi and colleagues analysed the host genotype, gut microbiome and blood metabolite levels in up to 12,653 participants from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) over a median follow-up period of six years. Dietary intake of milk was assessed with two 24-hour dietary recalls (participants were asked to recall all the food and drink they consumed in 24 hours) and a food propensity questionnaire. Milk intake increased by one serving (where a serving is 1 fluid cup of milk) was associated with an approximately 30% decreased risk of developing T2D only in participants with lactase non-persistence. The link between milk intake, LCT genotype and T2D risk was also validated in 167,172 individuals in the UK Biobank.

In the Hispanic and Latino cohort, milk intake was found to be associated with distinct changes in the abundance of gut bacteria species in lactase non-persistent individuals. The observed enrichment in Bifidobacterium species was correlated with reduced risk of T2D. Milk intake was also associated with specific changes in blood metabolite levels in lactase non-persistent participants, such as changes in branched chain amino acids and tryptophan metabolites, which were linked to reduced T2D risk. In lactase persistent participants, no association with T2D risk was observed. The authors found that changes in bacterial species abundance were correlated with changes in metabolite levels. This indicates that milk intake might affect the gut microbiota composition and blood metabolite profile in a specific manner depending on the host LCT genotype and that milk intake may protect against T2D among lactase-deficient individuals.

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