Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Matters Arising
  • Published:

Reply to: Milk intake, lactase non-persistence and type 2 diabetes risk in Chinese adults

The Original Article was published on 18 September 2024

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Adjustment for adiposity measures in the associations of milk-associated metabolites and gut bacterial species with incident T2D.

Data availability

The data in our original article2 were used to generate results in this paper. In brief, the genetics data of HCHS/SOL used in this paper are archived at the NIH repositories dbGap (accession no. phs000810.v1.p1) and BioLINCC (accession no. HLB01141418a), and gut microbiome sequence data in this study are deposited in QIITA (study ID 11666). HCHS/SOL has established a process for the scientific community to apply for access to participant data and materials, with such requests reviewed by the project’s Steering Committee. These policies are described at https://sites.cscc.unc.edu/hchs/ (accessed December 2022). Original data from the UKB used in the present study are available at https://www.ukbiobank.ac.uk/. Source data are provided with this paper.

Code availability

No custom codes or functions were generated for this manuscript. All codes regarding the main analyses or data visualization can be made available upon reasonable request to the corresponding author.

References

  1. Kakkoura, M. G., Walters, R. G., Clarke, R., Chen, Z. & Du, H. Milk intake, lactase non-persistance and type 2 diabetes risk in Chinese adults. Nat. Metab. https://doi.org/10.1038/s42255-024-01128-2 (2024).

  2. Luo, K. et al. Variant of the lactase LCT gene explains association between milk intake and incident type 2 diabetes. Nat. Metab. 6, 169–186 (2024).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Kakkoura, M. G. et al. Dairy consumption and risks of total and site-specific cancers in Chinese adults: an 11-year prospective study of 0.5 million people. BMC Med. 20, 134 (2022).

    Article  PubMed  PubMed Central  Google Scholar 

  4. Anguita-Ruiz, A., Aguilera, C. M. & Gil, A. Genetics of lactose intolerance: an updated review and online interactive world maps of phenotype and genotype frequencies. Nutrients 12, 2689 (2020).

  5. Segurel, L. & Bon, C. On the evolution of lactase persistence in humans. Annu. Rev. Genomics Hum. Genet. 18, 297–319 (2017).

    Article  CAS  PubMed  Google Scholar 

  6. Storhaug, C. L., Fosse, S. K. & Fadnes, L. T. Country, regional, and global estimates for lactose malabsorption in adults: a systematic review and meta-analysis. Lancet Gastroenterol. Hepatol. 2, 738–746 (2017).

    Article  PubMed  Google Scholar 

  7. Evershed, R. P. et al. Dairying, diseases and the evolution of lactase persistence in Europe. Nature 608, 336–345 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Kitaoka, M. Bifidobacterial enzymes involved in the metabolism of human milk oligosaccharides. Adv. Nutr. 3, 422S–429S (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Alvarez-Bueno, C. et al. Effects of milk and dairy product consumption on type 2 diabetes: overview of systematic reviews and meta-analyses. Adv. Nutr. 10, S154–S163 (2019).

    Article  PubMed  PubMed Central  Google Scholar 

  10. Gijsbers, L. et al. Consumption of dairy foods and diabetes incidence: a dose-response meta-analysis of observational studies. Am. J. Clin. Nutr. 103, 1111–1124 (2016).

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

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.C.K.) from the National Institute on Minority Health and Health Disparities. 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 National Heart, Lung, and Blood Institute (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). 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 https://sites.cscc.unc.edu/cscc/. The funding agencies had no role in the data analyses and results interpretation.

Author information

Authors and Affiliations

Authors

Contributions

K.L. and Y.Z. conducted the analyses. K.L. prepared the tables and figures and drafted the manuscript. R.C.K. and Q.Q. critically revised the manuscript.

Corresponding author

Correspondence to Qibin Qi.

Ethics declarations

Competing interests

The authors declare no competing interests.

Peer review

Peer review information

Nature Metabolism thanks the anonymous reviewers for their contribution to the peer review of this work. Primary Handling Editor: Ashley Castellanos-Jankiewicz, in collaboration with the Nature Metabolism team.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Source data

Source Data Fig. 1

Source data for results shown in Fig. 1.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Luo, K., Zhang, Y., Kaplan, R.C. et al. Reply to: Milk intake, lactase non-persistence and type 2 diabetes risk in Chinese adults. Nat Metab 6, 2057–2059 (2024). https://doi.org/10.1038/s42255-024-01129-1

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue date:

  • DOI: https://doi.org/10.1038/s42255-024-01129-1

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing