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Colon
Original research
Maternal obesity, pregnancy weight gain, and birth weight and risk of colorectal cancer
  1. Caitlin C Murphy1,
  2. Piera M Cirillo2,
  3. Nickilou Y Krigbaum2,
  4. Amit G Singal3,
  5. MinJae Lee4,
  6. Timothy Zaki3,
  7. Ezra Burstein3,
  8. Barbara A Cohn2
  1. 1 School of Public Health, The University of Texas Health Science Center at Houston, Houston, Texas, USA
  2. 2 Child Health and Development Studies, Public Health Institute, Oakland, California, USA
  3. 3 Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
  4. 4 Population and Data Sciences, University of Texas Southwestern Medical Center, Dallas, Texas, USA
  1. Correspondence to Dr Caitlin C Murphy, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; caitlin.c.murphy{at}uth.tmc.edu

Abstract

Objective Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide. Obesity is a well-established risk factor for CRC, and fetal or developmental origins of obesity may underlie its effect on cancer in adulthood. We examined associations of maternal obesity, pregnancy weight gain, and birth weight and CRC in adult offspring.

Design The Child Health and Development Studies is a prospective cohort of women receiving prenatal care between 1959 and 1966 in Oakland, California (N=18 751 live births among 14 507 mothers). Clinical information was abstracted from mothers’ medical records 6 months prior to pregnancy through delivery. Diagnoses of CRC in adult (age ≥18 years) offspring were ascertained through 2019 by linkage with the California Cancer Registry. We used Cox proportional hazards models to estimate adjusted HR (aHR); we examined effect measure modification using single-referent models to estimate the relative excess risk due to interaction (RERI).

Results 68 offspring were diagnosed with CRC over 738 048 person-years of follow-up, and half (48.5%) were diagnosed younger than age 50 years. Maternal obesity (≥30 kg/m2) increased the risk of CRC in offspring (aHR 2.51, 95% CI 1.05 to 6.02). Total weight gain modified the association of rate of early weight gain (RERI −4.37, 95% CI −9.49 to 0.76), suggesting discordant growth from early to late pregnancy increases risk. There was an elevated association with birth weight (≥4000 g: aHR 1.95, 95% CI 0.8 to 4.38).

Conclusion Our results suggest that in utero events are important risk factors for CRC and may contribute to increasing incidence rates in younger adults.

  • obesity
  • colorectal cancer
  • cancer epidemiology

Data availability statement

Data are available on reasonable request. Deidentified (anonymised) data are available on request from Barbara Cohn, PhD, Director of the Child Health and Development Studies. Requests will be reviewed by Dr Cohn, research staff and the Institutional Review Board at the Public Health Institute. Approval of requests for deidentified (anonymised) data requires execution of a data use agreement.

https://doi.org/10.1136/gutjnl-2021-325001

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    Data availability statement

    Data are available on reasonable request. Deidentified (anonymised) data are available on request from Barbara Cohn, PhD, Director of the Child Health and Development Studies. Requests will be reviewed by Dr Cohn, research staff and the Institutional Review Board at the Public Health Institute. Approval of requests for deidentified (anonymised) data requires execution of a data use agreement.

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    Footnotes

    • Twitter @caitlincmurphy

    • Contributors Study conception and design: CM, BAC. Acquisition of data: BAC, PMC, NYK. Analysis and interpretation of data: All authors. Statistical analysis: CM, PMC, ML. Drafting of manuscript: CM. Critical revision: all authors.

    • Funding This work was supported by the National Cancer Institute at the National Institutes of Health under award number R01CA242558 (CM).

    • Disclaimer The sponsor had no role in design and conduct of the study; collection, management, analysis and interpretation of the data; preparation, review or approval of the manuscript; and decision to submit the manuscript for publication.

    • Competing interests CM reports consulting for Freenome; AGS reports consulting/advisory boards for Bayer, Eisai, Genentech, BMS, Exelixis, Exact Sciences, and GRAIL; PMC, NYK, ML, TZ, EB and BAC have no financial disclosures or conflicts of interest.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.