Tier 4 — mechanistic

Dietary betaine and choline intake are not associated with risk of epithelial ovarian cancer

J Kotsopoulos, S E Hankinson, S S Tworoger
European journal of clinical nutrition 2010 64(1):111-114

Bibliography

PubMed
PMID 19707229
PubMed Central
PMC2892854
DOI
10.1038/ejcn.2009.109
Funding
Indexed grant support: R01 CA050385 — NCI NIH HHS — United States; P01 CA087969 — NCI NIH HHS — United States; R01 CA50385 — NCI NIH HHS — United States; P50 CA105009 — NCI NIH HHS — United States; P01 CA87969 — NCI NIH HHS — United States. The indexed list may not contain the complete funding declaration.
Competing interests
Reported disclosure: The authors declare no conflict of interest.

Study snapshot

DesignProspective cohorts
ModelHuman participants
Sample159957 women; 526 ovarian-cancer cases
InterventionHabitual dietary choline and/or betaine intake; no randomized TMG treatment
DurationUp to 22 years
EndpointsOvarian-cancer incidence

What the study showed, in plain terms

Published in 2010, this source examined human observational and biomarker research. Design: Prospective cohorts. Sample/model: 159957 women; 526 ovarian-cancer cases. The exposure or intervention was Habitual dietary choline and/or betaine intake; no randomized TMG treatment. Follow-up or treatment period: Up to 22 years.

Dietary betaine and choline were not associated with epithelial ovarian-cancer risk.

Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.

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Key findings

  • Dietary betaine and choline were not associated with epithelial ovarian-cancer risk.
  • The recorded outcome domains were Ovarian-cancer incidence.
  • The exposure was observed rather than assigned as an isolated supplement treatment.

What this study can and cannot tell us

  • Observational exposure analysis: residual confounding and reverse causation remain possible. Associations do not establish that betaine supplementation causes the same outcome.
  • Confounding, dietary patterns, illness, medication use and reverse causation can influence an association. Blood or dietary concentrations do not identify the effect of starting a capsule.
  • Source basis: Accessible full-text extract plus indexed bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology