Article | Published:

Carbohydrate and fiber intake and the risk of premenstrual syndrome

European Journal of Clinical Nutritionvolume 72pages861870 (2018) | Download Citation

Abstract

Background/objectives

Women with premenstrual syndrome (PMS) are encouraged to reduce sugar and increase fiber intake to reduce symptoms. However, research supporting these recommendations is limited, and their role in PMS development is unclear. This study examines the relation between carbohydrate and fiber intake and the risk of PMS nested within the prospective Nurses’ Health Study II cohort.

Subjects/methods

Carbohydrate and fiber intake were assessed at baseline and three additional times during follow up by food frequency questionnaire. Incident cases of PMS were identified by self-reported PMS diagnosis during 14 years of follow up and validated by supplemental questionnaire (n = 1234). Women were classified as controls if they did not report PMS diagnosis during follow up and confirmed minimal or no premenstrual symptoms (n = 2426). We estimated relative risks (RR) and 95% confidence intervals (CI) using multivariable logistic regression.

Results

Total carbohydrate intake 2–4 years before reference year was not associated with PMS development (RR quintile 5 versus 1 = 0.99; 95% CI = 0.74–1.33). Intakes of specific carbohydrates or fibers were not associated with PMS development, except maltose. Adjusting for body mass index, smoking, and other factors, women with the highest maltose intake (median = 3.0 g/day) had a RR of 1.45 (95% CI = 1.11–1.88) compared to those with the lowest intake (median = 1.2 g/day).

Conclusions

Overall, carbohydrate and fiber consumption was not associated with risk of PMS. As this is the first study to suggest that maltose may be associated with PMS development, further replication is needed.

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Acknowledgements

This work was supported by Public Health Services grants CA176726 and MH076274 from the National Institutes of Health, Department of Health and Human Services; a cy pres distribution from Rexall/Cellasene settlement litigation; and a grant from GlaxoSmithKline Consumer Healthcare.

Author contributions

J.E.M., S.E.H., and E.R.B.-J. designed the research; S.C.H. and E.R.B.-J. conducted the research; J.E.M. and S.E.H. provided essential materials; S.C.H. and E.R.B.-J. performed the statistical analysis; S.C.H. and E.R.B.-J. wrote the paper; B.W.W., L.M.T., and C.B. interpreted study results, reviewed manuscript for important intellectual content, and contributed knowledge of underlying biologic mechanisms; S.C.H., J.E.M., and E.R.B.-J. had primary responsibility for the final content. All authors read and approved the final manuscript.

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Affiliations

  1. Department of Biostatistics and Epidemiology, University of Massachusetts, Amherst, MA, USA

    • Serena C. Houghton
    • , Brian W. Whitcomb
    • , Susan E. Hankinson
    • , Carol Bigelow
    •  & Elizabeth R. Bertone-Johnson
  2. Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

    • JoAnn E. Manson
    •  & Susan E. Hankinson
  3. Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

    • JoAnn E. Manson
  4. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA

    • JoAnn E. Manson
  5. Department of Nutrition, University of Massachusetts, Amherst, MA, USA

    • Lisa M. Troy

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Conflict of interest

The authors declare that they have no conflict of interest.

Corresponding author

Correspondence to Serena C. Houghton.

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DOI

https://doi.org/10.1038/s41430-017-0076-8