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High Total/Saturated Fat Intake Associated With Increased Risk of Hormone Receptor–Positive Breast Cancer and HER2-Negative Breast Cancer

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Key Points

  • High total fat intake and saturated fat intake were associated with increased risk of estrogen receptor–positive/progesterone receptor–positive breast cancer.
  • High saturated fat intake was associated with increased risk of HER2-negative breast cancer.

In an analysis from the EPIC study reported in the Journal of the National Cancer Institute, Sieri et al found that high dietary intake of total fat and saturated fat were associated with increased risk of estrogen receptor–positive/progesterone receptor–positive breast cancer and that high saturated fat intake was associated with significantly increased risk of HER2-negative disease.

Study Details

The EPIC study (European Investigation Into Cancer and Nutrition) initially identified weak but statistically significant associations of saturated fat intake with breast cancer risk. Follow-up was expanded to prospectively evaluate associations of dietary fat with estrogen receptor, progesterone resceptor, and HER2 status.

Among 337,327 women in the cohort who completed dietary and lifestyle questionnaires, there were 10,062 cases of breast cancer after 11.5 years of follow-up. Estrogen receptor, progesterone receptor, and HER2 status from pathology reports were available for 70.6%, 59.0%, and 22.9% of patients, respectively. Analysis of risk was stratified by center and age; nonalcohol energy, energy from alcohol, smoking, education, age at menarche, full-term pregnancy, hormone therapy use, and body mass index/menopausal status interaction were covariates.

Increased Risk of Hormone Receptor–Positive Disease

Analysis in 5,601 case patient showed that compared with lowest (1st) quintile of total fat intake (43.2 g/d), the highest (5th) quintile (117.3 g/d) was associated with significantly increased risk of estrogen receptor–positive/progesterone receptor–positive disease (hazard ratio [HR = 1.20, 95% confidence interval [CI] = 1.00–1.45; P = .21 for trend). Compared with the lowest quintile of saturated fat intake (15.4 g/d), the 4th quintile (33.9 g/d; HR = 1.15, 95% CI = 1.01–1.32) and the 5th quintile (47.5 g/d; HR = 1.28, 95% CI = 1.09–1.52; P = .009 for trend) were associated with increased risk of estrogen receptor–positive/progesterone receptor–positive disease.

Saturated fat intake as a continuous variable was also associated with increased risk for estrogen receptor–positive/progesterone receptor–positive disease (HR = 1.03, 95% CI = 1.01–1.06) and for estrogen receptor–positive/progesterone receptor–negative disease (HR = 1.06, 95% CI = 1.01–1.11).

Increased Risk of HER2-Negative Disease

Analysis in 2,259 case patients showed that compared with the lowest quintile of saturated fat intake (15.7 g/d), the 2nd quintile (22.9 g/d; HR = 1.19, 95% CI = 1.01–1.39), 3rd quintile (28.3 g/d; HR = 1.20, 95% CI = 1.01–1.43), 4th quintile (34.8 g/d; HR = 1.27, 95% CI = 1.01–1.54), and highest quintile (48.6 g/d; HR = 1.29, 95% CI = 1.01–1.64; P = .04 for trend) were associated with significantly increased risk of HER2-negative disease.

Both total fat intake (HR = 1.05, 95% CI = 1.00–1.11) and saturated fat intake (HR = 1.04 95% CI = 1.00–1.09) as continuous variables were associated with increased risk of HER2-negative disease. The highest saturated fat quintile (HR = 1.14, 95% CI = 1.01–1.30; P = .03 for trend) and saturated fat intake as a continuous variable (HR = 1.03, 95% CI = 1.01–1.05) were also associated with increased risk of disease with unknown HER2 status.

The investigators concluded, “[T]he results of this prospective study on a large heterogeneous population of European women indicate that a high-fat diet increases [breast cancer] risk and, most conspicuously, that high saturated fat intake increases risk of receptor-positive disease, suggesting saturated fat involvement in the etiology of receptor-positive [breast cancer].”

Sabina Sieri, PhD, of Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, is the corresponding author for the Journal of the National Cancer Institute article.

The study was supported by the European Commission (DG-SANCO), International Agency for Research on Cancer, and others.

The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.


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