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  • br Only one study has

    2020-08-24


    Only one study has examined the pattern of offspring breastfed and its association with EOC, reporting that while breastfeeding in general is associated with reduced EOC risk, this protective association was lim-ited to women who breastfed their last child [22]. We did not replicate that finding. We observed that if breastfeeding any one child provides greater protection, it is the first child, which in our study was associated
    Table 3
    Association of breastfeeding duration with epithelial ovarian cancer, the HOPE Study 2003–2008.
    Factor Controls
    Cases
    Odds ratio 95% confidence interval Adjusted odds ratioa 95% confidence interval
    Total duration of breastfeeding (years)
    a Separate models and analyses for each factor. Each model adjusted for age, race, education, duration of oral contraceptive use, and number of pregnancies.
    Table 4
    Timing of breastfeeding and epithelial ovarian cancer, the HOPE Study 2003–2008.
    Factor Controls
    Cases
    Odds ratio 95% confidence interval Adjusted odds ratioa 95% confidence interval
    Age at first breastfeeding episode (years)
    Age at last breastfeeding episode (years)
    a Separate models and analyses for each factor. Each model adjusted for age, race, education, duration of oral contraceptive use, and number of pregnancies.
    with a (statistically non-significant) increased protection relative to breastfeeding any child but the first.
    A protective effect of breastfeeding is biologically plausible. Al-though the pathogenesis of EOC remains unclear, two prevailing theo-ries have dominated the literature. The incessant ovulation hypothesis posits that ovulation SCR-7 results in repeated trauma to ovarian surface epi-thelial cells, and subsequent repair opens the door for malignant trans-formation [9]. More recently, data suggest that some ovarian cancers may arise from the fimbreated end of the fallopian tube [5], where release of follicular fluid from ovulation may result in inflammation and DNA damage to tubal epithelial SCR-7 [10]. These transformed cells may then migrate and implant on the ovarian surface or within the peritoneal cav-ity [27]. Regardless of whether EOC arises in the ovary or fallopian tube, factors that decrease ovulation would reduce EOC risk. The gonadotropin hypothesis posits that high levels of gonadotropins increase ovarian es-trogen stimulation, thereby promoting ovarian surface and tubal epithe-lial cell proliferation and increasing the chance for malignant transformation [11]. Thus, factors that decrease gonadotropins would also reduce EOC risk. Breastfeeding suppresses gonadotropins (particu-larly luteinizing hormone), which reduces estrogen levels and leads to anovulation and amenorrhea [14]. In the absence of breastfeeding, ovula-tion typically resumes six weeks postpartum, whereas ovulation can be suppressed for several months with lactation [28,29].
    Alterations in the maternal hormonal milieu and/or metabolism are other potential biologic mechanisms whereby breastfeeding may im-pact EOC risk. Weaning, not birth, is the natural end to a pregnancy ep-isode in terms of pregnancy-associated physiologic changes [30]. Therefore, lactation may reset pregnancy-associated hormonal mecha-nisms, which could influence EOC risk [22]. It may also reset pregnancy-associated metabolic changes, such as insulin resistance and visceral fat accumulation, that may increase EOC risk [31,32]. Lon-ger breastfeeding duration reduces accumulated fat stores and results in other favorable metabolic changes that persist long after weaning [28]. In contrast, in women who do not breastfeed, adverse metabolic changes associated with EOC risk persist [30].
    A major strength of this study is that it is one of the largest population-based studies of EOC ever conducted in the US. In addition, data were collected through a standardized, structured interview ad-ministered by trained personnel, ensuring consistent and high-quality exposure measurements. 
    Despite these strengths, limitations must be noted. First, although the original HOPE subject population frequency matched cases and con-trols by 5-year age groupings, when restricting the data set to women reporting at least one live birth, controls were younger than cases (Table 1). Thus, because younger controls were overrepresented in the subset of participants included in the breastfeeding analyses reported herein, some of our findings may reflect the structure of the restricted dataset rather than a true association. For example, younger women may be more likely to breastfeed more recently. To address this concern, we controlled for age in our models. In addition, we repeated our anal-yses limiting subjects to women over 50 years of age, which showed similar results to analyses in the overall population.