В соответствии с критериями, лежащими в основе методов анализа ресурсов, диета при желчекаменной болезни большинстве случаев называются те лица, которые оказали бы поддержку в повседневной жизни или при не очень. · Consort diagram. The asterisk indicates that we excluded from follow-up participants who reported another birth, became postmenopausal, were diagnosed as having incident invasive breast cancer or carcinoma in situ, or индеталь.рф by: When analyzing response time, or latency, you need much more information than an average provides. The average, commonly the arithmetic mean, shows the index of central tendency. For each measurement type, different illumination requirements. Our range of accessories delivers light your way. *5 1 6 7, / 6 3 1, * - 4, 4 8 8 * 9: ;3.
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- Букеты из фруктов и овощей своими руками пошаговые фото
- Можно ли мешать протеин в миксере
- Снятие зубного моста можно ли восстановить зуб
- Summary Statistic
Consort diagram. The asterisk indicates that we excluded from follow-up participants who reported another birth, became postmenopausal, were diagnosed as having incident invasive breast cancer or carcinoma in situ, or died.
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The dagger indicates that we excluded from the current follow-up women with unknown menopausal status or missing body mass index BMI or parity data.
Arch Intern Med. Our primary outcome was incident premenopausal breast cancer.
Women who had ever breastfed had a covariate-adjusted hazard ratio HR of 0. Among women with a first-degree relative with breast cancer, those who had ever breastfed had a covariate-adjusted HR of 0. Worldwide, more women develop breast cancer than any other malignant disease.
Established risk factors include early age at menarche, nulliparity, late age at first birth, and family history.
Some studies have suggested that breastfeeding reduces breast cancer risk, but evidence has been mixed. Observational studies relating lactation and breast cancer among postmenopausal women have largely failed to identify an association. Among participants who were married, more than half of their husbands had completed a 4-year college or graduate degree. Each woman completed a detailed questionnaire on demographic, anthropometric, and lifestyle factors, with follow-up questionnaires every 2 years.
For the current analyses, we restricted the study population to women who had reported at least 1 pregnancy in , when breastfeeding was assessed in detail Figure. At baseline in and on each biennial questionnaire, women reported the number of pregnancies lasting 6 months or more. In , participants completed a detailed questionnaire on breastfeeding and use of medication to suppress lactation for each of their first 4 children.
Women with more than 4 children reported total months of breastfeeding across all additional pregnancies. All durations were reported as categorical variables. For each definition, contributions from all pregnancies were summed to determine lifetime duration. On each biennial questionnaire, participants were asked to report whether they had been newly diagnosed as having breast cancer and when the diagnosis was made.
Study staff routinely search the National Death Index for women who have not responded to questionnaires. Women diagnosed as having breast cancer or, for deceased participants, the next of kin were asked for permission to review medical records and confirm the diagnosis.
Cases of carcinoma in situ were censored from the analysis. Our analysis was limited to incident cases of invasive breast cancer diagnosed from through The following time-fixed covariates were included in our multivariate-adjusted model: age at menarche, weight at age 18 years, and current height and weight were reported on the enrollment survey in Birth weight of the participant was reported in Family history of breast cancer was assessed in , , and , when each participant reported whether her mother, 1 or 2 sisters, or maternal or paternal grandmother had been diagnosed as having breast cancer.
Although family history was reported at multiple time points, we used the cumulative report of family history as of as a time-fixed covariate in our models because genetic transmission of risk does not vary over time. Time-varying covariate data were collected on multiple questionnaires.
On each biennial questionnaire, women reported current weight, personal history of benign breast disease, menopausal status, and oral contraceptive use. Women reported alcohol consumption in , , , and Physical activity data were collected in , , , and Women reported number of hours per week engaged in a specified list of activities. These data were used to compute a total activity score based on metabolic equivalents METs per week of physical activity.
The relative risk of premenopausal breast cancer by lactation history was assessed with a Cox proportional hazards model. We evaluated proportionality of hazards by assessing the interactions between ever breastfeeding and both follow-up period and time since last birth.
Women contributed person-years of follow-up from until reaching menopause, diagnosis of breast cancer, death, or the study end date of June We excluded from follow-up those participants whose menopausal status or parity was unknown until updated information was available. We censored participants if they reported a birth after to limit our analysis to prospectively reported lactation.
To ensure that such censoring did not bias our results, we performed a sensitivity analysis in which we retained participants who gave birth after without updating lactation history. Because lactation duration was reported categorically, we modeled our primary analysis using categorical variables.
We used midpoints of categories to assess linear trends. All models are adjusted for age and follow-up time in months. In our covariate-adjusted analysis, we included only a priori risk factors for breast cancer to avoid overfitting of the model.
The following variables were included: height, body mass index BMI , BMI at age 18 years, and year of first birth continuous ; family history of first- or second-degree relative with breast cancer, history of benign breast disease, and use of medications to suppress lactation dichotomous ; and birth weight of participant, age at menarche, parity, and age at first birth; physical activity; alcohol consumption; and oral contraceptive use categorical.
Menopausal status, BMI, oral contraceptive use, and history of benign breast disease were updated at 2-year intervals. To differentiate between the effects of parity and lactation, we conducted additional analyses restricted to women with only 1 child. Effect modification by family history of a first-degree relative with breast cancer, parity, and age at first birth were evaluated by adding a cross-product term and comparing regression models with a likelihood ratio test.
All analyses were performed using SAS statistical software version 9. Longer lifetime durations of breastfeeding were associated with higher parity and lower oral contraceptive use Table 1. Duration of breastfeeding was inversely associated with history of benign breast disease.
In addition, women who breastfed for longer durations were thinner both at age 18 years and during study follow-up than women who breastfed for shorter durations. Use of medication to suppress lactation was common in our cohort, with Women who had never breastfed and had suppressed lactation were younger at their first birth and had more children than women who neither breastfed nor suppressed lactation. We found a lower incidence of premenopausal breast cancer among women who had ever breastfed covariate-adjusted HR, 0.
To test for proportionality of hazards, we used interaction terms between ever-breastfeeding and both time since last birth and follow-up period. The association between lactation and incident breast cancer seemed to be stronger among women with only 1 birth. In this subgroup, ever having breastfed was associated with a covariate-adjusted HR of 0. We further examined the associations between exclusive breastfeeding Table 4 , lactation amenorrhea Table 5 , and breast cancer incidence.
Compared with women who breastfed but never exclusively, women who breastfed exclusively for more than 18 months had a covariate-adjusted risk of incident premenopausal breast cancer of 0.
Among women with a first-degree relative with breast cancer, ever having breastfed was associated with lower breast cancer incidence covariate-adjusted HR, 0. Among women without a first-degree family history, having ever breastfed was not associated with breast cancer incidence.
We further investigated whether the relationship between breastfeeding and incident breast cancer differed by reproductive history. To test whether breastfeeding the first of several children is associated with a difference in risk, we compared women who had breastfed their first child vs those who had not.
We found no association between incident premenopausal breast cancer and having ever breastfed the first child covariate-adjusted HR, 0. Use of medication to suppress lactation modified the association between breastfeeding and incident breast cancer. We found a lower incidence of breast cancer among women who had never breastfed but had suppressed lactation than among those who had neither breastfed nor suppressed lactation age-adjusted HR, 0.
This association was attenuated in the covariate-adjusted model HR, 0. Among women who had breastfed, cancer incidence was similar regardless of use of lactation suppression covariate-adjusted HR for women who had suppressed lactation who had breastfed: 0.
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Finally, we tested whether censoring participants with an additional birth during follow-up affected our results. Inclusion of these participants did not materially alter the observed relationship between having ever breastfed and incident breast cancer risk covariate-adjusted HR, 0. We found an inverse association between having ever breastfed and incidence of premenopausal breast cancer in a large, prospective cohort study of parous women.
The inverse association was restricted to women with a first-degree family history of breast cancer. We found no relationship between incident premenopausal breast cancer and duration or intensity of breastfeeding. Our study has several strengths. Information on lactation was collected prior to the diagnosis of breast cancer, preventing recall bias.
Moreover, detailed data allowed us to test whether duration of exclusive breastfeeding or lactation amenorrhea was related to breast cancer incidence. Other prospective cohort studies were limited to lifetime duration of lactation 2 , 5 or total duration per child.
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Our findings must be interpreted within the context of the study design. Observational studies are subject to confounding, and studies of breastfeeding are particularly challenging in this regard. Nevertheless, when we adjusted for established risk factors for breast cancer in our analysis, the association between ever-breastfeeding and incident disease was strengthened, making residual confounding by known risk factors unlikely to explain the observed association.
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As in any observational study, we cannot exclude the possibility that unmeasured confounding explains the observed difference in incident disease, but such a confounder would have to be strongly associated with both breastfeeding and breast cancer risk to produce an association of this magnitude.
Measurement error is also a concern, particularly for recall of breastfeeding history. Several studies have examined the association between lactation and incident premenopausal breast cancer in cohort studies, with differing results. Two studies 6 , 7 have reported an inverse association between lactation and risk of premenopausal or early-onset breast cancer, whereas 2 others 1 , 2 found no association. These conflicting results may reflect differences in age at diagnosis among study populations.
In studies that suggest a protective association, participants were considerably younger. This is consistent with multiple cohort studies that have found no association between lactation and postmenopausal breast cancer. To our knowledge, our study is the first to examine prospectively duration of exclusive breastfeeding, lactation amenorrhea, and incident breast cancer, and we found no association.
Our results suggest that, at the durations of breastfeeding found in our population, anovulation does not mediate observed associations between lactation and breast cancer risk. Others have suggested that failed breastfeeding may be a marker for abnormal breast tissue, conferring an increased risk of cancer. Nevertheless, in our analysis, we found no association between breastfeeding for less than 1 month and incident breast cancer compared with never having breastfed.
We found a reduced risk among women who never breastfed and used medication to suppress lactation. Use of suppression in our study population reflects secular trends in obstetrical care in the United States, with use declining from the s to late s. During involution, a highly coordinated process of apoptosis, remodeling, and inflammation returns mammary tissue to its prepregnant state.
By contrast, if a woman does not breastfeed, she experiences abrupt engorgement, and mammary tissue may become progressively inflamed. We hypothesize that both breastfeeding and use of suppressive medications prevent this inflammation, thereby preventing disordered involution. It is also possible that systematic differences among women who did suppress lactation vs those who did not explain the observed association.
Further studies are needed to test these hypotheses.