Short-term weight gain and breast cancer risk by hormone receptor classification among pre- and postmenopausal women.
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ABSTRACT:
SUBMITTER: Rosner B
PROVIDER: S-EPMC4383816 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:PurposeRisk factors for obesity and weight gain are typically evaluated individually while "adjusting for" the influence of other confounding factors, and few studies, if any, have created risk profiles by clustering risk factors. We identified subgroups of postmenopausal women homogeneous in their clustered modifiable and non-modifiable risk factors for gaining ? 3% weight.MethodsThis study included 612 postmenopausal women 50-79 years old, enrolled in an ancillary study of the Women's Health Initiative Observational Study between February 1995 and July 1998. Classification and regression tree and stepwise regression models were built and compared.ResultsOf 27 selected variables, the factors significantly related to ? 3% weight gain were weight change in the past 2 years, age at menopause, dietary fiber, fat, alcohol intake, and smoking. In women younger than 65 years, less than 4 kg weight change in the past 2 years sufficiently reduced risk of ? 3% weight gain. Different combinations of risk factors related to weight gain were reported for subgroups of women: women 65 years or older (essential factor: < 9.8 g/day dietary factor), African Americans (essential factor: currently smoking), and white women (essential factor: ? 5 kg weight change for the past 2 years).ConclusionsOur findings suggest specific characteristics for particular subgroups of postmenopausal women that may be useful for identifying those at risk for weight gain. The study results may be useful for targeting efforts to promote strategies to reduce the risk of obesity and weight gain in subgroups of postmenopausal women and maximize the effect of weight control by decreasing obesity-relevant adverse health outcomes.
| S-EPMC4378852 | biostudies-literature
Project description:Breast density tends to decrease when women stop taking hormone therapy (HT). Some women find HT cessation difficult to tolerate, possibly because of fluctuations in endogenous hormone levels and vasomotor symptoms. We hypothesized that women with dense breasts might have lower tolerance for short-term HT suspension than do women with fatty breasts.As part of the Radiologic Evaluation And breast Density (READ) trial, we randomly assigned 881 women aged 45-80 with a prior screening (index) mammogram to suspend HT for 1 or 2 months before their next screening (study) mammogram. We measured continuous breast density on index mammograms using computer-assisted thresholding. At study mammograms, women indicated tolerance for stopping HT from 1 (extremely difficult) to 7 (very easy). Using linear regression, we evaluated the association between index breast density and tolerance after cessation, adjusting for age, body mass index (BMI), HT type, randomization group, and vasomotor symptoms.A higher percentage of breast density was associated with lower unadjusted mean tolerance scores (tolerance 4.27, 95% confidence interval [CI] 3.77-4.77 for women with > or =50% density, and 4.73, 95% CI 4.45-5.01 for women with <10% density, not a statistically significant difference). In adjusted analyses, neither percent breast density nor dense breast area was associated with tolerance for HT suspension.Although HT use affects breast density, tolerance for suspending HT is not associated with breast density. Women with dense breasts have the greatest potential for decreases in density after HT cessation; they should tolerate stopping HT as well as women with fatty breasts.
| S-EPMC2941404 | biostudies-literature
Project description:Body weight in lower animals and humans is highly stable despite a very large flux in energy intake and expenditure over time. Conversely, the existence of higher-than-average variability in weight may indicate a disruption in the mechanisms responsible for homeostatic weight regulation.In a sample chosen for weight-gain proneness, we evaluated whether weight variability over a 6-mo period predicted subsequent weight change from 6 to 24 mo.A total of 171 nonobese women were recruited to participate in this longitudinal study in which weight was measured 4 times over 24 mo. The initial 3 weights were used to calculate weight variability with the use of a root mean square error approach to assess fluctuations in weight independent of trajectory. Linear regression analysis was used to examine whether weight variability in the initial 6 mo predicted weight change 18 mo later.Greater weight variability significantly predicted amount of weight gained. This result was unchanged after control for baseline body mass index (BMI) and BMI change from baseline to 6 mo and for measures of disinhibition, restrained eating, and dieting.Elevated weight variability in young women may signal the degradation of body weight regulatory systems. In an obesogenic environment this may eventuate in accelerated weight gain, particularly in those with a genetic susceptibility toward overweight. Future research is needed to evaluate the reliability of weight variability as a predictor of future weight gain and the sources of its predictive effect. The trial on which this study is based is registered at clinicaltrials.gov as NCT00456131.
| S-EPMC4625595 | biostudies-literature
Project description:Obesity following breast cancer diagnosis is associated with poor overall survival. Understanding weight trajectories will help inform breast cancer survivors at greater risk of weight gain, and those who would benefit from earlier anti-obesity interventions. We performed a retrospective chart review of women from the Breast Cancer Program Longitudinal Repository (BCPLR) at Johns Hopkins diagnosed with hormone receptor-positive Stage I-III breast cancer from 2010 to 2020. We investigated obesity (measured by body mass index [BMI]) over time, patient and tumor characteristics, as well as treatment and recurrence. We observed a significant ≥5% increase in BMI from diagnosis to most recent follow-up (p = 0.009), particularly among those who were overweight at diagnosis (p = 0.003). Additionally, among those up to 5 years since diagnosis, there was a significant association between experiencing a ≥0.1 kg/m2 increase per year since diagnosis and baseline BMI status (p = 0.009). A ≥0.6 kg/m2 decrease in BMI was observed for participants with obesity at diagnosis (p = 0.006). Our study highlights (i) the significant burden of obesity in women with a history of breast cancer and (ii) higher risks for increases in BMI and shifts in class of obesity among women who are overweight at diagnosis.
| S-EPMC9222132 | biostudies-literature
Project description:Title: Transcriptome analysis of human endometrial tissues from healthy post-menoupausal women reflecting the endometrial response to 3-weeks treatment with tibolone, E2 and E2+MPA. In an observational, open, non-randomized, controlled study uterine tissues were collected in order to generate endometrial gene expression profiles. healthy postmenopausal women were enrolled into the following treatment groups: Control-group; Tibolone-group, 2,5 mg of tibolone (administered orally) every day, starting 21 days prior to surgery; Estradiol-group, 2 mg of estradiol (administered orally) every day, starting 21 days prior to surgery; Estradiol+progestagen-group, 2 mg of estradiol (administered orally) and 5 mg of MPA (Medroxy Progesteroneacetate, administered orally) every day, starting 21 days prior to surgery. Pure (100%) endometrium was isolated from the snap-frozen uterine tissues and used for RNA isolation. RNA was labeled and hybridized to whole genome Affymetrix U133plus2 GeneChips containing 54,614 probe sets, representing approximately 47,000 transcripts. Relative to the control group, 940 genes are regulated in the endometrium of E2 treated patients, whereas only 198 genes are significantly regulated in endometria from tibolone or E2+MPA treated patients. Furthermore, only 9% of E2 regulated genes are also regulated by tibolone (85 out of 940), only 5% are also regulated by E2+MPA treatment and the overlap between tibolone and E2+MPA treatment is about 10%. This indicated that tibolone-treatment results in a weak endometrial profile similarity to E2 treatment and no profile similarity to E2+MPA treatment. A more detailed analysis showed that down stream processes, such as regulation of the cell cycle, angiogenesis and cell proliferation are almost not affected by tibolone treatment but, in contrast, are significantly affected by E2. For example, upon staining with Ki67, a marker for mitotic activity, significantly increased stromal as well as glandular cell proliferation was observed in the endometria from the E2-only treated group, while tibolone treatment resulted only in a slight increase in stromal cell proliferation (and no increase in glandular cell proliferation). These results indicate that in contrast to long-term tibolone use, short-term (21-days) use results in some estrogenic stimulation of the endometrium, which is clearly far less and rather different from what is observed during E2 treatment. References: Klaassens et al., 2006 Hanifi-Moghaddam et al., 2007 Verheul et al., 2007
2008-08-21 | GSE12446 | GEO
Project description:ObjectiveWeight gain frequently occurs after smoking cessation. The objective of this study was to examine whether weight gain after smoking cessation was attenuated by physical activity (PA) in postmenopausal women.MethodsA total of 4,717 baseline smokers from the Women's Health Initiative were followed for 3 years. One thousand two hundred eighty-two women quit smoking, and 3,435 continued smoking. Weight was measured at baseline and at the year 3 visit. PA was assessed at both times by self-report, summarized as metabolic equivalent task-hours per week. Multiple linear regression models were used to assess the association between PA and postcessation weight gain, adjusting for potential confounding factors.ResultsCompared with continuing smokers, quitters gained an average of 3.5 kg (SD = 5.6) between the baseline and year 3 visit. Quitters with decreased PA had the highest amount of weight gain (3.88 kg, 95% CI: 3.22-4.54); quitters with increased PA (≥15 metabolic equivalent task-hours /week) had the lowest weight gain (2.55 kg, 95% CI: 1.59-3.52). Increased PA had a stronger beneficial association for postcessation weight gain for women with obesity compared to normal weight women. Quitters who had low PA at baseline and high PA at year 3 and were also enrolled in a dietary modification intervention had nonsignificant weight gain (1.88 kg, 95% CI: -0.21-3.96) compared with continuing smokers.ConclusionsOur data demonstrate that even a modest increase in PA (equivalent to current recommendations) can attenuate weight gain after quitting smoking among postmenopausal women, especially in combination with improved diet.
| S-EPMC6309933 | biostudies-literature
Project description:To test the hypothesis that greater chocolate-candy intake is associated with more weight gain in postmenopausal women.A prospective cohort study involved 107,243 postmenopausal American women aged 50-79 years (mean = 60.7) at enrollment in the Women's Health Initiative, with 3-year follow-up. Chocolate-candy consumption was assessed by food frequency questionnaire, and body weight was measured. Linear mixed models, adjusted for demographic, socio economic, anthropomorphic, and behavioral variables, were used to test our main hypotheses.Compared with women who ate a 1 oz (?28 g) serving of chocolate candy <1 per month, those who ate this amount 1 per month to <1 per week, 1 per week to?<?3 per week and ?3 per week showed greater 3-year prospective weight gains (kg) of 0.76 (95% CI: 0.66, 0.85), 0.95 (0.84, 1.06), and 1.40 (1.27, 1.53), respectively, (P for linear trend<0.0001). Each additional 1 oz/day was associated with a greater 3-year weight gain (kg) of 0.92 (0.80, 1.05). The weight gain in each chocolate-candy intake level increased as BMI increased above the normal range (18.5-25 kg/m(2)), and was inversely associated with age.Greater chocolate-candy intake was associated with greater prospective weight gain in this cohort of postmenopausal women.
| S-EPMC4351742 | biostudies-literature
Project description:BackgroundAlthough obesity is an established risk factor for postmenopausal breast cancer, the results of weight loss and breast cancer studies are inconsistent. Therefore, we evaluated associations between weight change and breast cancer risk in postmenopausal women in the Women's Health Initiative Observational Study.MethodsPostmenopausal women (n = 61,335) who had no prior breast cancer and a normal mammogram had body weight and height measured and body mass index (BMI) calculated at baseline and year 3. Weight change at year 3 was categorized as stable (<5%), loss (≥5%), or gain (≥5%) with further assessment of weight loss intentionality by self-report. Multivariable Cox proportional hazard regression models were used to evaluate relationships between weight change and subsequent breast cancer incidence.ResultsDuring a mean follow-up of 11.4 years with 3061 incident breast cancers, women with weight loss (n = 8175) had a significantly lower risk of breast cancer compared with women whose weight remained stable (n = 41,139) (hazard ratio [HR], 0.88; 95% confidence interval [CI], 0.78-0.98; P = .02) with no interaction by BMI. Adjustment for mammography did not alter findings (HR, 0.88; 95% CI, 0.78-0.99) with no significant difference by weight loss intentionality. Weight gain (≥5%) (n = 12,021) was not associated with breast cancer risk (HR, 1.02; 95% CI, 0.93-1.11) but was associated with higher triple-negative breast cancer incidence (HR, 1.54; 95% CI, 1.16-2.05).ConclusionsPostmenopausal women who lose weight have lower breast cancer risk than those with stable weight. These findings suggest that postmenopausal women who lose weight may reduce their breast cancer risk.
| S-EPMC6890496 | biostudies-literature
Project description:The Institute of Medicine (IOM) guidelines are the most widely used guidelines on gestational weight gain; however, accumulation of evidence that body composition in Asians differs from other races has brought concern regarding whether their direct application is appropriate. We aimed to study to what extent optimal gestational weight gain among women in Japan differs by pre-pregnancy body mass index (BMI) and to compare estimated optimal gestational weight gain to current Japanese and Institute of Medicine (IOM) recommendations.We retrospectively studied 104,070 singleton pregnancies among nulliparous women in 2005-2011 using the Japanese national perinatal network database. In five pre-pregnancy BMI sub-groups (17.0-18.4, 18.5-19.9, 20-22.9, 23-24.9, and 25-27.4 kg/m2), we estimated the association of the rate of gestational weight gain with pregnancy outcomes (fetal growth, preterm delivery, and delivery complications) using multivariate regression.Weight gain rate associated with the lowest risk of adverse outcomes decreased with increasing BMI (12.2 kg, 10.9 kg, 9.9 kg, 7.7 kg, and 4.3 kg/40 weeks) for the five BMI categories as described above, respectively. Current Japanese guidelines were lower than optimal gains, with the lowest risk of adverse outcomes for women with BMI below 18.5 kg/m2, and current IOM recommendations were higher than optimal gains for women with BMI over 23 kg/m2.Optimal weight gain during pregnancy varies largely by pre-pregnancy BMI, and defining those with BMI over 23 kg/m2 as overweight, as proposed by the World Health Organization, may be useful when applying current IOM recommendations to Japanese guidelines.
| S-EPMC5602799 | biostudies-other
Project description:BackgroundThe association between socioeconomic position in middle age and risk of subsequent, short-term weight gain is unknown. We therefore assessed this association in a prospective population based cohort study in Norfolk, UK.MethodsWe analysed data on 14,619 middle-aged men and women (aged between 40-75 at baseline) with repeated objective measures of weight and height at baseline (1993-1997) and follow up (1998-2000).ResultsDuring follow up 5,064 people gained more than 2.5 kg. Compared with the highest social class, individuals in the lowest social class had around a 30% greater risk of gaining more than 2.5 kg (OR 1.29; 95% CI 1.11-1.51; p for trend = 0.002). This association remained statistically significant following adjustment for sex, age, baseline BMI, smoking, and follow up time (OR 1.25; CI 1.07-1.46; p for trend <0.001). We also found no material difference between unadjusted models and those including all confounders and potential mediators.ConclusionIndividuals of low socioeconomic position are at greatest risk of gaining weight during middle age, which is not explained by classical correlates of socioeconomic position and risk factors for obesity.
| S-EPMC2323377 | biostudies-literature