Midlife weight gain is a risk factor for obesity-related cancer.
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ABSTRACT:
SUBMITTER: Chadid S
PROVIDER: S-EPMC6008441 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundExcess body weight and weight gain have been reported to independently increase the risk of several cancers. There are few published studies in nationally representative populations of women on specific, 'obesity-related' cancers in relation to prior weight change and relevant confounders.MethodsBased on self-reported anthropometry, we prospectively assessed body mass index (BMI), weight change over 6 years and subsequent obesity-related cancer risk in the Norwegian Women and Cancer study. We used Cox proportional hazard models to calculate hazard ratios and restricted cubic splines to model potential non-linear dose-response relationships.ResultsExcess body weight increased the risk of overall obesity-related cancer, postmenopausal breast, colorectal, colon, endometrial and kidney cancer, with endometrial cancer showing a threefold elevated risk. High weight gain (???10?kg) increased the risk of overall obesity-related cancer, postmenopausal breast, endometrial and pancreatic cancer. The association between high weight gain and pancreatic cancer was strong, with 91% increased risk.ConclusionsMaintaining stable weight in middle adulthood, irrespective of BMI category at baseline, and avoiding excess body weight are both important in the prevention of several obesity-related cancers in women. Our finding of increased risk of pancreatic cancer in women with moderate and high weight gain is novel.
| S-EPMC6162329 | biostudies-literature
Project description:ObjectiveColorectal cancer (CRC) is a leading cause of cancer-related death worldwide. Obesity is a well-established risk factor for CRC, and fetal or developmental origins of obesity may underlie its effect on cancer in adulthood. We examined associations of maternal obesity, pregnancy weight gain, and birth weight and CRC in adult offspring.DesignThe Child Health and Development Studies is a prospective cohort of women receiving prenatal care between 1959 and 1966 in Oakland, California (N=18 751 live births among 14 507 mothers). Clinical information was abstracted from mothers' medical records 6 months prior to pregnancy through delivery. Diagnoses of CRC in adult (age ≥18 years) offspring were ascertained through 2019 by linkage with the California Cancer Registry. We used Cox proportional hazards models to estimate adjusted HR (aHR); we examined effect measure modification using single-referent models to estimate the relative excess risk due to interaction (RERI).Results68 offspring were diagnosed with CRC over 738 048 person-years of follow-up, and half (48.5%) were diagnosed younger than age 50 years. Maternal obesity (≥30 kg/m2) increased the risk of CRC in offspring (aHR 2.51, 95% CI 1.05 to 6.02). Total weight gain modified the association of rate of early weight gain (RERI -4.37, 95% CI -9.49 to 0.76), suggesting discordant growth from early to late pregnancy increases risk. There was an elevated association with birth weight (≥4000 g: aHR 1.95, 95% CI 0.8 to 4.38).ConclusionOur results suggest that in utero events are important risk factors for CRC and may contribute to increasing incidence rates in younger adults.
| S-EPMC8866526 | biostudies-literature
Project description:BackgroundEpidemiologic studies regarding weight loss and subsequent cancer risk are sparse. The study aim was to evaluate the association between weight change by intentionality and obesity-related cancer incidence in the Women's Health Initiative Observational Study. Eleven cancers were considered obesity related: breast, ovary, endometrium, colon and rectum, esophagus, kidney, liver, multiple myeloma, pancreas, stomach, and thyroid.MethodsPostmenopausal women (n = 58 667) aged 50-79 years had body weight and waist circumference (WC) measured at baseline and year 3. Weight or WC change was categorized as stable (change < ±5%), loss (≥5%), and gain (≥5%). Self-report at year 3 characterized weight loss as intentional or unintentional. During the subsequent 12 years (mean) of follow-up, 6033 incident obesity-related cancers were identified. Relationships were evaluated using multivariable Cox proportional hazards regression models.ResultsCompared to women with stable weight, women with intentional weight loss had lower obesity-related cancer risk (hazard ratio [HR] = 0.88, 95% confidence interval [CI] = 0.80 to 0.98). A similar result was observed for intentional WC reduction (HR = 0.88, 95% CI = 0.80 to 0.96). Among all cancers, intentional weight loss was most strongly associated with endometrial cancer (HR = 0.61, 95% CI = 0.42 to 0.88). Intentional WC loss was also associated with lower colorectal cancer risk (HR = 0.79, 95% CI = 0.63 to 0.99). Unintentional weight loss or weight gain was not associated with overall obesity-related cancer risk.ConclusionIntentional weight or WC loss in postmenopausal women was associated with lower risk of obesity-related cancer. These findings suggest that postmenopausal women who intentionally lose weight can reduce their obesity-related cancer risk.
| S-EPMC6795232 | biostudies-literature
Project description:BACKGROUND: Elevated pregnancy estrogen levels are associated with increased risk of developing breast cancer in mothers. We studied whether pregnancy weight gain that has been linked to high circulating estrogen levels, affects a mother's breast cancer risk. METHODS: Our cohort consisted of women who were pregnant between 1954-1963 in Helsinki, Finland, 2,089 of which were eligible for the study. Pregnancy data were collected from patient records of maternity centers. 123 subsequent breast cancer cases were identified through a record linkage to the Finnish Cancer Registry, and the mean age at diagnosis was 56 years (range 35 - 74). A sample of 979 women (123 cases, 856 controls) from the cohort was linked to the Hospital Inpatient Registry to obtain information on the women's stay in hospitals. RESULTS: Mothers in the upper tertile of pregnancy weight gain (>15 kg) had a 1.62-fold (95% CI 1.03-2.53) higher breast cancer risk than mothers who gained the recommended amount (the middle tertile, mean: 12.9 kg, range 11-15 kg), after adjusting for mother's age at menarche, age at first birth, age at index pregnancy, parity at the index birth, and body mass index (BMI) before the index pregnancy. In a separate nested case-control study (n = 65 cases and 431 controls), adjustment for BMI at the time of breast cancer diagnosis did not modify the findings. CONCLUSIONS: Our study suggests that high pregnancy weight gain increases later breast cancer risk, independently from body weight at the time of diagnosis.
| S-EPMC535935 | biostudies-literature
Project description:BackgroundWe analyzed data from the Japan Collaborative Cohort Study (36 164 women aged 40-79 years at baseline in 1988-1990 with no previous diagnosis of breast cancer and available information on weight and height) to examine the association between baseline body mass index (BMI)/weight gain from age 20 years and breast cancer risk in a non-Western population.MethodsThe participants were followed prospectively from enrollment until 1999-2003 (median follow-up: 12.3 years). During follow-up, breast cancer incidence was mainly confirmed through record linkage to population-based cancer registries. A Cox proportional hazards model was used to calculate hazard ratios (HRs) and 95% CIs for the association between breast cancer risk and body size.ResultsIn 397 644.1 person-years of follow-up, we identified 234 breast cancer cases. Among postmenopausal women, the adjusted HR increased with BMI, with a significant linear trend (P < 0.0001). Risk was significantly increased among women with a BMI of 24 or higher (HR: 1.50, 95% CI: 1.09-2.08 for BMI of 24-28.9, and 2.13, 1.09-4.16 for BMI ≥ 29) as compared with women with a BMI of 20 to 23.9. Weight gain after age 20 years and consequent overweight/obesity were combined risk factors for postmenopausal breast cancer risk. This combined effect was stronger among women aged 60 years or older. However, the HRs were not significant in premenopausal women.ConclusionsOur findings support the hypothesis that weight gain and consequent overweight/obesity are combined risk factors for breast cancer among postmenopausal women, particularly those aged 60 years or older.
| S-EPMC3700246 | biostudies-literature
Project description:Second-generation antipsychotics can greatly improve symptoms of psychosis-spectrum disorders. Unfortunately, these drugs are associated with weight gain, which increases a patient's risk for developing chronic diseases including Type 2 diabetes, cardiovascular diseases or other obesity-related complications. There are interindividual differences in weight gain resulting from antipsychotic drug use that may be explained by pharmacodynamic characteristics of these agents as well as clinical factors. In addition, genetic variations in pathways associated with satiety are increasingly recognized as potential contributors to antipsychotic-associated weight gain. Polymorphisms in the leptin gene, as well as the leptin receptor gene, are potential pharmacogenetic markers associated with these outcomes. This article summarizes evidence for the associations of the leptin gene and the leptin receptor gene polymorphisms with antipsychotic-induced weight gain, potential mechanisms underlying these relationships, and discusses areas for future pharmacogenetic investigation.
| S-EPMC3792568 | biostudies-literature
Project description:BACKGROUND:Obesity and HIV disproportionately affect minorities and have significant health risks, but few studies have examined disparities in weight change in HIV-seropositive (HIV+) cohorts. OBJECTIVE:To determine racial and health insurance disparities in significant weight gain in a predominately Hispanic HIV+ cohort. METHODS:Our observational cohort study of 1214 nonunderweight HIV+ adults from 2007 to 2010 had significant weight gain [?3% annual body mass index (BMI) increase] as the primary outcome. The secondary outcome was continuous BMI over time. A 4-level race-ethnicity/insurance predictor reflected the interaction between race-ethnicity and insurance: insured white (non-Hispanic), uninsured white, insured minority (Hispanic or black), or uninsured minority. Logistic and mixed-effects models adjusted for baseline BMI, age, gender, household income, HIV transmission category, antiretroviral therapy type, CD4 count, plasma HIV-1 RNA, observation months, and visit frequency. RESULTS:The cohort was 63% Hispanic and 14% black; 13.3% were insured white, 10.0% uninsured white, 40.9% insured minority, and 35.7% uninsured minority. At baseline, 37.5% were overweight, 22.1% obese. Median observation was 3.25 years. Twenty-four percent of the cohort had significant weight gain, which was more likely for uninsured minority patients than insured whites [adjusted odds ratio = 2.85, 95% confidence intervals (CIs): 1.66 to 4.90]. The rate of BMI increase in mixed-effects models was greatest for uninsured minorities. Of 455 overweight at baseline, 29% were projected to become obese in 4 years. CONCLUSIONS AND RELEVANCE:In this majority Hispanic HIV+ cohort, 60% were overweight or obese at baseline, and uninsured minority patients gained weight more rapidly. These data should prompt greater attention by HIV providers for prevention of obesity.
| S-EPMC3957274 | biostudies-literature
Project description:Dynamic changes in body weight have long been recognized as important indicators of risk for human health. Many population-based observational studies have shown that rapid weight gain during infancy, including a catch-up growth phenomenon or adiposity rebound in early childhood, predisposes a person to the development of obesity, type 2 diabetes, and cardiovascular diseases later in life. However, a consensus has not been established regarding which period of weight gain contributes to future risks. This review evaluates recent evidence on the relationship between early rapid growth and future obesity and cardiometabolic risk, with a focus on the differential significance of rapid weight gain in infancy and early childhood. Although there is a need for attention to childhood growth during early infancy before 1 yr of age as it may be related to future obesity, emerging evidence strongly suggests that toddlers showing an increase in body mass index (BMI) before 3 yr of age, a period normally characterized by decreased BMI, are prone to developing later cardiometabolic risk.
| S-EPMC7534524 | biostudies-literature
Project description:ObjectiveAssessment of the joint and independent relationships of gestational weight gain and prepregnancy body mass index (BMI) on risk of infant mortality was performed.MethodsThis study used Pennsylvania linked birth-infant death records (2003-2011) from infants without anomalies born to mothers with prepregnancy BMI categorized as underweight (n = 58,973), normal weight (n = 610,118), overweight (n = 296,630), grade 1 obesity (n = 147,608), grade 2 obesity (n = 71,740), and grade 3 obesity (n = 47,277). Multivariable logistic regression models stratified by BMI category were used to estimate dose-response associations between z scores of gestational weight gain and infant death after confounder adjustment.ResultsInfant mortality risk was lowest among normal-weight women and increased with rising BMI category. For all BMI groups except for grade 3 obesity, there were U-shaped associations between gestational weight gain and risk of infant death. Weight loss and very low weight gain among women with grades 1 and 2 obesity were associated with high risks of infant mortality. However, even when gestational weight gain in women with obesity was optimized, the predicted risk of infant death remained higher than that of normal-weight women.ConclusionsInterventions aimed at substantially reducing preconception weight among women with obesity and avoiding very low or very high gestational weight gain may reduce risk of infant death.
| S-EPMC4731302 | biostudies-literature
Project description:Background and objectiveEnvironmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring.MethodsWe included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates.ResultsFourteen studies were included (N = 108 321 mother-child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16-1.49) or current (OR = 1.21; 95% CI, 1.07-1.37); each 1-kg/m(2) increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001-1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic.ConclusionsMOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed.
| S-EPMC4187236 | biostudies-literature