Body mass index (BMI) trajectories and risk of colorectal cancer in the PLCO cohort.
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ABSTRACT:
SUBMITTER: Zheng R
PROVIDER: S-EPMC6035226 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Evidence suggests that obesity in adulthood is associated with increased risk of "clinically significant" prostate cancer. However, studies of body mass index (BMI) across the adult life course and prostate cancer risks remain limited. In a prospective cohort of 69 873 men in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, we examined associations of prediagnostic BMI across the adult life course with risk of incident prostate cancer and fatal prostate cancer (prostate cancer-specific mortality). At 13 years of follow-up, we identified 7822 incident prostate cancer cases, of which 3078 were aggressive and 255 fatal. BMI trajectories were determined using latent-class trajectory modeling. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). BMI at age 20 years, 50 years, and baseline questionnaire (mean age = 63 years) were associated with increased risks of fatal prostate cancer (HRs = 1.27-1.32 per five-unit increase). In five BMI trajectories identified, fatal prostate cancer risk was increased in men who had a normal BMI (HR = 1.95, 95% CI = 1.21 to 3.12) or who were overweight (HR = 2.65, 95% CI = 1.35 to 5.18) at age 20 years and developed obesity by baseline compared with men who maintained a normal BMI. Aggressive and nonaggressive prostate cancer were not associated with BMI, and modest inverse associations were seen for total prostate cancer. Our results suggest that BMI trajectories during adulthood that result in obesity lead to an elevated risk of fatal prostate cancer.
| S-EPMC5074530 | biostudies-literature
Project description:Previously, we found that excess weight already in childhood has positive associations with endometrial cancer; however, associations with changes in body mass index (BMI) during childhood are not well understood. Therefore, we examined whether growth in childhood BMI is associated with endometrial cancer and its sub-types. A cohort of 155,505 girls from the Copenhagen School Health Records Register with measured weights and heights at the ages of 6-14 years and born 1930-1989 formed the analytical population. BMI was transformed to age-specific z scores. Using linear spline multilevel models, each girl's BMI growth trajectory was estimated as the deviance from the average trajectory for three different growth periods (6.25-7.99, 8.0-10.99, 11.0-14.0 years). Via a link to health registers, 1,020 endometrial cancer cases were identified, and Cox regressions were performed. A greater gain in BMI during childhood was positively associated with endometrial cancer but no differences between the different growth periods were detected in models adjusted for baseline BMI. The hazard ratios for the associations with overall growth during childhood per 0.1 z score increase were 1.15 (95% confidence interval [CI]: 1.07-1.24) for all endometrial cancers, 1.12 (95% CI: 1.04-1.21) for estrogen-dependent cancers, 1.16 (95% CI: 1.06-1.26) for endometrioid adenocarcinomas and 1.46 (95% CI: 1.16-1.84) for non-estrogen-dependent cancers. Growth in BMI in early life is positively linked to later endometrial cancer risk. We did not identify any sensitive childhood growth period, which suggests that excess gain in BMI during the entire childhood period should be avoided.
| S-EPMC5132154 | biostudies-literature
Project description:Obesity is a serious public health problem in China. The relationship between obesity and socio-economic status (SES) is changing and affected by uncertainty, particularly, in developing countries. The sex-related differences in body mass index (BMI) trajectories are controversial and require substantial empirical data for updating and enriching.This study examined the relationship between SES and BMI in Chinese adults from a dynamic perspective using longitudinal data (1991-2011) from the China Health and Nutrition Survey (CHNS). Then, sex-related differences were determined. A hierarchical linear model was used.SES positively affected the male BMI changes, with faster BMI growth rates in the high-SES males over the past 20 years. By contrast, female BMI was only affected by BMI baseline and residential area. Specifically, greater BMI baseline led to greater BMI growth rate and earlier BMI decline. In the past 20 years, the BMI growth rate has been greater in the urban females than in the rural females.The relationship between SES and obesity is complex in China, and a substantial sex-related difference exists. We argue that this large sex-related difference is due to the rapid economic and social changes that have affected national health and increased the gender inequality and social role restrictions in females. We provide insights for further research and policy recommendations.
| S-EPMC5559788 | biostudies-other
Project description:It is unclear whether there are different body mass index (BMI) trajectories among a population with normal BMI levels, and the association between BMI patterns and incident hypertension is not well characterized. This prospective cohort study includes surveys conducted at baseline and three follow-ups. 3939 participants who are free of hypertension at baseline or first two follow-ups were enrolled. At baseline, the age of participants ranged from 35 to 82 years and the mean age was 45.9 years. The BMI trajectories were identified using latent mixture modeling with data from the baseline and first two follow-ups. The effects of different BMI trajectories on the development of hypertension were analyzed using a Cox proportional hazard model. Four distinct BMI trajectories were identified over the study period (2004-2010): normal-stable (n = 1456), normal-increasing (n = 2159), normal-fluctuated (n = 166), and normal-sharp-increasing (n = 158). Relative to the normal-stable BMI group, the hazard ratios (HRs) and 95% confidence intervals (CIs) after adjustment for confounding factors of the normal-increasing, normal-fluctuated, and normal-sharp-increasing groups were 1.244 (1.103-1.402), 1.331 (1.008-1.756), and 1.641 (1.257-2.142), respectively. Additionally, subgroup analysis showed that the normal-fluctuated BMI trajectory was associated with a significantly higher risk of hypertension only in women (HR = 1.362; 95% CI = 1.151-1.611). The BMI trajectories were significant predictors of hypertension incidence, and increasing BMI trajectories within the currently designated normal range were associated with an increased hypertension risk, especially in women.
| S-EPMC8678668 | biostudies-literature
Project description:BackgroundStudies on the relationship between lifetime body mass index (BMI) trajectory and colorectal premalignant precursor lesions are limited. This study aimed to assess the relationship between prediagnostic adulthood BMI trajectory and the risk of colorectal adenomas using data from the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial.MethodsIn total, 39,824 participants in the intervention arm of the prospective PLCO cohort, who have undergone at least one colonoscopy or sigmoidoscopy examination with a confirmed diagnosis of colorectal adenomas, were enrolled and divided into four groups (underweight, normal weight, overweight, and obese) according to BMI during each age period. SAS Proc Traj was used to establish the BMI trajectory model. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsCompared with normal weight, overweight or obesity significantly increased colorectal adenomas risk in each age period after 30 years. Specifically, obesity in the 50s was most closely related to colorectal adenomas risk [HR: 1.32, 95% CI: (1.22, 1.43)]. BMI gain from the age of 40 to 50 [HR: 1.25, 95% CI: (1.11, 1.42)] showed the strongest correlation with an increased incidence of colorectal adenomas, followed by that from the age of 30 to 50 [HR: 1.19, 95% CI: (1.10, 1.29)], the age of 20 to 50 [HR: 1.16, 95% CI: (1.10, 1.24)], the age of 20 to 40 [HR: 1.14, 95% CI: (1.05, 1.23)], and the age of 20 to 30 [HR: 1.13, 95% CI: (1.02, 1.26)]. Additionally, compared with those who maintained normal weight throughout adulthood, those who progressed from normal weight to obesity [HR: 1.15, 95% CI: (1.06, 1.25)], or from overweight to obesity [HR: 1.33, 95% CI: (1.11, 1.61)], had a higher risk of colorectal adenomas.ConclusionsOverweight and obesity increased the risk of colorectal adenomas, and this risk increased with advancing age.
| S-EPMC7396232 | biostudies-literature
Project description:Little research has addressed the heterogeneity and mortality risk in body mass index (BMI) trajectories among older populations. Applying latent class trajectory models to 9,538 adults aged 51 to 77 years from the US Health and Retirement Study (1992-2008), we defined 6 latent BMI trajectories: normal weight downward, normal weight upward, overweight stable, overweight obesity, class I obese upward, and class II/III obese upward. Using survival analysis, we found that people in the overweight stable trajectory had the highest survival rate, followed by those in the overweight obesity, normal weight upward, class I obese upward, normal weight downward, and class II/III obese upward trajectories. The results were robust after controlling for baseline demographic and socioeconomic characteristics, smoking status, limitations in activities of daily living, a wide range of chronic illnesses, and self-rated health. Further analysis suggested that BMI trajectories were more predictive of mortality risk than was static BMI status. Using attributable risk analysis, we found that approximately 7.2% of deaths after 51 years of age among the 1931-1941 birth cohort were due to class I and class II/III obese upward trajectories. This suggests that trajectories of increasing obesity past 51 years of age pose a substantive threat to future gains in life expectancy.
| S-EPMC3842899 | biostudies-other
Project description:BackgroundBody mass index (BMI) during adulthood has been associated with pancreatic ductal adenocarcinoma (PDAC), however, patterns of body size across the adult life course have not been studied extensively. We comprehensively evaluated the association between adiposity across adulthood and PDAC.MethodsWe conducted a prospective analysis of 269 480 (162 735 males, 106 745 females) National Institutes of Health-AARP Diet and Health Study participants, aged 50-71 years (1995-1996) who self-reported height and weight history. Participants were followed through December 31, 2011. We examined associations between BMI (kg/m2) at ages 18, 35, 50, and 50-71 (baseline) years, their trajectories determined from latent-class trajectory modeling, and incident PDAC. Cox proportional hazard models were used to calculate multivariable adjusted hazards ratios (HRs) and 95% confidence intervals (CIs).ResultsDuring up to 15.2 years of follow-up, 3092 (2020 males, 1072 females) patients with incident PDAC were identified. BMI at all 4 ages were statistically significantly associated with increased PDAC (per 5-unit increase, HR = 1.09-1.13) with higher magnitude associations in males than females at ages 35 years and older (Pinteraction < .05). Four BMI trajectories were created. Compared with normal-weight maintainers, normal-to-overweight, normal-to-obese class I, and overweight-to-obese class III trajectories had hazard ratios of 1.15 (95% CI = 1.06 to 1.25), 1.39 (95% CI = 1.25 to 1.54), and 1.48 (95% CI = 1.18 to 1.87), respectively (Pinteraction by sex = .07).ConclusionsHigh BMI and BMI trajectories that result in overweight or obesity during adulthood were positively associated with PDAC, with stronger associations among those with early onset adiposity and those with male sex. Avoidance of excess body weight throughout the adult life course may prevent PDAC.
| S-EPMC9651977 | biostudies-literature
Project description:Traditional observational studies have reported a positive association between higher body mass index (BMI) and the risk of colorectal cancer (CRC). However, evidence from other approaches to pursue the causal relationship between BMI and CRC is sparse. A two-sample Mendelian randomization (MR) study was undertaken using 68 single nucleotide polymorphisms (SNPs) from the Japanese genome-wide association study (GWAS) and 654 SNPs from the GWAS catalogue for BMI as sets of instrumental variables. For the analysis of SNP-BMI associations, we undertook a meta-analysis with 36 303 participants in the Japanese Consortium of Genetic Epidemiology studies (J-CGE), comprising normal populations. For the analysis of SNP-CRC associations, we utilized 7636 CRC cases and 37 141 controls from five studies in Japan, and undertook a meta-analysis. Mendelian randomization analysis of inverse-variance weighted method indicated that a one-unit (kg/m2 ) increase in genetically predicted BMI was associated with an odds ratio of 1.13 (95% confidence interval, 1.06-1.20; P value <.001) for CRC using the set of 68 SNPs, and an odds ratio of 1.07 (1.03-1.11, 0.001) for CRC using the set of 654 SNPs. Sensitivity analyses robustly showed increased odds ratios for CRC for every one-unit increase in genetically predicted BMI. Our MR analyses strongly support the evidence that higher BMI influences the risk of CRC. Although Asians are generally leaner than Europeans and North Americans, avoiding higher BMI seems to be important for the prevention of CRC in Asian populations.
| S-EPMC8019210 | biostudies-literature
Project description:BackgroundHigh body mass index (BMI) is consistently linked to increased risk of colorectal cancer for men, whereas the association is less clear for women. As risk estimates from observational studies may be biased and/or confounded, we conducted a Mendelian randomization study to estimate the causal association between BMI and colorectal cancer.MethodsWe used data from 10,226 colorectal cancer cases and 10,286 controls of European ancestry. The Mendelian randomization analysis used a weighted genetic risk score, derived from 77 genome-wide association study-identified variants associated with higher BMI, as an instrumental variable (IV). We compared the IV odds ratio (IV-OR) with the OR obtained using a conventional covariate-adjusted analysis.ResultsIndividuals carrying greater numbers of BMI-increasing alleles had higher colorectal cancer risk [per weighted allele OR, 1.31; 95% confidence interval (CI), 1.10-1.57]. Our IV estimation results support the hypothesis that genetically influenced BMI is directly associated with risk for colorectal cancer (IV-OR per 5 kg/m(2), 1.50; 95% CI, 1.13-2.01). In the sex-specific IV analyses higher BMI was associated with higher risk of colorectal cancer among women (IV-OR per 5 kg/m(2), 1.82; 95% CI, 1.26-2.61). For men, genetically influenced BMI was not associated with colorectal cancer (IV-OR per 5 kg/m(2), 1.18; 95% CI, 0.73-1.92).ConclusionsHigh BMI was associated with increased colorectal cancer risk for women. Whether abdominal obesity, rather than overall obesity, is a more important risk factor for men requires further investigation.ImpactOverall, conventional epidemiologic and Mendelian randomization studies suggest a strong association between obesity and the risk of colorectal cancer.
| S-EPMC4490960 | biostudies-literature
Project description:BACKGROUND:Accurately characterizing children's body mass index (BMI) trajectories and studying their determinants is a statistical challenge. There is a need to identify early public health measures for obesity prevention. We describe a method that allows studies of the determinants of height, weight and BMI growth up to five years of age. We illustrated this method using maternal smoking during pregnancy as one of the early-life factors that is potentially involved in prenatal programming of obesity. METHODS:Individual height and weight trajectories were fitted using the Jenss-Bayley model on 28,381 and 30,515 measurements, respectively, from 1,666 children to deduce BMI trajectories. We assessed global associations between smoking and growth trajectories and cross-sectional associations at specific ages. RESULTS:Children exposed in late pregnancy had a 0.24 kg/m2 (95% confidence interval: 0.07, 0.41) higher BMI at 5 years of age compared with non-exposed children. Although the BMIs of children exposed during late pregnancy became significantly higher compared with those of non-exposed children from 2 years onwards, the trajectories began to diverge during the first weeks of life. CONCLUSION:Our method is relevant for studies on the relationships between individual-level exposures and the dynamics and shapes of BMI growth during childhood, including key features such as instantaneous growth velocities and the age or BMI value at the BMI infancy peak that benefit from the monotonic pattern of height and weight growth.
| S-EPMC4915665 | biostudies-other