Body Mass Index In Early Adulthood Research Articles

Late midlife C-reactive protein and interleukin-6 in middle aged danish men in relation to body size history within and across generations.

The aim was to estimate the effects of ponderal index at birth and body mass index (BMI) in early adulthood on C-reactive protein (CRP) and interleukin-6 (IL-6) and to quantify the effects through subsequent measures of body size. In a subanalysis, the contributions of maternal BMI to the inflammatory status of offspring were investigated. The study was based on 2,986 Danish males from the Copenhagen Aging and Midlife Biobank. Path analysis was employed to estimate direct and indirect effects. A 10% higher maternal BMI was associated with 7% higher CRP and 3% higher IL-6 among offspring. A 10% higher ponderal index at birth was associated with 4% lower CRP in late midlife; this effect was only partially mediated by later growth. A 10% higher BMI in early adulthood was associated with 8% higher CRP and 4% higher IL-6 in late midlife. The findings suggest that weight gain in adulthood is associated with low-grade inflammation in late midlife. Ponderal index at birth is associated with CRP in later life independently of adult BMI. The findings additionally suggest that preventing weight gain in early adulthood would be beneficial for inflammatory status in later life.

Obesity and Risk of Monoclonal Gammopathy of Undetermined Significance: A Population-Based Study

BackgroundNearly all multiple myelomas (MM) are preceded by the premalignant state, monoclonal gammopathy of undetermined significance (MGUS), an asymptomatic condition that needs no treatment. The etiology of MGUS and MM is to a large extent unknown. Two studies on the association between obesity and MGUS have been conducted with conflicting results, despite a reported association between obesity and MM. The aim of this study was to determine if obesity is associated with an increased risk of MGUS and light-chain MGUS (LC-MGUS) in a population-based screened cohort of individuals above the age of 65 years using extensive number of markers for current and early life obesity.MethodsThis study was based on participants from the Age, Gene/Environment Susceptibility – Reykjavik Study (AGES-RS), which is a continuation of the Reykjavik Study, a population-based study performed by the Icelandic Heart Association. In 1967, the Reykjavik Study began recruiting a sample of over 30,000 residents of Reykjavik from the 1907-1935 birth cohorts. In 2002, the AGES-RS began recruiting 5,764 of the surviving members. Serum protein electrophoresis (SPEP) and serum free light-chain assay were performed on all subjects. Obesity measures were performed at baseline, and participants were additionally asked about their weight at the age of 25 years. The measures at baseline included were weight (kg), body mass index (BMI) (kg/m2), percent body fat, fat (kg), and fat-free mass (kg) from bioimpedance, total body fat area (cm2), visceral and subcutaneous fat area (cm2), and waist circumference (cm). The association with MGUS and LC-MGUS was analyzed using logistic regression and adjustment was made for age and sex. Cox proportional-hazard regression was performed to test whether obesity was a risk factor for progression from MGUS to MM and lymphoproliferative diseases.ResultsA total of 304 (5.3%) MGUS cases and 118 participants (2.1%) with LC-MGUS were identified. No association was found between any of the obesity markers and MGUS (Table). A statistically significant positive association was found between obesity (BMI ≥ 30 kg/m2) at study baseline and LC-MGUS (Table). Weak but statistically significant association was found between LC-MGUS and BMI at baseline, weight, max weight, percent body fat, fat in kg, fat-free mass, and waist circumference (Table). No association was found on risk of MGUS using joint effect of early adulthood BMI and BMI at study entry. Analysis on the effect of the obesity markers on the progression from MGUS to MM and lymphoproliferative diseases showed no association.ConclusionIn this large population-based cross-sectional study aimed at evaluating the association between obesity and MGUS and LC-MGUS, we found obesity (BMI ≥ 30 kg/m2) to be associated with 2-fold excess risk for LC-MGUS. An association was additionally found between several of the obesity markers used and LC-MGUS. Future studies are needed to clarify underlying mechanisms for this finding. However, we did not find an association between any of the obesity markers and MGUS. Taken together, we were unable to confirm the previously reported association between MGUS and obesity.Abstract 5706. Table:Obesity and risk of MGUS or light-chain MGUS (LC-MGUS)No MGUSMGUSLC-MGUSNo MGUS vs. MGUS OR* (95%CI)No MGUS vs. LC MGUS OR* (95%CI)BMI (n)<25178310226ReferenceReference25-302286147551.15 (0.88 - 1.50)1.55 (0.97 - 2.49)≥30117651340.85 (0.60 - 1.20)2.12 (1.26 - 3.58)BMI 25y (n)<25394922083ReferenceReference≥2580944250.87 (0.62-1.22)1.13 (0.71-1.79)BMI (kg/m2)27.026.728.31.00 (0.97 - 1.02)1.07 (1.03 - 1.12)BMI 25y (kg/m2)22.822.922.90.99 (0.94 - 1.04)0.93 (0.86 - 1.01)Weight (kg)75.275.384.11.00 (0.99 - 1.01)1.03 (1.02 - 1.04)Max weight (kg)80.682.389.11.00 (0.99 - 1.01)1.02 (1.01 - 1.03)Percent body fat (%)28.926.827.20.99 (0.97 - 1.02)1.04 (1.01 - 1.07)Fat (kg)21.920.522.71.00 (0.98 - 1.02)1.04 (1.01 - 1.07)Fat free mass (kg)53.455.460.31.00 (0.98 - 1.02)1.04 (1.01 - 1.07)Total body fat area (cm2)493.1481.8543.21.00 (1.00 - 1.00)1.00 (1.00 - 1.00)Visceral fat area (cm2)171.8174.4209.41.00 (1.00 - 1.00)1.00 (1.00 - 1.00)Subcutaneous fat area (cm2)256.3241.6260.11.00 (1.00 - 1.00)1.00 (1.00 - 1.00)CT waist circumference (cm)125.7125.7131.11.00 (0.99 - 1.01)1.03 (1.01 - 1.04)Waist circumference (cm)100.7100.8105.61.00 (0.99 - 1.01)1.03 (1.01 - 1.05)*Adjusted for age and sex DisclosuresNo relevant conflicts of interest to declare.

Higher weight in adolescence and young adulthood is associated with an earlier age at multiple sclerosis onset

Background: Growing evidence suggests an association between adolescent obesity and increased risk of multiple sclerosis (MS). Objective: The objective of this paper is to investigate whether weight or body mass index (BMI) in adolescence and young adulthood was associated with age at MS symptom onset. Methods: Our cohort is comprised of a sub-group of 184 women enrolled in the New York State MS Consortium registry. Individuals were asked to recall their weight at the time of first menstruation and at age 25. BMI was calculated accordingly for age 25. Regression analyses were carried out to investigate the association between weight or BMI and age at onset. Results: Weight at menarche was significantly related to younger age at symptom onset (β = −0.073, p = 0.001). These results were also found at age 25 for weight (β = −0.080, p < 0.001) and BMI (β = −0.448, p = 0.001). Significantly earlier disease onset (26.9 years ±9.9) was observed in individuals who were overweight at 25 compared to those who were not overweight (32.1 years ±9.2, p = 0.006). Conclusions: Women who reported higher weight in adolescence and BMI in early adulthood were younger at MS onset. Future research should investigate whether there is a causal link between body weight and MS, as prevention lifestyle and dietary interventions could be implemented.

Prenatal vitamin intake during pregnancy and offspring obesity.

Background/ObjectivesIn animal studies, exposure to multi-vitamins may be associated with obesity in the offspring; however, data in humans is sparse. We therefore examined the association between prenatal vitamin intake during pregnancy and offspring obesity.Subjects/MethodsWe investigated the association between prenatal vitamin intake and obesity among 29 160 mother-daughter dyads in the Nurses’ Health Study II. Mothers of participants provided information on prenatal vitamin use during pregnancy with the nurse daughter. Information on body fatness at ages 5 and 10, body mass index (BMI) at age 18, weight in 1989 and 2009, waist circumference, and height was obtained from the daughter. Polytomous logistic regression was used to predict BMI in early adulthood and adulthood, and body fatness in childhood. Linear regression was used to predict waist circumference in adulthood.ResultsIn utero exposure to prenatal vitamins was not associated with body fatness, either in childhood or adulthood. Women whose mothers took prenatal vitamins during pregnancy had a covariate-adjusted odds ratio of being obese in adulthood of 0.99 (95% CI 0.92 – 1.05, P-value = 0.68) compared to women whose mothers did not take prenatal vitamins. Women whose mothers took prenatal vitamins during pregnancy had a covariate-adjusted odds ratio of having the largest body shape at age 5 of 1.02 (95% CI 0.90 – 1.15, P-value = 0.78). In additional analyses, in utero exposure to prenatal vitamins was also unrelated to adult abdominal adiposity.ConclusionsExposure to prenatal vitamins was not associated with body fatness either in childhood or in adulthood.

Early adulthood body mass index, cumulative smoking, and esophageal adenocarcinoma survival.

10 Background: Little is known about the individual and combined effect of early-adulthood obesity and cumulative smoking on the survival of esophageal adenocarcinoma (EAC) patients. Methods: We analyzed two independent cohorts of EAC patients: 235 patients from Toronto, Canada (TO, 2006-2011) and 329 patients from Boston, USA (BO,1999-2004). Associations between early adulthood body mass index (EA-BMI) and smoking with overall survival (OS) were assessed using Cox proportional hazard models, adjusted for stage, treatment, and other relevant covariates. Results: Median age (range) for TO dataset was 64(29-88)yrs; for BO dataset, 64(21-91)yrs. Males comprised 86% of TO and 89% of BO datasets. 90% of TO and 98% of BO patients were Caucasians. The Median (range) for packyears was 34 (0.2-118; TO) and 34 (0.2-212; BO). The Median (range) for EA-BMI was 24(15-44; TO) and 24(15-47; BO). Median BMI 1 yr prior to diagnosis was 25(16-43; TO) and 25(20-49; BO). 92% of TO and 88% of BO patients had ECOG 0 or 1. Disease stage distribution (early/locally-advanced/metastatic) was 11%/64%/25% (TO) and 30%/52%/18% (BO). For TO, the aHR for smoking was 1.03 (95%CI: 1.02-1.04; p=8E-08) per packyear, while for BO, smoking also independently conferred worse OS, with aHR of 1.007 (95%CI: 1.002-1.01; p=0.003) for each packyear increase. The aHRs for being underweight (EA-BMI&lt;18.5), overweight (EA-BMI 25-30), and obese (EA-BMI&gt;30) in early adulthood were 2.19 (95%CI: 1.0-4.6), 1.89 (95%CI:1.2-3.0), and 2.49 (95%CI:1.5-4.2), respectively for the TO dataset (global p=0.003 for EA-BMI). In BO, the corresponding values were 1.30 (95%CI: 0.8-2.2), 1.45 (95%CI: 1.0-2.5), and 2.39 (95%CI:1.5-3.8), respectively (global p=0.002). In contrast, BMI at one year prior to diagnosis had no association with OS in either study. Conclusions: Elevated BMI in early adulthood and heavy cumulative smoking history are independently associated with increased mortality risk in two North American EAC populations. These survival differences may reflect comorbidity differences, biological differences or both, and offer insight into how key modifiable behaviors in prevention can also affect cancer prognoses. AS, LC, DCC and GL contributed equally.

Adolescent and young adult exposure to physical activity and breast density.

The objective of this study is to examine the role of early lifetime exposure to physical activity on magnetic resonance imaging-determined breast density measures. Associations of adolescent (high school (ages 14-17 yr) and early adulthood, post-high school (ages 18-21 yr) and past year) leisure-time physical activity, as well as a principal component score including all three estimates, were examined with percent dense breast volume (%DBV) and absolute dense breast volume (ADBV) in a cross-sectional analysis of 182 healthy women, ages 25-29 yr, enrolled in the Dietary Intervention Study in Children Follow-up Study (DISC06). Generalized linear mixed models were used to examine associations after adjustment for relevant covariates for the entire analytic sample. Analyses were repeated in nulliparous women and hormonal contraceptive nonusers. Physical activity during high school and post-high school were not statistically significantly related to %DBV or ADBV in multivariable models. Past year physical activity was positively related to %DBV in the unadjusted and partially adjusted models (P < 0.001 and P = 0.01, respectively), which did not adjust for body mass index (BMI). After additional adjustment for childhood and early adulthood BMI, this association became nonstatistically significant. The relation between past year physical activity and ADBV was not statistically significant. These findings were similar in nonusers of hormonal contraceptives. No statistically significant relations were found in nulliparous women or between the principal component score and %DBV or ADBV. Results from this study are consistent with previous research suggesting that physical activity during adolescence and early adulthood is unrelated to breast density.

Childhood and family influences on body mass index in early adulthood: findings from the Ontario Child Health Study

BackgroundOverweight and obesity are steadily increasing worldwide with the greatest prevalence occurring in high-income countries. Many factors influence body mass index (BMI); however multiple influences assessed in families and individuals are rarely studied together in a prospective design. Our objective was to model the impact of multiple influences at the child (low birth weight, history of maltreatment, a history of childhood mental and physical conditions, and school difficulties) and family level (parental income and education, parental mental and physical health, and family functioning) on BMI in early adulthood.MethodsWe used data from the Ontario Child Health Study, a prospective, population-based study of 3,294 children (ages 4–16 years) enrolled in 1983 and followed up in 2001 (N = 1,928; ages 21–35 years). Using multilevel models, we tested the association between family and child-level variables and adult BMI after controlling for sociodemographic variables and health status in early adulthood.ResultsAt the child level, presence of psychiatric disorder and school difficulties were related to higher BMI in early adulthood. At the family level, receipt of social assistance was associated with higher BMI, whereas family functioning, having immigrant parents and higher levels of parental education were associated with lower BMI. We found that gender moderated the effect of two risk factors on BMI: receipt of social assistance and presence of a medical condition in childhood. In females, but not in males, the presence of these risk factors was associated with higher BMI in early adulthood.ConclusionOverall, these findings indicate that childhood risk factors associated with higher BMI in early adulthood are multi-faceted and long-lasting. These findings highlight the need for preventive interventions to be implemented at the family level in childhood.

Body mass index and mortality in an ethnically diverse population: the Multiethnic Cohort Study

Body mass index (BMI) has been strongly related to overall mortality, but the consistency of this association across diverse ethnic groups and the effects of early adult BMI versus BMI in later adulthood have not been adequately studied. A prospective analysis was performed using data from 183,211 adults aged 45-75 who enrolled the population-based Multiethnic Cohort Study by completing a questionnaire that included self-reported weight and height information in 1993-1996. Participants were African Americans, Native Hawaiians, Japanese Americans, Latinos, and whites living in Hawaii and California. During an average 12.5years of follow-up, 35,664 deaths were identified. To control for confounding caused by conditions that lead to weight loss and mortality, we excluded participants with a history of cancer or heart disease, who ever smoked, and who died within the first 3years of follow-up. An increased risk of mortality was observed in participants with a BMI≥27.5 in both men and women compared with the reference category of BMI 23.0-24.9; a BMI≥35.0 carried a greater risk of mortality in men than in women. Although the findings were generally similar across ethnic groups, the association of higher BMI with mortality in Latino men appeared to be weaker than in the other groups. A BMI of 25.0-34.9 at age 21 showed a stronger positive association, with no further increase in risk for a BMI≥35.0, than did BMI in later adulthood. These results indicate that the association of BMI with mortality is generally consistent across sex and ethnic groups, with some variation in the strength of the effect. Most notably, the effect of overweight in young adulthood appears to be much stronger than that of overweight in later adulthood on mortality in later life. This emphasizes the importance of weight management in childhood and adolescence.

Lactation and maternal subclinical cardiovascular disease among premenopausal women

The objective of the study was to examine the association between lactation and maternal subclinical cardiovascular disease. The Women and Infants Study of Healthy Hearts enrolled 607 mothers who delivered a singleton between 1997 and 2002. In 2007, participating mothers underwent measurements of carotid intima-media thickness, lumen diameter, adventitial diameter, and carotid-femoral pulse wave velocity. Multivariable linear and logistic regressions were used to estimate the associations between lactation and subclinical cardiovascular disease. Compared with mothers who breastfed for 3 or more months after every birth, mothers who never breastfed exhibited a 0.13 mm larger lumen diameter (95% confidence interval, 0.04-0.22) and a 0.12 mm larger adventitial diameter (95% confidence interval, 0.02-0.22) in models adjusting for age, parity, birth outcome, sociodemographic variables, health-related behaviors, family history, gestational weight gain, early adult body mass index, current body mass index, C-reactive protein, blood pressure, cholesterol, triglyceride, high-density lipoprotein, glucose, and insulin levels. Mothers who do not breastfeed have vascular characteristics associated with a greater risk of cardiovascular disease.

Association of body mass index in early adulthood and middle age with future site-specific cancer mortality: the Harvard Alumni Health Study

Background:The association between adiposity in early adulthood and subsequent development of specific malignancies is unclear. Further, the potential for mediation by adiposity in middle age has not been well examined. In a rare study, we investigated the association of body mass index (BMI) in early adulthood with mortality from several site-specific cancers.Design:In the Harvard Alumni Health Study cohort, 19 593 males had a physical examination at the university between 1914 and 1952 (mean age: 18.4 years) and returned a questionnaire in 1962 or 1966 (mean age = 45.1 years). BMI was computed using weight (kg)/height2 (m2) at both time points. Vital status follow up continued for a maximum of 82 years.Results:Positive early adulthood cancer mortality gradients by BMI were found for all malignancies combined (adjusted hazard ratio [HR] = 1.11; 95% confidence interval [CI]: 1.05–1.17 for a one standard deviation increase in early adulthood BMI), and for lung (HR = 1.24; 95% CI = 1.10–1.40) and skin (HR = 1.29; 95% CI = 0.96–1.75) cancers. There were also apparent associations for cancers of the oesophagus and urogenital sites. Mediation by BMI in middle age was found to be minimal.Conclusion:Higher BMI in early adulthood appears to be a direct risk factor for selected malignancies several decades later.

Abstract A72: Patterns of cancer risk according to weight in early, middle, and older adult life

Abstract Background: Body mass index (BMI) assessed in middle and older adulthood is positively associated with risk of multiple cancer types. Whether BMI in early adulthood is similarly associated with the risk of these cancers has not been established. We therefore examined BMI in early, middle, and older adulthood in relation to site-specific cancer risk among 160,867 men and 97,853 postmenopausal women enrolled in the prospective NIH-AARP Diet and Health Study. We additionally examined the joint association of BMI at age 18 and adulthood weight change (from ages 18 to 50) to determine the independent association of each with cancer risk. Methods: Participants completed an initial self-administered questionnaire (sent in 1995–1996) inquiring about current weight and height, demographics, and other health behaviors and a second questionnaire (1996–1997) inquiring about weight at ages 18, 35, and 50. We used Cox regression to estimate hazard ratios (HR) for the associations of BMI at different ages, as well as the joint association between BMI at age 18 and adulthood weight change, with site-specific cancer risk, adjusting for potential confounders. Cancer outcomes were restricted to those previously identified from prospective cohort studies as having consistent positive associations with obesity. Results: During the follow-up period from 1996 through 2006 (median=10.1 years), 11,268 women and 27,707 men were diagnosed with a first primary cancer. Among women, risk of pancreatic and ovarian cancers and multiple myeloma were more strongly associated with BMI at age 18 than BMI later in life (e.g., HRs for pancreatic cancer=1.21, 1.08, 1.03, and 1.02 for BMI at ages 18, 35, 50, and at enrollment, respectively, per 5 kg/m2). This finding was largely confirmed in the analysis of joint effects of BMI at age 18 (&amp;lt;25 vs ≥25 kg/m2) and adulthood weight change (&amp;lt;4 vs ≥4 kg/m2): among women who gained &amp;lt;4 kg/m2 between age 18 and 50, higher BMI at age 18 was positively associated with risk of pancreatic cancer (HR=1.46, 95% CI: 0.93–2.29), and greater adulthood weight gain did not further increase this risk. In contrast, we found stronger positive associations between BMI at older versus younger ages and risk of endometrial and breast cancers and leukemia (e.g. endometrial HRs=1.24, 1.46, 1.50, and 1.55 for BMI at ages 18, 35, 50, and at enrollment). In line with these results, adulthood weight gain was positively associated with risk of breast cancer and leukemia in women irrespective of BMI at age 18, while BMI at age 18 was not positively associated with risk of these cancers after controlling for weight gain. For endometrial cancer, however, we observed independent positive associations for BMI at age 18 (≥25 vs &amp;lt;25 kg/m2) and adulthood weight gain (≥4 vs &amp;lt;4 kg/m2) (joint HR=3.01, 95% CI: 2.09–4.32). In men, associations for BMI at ages 18, 35, 50, and at enrollment were similar by cancer site (e.g., kidney cancer HRs=1.25, 1.36, 1.39, 1.32, respectively). Also in men, we found that BMI at age 18 and adulthood weight gain were independently positively associated with risk for most of the cancer sites examined, including NHL and kidney, thyroid, liver, gastric cardia cancers. Conclusion: There may be sensitive periods in the life course during which body weight has a particularly important role in cancer development; these influences may be site- and gender-specific. For many obesity-related cancers, higher BMI at age 18 and greater weight gain by age 50 had independent positive associations with risk. Citation Information: Cancer Prev Res 2011;4(10 Suppl):A72.

Early adulthood obesity, cumulative smoking, and esophageal cancer survival.

1546 Background: Obesity and smoking have been associated with worsening outcomes of several cancer types. However, little is known about the combined impact of early adulthood obesity (decades prior to diagnosis) and smoking on mortality of esophageal cancer (EC). Methods: We analyzed data from a cohort of 345 patients with EC from Boston, USA enrolled from 1999 to 2004. Associations between early adulthood body mass index (EABMI) (not at time of diagnosis) and smoking and overall survival (OS) were assessed using Cox proportional hazard models, adjusted for age, stage, performance status. Results: EABMI was independently associated with worse OS (HRadj=1.04; 95% CI, 1.01-1.07; p=0.009; continuous variable (CV)). When patients were evaluated in quartiles, the highest quartile of EABMI (>26.9) had the worst survival (HRadj=1.52; 1.1-2.1; p=0.01). In contrast, BMI 1 year prior to diagnosis had no association with OS. Cumulative smoking also independently conferred worse OS (HRadj=1.01; 1.00-1.01; p=0.005; CV); when evaluated using quintiles, OS was worst in the heaviest smoking quintile (>85 pack-years) (HRadj=1.60; 95% CI, 1.1-2.3; p=0.007). Compared with the lowest weight patients (during their early adulthood years) who were never smokers, HRadj for mortality increased progressively with increasing quintiles of both smoking and quartiles of EABMI. In joint effects analysis, within the highest BMI quartile (>26.9), the HRadj rose from 0.4 (0.1-1.5; lowest smoking quintile, consisting of lifetime never-smokers) through 1.8 (0.8-3.9; highest smoking quintile of >56 pack-years). Likewise, within the highest smoking quintile (>56 pack-years), the HRadj rose from 1.0 (0.4-2.3; lowest BMI quartile of <21) through to 1.8 (0.8-3.9; highest BMI quartile >26.9). Conclusions: Among EC patients, elevated BMI in early adulthood and heavy cumulative smoking history are independently associated with increased mortality risk. The combination of obesity and smoking is related to an especially higher mortality risk. These differences may reflect differences in obesity- or smoking-related comorbidities, but may also be due to biologic differences arising from different, adiposity-related carcinogenic pathways.

A pooled analysis of 14 cohort studies of anthropometric factors and pancreatic cancer risk.

Epidemiologic studies of pancreatic cancer risk have reported null or nonsignificant positive associations for obesity, while associations for height have been null. Waist and hip circumference have been evaluated infrequently. A pooled analysis of 14 cohort studies on 846,340 individuals was conducted; 2,135 individuals were diagnosed with pancreatic cancer during follow-up. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Compared to individuals with a body mass index (BMI) at baseline between 21-22.9 kg/m(2) , pancreatic cancer risk was 47% higher (95%CI:23-75%) among obese (BMI ≥ 30 kg/m(2) ) individuals. A positive association was observed for BMI in early adulthood (pooled multivariate [MV]RR = 1.30, 95%CI = 1.09-1.56 comparing BMI ≥ 25 kg/m(2) to a BMI between 21 and 22.9 kg/m(2) ). Compared to individuals who were not overweight in early adulthood (BMI < 25 kg/m(2) ) and not obese at baseline (BMI < 30 kg/m(2) ), pancreatic cancer risk was 54% higher (95%CI = 24-93%) for those who were overweight in early adulthood and obese at baseline. We observed a 40% higher risk among individuals who had gained BMI ≥ 10 kg/m(2) between BMI at baseline and younger ages compared to individuals whose BMI remained stable. Results were either similar or slightly stronger among never smokers. A positive association was observed between waist to hip ratio (WHR) and pancreatic cancer risk (pooled MVRR = 1.35 comparing the highest versus lowest quartile, 95%CI = 1.03-1.78). BMI and WHR were positively associated with pancreatic cancer risk. Maintaining normal body weight may offer a feasible approach to reducing morbidity and mortality from pancreatic cancer.

Childhood, adolescent and early adult body mass index in relation to adult mortality: results from the British 1946 birth cohort

BackgroundAdult body mass index (BMI) has been consistently related to mortality, but little is known about the impact of earlier life BMI on adult mortality. The aim is to investigate...

Abstract 1833: Body mass index and physical activity in relation to risk of non-Hodgkin lymphoma (NHL)

Abstract Background: Obesity has been linked to NHL risk in some studies, and may be stronger for obesity in early adulthood (ages 18-20). There has only been limited evaluation of physical activity and risk of NHL, particularly physical activity earlier in life. The purpose of this study was to evaluate the association of body mass index (BMI), physical activity (PA), and NHL risk during adulthood and at age 18. Methods: Self-reported anthropometrics and PA were collected in a clinic-based study of 954 newly diagnosed NHL cases and 1146 controls enrolled at the Mayo Clinic from 2002-2008. PA variables included duration and frequency of mild, moderate, and strenuous PA two years prior to case diagnosis or control selection, strenuous activity at age 18 (any vs. none), and height and weight at both time periods. An overall PA index was estimated by weighting the reported duration and frequency of each PA intensity by the average energy requirement (defined in METs) to obtain an average MET-minutes/week for each participant. BMI was calculated as weight (kg) divided by height (m) squared. Odds Ratios (OR), 95% confidence intervals (CI), and test for trend were estimated using unconditional logistic regression adjusted for the age, gender, and residence. Continuous variables were divided into quartiles according to the distribution among the controls; results are reported for the highest vs. lowest category or quartile unless otherwise specified. Results: The mean age at diagnosis/enrollment was 61 for both cases and controls; 47% and 43% of the cases and controls, respectively, were female. The most common NHL subtypes were CLL/SLL (32%), follicular lymphoma (FL; 26%), and diffuse large B-cell lymphoma (DLBCL; 21%). BMI 2 years prior to diagnosis was not associated with NHL risk (OR=1.21, p-trend=0.13), while there was a positive association with BMI at age 18 (OR=1.40, p-trend=0.001). There was no association of the PA index with risk (OR=0.91, p-trend=0.29). Furthermore, frequency of walking (OR=0.71, p-trend 0.43), mild (OR=1.30, p-trend=0.64), moderate (OR=0.99, p-trend=0.75), and strenuous (OR=0.77, p-trend=0.20) PA were not associated with NHL risk when evaluated individually. However, there was a suggestive weak inverse association between strenuous activity at age 18 and NHL risk (OR=0.85, 95% CI 0.71-1.05). On exploratory analysis, the association of BMI at age 18 with NHL risk was specific to DLBCL (OR=1.84, p-trend=0.002) and CLL/SLL (OR=1.25, p-trend=0.044) but not FL; all other results were similar across these subtypes. Conclusions: We did not observe an association between adult BMI and NHL risk; however a higher BMI in early adulthood was associated with NHL risk, consistent with limited prior reports. We found little evidence to support an association between PA in either early adulthood or later in life and NHL risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1833.

Association between obesity and the risk of malignant lymphoma in Japanese: a case–control study

Although marked differences in anthropometric characteristics and malignant lymphoma (ML) incidence suggest that the association between obesity and ML risk in Asian and non-Asian populations may differ, few studies have investigated this association in Asian populations. Here, we conducted a sex- and age-matched case-control study in a Japanese population using 782 cases and 3,910 noncancer controls in the hospital-based Epidemiological Research Program at Aichi Cancer Center Hospital. Odds ratios (ORs) and 95% confidence intervals (CIs) for anthropometric characteristics were estimated using a conditional logistic regression model that incorporated smoking and alcohol intake. Recent body weight and body mass index (BMI) showed marginally significant association with ML risk (ORs [95% CIs] per 5-unit increase in recent weight and BMI; 1.04 [0.99-1.09] and 1.11 [0.98-1.27], respectively). On the other hand, weight and BMI in early adulthood exhibited a strong association with ML risk (ORs [95% CIs] per 5-unit increase in early adulthood weight and BMI; 1.11 [1.05-1.18] and 1.33 [1.13-1.55], respectively). Further, in women, a BMI of 25.0-29.9 kg/m(2), defined as obesity in Asian populations, during early adulthood was significantly associated with ML risk compared to the normal range of 18.5-22.9 kg/m(2). By histological ML subtype, the point estimates of ORs for obesity relative to normal weight in early adulthood were over unity for non-Hodgkin lymphoma (NHL) as a whole and significant for diffuse large B-cell lymphoma (DLBCL). In conclusion, our study in Japanese subjects suggested that early adulthood obesity is associated with the risk of NHL, particularly DLBCL.

Body mass index through life and adult mortality: results from the British 1946 birth cohort

Adult body mass index (BMI) has been consistently related to mortality, but little is known about the impact of earlier life BMI on adult mortality. Investigate the impact of childhood,...

Obesity and restless legs syndrome in men and women

Obesity and restless legs syndrome (RLS) are both associated with hypofunction of dopamine in the CNS. We therefore examined whether individuals who are obese have an increased risk of RLS in two ongoing US cohorts, the Nurses' Health Study II and the Health Professional Follow-up Study. We included 65,554 women and 23,119 men free of diabetes, arthritis, and pregnancy in the current analyses. Information on RLS was assessed using a set of standardized questions. Participants were considered to have RLS if they met four RLS diagnostic criteria recommended by the International RLS Study Group and had restless legs > or =5 times/month. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed using logistic regression models adjusting for age, smoking, use of antidepressant, phobic anxiety score, and other covariates. Log ORs from the two cohorts were pooled by a fixed-effects model. There were 6.4% of women and 4.1% of men who were considered to have RLS. Multivariate adjusted ORs for RLS were 1.42 (95% CI: 1.3, 1.6; p trend <0.0001) for participants with body mass index (BMI) >30 vs <23 kg/m(2) and 1.60 (95% CI: 1.5, 1.8; p trend <0.0001) for highest vs lowest waist circumference quintiles. Greater BMI in early adulthood (age 18-21 years) and weight gain were also associated with a higher prevalence of RLS (p trend <0.01 for both). Both overall and abdominal adiposity are associated with increased likelihoods of having restless legs syndrome (RLS). Further prospective studies are warranted to clarify causative association between obesity and risk of developing RLS.

Height, Body Mass Index, and Ovarian Cancer: A Pooled Analysis of 12 Cohort Studies

Although many studies have investigated the association between anthropometry and ovarian cancer risk, results have been inconsistent. The associations of height, body mass index (BMI), and ovarian cancer risk were examined in a pooled analysis of primary data from 12 prospective cohort studies from North America and Europe. The study population consisted of 531,583 women among whom 2,036 epithelial ovarian cancer cases were identified. To summarize associations, study-specific relative risks (RR) were estimated using the Cox proportional hazards model and then combined using a random-effects model. Women with height > or =1.70 m had a pooled multivariate RR of 1.38 [95% confidence interval (95% CI), 1.16-1.65] compared with those with height <1.60 m. For the same comparison, multivariate RRs were 1.79 (95% CI, 1.07-3.00) for premenopausal and 1.25 (95% CI, 1.04-1.49) for postmenopausal ovarian cancer (P(interaction) = 0.14). The multivariate RR for women with a BMI > or =30 kg/m(2) was 1.03 (95% CI, 0.86-1.22) compared with women with a BMI from 18.5 to 23 kg/m(2). For the same comparison, multivariate RRs were 1.72 (95% CI, 1.02-2.89) for premenopausal and 1.07 (95% CI, 0.87-1.33) for postmenopausal women (P(interaction) = 0.07). There was no statistically significant heterogeneity between studies with respect to height or BMI. BMI in early adulthood was not associated with ovarian cancer risk. Height was associated with an increased ovarian cancer risk, especially in premenopausal women. BMI was not associated with ovarian cancer risk in postmenopausal women but was positively associated with risk in premenopausal women.

Systematic review of prostate cancer’s association with body size in childhood and young adulthood

Body size relatively early in life may influence men's later rate of prostate cancer. We searched for published, English-language studies of the association between prostate cancer incidence or mortality and body size between ages 5 and 29 years. We summarized analyses of childhood body size, early-adult waist circumference, and early-adult body mass index (BMI). Most study designs were case-control or retrospective cohort studies, in which body size was self-reported and recalled. The few studies of childhood body size and early-adult waist circumference indicated null or weak associations. The results from studies of early-adult BMI were heterogeneous (p = 0.04) and showed evidence of funnel plot asymmetry. The random-effects rate ratio (RR) was 1.06 (95% confidence interval [CI]: 0.99, 1.14) per five-unit increase in BMI. Studies using measured (as opposed to self-recalled) height and weight (n = 3) tended to produce stronger associations: fixed-effects summary RR = 1.22 (1.06, 1.39). The same was true for studies that did not adjust for later-life BMI (n = 13): fixed-effects RR = 1.13 (1.06, 1.21). Examining only analyses of advanced or high-grade prostate cancers, results were heterogeneous (p < 0.01). The random-effects summary RR per five units of BMI was 1.01 (95% CI: 0.89, 1.15). In all the reviewed studies, the vast majority of men were of normal weight in childhood and early adulthood. Few studies presented data describing the association between prostate cancer and obesity (e.g., early-adult BMI > or = 30). The exact relationships between early-life body size and prostate cancer remain unclear but appear to be weak.