Long-Term Aspirin Use and Self-Reported Walking Speed in Older Men: The Physicians' Health Study.

BACKGROUND: Mobility limitation is a component of frailty that shares a bidirectional relationship with cardiovascular disease (CVD). Data are limited on the role of established CVD prevention therapies, such as aspirin, for prevention of frailty and mobility limitation. OBJECTIVES: Examine the association between long-term aspirin use and walking speed. DESIGN, SETTING, PARTICIPANTS: Prospective cohort of 14,315 men who participated in the Physicians' Health Study I, a completed randomized controlled trial of aspirin (1982-1988), with extended post-trial follow-up. MEASUREMENTS: Annual questionnaires collected data on aspirin use, lifestyle and other factors. Average annual aspirin use was categorized for each participant: ≤60 days/year and >60 days/year. Mobility was defined according to self-reported walking pace, categorized as: don't walk regularly (reference), easy/casual <2mph, normal ≥2-2.9mph, or brisk/very brisk ≥3mph. Propensity scoring balanced covariates between aspirin categories. Multinomial logistic regression models estimated odds of being in each self-reported walking category. RESULTS: Mean age was 70±8 years; mean aspirin use 11 years. There were 2,056 (14.3%) participants who reported aspirin use ≤60 days/year. Aspirin use >60 days/year was associated with drinking alcohol, smoking, hypertension, heart disease and stroke, while ≤60 days/year was associated with anticoagulation use and bleeding history. In all, 13% reported not walking regularly, 12% walked <2 mph, 44% walked ≥2-2.9 mph, and 31% walked ≥3 mph. After propensity score adjustment, regular aspirin use was associated with a faster walking speed. Odds ratios (95% confidence intervals) were 1.16 (0.97 to 1.39), 1.24 (1.08 to 1.43), and 1.40 (1.21 to 1.63) for <2 mph, ≥2-2.9 mph and ≥3 mph, respectively, compared to not walking regularly (p-trend<0.001). CONCLUSIONS: In this cohort of older men, long-term aspirin use is associated with a greater probability of faster walking speed later in life.

No association between circulating concentrations of vitamin D and risk of lung cancer: an analysis in 20 prospective studies in the Lung Cancer Cohort Consortium (LC3).

Background: There is observational evidence suggesting that high vitamin D concentrations may protect against lung cancer. To investigate this hypothesis in detail, we measured circulating vitamin D concentrations in prediagnostic blood from 20 cohorts participating in the Lung Cancer Cohort Consortium (LC3). Patients and methods: The study included 5313 lung cancer cases and 5313 controls. Blood samples for the cases were collected, on average, 5 years before lung cancer diagnosis. Controls were individually matched to the cases by cohort, sex, age, race/ethnicity, date of blood collection, and smoking status in five categories. Liquid chromatography coupled with tandem mass spectrometry was used to separately analyze 25-hydroxyvitamin D2 [25(OH)D2] and 25-hydroxyvitamin D3 [25(OH)D3] and their concentrations were combined to give an overall measure of 25(OH)D. We used conditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for 25(OH)D as both continuous and categorical variables. Results: Overall, no apparent association between 25(OH)D and risk of lung cancer was observed (multivariable adjusted OR for a doubling in concentration: 0.98, 95% CI: 0.91, 1.06). Similarly, we found no clear evidence of interaction by cohort, sex, age, smoking status, or histology. Conclusion: This study did not support an association between vitamin D concentrations and lung cancer risk.

Systematic review with meta-analysis: the comparative effectiveness of aspirin vs. screening for colorectal cancer prevention.

BACKGROUND: Both aspirin use and screening with flexible sigmoidoscopy or guaiac faecal occult blood testing (FOBT) may reduce mortality from colorectal cancer, but comparative effectiveness of these interventions is unknown. AIM: To compare aspirin to guaiac FOBT screening with regard to incidence and mortality of colorectal cancer in a network meta-analysis. METHODS: We searched Medline, EMBASE and the COCHRANE central register (CENTRAL) for relevant randomised trials identified until 31 October 2015. Randomised trials in average-risk populations that reported colorectal cancer mortality, colorectal cancer incidence, or both, with a minimum follow-up of 2 years, and more than 100 randomised individuals were included. Three investigators independently extracted data. We calculated relative risks [RR with 95% predictive intervals (PrIs)] for the comparison of the interventions by frequentist network meta-analyses. RESULTS: The effect of aspirin on colorectal cancer mortality was similar to FOBT (RR 1.03; 95% PrI 0.76-1.39) and flexible sigmoidoscopy (RR 1.16; 95% PrI 0.84-1.60). Aspirin was more effective than FOBT (RR 0.36; 95% PrI 0.22-0.59) and flexible sigmoidoscopy (RR 0.37; 95% PrI 0.22-0.62) in preventing death from or cancer in the proximal colon. Aspirin was equally effective as screening in reducing colorectal cancer incidence, while flexible sigmoidoscopy was superior to FOBT (RR 0.84; 95% PrI 0.72-0.97). CONCLUSIONS: Low-dose aspirin seems to be equally effective as flexible sigmoidoscopy or guaiac FOBT screening to reduce colorectal cancer incidence and mortality, and more effective for cancers in the proximal colon. A randomised comparative effectiveness trial of aspirin vs. screening is warranted.

Common variation in BRCA1 may have a role in progression to lethal prostate cancer after radiation treatment.

BACKGROUND: To evaluate whether single-nucleotide polymorphisms (SNPs) reflecting common variation in the tumor suppressor BRCA1 affect prostate cancer outcomes. Because radiation therapy (RT) induces DNA damage, we hypothesized that common variation in BRCA1 has a role in progression to lethal prostate cancer, particularly in patients receiving RT. METHODS: We followed 802 men diagnosed with localized prostate cancer (cT1-T3/N0/M0) who were treated with RT in the US Health Professionals Follow-up Study (HPFS) and Physicians' Health Study (PHS), for progression to lethal prostate cancer. Six SNPs (rs3737559, rs1799950, rs799923, rs915945, rs4474733 and rs8176305) were genotyped in HPFS to capture common variation across BRCA1. rs4474733 and rs8176305 were also evaluated in the PHS cohort. Cox proportional hazards models were used to estimate per-allele hazard ratios (HR) and 95% confidence intervals (CI) stratified by primary treatment. RESULTS: In the RT group (n=802), 71 men progressed to lethal disease during a mean follow-up of 12 years. We found that two SNPs, rs4473733 (HR: 0.65; 95% CI 0.42-0.99) and rs8176305 (HR: 2.03; 95% CI 1.33-3.10), were associated with lethal prostate cancer in men receiving RT. CONCLUSIONS: Common variation in BRCA1 may influence clinical outcomes in patients receiving RT for localized prostate cancer by modifying the response to RT. Our findings merit further follow-up studies to validate these SNPs and better understand their functional and biological significance.

Central adiposity, obesity during early adulthood, and pancreatic cancer mortality in a pooled analysis of cohort studies.

BACKGROUND: Body mass index (BMI), a measure of obesity typically assessed in middle age or later, is known to be positively associated with pancreatic cancer. However, little evidence exists regarding the influence of central adiposity, a high BMI during early adulthood, and weight gain after early adulthood on pancreatic cancer risk. DESIGN: We conducted a pooled analysis of individual-level data from 20 prospective cohort studies in the National Cancer Institute BMI and Mortality Cohort Consortium to examine the association of pancreatic cancer mortality with measures of central adiposity (e.g. waist circumference; n = 647 478; 1947 pancreatic cancer deaths), BMI during early adulthood (ages 18-21 years) and BMI change between early adulthood and cohort enrollment, mostly in middle age or later (n = 1 096 492; 3223 pancreatic cancer deaths). Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression models. RESULTS: Higher waist-to-hip ratio (HR = 1.09, 95% CI 1.02-1.17 per 0.1 increment) and waist circumference (HR = 1.07, 95% CI 1.00-1.14 per 10 cm) were associated with increased risk of pancreatic cancer mortality, even when adjusted for BMI at baseline. BMI during early adulthood was associated with increased pancreatic cancer mortality (HR = 1.18, 95% CI 1.11-1.25 per 5 kg/m(2)), with increased risk observed in both overweight and obese individuals (compared with BMI of 21.0 to <23 kg/m(2), HR = 1.36, 95% CI 1.20-1.55 for BMI 25.0 < 27.5 kg/m(2), HR = 1.48, 95% CI 1.20-1.84 for BMI 27.5 to <30 kg/m(2), HR = 1.43, 95% CI 1.11-1.85 for BMI ≥30 kg/m(2)). BMI gain after early adulthood, adjusted for early adult BMI, was less strongly associated with pancreatic cancer mortality (HR = 1.05, 95% CI 1.01-1.10 per 5 kg/m(2)). CONCLUSIONS: Our results support an association between pancreatic cancer mortality and central obesity, independent of BMI, and also suggest that being overweight or obese during early adulthood may be important in influencing pancreatic cancer mortality risk later in life.

Replication of a genetic variant for prostate cancer-specific mortality.

BACKGROUND: Few genetic variants have been confirmed as being associated with prostate cancer-specific mortality (PCSM). A recent study identified 22 candidate single-nucleotide polymorphisms (SNPs) associated with PCSM in a Seattle-based patient cohort. Five of these associations were replicated in an independent Swedish cohort. METHODS: We genotyped these 22 SNPs in Physicians' Health Study (PHS) participants diagnosed with prostate cancer (PCa). Using the same model that was found to be most significant in the Seattle cohort, we examined the association of these SNPs with lethal disease with Cox proportional hazards models. RESULTS: One SNP, rs5993891 in the ARVCF gene on chromosome 22q11, which had also replicated in the Swedish cohort, was also significantly associated with PCSM in the PHS cohort (hazard ratio (HR)=0.32; P=0.01). When we tested this SNP in an additional cohort (Health Professionals Follow-up Study, HPFS), the association was null (HR=0.95, P=0.90); however, a meta-analysis across all studies showed a statistically significant association with a HR of 0.52 (0.29-0.93, P=0.03). CONCLUSIONS: The association of rs5993891 with PCSM was further replicated in PHS and remains significant in a meta-analysis, though there was no association in HPFS. This SNP may contribute to a genetic panel of SNPs to determine at diagnosis whether a patient is more likely to exhibit an indolent or aggressive form of PCa. This study also emphasizes the importance of multiple rounds of replication.

Reproductive factors, exogenous hormone use and risk of hepatocellular carcinoma among US women: results from the Liver Cancer Pooling Project.

BACKGROUND: Hepatocellular carcinoma (HCC) occurs less commonly among women than men in almost all regions of the world. The disparity in risk is particularly notable prior to menopause suggesting that hormonal exposures during reproductive life may be protective. Exogenous oestrogenic exposures such as oral contraceptives (OCs), however, have been reported to increase risk, suggesting that estrogens may be hepatocarcinogenic. To examine the effects of reproductive factors and exogenous hormones on risk, we conducted a prospective analysis among a large group of US women. METHODS: In the Liver Cancer Pooling Project, a consortium of US-based cohort studies, data from 799,500 women in 11 cohorts were pooled and harmonised. Cox proportional hazards regression models were used to generate hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of reproductive factors and exogenous hormones with HCC (n=248). RESULTS: Bilateral oophorectomy was associated with a significantly increased risk of HCC (HR=2.67, 95% CI=1.22-5.85), which did not appear to be related to a shorter duration of exposure to endogenous hormones or to menopausal hormone therapy use. There was no association between OC use and HCC (HR=1.12, 95% CI=0.82-1.55). Nor were there associations with parity, age at first birth, age at natural menopause, or duration of fertility. CONCLUSIONS: The current study suggests that bilateral oophorectomy increases the risk of HCC but the explanation for the association is unclear. There was no association between OC use and HCC risk. Examination of endogenous hormone levels in relation to HCC may help to clarify the findings of the current study.

Physical activity and weight gain prevention in older men.

BACKGROUND: Physical activity and adiposity are important predictors of mortality, even in older individuals. However, it is unclear how much physical activity is needed to prevent weight gain in older persons. PURPOSE: To examine the associations of different amounts of physical activity with weight gain prevention in older men. METHODS: A total of 5973 healthy men (mean age, 65.0 years) from the Harvard Alumni Health Study were followed from 1988 to 1998. At baseline (1988), in 1993 and 1998, men reported their recreational physical activity and body weight. Physical activity was categorized as: <7.5 metabolic equivalent (MET)-h per week (7.5 MET-h per week corresponds to the minimum required by the 2008 US federal guidelines), 7.5 to <21 MET-h per week (21 MET-h per week corresponds to the 2002 Institute of Medicine (IOM) guideline) and 21 MET-h per week. Meaningful weight gain was defined as an increase of ≥3% of body weight. RESULTS: Overall, weight tended to be stable over any 5-year period; mean change, -0.08 (s.d.=4.44) kg. However, ∼21% of men experienced meaningful weight gain over any 5-year period. In multivariate analyses, compared with men expending ≥ 21 MET-h per week, those expending 7.5 to <21 MET-h per week had an odds ratio (OR) of 1.35 (95% confidence interval: 1.03, 1.77) for meaningful weight gain, and men expending <7.5 MET-h per week, an OR of 1.16 (1.01, 1.33; P trend=0.09). CONCLUSIONS: Among older men, those with lesser levels of physical activity were more likely to gain weight than men satisfying the 2002 IOM guidelines of ≥21 MET-h per week (∼60 min day(-1) of moderate-intensity physical activity).

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)/height(2) (m(2)) 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.

Dairy products, calcium and prostate cancer risk.

In a prospective study of 10,011 men with 815 prostate cancer cases, despite plausible biological mechanisms, neither increasing intake levels of dairy products nor calcium from dairy products (P trend; 0.23 and 0.64, respectively), or calcium supplements was associated with prostate cancer risk (relative risk, 1.05; 95% confidence interval, 0.84-1.31).

Blood pressure measures and risk of total, ischemic, and hemorrhagic stroke in men.

OBJECTIVE: To evaluate which blood pressure measure is the best predictor of risk of total, ischemic, and hemorrhagic stroke. METHODS: The authors used a prospective cohort study among 11,466 men followed for incident stroke during a median of 19.4 years in the Physicians' Health Study. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were self-reported. They calculated relative risks (RRs) and 95% CIs for total, ischemic, and hemorrhagic stroke using Cox proportional hazards models. Model fit was compared using the chi(2) test statistic from likelihood ratio tests. RESULTS: During follow-up, 508 strokes occurred (411 ischemic, 89 hemorrhagic, and eight of unknown etiology). For each 10-mm Hg increase in SBP, the multivariable RRs were 1.31 (95% CI: 1.20 to 1.42) for total stroke, 1.28 (95% CI: 1.16 to 1.40) for ischemic stroke, and 1.38 (95% CI: 1.13 to 1.68) for hemorrhagic stroke. Although DBP, pulse pressure, and mean arterial pressure were all significant predictors of stroke risk, none was a significantly better predictor than SBP alone. Adding DBP did not significantly improve the model fit of SBP alone for any stroke type. CONCLUSION: In this large cohort of initially healthy men, systolic blood pressure was a consistent and significant predictor of total, ischemic, and hemorrhagic stroke. Systolic blood pressure alone was the only measure necessary to predict risk of total stroke or its major subtypes.

Physical activity and risk of Parkinson's disease: a prospective cohort study.

BACKGROUND: Despite the fact that Parkinson's disease is the second most common neurodegenerative disease, little is known about risk factors for the disease. Laboratory experiments indicate that physical activity may have a neuroprotective effect; however, there are few data on whether physical activity is associated with decreased risk of Parkinson's disease. AIM: To investigate the relationship between physical activity and Parkinson's disease in 10,714 men (mean age, 67.6 years) from the Harvard Alumni Health Study, who were diagnosed as free of self-reported Parkinson's disease in 1988. METHODS: Physical activity was assessed in 1988 by asking about the daily number of blocks walked and stairs climbed, and participation in sports and recreational activities in the past week. Energy expenditure was then estimated and men were categorised into four groups: < 1000, 1000-1999, 2000-2999 or > or = 3000 kcal/week. In addition, physical activity data were available for three past time points: during college, 1962 or 1966, and 1977. Incident cases of Parkinson's disease occurring after 1988 (n = 101) were identified through a follow-up health questionnaire in 1993 and death certificates obtained until 1997. RESULTS: In multivariate analyses, the relative risks (RR) for Parkinson's disease associated with < 1000, 1000-1999, 2000-2999 and > or = 3000 kcal/week of physical activity were 1 (referent), 1.15 (95% confidence interval (95% CI) 0.71 to 1.88), 0.92 (0.50 to 1.71) and 0.63 (0.36 to 1.12), respectively; p for trend was 0.12. When walking was examined separately, somewhat lower, but not significant, risks were observed for Parkinson's disease. The multivariate RRs (95% CI) for walking < 5, 5-10, 10-20 and > 20 km/week were 1 (referent), 0.67 (0.37 to 1.23), 0.81 (0.50 to 1.31) and 0.72 (0.39 to 1.34), respectively; p for trend was 0.26. Analyses that considered physical activity at other time points before 1988 did not show any significant associations. CONCLUSIONS: These data do not strongly support the hypothesis that physical activity lowers the risk of Parkinson's disease. However, as the number of patients with Parkinson's disease in this study was not large, statistical power may have been limited and further large studies are needed to provide additional data.

Homocysteine and risk of developing hypertension in men.

In cross-sectional studies, elevated homocysteine levels are associated with higher blood pressure, but it remains unclear whether plasma homocysteine is a risk factor for hypertension. In a prospective nested case-control study, participants who developed hypertension (n=396) had significantly higher levels of baseline plasma homocysteine (12.6 mol/l) than matched controls (11.8 mol/l, P=0.03); compared to those in the lowest quintile, those in the highest quintile had a crude relative risk (RR) of 1.56 (95% confidence interval (CI), 0.98-2.48; P for trend=0.10) and a multivariable RR of 1.63 (95% CI, 0.97-2.74; P for trend=0.13). Higher plasma homocysteine levels at baseline were associated with an increased but non-significant risk of incident hypertension that was minimally affected by multivariable adjustment.

History of diabetes mellitus and risk of prostate cancer in physicians.

Some studies have suggested that diabetes mellitus may decrease the risk of prostate cancer because of lower insulin levels. To further investigate the relation between diabetes and prostate cancer, a nested case-control study was conducted within the US Physicians' Health Study. Cases (n = 1,110) had been diagnosed with prostate cancer, confirmed on medical record review, during follow-up in 1982-1995. Controls (n = 1,110) were selected randomly from men free of prostate cancer and were matched on age and date of randomization. Information on personal history of diabetes and other diseases, lifestyle habits, and body weight/height was self-reported. Logistic regression analysis showed that the odds ratio for prostate cancer was 0.64 (95% confidence interval (CI): 0.43, 0.95) for men with diabetes, relative to those without the disease, after adjustment for potential confounders. Odds ratio estimates were 0.63 (95% CI: 0.35, 1.14), 0.77 (95% CI: 0.35, 1.72), 0.59 (95% CI: 0.21, 1.66), and 0.59 (95% CI: 0.27, 1.27) for diabetes diagnosed 1-5, 6-10, 11-15, and > or = 16 years prior to prostate cancer diagnosis (p for trend < 0.05). Adjusted odds ratios were 1.44 (95% CI: 0.34, 6.17) for stage A prostate cancer and 0.48 (95% CI: 0.28, 0.83) for stages B-D. Results suggest that history of diabetes may be associated with a decreased risk of prostate cancer, especially late-stage tumors.

Physical activity, body weight, and pancreatic cancer mortality.

In a study of 32 687 subjects with data on physical activity and body mass index (BMI) collected serially over time, we examined associations with pancreatic cancer mortality (n=212). Despite plausible biologic mechanisms, neither physical activity (multivariate relative risks for increasing levels: 1.00, 0.98, 0.92, and 1.31, respectively) nor BMI (corresponding findings: 1.00, 0.84, 1.08, and 0.99, respectively) significantly predicted pancreatic cancer mortality.

Physical activity and all cause mortality in women: a review of the evidence.

A computer assisted literature search was performed (Medline, 1966-2000) to examine the association of physical activity with all cause mortality in women. It was concluded that, by adhering to current guidelines for physical activity and expending about 4200 kJ of energy a week, women can postpone mortality. The magnitude of benefit experienced by women is similar to that seen in men.

Alcohol consumption and risk of prostate cancer: The Harvard Alumni Health Study.

BACKGROUND: Although many studies suggest that consumption of alcohol increases the risk of several site-specific cancers, the evidence remains unclear for prostate cancer. Few data exist on beverage-specific associations as well as lifetime patterns of alcohol consumption and prostate cancer risk. METHODS: We prospectively followed 7612 Harvard alumni (mean age 66.6 years) from 1988 through 1993, during which 366 cases of incident prostate cancer occurred. Self-reported alcohol consumption was assessed at baseline from wine, beer, and liquor intake. Previous assessments during college and in 1977 were also available. RESULTS: Overall, the mean total alcohol consumption in 1988 was 123.1 g/week, of which 28.6% was from wine, 15.8% from beer, and 55.6% from liquor. Compared to men reporting almost never drinking alcohol in 1988, the multivariate relative risks (95% CI) for 1 drink/month to < 3 drinks/week, 3 drinks/week to < 1 drink/ day, 1 to < 3 drinks/day, and > or = 3 drinks/day were 1.33 (0.88-2.01), 1.65 (1.12-2.44), 1.85 (1.29-2.64), and 1.33 (0.86-2.05), respectively. Wine or beer consumption was unassociated with prostate cancer; however, moderate liquor consumption was associated with a significant 61-67% increased risk of prostate cancer (P, non-linear trend < 0.001). Men initiating alcohol consumption between 1977 and 1988 had a twofold increased risk of prostate cancer compared to men with almost no alcohol consumption at both times. CONCLUSIONS: In contrast to the majority of previous studies, we found a positive association between moderate alcohol consumption and the risk of prostate cancer. Liquor, but not wine or beer, consumption was positively associated with prostate cancer.

Maternal and paternal history of myocardial infarction and risk of cardiovascular disease in men and women.

BACKGROUND: Few studies have examined the effects of paternal and maternal history of myocardial infarction (MI), including age at MI, on cardiovascular disease (CVD) risk, particularly among women. METHODS AND RESULTS: We prospectively studied 22 071 men from the Physicians' Health Study and 39 876 women from the Women's Health Study with data on parental history and age at MI. Among men, 2654 CVD cases developed over 13.0 years; among women, 563 CVD cases occurred over 6.2 years. Compared with men with no parental history, only maternal, only paternal, and both maternal and paternal history of MI conferred relative risks (RRs) of CVD of 1.71, 1.40, and 1.85; among women, the respective RRs were 1.46, 1.15, and 2.05. For men, maternal age at MI of <50, 50 to 59, 60 to 69, 70 to 79, and >/=80 years had RRs of 1.00, 1.88, 1.88, 1.67, and 1.17; for women, the RRs for maternal age at MI of <50, 50 to 59, and >/=60 years were 2.57, 1.33, and 1.52. Paternal age at MI of <50, 50 to 59, 60 to 69, 70 to 79, and >/=80 years in men had RRs of 2.19, 1.64, 1.42, 1.16, and 0.92; in women, for paternal age at MI of <50, 50 to 59, and >/=60 years, the RRs were 1.63, 1.33, and 1.13. CONCLUSIONS: An early history of parental MI (<60 years) conferred a greater risk of CVD than did MI at older ages. However, an increased risk of CVD remained for maternal age at MI of 70 to 79 years in men and >/=60 years in women, which suggests that any maternal history of MI may be important.

A prospective cohort study of physical activity and body size in relation to prostate cancer risk (United States).

OBJECTIVES: To examine the associations of physical activity and body size with risk of prostate cancer. METHODS: At baseline in 1988, 8922 men (mean age 67 years) completed a health questionnaire which included information on physical activity, body weight, and waist girth. In a subgroup (74% of men), physical activity data also had been provided in 1962 or 1966 and again in 1977. Additionally, body weight measured at age 18 was available for 92% of men. During follow-up from 1988 through 1993, 439 men developed prostate cancer. RESULTS: In multivariate analyses that accounted for potential confounders, the RRs (95% CI) for < 4200, 4200-8399, 8400-12,599, and > or = 12,600 kJ/week of physical activity at baseline were 1.00 (referent), 1.13 (0.84-1.52), 0.96 (0.68-1.35), and 1.04 (0.79-1.38), respectively. For body mass indexes (BMI) of < 22.5, 22.5-24.9, 25.0-27.4, and > or = 27.5 kg/m2 at baseline, corresponding results were 1.00 (referent), 1.27 (0.94-1.71), 1.26 (0.92-1.72), and 1.02 (0.68-1.53), respectively. For waist girths of < or = 86.4, 86.5-91.4, 91.5-96.5, and > 96.5 cm, they were 1.00 (referent), 1.30 (0.96-1.76), 1.31 (0.96-1.80), and 1.19 (0.85-1.65), respectively. Combining physical activity measures from the past, or examining vigorous activities only, did not yield any significant associations. BMI at age 18 also was not related to risk. CONCLUSION: These findings do not support a role of physical activity or body weight in prostate cancer etiology.