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Meir J Stampfer

Publications and source records attributed to Meir J Stampfer.

At least 19 recordsLinked to original sources
PubMed2025

Cross-omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging.

Inflammation is a critical component of chronic diseases, aging progression, and lifespan. Omics signatures may characterize inflammation status beyond blood biomarkers. We leveraged genetics (polygenic risk score [PRS]), metabolomics (metabolomic risk score [MRS]), and epigenetics (epigenetic risk score [ERS]) to build multi-omics-multi-marker risk scores for inflammation status represented by the level of circulating C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α). We found that multi-omics risk scores generally outperformed single-omics risk scores in predicting all-cause mortality in the Canadian Longitudinal Study on Aging. Compared with circulating inflammation biomarkers, some multi-omics risk scores had a higher hazard ratio (HR) for all-cause mortality when including both score and circulating IL-6 in the same model (1-SD IL-6 MRS-ERS: HR = 2.20 [1.55-3.13] vs. 1-SD circulating IL-6 HR = 0.94 [0.67,1.32]. 1-SD IL-6 PRS-MRS: HR = 1.47 [1.35,1.59] vs. 1-SD circulating IL-6 HR = 1.33 [1.18, 1.51]. 1-SD PRS-MRS-ERS: HR = 1.95 [1.40, 2.70] vs. 1-SD circulating IL-6: HR = 0.99 [0.71, 1.39]). In the Nurses' Health Study (NHS), NHS II, and Health Professional Follow-up Study with available omics, 1 SD of IL-6 PRS and 1-SD IL-6 PRS-MRS had HR = 1.12 [1.00,1.26] and HR = 1.13 [1.01,1.26] among individuals >65 years old without mutual adjustment of the score and circulating IL-6. Our study demonstrates that some multi-omics scores for inflammation markers may characterize important inflammation burden for an individual beyond those represented by blood biomarkers and improve our prediction capability for the aging process and lifespan.

Humans↗
PubMed2007

A prospective cohort study of red wine consumption and risk of prostate cancer.

In light of recent, strong inverse findings between lifetime red wine consumption and prostate cancer among younger men, we revisited our previous cohort analysis to more thoroughly investigate red wine consumption and prostate cancer in the Health Professionals Follow-up Study (HPFS). In 1986, HPFS participants reported their average consumption of red wine, white wine, beer and liquor during the past year, and their change in alcohol consumption over the prior 10 years. Prostate cancer diagnoses were ascertained on each biennial questionnaire and confirmed by medical record review. Between 1986 and 2002, 3,348 cases of prostate cancer were diagnosed among 45,433 eligible participants. Using men who did not consume red wine as the reference, no linear trend was observed between red wine consumption and prostate cancer in the full analytic cohort (p-trend = 0.57). Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed 4 glasses/week, resulting in a lack of linear trend. These findings suggest that red wine does not contribute appreciably to the etiology of prostate cancer.

Adult↗
PubMed2007

Prospective study of body mass index, height, physical activity and incidence of bladder cancer in US men and women.

We evaluated prospectively the association between body mass index (BMI), height, recreational physical activity and the risk of bladder cancer among US adults. Data were used from 2 ongoing cohorts, the Health Professionals Follow-up Study and the Nurses' Health Study, with 3,542,012 years of follow-up and 866 incident bladder cancer cases (men = 507; women = 359) for the anthropometric analysis and 1,890,476 years of follow-up and 706 incident bladder cancer cases (men = 502; women = 204) for the physical activity analysis. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between BMI, height, physical activity and bladder cancer risk adjusting for age, pack-years of cigarette smoking and current smoking. Estimates from each cohort were pooled using a random-effects model. We observed no association between baseline BMI and bladder cancer risk, even when we compared a BMI of > or =30 kg/m(2) to a BMI of 18-22.9 kg/m(2) [pooled multivariate (MV) RR, 1.16; 95% CI: 0.89-1.52]. A weak, but statistically significant, association was observed for the same comparison after excluding bladder cancer cases diagnosed within the first 4 years of follow-up (pooled MV RR, 1.33; 95% CI: 1.01-1.76). Height was not related to bladder cancer risk (pooled MV RR, 0.82; 95% CI: 0.65-1.03, top vs. bottom quintile). Total recreational physical activity also was not associated with the risk of bladder cancer (pooled MV RR, 0.97; 95% CI: 0.77-1.24, top vs. bottom quintile). Our findings do not support a role for BMI, height or physical activity in bladder carcinogenesis.

Adult↗
PubMed2006

Statin drugs and risk of advanced prostate cancer.

BACKGROUND: Statins are commonly used cholesterol-lowering drugs that have proapoptotic and antimetastatic activities that could affect cancer risk or progression. Results from previous epidemiologic studies of the association between statin use and cancer have been inconsistent. We investigated the association of statin use with total and advanced prostate cancer, the latter being the most important endpoint to prevent. METHODS: We analyzed data from an ongoing prospective cohort study of 34,989 US male health professionals who were cancer free in 1990 and were followed to 2002. Participants reported their use of cholesterol-lowering drugs on biennial questionnaires. Prostate cancer diagnosis was confirmed by medical record review. Multivariable-adjusted relative risks (RRs) were estimated from Cox proportional hazards regression models. Statistical tests were two-sided. RESULTS: During 376,939 person-years of follow-up, we ascertained 2579 prostate cancer cases, 316 of which were advanced (regionally invasive, metastatic, or fatal). The age-standardized incidence rates of advanced prostate cancer were 38 and 89 per 100,000 person-years in current statin users and in past or never users, respectively. The multivariable-adjusted relative risk of advanced disease was 0.51 (95% confidence interval [CI] = 0.30 to 0.86) and of metastatic or fatal disease was 0.39 (95% CI = 0.19 to 0.77) for current statin use compared with no current use. The associations remained after adjusting for prostate-specific antigen screening history (advanced disease: RR = 0.57, 95% CI = 0.30 to 1.11; metastatic or fatal disease: RR = 0.35, 95% CI = 0.14 to 0.92). Risk of advanced disease was lower with longer statin use (P(trend) = .003); compared with never use, the relative risk for less than 5 years of use was 0.60 (95% CI = 0.35 to 1.03) and for 5 or more years of use was 0.26 (95% CI = 0.08 to 0.83). We found no association between statin use and risk of total prostate cancer (RR = 0.96, 95% CI = 0.85 to 1.09). CONCLUSIONS: In this cohort of male health professionals, use of statin drugs was not associated with risk of prostate cancer overall but was associated with a reduced risk of advanced (especially metastatic or fatal) prostate cancer.

Aged↗
PubMed2006

Coffee consumption and risk of myocardial infarction among older Swedish women.

Numerous studies have examined the association between coffee consumption and risk of myocardial infarction (MI), but results have been inconsistent. Case-control studies generally suggest a harmful effect of coffee drinking, whereas cohort studies have mostly shown no association. Recent studies found that coffee may lower the risk of diabetes, a major coronary risk factor. The authors prospectively examined the effect of coffee consumption on MI risk in 32,650 older Swedish women, aged 40-74 years, participating in the Swedish Mammography Cohort; 459 cases of MI developed during 165,896 person-years of follow-up from 1997 to 2002. After adjustment for age, coronary heart disease risk factors, and dietary variables, the relative risk of MI associated with drinking >/=5 cups/week versus 0-4 cups/week was 0.68 (95% confidence interval (CI): 0.43, 1.07). The authors observed a nonsignificant trend toward lower risk with higher consumption levels. Compared with that for 0-4 cups/week, the relative risks of MI were 0.84 (95% CI: 0.51, 1.38) for 5-7 cups/week, 0.65 (95% CI: 0.41, 1.03) for 2-3 cups/day, 0.64 (95% CI: 0.39, 1.04) for 4-5 cups/day, and 0.65 (95% CI: 0.37, 1.12) for >/=6 cups/day (p-trend = 0.07). Contrary to previous case-control studies, the authors concluded that coffee consumption does not increase MI risk. Coffee consumption of >/=5 cups/week was nonsignificantly inversely associated with MI risk among older Swedish women.

Adult↗
PubMed2006

Red meat intake and risk of breast cancer among premenopausal women.

BACKGROUND: The association between red meat intake and breast cancer is unclear, but most studies have assessed diet in midlife or later. Although breast tumors differ clinically and biologically by hormone receptor status, few epidemiologic studies of diet have made this distinction. METHODS: Red meat intake and breast cancer risk were assessed among premenopausal women aged 26 to 46 years in the Nurses' Health Study II. Red meat intake was assessed with a food frequency questionnaire administered in 1991, 1995, and 1999, with respondents followed up through 2003. Breast cancers were self-reported and confirmed by review of pathologic reports. RESULTS: During 12 years of follow-up of 90,659 premenopausal women, we documented 1021 cases of invasive breast carcinoma. Greater red meat intake was strongly related to elevated risk of breast cancers that were estrogen and progesterone receptor positive (ER+/PR+; n = 512) but not to those that were estrogen and progesterone receptor negative (ER-/PR-; n = 167). Compared with those eating 3 or fewer servings per week of red meat, the multivariate relative risks (95% confidence intervals) for ER+/PR+ breast cancer with increasing servings of red meat intake were 1.14 (0.90-1.45) for more than 3 to 5 or fewer servings per week, 1.42 (1.06-1.90) for more than 5 per week to 1 or fewer servings per day, 1.20 (0.89-1.63) for more than 1 to 1.5 or fewer servings per day, and 1.97 (1.35-2.88) for more than 1.5 servings per day (test for trend, P = .001). The corresponding relative risks for ER-/PR- breast cancer were 1.34 (0.89-2.00), 1.21 (0.73-2.00), 0.69 (0.39-1.23), and 0.89 (0.43-1.84) (test for trend, P = .28). Higher intakes of several individual red meat items were also strongly related to elevated risk of ER+/PR+ breast cancer. CONCLUSION: Higher red meat intake may be a risk factor for ER+/PR+ breast cancer among premenopausal women.

Adult↗
PubMed2006

Aspirin and decreased adult-onset asthma: randomized comparisons from the physicians' health study.

RATIONALE: In an observational cohort study, women who self-selected for frequent aspirin use developed less newly diagnosed asthma than women who did not take aspirin. OBJECTIVE: To explore whether low-dose aspirin decreased the risk of newly diagnosed asthma in a randomized, double-blind, placebo-controlled trial. METHODS: The Physicians' Health Study randomized 22,071 apparently healthy male physicians, aged 40-84 yr at baseline and tolerant of aspirin, over an 18-wk run-in period, to 325 mg aspirin or placebo on alternate days. The aspirin component was terminated after 4.9 yr due principally to the emergence of a statistically extreme 44% reduction in risk of first myocardial infarction among those randomly assigned to aspirin. MEASUREMENTS: Physicians could self-report an asthma diagnosis on questionnaires at baseline, 6 mo, and annually thereafter. Asthma was not an a priori endpoint of the trial. RESULTS: Among 22,040 physicians without reported asthma at randomization, there were 113 new asthma diagnoses in the aspirin group and 145 in the placebo group. The hazard ratio was 0.78 (95% confidence interval, 0.61-1.00; p = 0.045). This apparent 22% lower risk of newly diagnosed asthma among those assigned to aspirin was not modified by baseline characteristics including smoking, body mass index, or age. CONCLUSIONS: Aspirin reduced the risk of newly diagnosed adult-onset asthma in a large, randomized clinical trial of apparently healthy, aspirin-tolerant men. This result requires replication in randomized trials designed a priori to test this hypothesis; it does not imply that aspirin improves symptoms in patients with asthma.

Adult↗
PubMed2006

p53 Arg72Pro polymorphism and risk of colorectal adenoma and cancer.

A single nucleotide polymorphism (SNP) at codon 72 of the p53 gene (Arg72Pro) alters the p53 protein structure and affects its activity. We investigated this SNP in relation to colorectal adenoma and cancer among men and women from case-control studies nested within the Nurses' Health Study, the Health Professionals Follow-up Study and the Physicians' Health Study. Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg). This association did not vary by colorectal site or by sex. Among 442 colorectal cancer cases and 904 controls, we observed no significant overall association between p53 Arg72Pro genotype and colorectal cancer (multivariate OR = 1.14, 95% CI = 0.90-1.45). However, when colorectal site and sex was accounted for, the Pro carrier genotypes compared to Arg/Arg were associated with an increased risk of proximal colon cancers in women (multivariate OR = 2.59, 95% CI = 1.49-4.52) though not with distal colon or rectal cancers, while among men the same genotypes were associated with an increased risk of distal colon cancers (multivariate OR = 2.09, 95% CI = 1.28-3.40) but not proximal colon or rectal cancers. Our results suggest that Arg72Pro may play a role in the early stages of colorectal neoplasia and possibly in progression to invasive disease, depending on site and sex.

Adenoma↗
PubMed2006

Dietary fat and risk of postmenopausal breast cancer in a 20-year follow-up.

Dietary fat in midlife has not been associated with breast cancer risk in most studies, but few have followed women beyond one decade. The authors examined the relation of dietary fat, assessed by repeated questionnaires, to incidence of postmenopausal breast cancer in a cohort of 80,375 US women (3,537 new cases) prospectively followed for 20 years between 1980 and 2000. The multivariable relative risk for an increment of 5% of energy from total dietary fat intake was 0.98 (95% confidence interval: 0.95, 1.00). Additionally, specific types of fat were not associated with an increased risk of breast cancer. Furthermore, secondary analyses indicated no differences in breast cancer risk by estrogen receptor or progesterone receptor status. However, stratification by waist circumference indicated a significant decrease in breast cancer risk for participants with a waist circumference of 35 inches (88.9 cm) or greater (p-trend = 0.04). None of the latency intervals investigated were associated with an increased risk of breast cancer. In addition, fat intake before menopause was not related to risk of postmenopausal breast cancer. These results suggest a reduction in breast cancer risk for women with insulin resistance syndrome who consume high-fat diets and no association between specific sources of fat during midlife and risk of postmenopausal breast cancer.

Aged↗
PubMed2006

Healthy lifestyle and the risk of stroke in women.

BACKGROUND: Healthy lifestyle has been associated with decreased risk of coronary heart disease. In contrast, little is known about its association with stroke risk. METHODS: This is a prospective cohort study among 37 636 women 45 years or older participating in the Women's Health Study. Stroke was self-reported and confirmed by means of medical record review. We considered the following self-reported lifestyle factors: smoking, alcohol consumption, exercise, body mass index, and diet. The health index was calculated from these variables by assigning scores from 0 to 4 to the respective variable categories, with a higher score indicating healthier behavior. Healthy behavior was defined as never smoking, alcohol consumption between 4 and 10.5 drinks per week, exercise 4 or more times per week, body mass index (calculated as weight in kilograms divided by the square of height in meters) less than 22, and a diet high in cereal fiber, folate, and omega-3 fatty acids, with a high ratio of polyunsaturated to saturated fat, and low in trans fat and glycemic load. RESULTS: During 10 years of follow-up, 450 strokes (356 ischemic, 90 hemorrhagic, and 4 undefined) were confirmed. Compared with participants with 0 to 4 health index points (4.3%), women with 17 to 20 health index points (4.7%) had multivariable-adjusted hazard ratios (95% confidence interval) of 0.45 (0.24-0.83; P<.001 for trend) for total stroke, 0.29 (0.14-0.63; P<.001 for trend) for ischemic stroke, and 1.27 (0.37-4.29; P = .62 for trend) for hemorrhagic stroke. CONCLUSIONS: In this large prospective cohort of apparently healthy women, a healthy lifestyle consisting of abstinence from smoking, low body mass index, moderate alcohol consumption, regular exercise, and healthy diet was associated with a significantly reduced risk of total and ischemic stroke but not of hemorrhagic stroke. Our findings underscore the importance of healthy behaviors in the prevention of stroke.

Aged↗
PubMed2006

Coffee consumption and coronary heart disease in men and women: a prospective cohort study.

BACKGROUND: We examined the association between long-term habitual coffee consumption and risk of coronary heart disease (CHD). METHODS AND RESULTS: We performed a prospective cohort study with 44,005 men and 84,488 women without history of cardiovascular disease or cancer. Coffee consumption was first assessed in 1986 for men and in 1980 for women and then repeatedly every 2 to 4 years; the follow-up continued through 2000. We documented 2173 incident cases of coronary heart disease (1449 nonfatal myocardial infarctions and 724 fatal cases of CHD) among men and 2254 cases (1561 nonfatal myocardial infarctions and 693 fatal cases of CHD) among women. Among men, after adjustment for age, smoking, and other CHD risk factors, the relative risks (RRs) of CHD across categories of cumulative coffee consumption (<1 cup/mo, 1 cup/mo to 4 cups/wk, 5 to 7 cups/wk, 2 to 3 cups/d, 4 to 5 cups/d, and > or =6 cups/d) were 1.0, 1.04 (95% confidence interval 0.91 to 1.17), 1.02 (0.91 to 1.15), 0.97 (0.86 to 1.11), 1.07 (0.88 to 1.31), and 0.72 (0.49 to 1.07; P for trend=0.41); among women, the RRs were 1.0, 0.97 (0.83 to 1.14), 1.02 (0.90 to 1.17), 0.84 (0.74 to 0.97), 0.99 (0.83 to 1.17), and 0.87 (0.68 to 1.11; P for trend=0.08). Stratification by smoking status, alcohol consumption, history of type 2 diabetes mellitus, and body mass index gave similar results. Similarly, we found no effect when the most recent coffee consumption was examined. RRs for quintiles of caffeine intake varied from 0.97 (0.84 to 1.10) in the second quintile to 0.97 (0.84 to 1.11) in the highest quintile (P for trend=0.82) in men and from 1.02 (0.90 to 1.16) to 0.97 (0.85 to 1.11; P for trend=0.37) in women. CONCLUSIONS: These data do not provide any evidence that coffee consumption increases the risk of CHD.

Caffeine↗
PubMed2006

Prospective study of predictors of vitamin D status and cancer incidence and mortality in men.

BACKGROUND: Vitamin D has potent anticancer properties, especially against digestive-system cancers. Many human studies have used geographic residence as a marker of solar ultraviolet B and hence vitamin D exposure. Here, we considered multiple determinants of vitamin D exposure (dietary and supplementary vitamin D, skin pigmentation, adiposity, geographic residence, and leisure-time physical activity-to estimate sunlight exposure) in relation to cancer risk in the Health Professionals Follow-Up Study. METHODS: Among 1095 men of this cohort, we quantified the relation of these six determinants to plasma 25-hydroxy-vitamin D [25(OH)D] level by use of a multiple linear regression model. We used results from the model to compute a predicted 25(OH)D level for each of 47,800 men in the cohort based on these characteristics. We then prospectively examined this variable in relation to cancer risk with multivariable Cox proportional hazards models. RESULTS: From 1986 through January 31, 2000, we documented 4286 incident cancers (excluding organ-confined prostate cancer and nonmelanoma skin cancer) and 2025 deaths from cancer. From multivariable models, an increment of 25 nmol/L in predicted 25(OH)D level was associated with a 17% reduction in total cancer incidence (multivariable relative risk [RR] = 0.83, 95% confidence interval [CI] = 0.74 to 0.92), a 29% reduction in total cancer mortality (RR = 0.71, 95% CI = 0.60 to 0.83), and a 45% reduction in digestive-system cancer mortality (RR = 0.55, 95% CI = 0.41 to 0.74). The absolute annual rate of total cancer was 758 per 100,000 men in the bottom decile of predicted 25(OH)D and 674 per 100,000 men for the top decile; these respective rates were 326 per 100,000 and 277 per 100,000 for total cancer mortality and 128 per 100,000 and 78 per 100,000 for digestive-system cancer mortality. Results were similar when we controlled further for body mass index or physical activity level. CONCLUSIONS: Low levels of vitamin D may be associated with increased cancer incidence and mortality in men, particularly for digestive-system cancers. The vitamin D supplementation necessary to achieve a 25(OH)D increment of 25 nmol/L may be at least 1500 IU/day.

Adult↗