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Articles by M. J Stampfer
Total Records ( 8 ) for M. J Stampfer
  E. E Devore , F. J van Rooij , A Hofman , B Rosner , M. J Stampfer and M. M. Breteler

Background: Greater fish and omega-3 (n–3) polyunsaturated fatty acid (PUFA) intake may reduce dementia risk; however, previous studies have reported conflicting results, which were largely based on short-term follow-up.

Objective: The objective was to study the dietary consumption of fish and omega-3 PUFAs in relation to long-term dementia risk.

Design: We studied 5395 participants aged ≥55 y in the Rotterdam Study who were free of dementia and reported dietary information at baseline. We used age- and sex-adjusted Cox proportional hazard and multivariate-adjusted models to evaluate the relative risk of dementia and Alzheimer disease (AD) across categories of typical fish intake (none, low, and high) and fish type consumed (none, lean, and fatty). We also evaluated dementia and AD risk across tertiles of omega-3 PUFA intake, specifically, total long-chain omega-3 fatty acids: eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), -linolenic acid, and EPA and DHA individually.

Results: During an average follow-up of 9.6 y, dementia developed in 465 participants (365 with a diagnosis of AD). In multivariate-adjusted models, total fish intake was unrelated to dementia risk (P for trend = 0.7). Compared with participants who typically ate no fish, those with a high fish intake had a similar dementia risk (hazard ratio: 0.95; 95% CI: 0.76, 1.19), as did those who typically ate fatty fish (hazard ratio: 0.98; 95% CI: 0.77, 1.24). Dietary intakes of omega-3 PUFAs were also not associated with dementia risk, and the results were similar when we considered AD specifically.

Conclusion: In this Dutch cohort, who had a moderate consumption of fish and omega-3 PUFAs, these dietary factors do not appear to be associated with long-term dementia risk.

  J. R Stark , F Wiklund , H Gronberg , F Schumacher , J. A Sinnott , M. J Stampfer , L. A Mucci and P. Kraft

An understanding of factors associated with prostate cancer (PCa) mortality is increasingly important given the biological heterogeneity of disease. Previous studies have shown that genetic variation in the Toll-like receptor (TLR) signaling pathway is associated with PCa incidence, but any role in progression and mortality is unclear. Among 1,252 PCa cases from the Cancer Prostate in Sweden study, we conducted time-to-event analyses of PCa mortality for 99 individual tagging SNPs and haploytpes from 20 genes in the TLR pathway. Cox proportional hazards models were used to estimate hazard ratios (HR) and 99% confidence intervals (99% CI). Global P values were estimated from a likelihood ratio test. During a median follow-up of 5.1 years, 191 PCa deaths occurred. Controlling for age and geographic location, two polymorphisms were statistically significantly associated with PCa mortality (P < 0.01). Compared with homozygous wild-type carriers of the TLR-9 polymorphism (rs187084), the HR (99% CI) was 1.57 (1.02, 2.41) for heterozygotes and 1.02 (0.57, 1.84) for rare homozygotes (P = 0.009). For a MIC-1 SNP (rs1227732), the HR comparing carriers of at least one copy of the minor allele to wild-type homozygotes was 0.54 (99% CI: 0.34, 0.87). Only the MIC-1 SNP remained significant after additional adjustment for treatment. No significant associations were observed for common haplotypes and PCa mortality. This study highlights the importance of studies of PCa mortality because risk factors for incidence and mortality may differ. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1859–63)

  K. L Penney , F. R Schumacher , H Li , P Kraft , J. S Morris , T Kurth , L. A Mucci , D. J Hunter , P. W Kantoff , M. J Stampfer and J. Ma

The role of selenium in prostate cancer (PCa) risk remains controversial, but many epidemiologic studies suggest an inverse association with more aggressive disease. A recently discovered selenoprotein, SEP15, which is highly expressed in the prostate, may play a role either independently or by modifying the effects of selenium. We genotyped four common single-nucleotide polymorphisms capturing common variation (frequency >5%; R2 > 0.8) within SEP15, as well as rs5859 in the 3' untranslated region, previously reported to reduce the efficiency of selenium incorporation into SEP15. We examined the association of these single-nucleotide polymorphisms with PCa risk and PCa-specific mortality, as well as their interactions with plasma selenium levels, in the Physicians' Health Study. In this nested case-control study (1,286 cases and 1,267 controls), SEP15 polymorphisms were not significantly associated with PCa risk. However, among the cases, three variants were significantly associated with PCa-specific mortality [rs479341 hazard ratio (HR), 1.94; 95% confidence interval (95% CI), 1.15-3.25; rs1407131 HR, 2.85; 95% CI, 1.45-5.59; rs561104 HR, 1.54; 95% CI, 1.12-2.11] with a recessive model. Additionally, rs561104 significantly modified the association of plasma selenium with PCa survival (Pinteraction = 0.02); an inverse relationship of high levels of selenium with PCa mortality was apparent only among those without the increased risk genotype. This study provides evidence that SEP15 genetic variation may influence PCa mortality. Additionally, the association of selenium with PCa mortality was modified by a variant, suggesting the possibility that some men with PCa may benefit more from selenium than others, depending on their genotype. Cancer Prev Res; 3(5); 604–10. ©2010 AACR.

  J. H Page , J Ma , S. E Chiuve , M. J Stampfer , J Selhub , J. E Manson and E. B. Rimm

Background— We prospectively evaluated the relationships between fasting plasma levels of vitamin B6, as pyridoxal phosphate, and subsequent myocardial infarction risk in women.

Methods and Results— Among 32 826 women who provided blood samples between 1989 and 1990 (27% of the original 1976 cohort), 239 were diagnosed with incident myocardial infarction (fatal and nonfatal) after blood collection but before July 1998. Of these women, 144 had provided a sample after fasting >10 hours. Cases were matched 1:2 by age, cigarette smoking status, and month of and fasting status at the time of blood collection with controls from the same cohort. Conditional logistic regression was used to adjust for potential confounders, including traditional coronary risk factors, anthropometric factors, dietary intake, and selected biomarkers. Median age at blood collection was 63 years. Plasma levels of pyridoxal phosphate were inversely associated with risk of myocardial infarction; the multivariable-adjusted rate ratio for the highest compared with the lowest quartiles (>70 versus <27.9 pmol/mL) was 0.22 (95% confidence interval, 0.09 to 0.55; P for trend=0.05). The association varied by age: among women who were <60 years of age at blood sampling, the rate ratio comparing the highest and lowest quartiles was 0.05 (95% confidence interval, 0.004 to 0.61), whereas among older women, the corresponding rate ratio was 0.36 (95% confidence interval, 0.13 to 1.02).

Conclusions— Fasting plasma concentration of pyridoxal phosphate was inversely associated with myocardial infarction risk, an effect that was in part independent of dietary B6 intake. In addition to dietary vitamin B6 intake, there are other determinants of plasma vitamin B6 status, and these factors warrant further research.

  H Li , M. J Stampfer , L Mucci , N Rifai , W Qiu , T Kurth and J. Ma

Background: Adipocytokines may mediate the association between adiposity and lethal prostate cancer outcomes.

Methods: In the Physicians’ Health Study, we prospectively examined the association of prediagnostic plasma concentrations of adiponectin and leptin with risk of developing incident prostate cancer (654 cases diagnosed 1982–2000 and 644 age-matched controls) and, among cases, risk of dying from prostate cancer by 2007.

Results: Adiponectin concentrations were not associated with risk of overall prostate cancer. However, men with higher adiponectin concentrations had lower risk of developing high-grade or lethal cancer (metastatic or fatal disease). The relative risk (95% CI) comparing the highest quintile to the lowest (Q5 vs Q1) was 0.25 (95% CI 0.07–0.87; Ptrend = 0.02) for lethal cancer. Among all the cases, higher adiponectin concentrations predicted lower prostate cancer–specific mortality [hazard ratio (HR)Q5 vs Q1= 0.39; 95% CI 0.17–0.85; Ptrend = 0.02], independent of body mass index (BMI), plasma C-peptide (a marker of insulin secretion), leptin, clinical stage, and tumor grade. This inverse association was apparent mainly among men with a BMI ≥25 kg/m2 (HRQ5 vs Q1= 0.10; 95% CI 0.01–0.78; Ptrend = 0.02), but not among men of normal weight (Ptrend = 0.51). Although the correlation of leptin concentrations with BMI (r = 0.58, P < 0.001) was stronger than that of adiponectin (r = –0.17, P < 0.001), leptin was unrelated to prostate cancer risk or mortality.

Conclusions: Higher prediagnostic adiponectin (but not leptin) concentrations predispose men to a lower risk of developing high-grade prostate cancer and a lower risk of subsequently dying from the cancer, suggesting a mechanistic link between obesity and poor prostate cancer outcome.

  E. N Taylor , M. J Stampfer , D. B Mount and G. C. Curhan

Background and objectives: We previously observed associations between a Dietary Approaches to Stop Hypertension (DASH)-style diet and large reductions in kidney stone risk. This study examined associations between a DASH-style diet and 24-hour excretions of urinary lithogenic factors.

Design, setting, participants, & measurements: We studied 3426 participants with and without nephrolithiasis in the Health Professionals Follow-up Study (HPFS) and the Nurses' Health Studies (NHS) I and II. A dietary DASH score was based on seven components: high intake of fruits, vegetables, nuts and legumes, dairy products, and whole grains and low intake of sweetened beverages and red and processed meats. We used analysis of covariance to adjust for age, stone history, body size, and other factors.

Results: Comparing participants in the highest to lowest quintiles of DASH score, multivariate-adjusted urinary calcium excretion was 3% greater in HPFS (P trend 0.12), 10% greater in NHS I (P trend <0.01), and 12% greater in NHS II (P trend 0.05). Urinary oxalate was 4% to 18% greater (P trend all ≤0.03), urinary citrate was 11% to 16% greater (P trend all <0.01), and urinary volume was 16% to 32% greater (P trend all <0.001). Higher DASH score was associated with higher urine potassium, magnesium, phosphate, and pH, and lower relative supersaturations (RSS) of calcium oxalate (women only) and uric acid.

Conclusions: A DASH-style diet may reduce stone risk by increasing urinary citrate and volume. The small associations between higher DASH score and lower RSS suggest unidentified stone inhibitors in dairy products and/or plants.

  J. R Stark , G Judson , J. F Alderete , V Mundodi , A. S Kucknoor , E. L Giovannucci , E. A Platz , S Sutcliffe , K Fall , T Kurth , J Ma , M. J Stampfer and L. A. Mucci

A recent nested case–control study found that the presence of antibodies against Trichomonas vaginalis, a common nonviral sexually transmitted infection, was positively associated with subsequent incidence of prostate cancer. We confirmed these findings in an independent population and related serostatus for antibodies against T vaginalis to prostate cancer incidence and mortality.


We conducted a case–control study nested within the Physicians’ Health Study that included 673 case subjects with prostate cancer and 673 individually matched control subjects who had available plasma samples. Plasma from blood samples collected at baseline was assayed for antibodies against T vaginalis with an enzyme-linked immunosorbent assay. We used conditional logistic regression to estimate the odds ratios (ORs) of incident prostate cancer, extraprostatic prostate cancer, and cancer that would ultimately progress to bony metastases or prostate cancer–specific death.


Although not statistically significant, the magnitude of the association between T vaginalis–seropositive status and overall prostate cancer risk (OR = 1.23, 95% confidence interval [CI] = 0.94 to 1.61) was similar to that reported previously. Furthermore, a seropositive status was associated with statistically significantly increased risks of extraprostatic prostate cancer (OR = 2.17, 95% CI = 1.08 to 4.37) and of cancer that would ultimately progress to bony metastases or prostate cancer–specific death (OR = 2.69, 95% CI = 1.37 to 5.28).


This large prospective case–control study obtained further support for an association between a seropositive status for antibodies against T vaginalis and the risk of prostate cancer, with statistically significant associations identified for the risk of extraprostatic prostate cancer and for clinically relevant, potentially lethal prostate cancer.

  F Fang , N. L Keating , L. A Mucci , H. O Adami , M. J Stampfer , U Valdimarsdottir and K. Fall

Receiving a cancer diagnosis is a stressful event that may increase risks of suicide and cardiovascular death, especially soon after diagnosis.


We conducted a cohort study of 342 497 patients diagnosed with prostate cancer from January 1, 1979, through December 31, 2004, in the Surveillance, Epidemiology, and End Results Program. Follow-up started from the date of prostate cancer diagnosis to the end of first 12 calendar months after diagnosis. The relative risks of suicide and cardiovascular death were calculated as standardized mortality ratios (SMRs) comparing corresponding incidences among prostate cancer patients with those of the general US male population, with adjustment for age, calendar period, and state of residence. We compared risks in the first year and months after a prostate cancer diagnosis. The analyses were further stratified by calendar period at diagnosis, tumor characteristics, and other variables.


During follow-up, 148 men died of suicide (mortality rate = 0.5 per 1000 person-years) and 6845 died of cardiovascular diseases (mortality rate = 21.8 per 1000 person-years). Patients with prostate cancer were at increased risk of suicide during the first year (SMR = 1.4, 95% confidence interval [CI] = 1.2 to 1.6), especially during the first 3 months (SMR = 1.9, 95% CI = 1.4 to 2.6), after diagnosis. The elevated risk was apparent in pre–prostate-specific antigen (PSA) (1979–1986) and peri–PSA (1987–1992) eras but not since PSA testing has been widespread (1993–2004). The risk of cardiovascular death was slightly elevated during the first year (SMR = 1.09, 95% CI = 1.06 to 1.12), with the highest risk in the first month (SMR = 2.05, 95% CI = 1.89 to 2.22), after diagnosis. The first-month risk was statistically significantly elevated during the entire study period, and the risk was higher for patients with metastatic tumors (SMR = 3.22, 95% CI = 2.68 to 3.84) than for those with local or regional tumors (SMR = 1.57, 95% CI = 1.42 to 1.74).


A diagnosis of prostate cancer may increase the immediate risks of suicide and cardiovascular death.

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