scholarly journals Dietary nicotine intake and risk of Parkinson disease: a prospective study

2020 ◽  
Vol 112 (4) ◽  
pp. 1080-1087
Author(s):  
Chaoran Ma ◽  
Samantha Molsberry ◽  
Yanping Li ◽  
Michael Schwarzschild ◽  
Alberto Ascherio ◽  
...  

ABSTRACT Background Tobacco use was observed to be associated with a lower risk of Parkinson disease (PD) in previous epidemiologic studies, with nicotine as a potential candidate. The association between dietary nicotine and PD risk has, however, not been examined in prospective studies yet. Objectives We aimed to examine prospectively the association between dietary nicotine intake and subsequent PD risk among never-smokers. Methods The current study was based on never-smoker participants from 2 large prospective cohorts: the Nurses’ Health Study (n = 31,615) and the Health Professionals Follow-up Study (n = 19,523). The studies contained information on dietary nicotine intake from 1986 from validated FFQs. Dietary nicotine intake was calculated based on consumption of peppers, tomatoes, processed tomatoes, potatoes, and tea. Incident cases of PD were identified via questionnaires and subsequently confirmed by reviewing medical records. We used Cox proportional hazard models to calculate cohort-specific HRs, and used fixed-effects models to calculate the pooled HR. Results During 26 y of follow-up, we identified 601 incident PD cases (296 women and 305 men). After adjusting for potential covariates, the pooled HR for the highest compared with the lowest quintile of dietary nicotine intake was 0.70 (95% CI: 0.51, 0.94). The significant inverse association was, however, only observed in women (adjusted HR: 0.64; 95% CI: 0.42, 0.96), not in men (adjusted HR: 0.77; 95% CI: 0.50, 1.20). Further adjusting for environmental tobacco smoke exposure, family history of PD, and use of ibuprofen generated similar significant results in women. Consistently, greater consumption of peppers was associated with lower risk of PD (adjusted HR for ≥5 times/wk compared with ≤3 times/mo: 0.49; 95% CI: 0.25, 0.94) in women but not in men (adjusted HR: 1.04; 95% CI: 0.57, 1.90). Conclusions Women with greater dietary nicotine intake had a lower risk of PD than those with lower intake.

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1222-1222
Author(s):  
Chaoran Ma ◽  
Samantha Molsberry ◽  
Yanping Li ◽  
Michael Schwarzschild ◽  
Alberto Ascherio ◽  
...  

Abstract Objectives To prospectively examine the association between dietary nicotine intake and subsequent PD risk among never-smokers. Methods The current study was based on never-smoker participants from two large prospective cohorts: the Nurses’ Health Study (n = 31,615) and the Health Professionals’ Follow-up Study (n = 19,523). The studies contained information on dietary nicotine intake from 1986 from validated food frequency questionnaires. Dietary nicotine intake was calculated based on consumption of peppers, tomatoes, processed tomatoes, potatoes, and tea. Incident cases of PD were identified via questionnaires and subsequently confirmed by reviewing medical records. We used Cox proportional hazard models to calculate cohort-specific hazard ratios (HRs), and used fix-effects models to calculate the pooled hazard ratio. Results During 26 years of follow-up, we identified 601 incident PD cases (296 women, and 305 men). After adjusting for potential covariates, the pooled HR for the highest vs. lowest quintile of dietary nicotine intake was 0.70 (95% confidence interval [CI], 0.51–0.94). The significant inverse association was, however, only observed in women (adjusted HR, 0.64; 95% CI, 0.42–0.96), but not in men (adjusted HR, 0.77; 95% CI, 0.50–1.20). Further adjusting for environmental tobacco smoke exposure generated similar significant results in women. Consistently, greater consumption of peppers was associated with lower risk of PD (adjusted HR for ≥5 times/week vs. ≤3 times/month, 0.49; 95% CI, 0.25–0.94) in women but not in men (adjusted HR, 1.04; 95% CI, 0.57–1.90). Conclusions Women with greater consumption of dietary nicotine intake had a lower risk of PD, relative to those with lower consumption. Funding Sources This work was supported by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health (NINDS 1R03NS093245–01A1 to X.G.). The NHS is funded by the National Institute of Health through grant UM1 CA186107. The HPFS cohort is funded by the National Institute of Health through grant UM1 CA 167,552.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Catherine Rahilly-Tierney ◽  
Howard D Sesso ◽  
J. Michael Gaziano ◽  
Luc Djousse

BACKGROUND: Few studies have examined prospectively the relationship between baseline high-density lipoprotein (HDL) cholesterol and longevity. OBJECTIVES: We sought to examine whether higher HDL levels were associated with lower risk of all-cause, cardiovascular (CVD), and non-CVD mortality prior to age 90 in the Physicians’ Health Study (PHS). METHODS: We considered a baseline cohort of 1351 PHS participants who provided bloods between 1997 and 2001 and were old enough to reach age 90 by March 4, 2009. Included subjects had complete baseline data on HDL and total cholesterol; lifestyle factors including smoking, exercise, alcohol consumption, and BMI; and comorbidities including hypertension, diabetes mellitus, congestive heart failure, cancer, and stroke. We used Cox proportional hazards to determine the HRs and 95% CIs for all-cause, CVD, and non-CVD mortality prior to age 90, adjusting for baseline age, co-morbidities, and non-HDL cholesterol. RESULTS: At baseline, the cohort had a mean (SD) age of 81.9 (2.9) years and a mean (SD) HDL cholesterol of 44.8(16.5) mg/dL. After a mean follow-up of 6.8 years (maximum 12.3 years), 501 (37.1%) of men died prior to age 90. In multi-variable adjusted analyses, men in the highest HDL-C quartile (≥54.1 mg/dL) had a 28% lower risk (HR 0.72, 95% CI 0.55-0.95) of all-cause mortality prior to age 90 compared to men in the lowest HDL-C quartile (<32.8 mg/dL). From the lowest to highest HDL quartile, age-adjusted HR(95%CI) for CVD mortality prior to age 90 were 0.66 (0.44-0.99), 0.58 (0.38-0.90), and 0.53 (0.34-0.82) (p for trend 0.004). There was no significant association between baseline HDL cholesterol and non-CVD death. CONCLUSION: In a cohort of older male physicians with long-term follow-up, baseline HDL cholesterol was inversely associated with the risk of dying prior to age 90, largely explained by an inverse association between HDL and CVD mortality.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Susanne Rautiainen ◽  
Robert J Glynn ◽  
Julie E Buring ◽  
J. Michael Gaziano ◽  
Howard D Sesso

Background: Although multivitamins are widely used by US adults, few prospective studies have investigated their association with the long- and short-term risk of cardiovascular disease (CVD). The aim of this study was to investigate how multivitamin use is associated with the risk of CVD in initially healthy men free of CVD at baseline. Methods: We studied 21,981 male physicians aged ≥40y from the Physicians Health Study I cohort who were free of CVD and cancer at baseline starting in 1982. All men provided a wide range of self-reported lifestyle and clinical factors plus intake of selected food and dietary supplements. Men were categorized at baseline as (1) no current use and (2) current use of multivitamins. Men were followed from baseline to the end of PHS I follow-up. Cox proportional hazards models were used to calculate multivariable-adjusted rate ratios (RR) (95% confidence intervals (CI)). Results: During an average of 13.7 y (total of 301,480 person-years) of follow-up, there were 1,269 incident cases of major CVD (defined as nonfatal myocardial infarction (MI), nonfatal stroke, and CVD death). In multivariable analyses, there were no statistically significant RRs (95% CIs) observed when comparing current multivitamin use versus no use for the risk of major CVD events (0.97 (0.79-1.04)), MI (0.94 (0.76-1.16), stroke (0.97 (0.77-1.23), or CVD death (1.02 (0.83-1.14)) but an inverse association was observed for cardiac revascularization (0.87 (0.75-1.00)). Conclusion: In this long-term prospective study among initially healthy men, baseline multivitamin use was not associated with the long-term risk of major CVD events.


2020 ◽  
Vol 112 (6) ◽  
pp. 1540-1546 ◽  
Author(s):  
Teresa T Fung ◽  
Ellen A Struijk ◽  
Fernando Rodriguez-Artalejo ◽  
Walter C Willett ◽  
Esther Lopez-Garcia

ABSTRACT Background Prior research has suggested that the antioxidative and anti-inflammatory potential of fruits and vegetables may ameliorate aging-related frailty. Objective We sought to prospectively examine the association between fruit and vegetable intake and incident frailty in older women. Design We followed 78,366 nonfrail women aged ≥60 y from the Nurses’ Health Study from 1990 to 2014. In this analysis, the primary exposure was the intake of total fruits and vegetables, assessed with an FFQ administered 6 times during follow-up. Frailty was defined as having ≥3 of the following 5 criteria from the FRAIL scale: fatigue, poor strength, low aerobic capacity, having ≥5 illnesses, and ≥5% weight loss. Cox models adjusted for potential confounders were used to estimate HRs and 95% CIs for the association between fruit and vegetable intake and incident frailty. Results In total, 12,434 (15.9%) incident frailty cases were accrued during follow-up. Total fruit and vegetable intakes were associated with a lower risk of frailty (adjusted HR comparing 7+ servings/d compared with &lt;3 servings/d: 0.92; 95% CI: 0.85, 0.99). The inverse association appeared to be stronger for those with physical activity above the median (P-interaction &lt; 0.05). Among physically active women, compared with those who consumed &lt;3 servings/d, the HR for 7+ servings/d was 0.68 (95% CI: 0.57, 0.81). Conclusion Higher fruit and vegetable intake was associated with a lower risk of frailty in this cohort of US women aged ≥60 y. Because of limited evidence on intakes of fruits and vegetables and the development of frailty, more data are needed to confirm our results.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Stephanie E Chiuve ◽  
Kathryn M Rexrode ◽  
Qi Sun ◽  
Eric N Taylor ◽  
Gary C Curhan ◽  
...  

Background: Plasma magnesium (Mg) has been strongly associated with lower risk of fatal coronary heart disease (CHD) and sudden cardiac death, which may be due to its anti-arrhythmic properties. Mg also affects endothelial function, inflammation, blood pressure and diabetes and thus may impact atherosclerosis in general. We examined the association between magnesium, measured in diet and plasma, and risk of fatal, nonfatal and total CHD among women in the Nurses’ Health Study. Design: The association for Mg intake was examined prospectively among 86,361 women free of disease in 1980. Mg intake and other covariates were ascertained updated every 2-4 years through questionnaires and 3661 cases of CHD (1214 fatal/2447 nonfatal) were documented through 2008. For plasma Mg, we conducted a nested case-control analysis with 405 CHD (63 fatal/342 nonfatal) cases, matched to controls (1:1) on age, smoking, fasting status, and date of blood sampling. Results: Dietary magnesium was inversely associated with risk of CHD, even after controlling for diet and CHD risk factors (RR comparing extreme quintiles: 0.75; 95%CI: 0.64, 0.89; P trend=0.002) (Table 1). The relationship with plasma Mg was less linear ( P trend=0.09) with a potential threshold effect at the 2 nd quintile. The RR of CHD comparing plasma Mg >2.0 v. ≤2.0 mg/dl was 0.49 (95%CI: 0.32, 0.74). The associations for dietary and plasma Mg appeared stronger for fatal versus nonfatal CHD. The RR (95%CI; P trend) comparing the highest to lowest quintile of dietary Mg was 0.60 (0.45, 0.79; p <0.001) for fatal and 0.85 (0.70, 1.04; p = 0.14) for nonfatal CHD. The RR (95%CI) comparing plasma Mg >2.0 v. ≤2.0 mg/dl was 0.23 (0.07, 0.81) for fatal and 0.55 (0.35, 0.86) for nonfatal CHD. Conclusions: Higher levels of Mg, in diet and plasma, were associated with lower risk of total CHD among women. The consistent inverse association found between two measures of Mg and CHD risk supports the hypothesis that Mg might lower CHD risk through multiple mechanisms, and may be most strongly protective for fatal events.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
An Pan ◽  
Gim Gee Teng ◽  
Jian-Min Yuan ◽  
Woon-Puay Koh

Introduction: Although it has been hypothesized that the hypertension-gout relation is bidirectional, few studies have addressed this hypothesis in a prospective setting, particularly in the Asian populations. Methods: We analyzed data from the Singapore Chinese Health Study (SCHS), a cohort of 63,257 Chinese aged 45-74 years at recruitment from 1993-98. The information about self reports of physician-diagnosed hypertension and gout was enquired at follow-ups I (1999-2004) and II (2006-2010). We included participants with complete data for both follow-ups and who were free of heart disease, stroke and cancer at follow-up I. For the analysis of hypertension and risk of incident gout, participants with prevalent gout were further excluded and the final analysis included 31,694 participants. For the analysis of gout and risk of incident hypertension, participants with prevalent hypertension were further excluded and the final analysis included 20,490 participants. Cox proportional hazards models were used to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) with adjustment for age, sex, years of interview, dialect group, education, smoking status, alcohol intake, physical activity, body mass index (BMI) and history of diabetes. Results: The mean age of the participants at baseline was 60.1 (SD 7.3) years, and the average follow-up year was 6.8 (SD 1.4) years. In the analysis of hypertension and risk of gout, 836 incident cases were identified. Compared to normotensive participants, hypertensive patients had a 93% increased risk of developing gout (RR 1.93; 95% CI 1.66-2.24). The association was slightly stronger in women (RR 2.09; 95% CI 1.69-2.58) compared to men (RR 1.72; 95% CI 1.39-2.14; P for interaction=0.056). The association was also stronger in normal weight adults (BMI <24 kg/m2; RR 2.25; 95% CI 1.82-2.77) compared to overweight/obese individuals (BMI ≥24 kg/m2; RR 1.66; 95% CI 1.34-2.04; P for interaction=0.03). In the parallel analysis of gout and risk of hypertension, 5491 participants reported to have newly diagnosed hypertension during the follow-up. Compared to participants without gout, those with gout had a 17% increased risk of developing hypertension (RR 1.17; 95% CI 1.01-1.35). The association was evident in men (RR 1.29; 95% CI 1.07-1.55) but not in women (RR 0.94; 95% CI 0.73-1.20; P for interaction=0.03). The association was present in normal weight adults (RR 1.34; 95% CI 1.09-1.64) but not among overweight/obese individuals (RR 0.99; 95% CI 0.80-1.23; P for interaction=0.03). Conclusions: Our results provide compelling evidence that the hypertension-gout association is bidirectional in Chinese population. The potential interactions of the bidirectional association with sex and obesity deserve further investigations.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S387-S388
Author(s):  
Elizabeth Salerno ◽  
Pedro Saint Maurice ◽  
Erik Willis ◽  
Loretta DiPietro ◽  
Charles Matthews

Abstract We examined the association between self-reported walking pace and all-cause mortality among cancer survivors in the NIH-AARP Diet and Health Study. Participants included 30,110 adults (Mage=62.4+/-5.14 years) diagnosed with cancer between study enrollment and follow-up, when they self-reported walking pace. Individuals were followed until death or administrative censoring in 2011. We estimated the hazards ratios (HR) and 95% confidence intervals (CI) for walking pace and all-cause mortality adjusting for age, sex, race, BMI, health status, physical activity and cancer type. Cancer survivors reporting faster walking paces had significantly reduced mortality risk. Relative to those reporting an ‘easy’ walking pace, walking at a ‘normal,’ ‘brisk,’ or ‘very brisk’ pace was associated with significantly lower risk: [HR=0.74 (0.70,0.78)], [HR=0.66 (0.61,0.71)], and [HR=0.73 (0.60,0.89)], respectively. Being ‘unable to walk’ was associated with 30% increased mortality [HR=1.30 (1.15,1.46)]. These findings provide novel support for the association between self-reported walking pace and survival after cancer.


2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 394-394 ◽  
Author(s):  
Amanda Phipps ◽  
Xabier Garcia-Albeniz ◽  
Carolyn Hutter ◽  
Emily White ◽  
Charles S. Fuchs ◽  
...  

394 Background: Beyond clinicopathologic stage, there are few established markers of prognosis in colorectal cancer (CRC). Recent genome-wide association studies have identified 17 germline single nucleotide polymorphisms (SNPs) significantly associated with incident CRC. However, it is unclear if these CRC susceptibility SNPs influence survival after CRC diagnosis. Although the functionality of many of these SNPs remains unknown, a few, including rs4939827 in SMAD7, map to genes with plausible biological mechanisms associated with both cancer risk and prognosis. We examined 17 CRC susceptibility SNPs in relation to survival after CRC diagnosis. Methods: We genotyped 2,611 men and women enrolled in five prospective cohort studies who were diagnosed with invasive CRC during study follow-up: the Physicians’ Health Study (N=281), Health Professionals Follow-up Study (N=268), Nurses’ Health Study (N=367), Vitamins and Lifestyle Study (N=281), and the Women’s Health Initiative (N=1414). Analyses were limited to Caucasians with known vital status, cause of death, and survival time. We used Cox proportional hazards regression to assess associations between each SNP and CRC-specific and overall survival in study-specific models adjusted for age, sex, and stage; SNPs were modeled additively to reflect associations per copy of the minor allele. Study-specific results were combined via fixed-effects meta-analysis. Results: The G allele in rs4939827 was associated with poorer CRC-specific survival [hazard ratio (HR)=1.16, p=0.02] and overall survival (HR=1.13, p=0.03) in CRC patients. The A alleles in rs10795668 and in rs4925386 were associated with a 1.14-fold increased risk of overall mortality (both p-values=0.03) but not CRC-specific mortality. Other evaluated SNPs were not associated with survival. Conclusions: Genetic variation in rs4939827 (SMAD7) is associated with CRC-specific and overall survival. These results suggest that SMAD7 may have a role in CRC progression, and provide proof-of-principle that common germline variation may provide prognostic information beyond traditional considerations such as stage.


2014 ◽  
Vol 112 (5) ◽  
pp. 735-743 ◽  
Author(s):  
Mia Sadowa Vedtofte ◽  
Marianne U. Jakobsen ◽  
Lotte Lauritzen ◽  
Eilis J. O'Reilly ◽  
Jarmo Virtamo ◽  
...  

The intake of the mainly plant-derived n-3 PUFA α-linolenic acid (ALA) has been reported to be associated with a lower risk of CHD. However, the results have been inconsistent. Therefore, the objective of the present study was to examine the association between the intake of ALA and the risk of CHD. Potential effect modification by the intake of long-chain n-3 PUFA (n-3 LCPUFA) was also investigated. Data from eight American and European prospective cohort studies including 148 675 women and 80 368 men were used. The outcome measure was incident CHD (CHD event and death). During 4–10 years of follow-up, 4493 CHD events and 1751 CHD deaths occurred. Among men, an inverse association (not significant) between the intake of ALA and the risk of CHD events and deaths was observed. For each additional gram of ALA consumed, a 15 % lower risk of CHD events (hazard ratios (HR) 0·85, 95 % CI 0·72, 1·01) and a 23 % lower risk of CHD deaths (HR 0·77, 95 % CI 0·58, 1·01) were observed. No consistent association was observed among women. No effect modification by the intake of n-3 LCPUFA was observed.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1036-1036
Author(s):  
Marta Guasch-Ferre ◽  
Yanping Li ◽  
Walter Willett ◽  
Qi Sun ◽  
Laura Sampson ◽  
...  

Abstract Objectives The association between olive oil intake and the risk of mortality has not been evaluated before in the US population. Our objective was to examine whether olive oil intake is associated with total and cause-specific mortality in two prospective cohorts of US men and women. We hypothesize that higher olive oil consumption is associated with lower risk of total and cause-specific mortality. Methods We followed 61,096 women (Nurses’ Health Study, 1990–2016) and 31,936 men (Health Professionals Follow-up Study, 1990–2016) who were free of diabetes, cardiovascular disease and cancer at baseline. Diet was assessed by a semi quantitative food frequency questionnaire at baseline and then every 4 years. Cox proportional hazards regressions were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results During 26 years of follow-up, 32,868 deaths occurred. Compared with those participants who never consumed olive oil, those with higher olive oil intake (&gt;1/2 tablespoon/d or &gt;8g/d) had 15% lower risk of total mortality [pooled hazard ratio (95% confidence interval): 0.85 (0.81, 0.88)] after adjustment for potential confounders. Higher olive oil intake was associated with 15% lower risk of CVD death [0.85 (0.78, 0.92)], 38% lower risk of neurodegenerative disease death [0.62 (0.54, 0.71)], and 12% lower risk of respiratory death [0.88 (0.77, 1.00)]. Replacing 10 g of margarine, mayonnaise, and dairy fat with the equivalent amount of olive oil was associated with 7–20% lower risk of total mortality, and death from CVD, cancer, neurodegenerative, and respiratory diseases. No significant associations were observed when olive oil was replacing other vegetable oils combined (corn, safflower, soybean and canola oil). Conclusions We observed that higher olive oil intake was associated with a lower risk of total mortality and cause-specific mortality in a large prospective cohort of U.S. men and women. The substitution of margarine, mayonnaise, and dairy fat with olive oil was associated with a reduced risk of mortality. Funding Sources This work was supported by grants from the National Institutes of Health.


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