Eilis J O'Reilly

Harvard Medical School, Boston, Massachusetts, United States

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Publications (65)442.92 Total impact

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    ABSTRACT: Caffeine is thought to be neuroprotective by antagonizing the adenosine A2A receptors in the brain and thereby protecting motor neurons from excitotoxicity. We examined the association between consumption of caffeine, coffee and tea and risk of amyotrophic lateral sclerosis (ALS). Longitudinal analyses based on over 1,010,000 males and females in five large cohort studies (the Nurses' Health Study, the Health Professionals Follow-up Study, the Cancer Prevention Study II Nutrition Cohort, the Multiethnic Cohort Study, and the National Institutes of Health-AARP Diet and Health Study). Cohort-specific multivariable-adjusted risk ratios (RR) and 95% confidence intervals (CI) estimates of ALS incidence or death were estimated by Cox proportional hazards regression and pooled using random-effects models. Results showed that a total of 1279 cases of ALS were documented during a mean of 18 years of follow-up. Caffeine intake was not associated with ALS risk; the pooled multivariable-adjusted RR comparing the highest to the lowest quintile of intake was 0.96 (95% CI 0.81-1.16). Similarly, neither coffee nor tea was associated with ALS risk. In conclusion, the results of this large study do not support associations of caffeine or caffeinated beverages with ALS risk.
    03/2015; DOI:10.3109/21678421.2015.1020813
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    ABSTRACT: IMPORTANCE Amyotrophic lateral sclerosis (ALS) is a severe progressive disease that cannot be prevented or cured. Diet-derived long-chain polyunsaturated fatty acids (PUFAs) are incorporated in brain lipids and modulate oxidative and inflammatory processes and could thus affect ALS risk and progression. OBJECTIVE To examine the association between omega-6 and omega-3 PUFA consumption and ALS risk. DESIGN, SETTING, AND PARTICIPANTS Longitudinal analyses based on 1 002 082 participants (479 114 women and 522 968 men) in 5 prospective cohorts: the National Institutes of Health-AARP Diet and Health Study, the Cancer Prevention Study II Nutrition Cohort, the Health Professionals Follow-up Study, the Multiethnic Cohort Study, and the Nurses' Health Study. Diet was assessed via food frequency questionnaire developed or modified for each cohort. Participants were categorized into cohort-specific quintiles of intake of energy-adjusted dietary variables. MAIN OUTCOMES AND MEASURES Cohort-specific multivariable-adjusted risk ratios (RRs) of ALS incidence or death estimated by Cox proportional hazards regression and pooled using random-effects methods. RESULTS A total of 995 ALS cases were documented during the follow-up. A greater omega-3 PUFA intake was associated with a reduced risk for ALS. The pooled, multivariable-adjusted RR for the highest to the lowest quintile was 0.66 (95% CI, 0.53-0.81; P < .001 for trend). Consumption of both a-linolenic acid (RR, 0.73; 95% CI, 0.59-0.89; P = .003 for trend) and marine omega-3 PUFAs (RR, 0.84; 95% CI, 0.65-1.08; P = .03 for trend) contributed to this inverse association. Intakes of omega-6 PUFA were not associated with ALS risk. CONCLUSIONS AND RELEVANCE Consumption of foods high in omega-3 PUFAs may help prevent or delay the onset of ALS.
    JAMA Neurology 07/2014; 71(9). DOI:10.1001/jamaneurol.2014.1214 · 7.01 Impact Factor
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    ABSTRACT: 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.
    British Journal Of Nutrition 06/2014; 112(05):1-9. DOI:10.1017/S000711451400138X · 3.34 Impact Factor
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    ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a fast-progressing neurodegenerative disease with a median survival time from diagnosis of 1.5-3 years. The cause of ALS is unknown, but inflammation may play a role. Fiber has been shown to lower inflammatory markers, and a high fiber intake was associated with a lower risk of ALS in a case-control study; however, prospective studies are lacking. We explored the relation between dietary intake of fiber and the risk of ALS in 5 large prospective cohort studies comprising over 1,050,000 US citizens who contributed 1,133 ALS cases during a mean of 15 years of follow-up (1980-2008). Cox proportional hazards models were used within each cohort, and cohort-specific estimates were subsequently pooled using a random-effects model. We found that intakes of total fiber, cereal fiber, vegetable fiber, and fruit fiber were not associated with ALS risk when comparing the highest quintile of intake with the lowest (for total fiber, pooled multivariable relative risk (RR) = 0.99, 95% confidence interval (CI): 0.80, 1.24; for cereal fiber, RR = 1.13, 95% CI: 0.94, 1.37; for vegetable fiber, RR = 0.97, 95% CI: 0.77, 1.23; and for fruit fiber, RR = 1.05, 95% CI: 0.86, 1.29). These findings do not support the hypothesis that fiber intake is a major determinant of ALS risk.
    American journal of epidemiology 05/2014; 179(12). DOI:10.1093/aje/kwu089 · 4.98 Impact Factor
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    ABSTRACT: Intake of n-3 and n-6 polyunsaturated fatty acids (PUFAs) has been implicated in the pathogenesis of depression. We sought to estimate the association between intake of fish and n-3 and n-6 PUFAs and suicide mortality over the course of long-term follow-up. In this prospective cohort study, biennial questionnaires were administered to 42,290 men enrolled in the Health Professionals Follow-up Study (1988-2008), 72,231 women enrolled in the Nurses' Health Study (1986-2008), and 90,836 women enrolled in Nurses' Health Study II (1993-2007). Dietary fish and n-3 and n-6 PUFA intakes were assessed every 4 years using a validated food-frequency questionnaire. Suicide mortality was ascertained through blind physician review of death certificates and hospital or pathology reports. Adjusted relative risks of suicide mortality were estimated with multivariable Cox proportional hazards models and pooled across cohorts using random-effects meta-analysis. The pooled multivariable relative risks for suicide among persons in the highest quartile of intake of n-3 or n-6 PUFAs, relative to the lowest quartile, ranged from 1.08 to 1.46 for n-3 PUFAs (Ptrend = 0.11-0.52) and from 0.68 to 1.19 for n-6 PUFAs (Ptrend = 0.09-0.54). We did not find evidence that intake of n-3 PUFAs or fish lowered the risk of completed suicide.
    American journal of epidemiology 05/2014; 179(12). DOI:10.1093/aje/kwu086 · 4.98 Impact Factor
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    ABSTRACT: The relation between body weight and mortality among persons with type 2 diabetes remains unresolved, with some studies suggesting decreased mortality among overweight or obese persons as compared with normal-weight persons (an "obesity paradox"). We studied participants with incident diabetes from the Nurses' Health Study (8970 participants) and Health Professionals Follow-up Study (2457 participants) who were free of cardiovascular disease and cancer at the time of a diagnosis of diabetes. Body weight shortly before diagnosis and height were used to calculate the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters). Multivariable Cox models were used to estimate the hazard ratios and 95% confidence intervals for mortality across BMI categories. There were 3083 deaths during a mean period of 15.8 years of follow-up. A J-shaped association was observed across BMI categories (18.5 to 22.4, 22.5 to 24.9 [reference], 25.0 to 27.4, 27.5 to 29.9, 30.0 to 34.9, and ≥35.0) for all-cause mortality (hazard ratio, 1.29 [95% confidence interval {CI}, 1.05 to 1.59]; 1.00; 1.12 [95% CI, 0.98 to 1.29]; 1.09 [95% CI, 0.94 to 1.26]; 1.24 [95% CI, 1.08 to 1.42]; and 1.33 [95% CI, 1.14 to 1.55], respectively). This relationship was linear among participants who had never smoked (hazard ratios across BMI categories: 1.12, 1.00, 1.16, 1.21, 1.36, and 1.56, respectively) but was nonlinear among participants who had ever smoked (hazard ratios across BMI categories: 1.32, 1.00, 1.09, 1.04, 1.14, and 1.21) (P=0.04 for interaction). A direct linear trend was observed among participants younger than 65 years of age at the time of a diabetes diagnosis but not among those 65 years of age or older at the time of diagnosis (P<0.001 for interaction). We observed a J-shaped association between BMI and mortality among all participants and among those who had ever smoked and a direct linear relationship among those who had never smoked. We found no evidence of lower mortality among patients with diabetes who were overweight or obese at diagnosis, as compared with their normal-weight counterparts, or of an obesity paradox. (Funded by the National Institutes of Health and the American Diabetes Association.).
    New England Journal of Medicine 01/2014; 370(3):233-44. DOI:10.1056/NEJMoa1304501 · 54.42 Impact Factor
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    ABSTRACT: Inflammation is considered as a mechanism leading to depression, but the association between inflammatory dietary pattern and depression risk is unknown. Using reduced-rank regression, we identified a dietary pattern that was related to plasma levels of inflammatory markers (C-reactive protein, interleukin-6, tumor necrosis factor receptor 2), and we conducted a prospective analysis of the relationship of this pattern and depression risk among participants in the Nurses' Health Study. A total of 43,685 women (aged 50-77) without depression at baseline (1996) were included and followed up until 2008. Diet information was obtained from food frequency questionnaires completed between 1984 through 2002 and computed as cumulative average of dietary intakes with a 2-year latency applied. We used a strict definition of depression that required both self-reported physician-diagnosed depression and use of antidepressants, and a broader definition that included women who reported either clinical diagnosis or antidepressant use. During the 12-year follow-up, we documented 2,594 incident cases of depression using the stricter definition and 6,446 using the broader definition. After adjustment for body mass index and other potential confounders, relative risks comparing extreme quintiles of the inflammatory dietary pattern were 1.41 (95% confidence interval [CI], 1.22, 1.63; P-trend <.001) for the strict definition and 1.29 (95% CI, 1.18, 1.41; P-trend <.001) for the broader definition of depression. The inflammatory dietary pattern is associated with a higher depression risk. This finding suggests that chronic inflammation may underlie the association between diet and depression.
    Brain Behavior and Immunity 10/2013; 36. DOI:10.1016/j.bbi.2013.09.014 · 6.13 Impact Factor
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    ABSTRACT: Prior reports have indicated a potential dose-response relationship between smoking and suicide. However, this relationship is controversial. This study evaluated the association between smoking and risk of death from suicide in three large-scale cohorts of U.S. men and women (n=253,033). Suicides were identified from death certificates among 43,816 men enrolled in the Health Professionals Follow-up Study (HPFS) between 1986 and 2008, 116,566 women in the Nurses' Health Study (NHS) between 1976 and 2008, and 92,651 women in the NHS II between 1989 and 2007. Information on smoking was obtained at baseline and updated every 2 years. Relative risks (RRs) of suicide were estimated using Cox proportional hazards regression models. Cohort specific RRs were pooled using random-effects models. Suicide deaths were determined by physician review of death certificates. A total of 457 deaths from suicide were documented. Compared to never smokers, the pooled multivariate RR (95% confidence interval [CI]) of suicide was 1.15 (0.91-1.45) for former smokers and 2.69 (2.11-3.42) for current smokers. A nonmonotonic dose-response relationship was noted between the number of cigarettes smoked per day (CPD) and suicide risk (Ptrend<0.001). Compared to never smokers, the pooled multivariate RR (95% CI) was 2.59 (1.77-3.79) for those with 1-14 CPD, 2.03 (1.39-2.94) for those with 15-24 CPD, and 4.13 (2.96-5.78) for those with ≥25 CPD. Smoking was self-reported and had some degree of measurement error. Participants were not a representative sample of the U.S. population. Results from three large cohorts suggest a nonmonotonic dose-response association between smoking and suicide risk.
    Journal of Affective Disorders 09/2013; 151(3). DOI:10.1016/j.jad.2013.08.033 · 3.71 Impact Factor
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    ABSTRACT: A recent meta-analysis of 7 genome-wide association studies on early balding (alopecia) revealed single nucleotide polymorphism variants in the region of the amyotrophic lateral sclerosis (ALS) gene TAR DNA-binding protein 43 (TARDBP/TDP-43). We therefore explored the association of early-onset alopecia and ALS in the Health Professionals Follow-up Study, a large cohort of 51,529 US men. In 1992, the participants (then aged 46-81 years) were asked to report their hair line pattern at age 45 years. During the follow-up period (1992-2008), 42 men were diagnosed with ALS. Of those, 13 had reported no alopecia, 18 had reported moderate alopecia, and 11 had reported extensive alopecia at age 45 years. Those who reported extensive alopecia had an almost 3-fold increased risk of ALS compared with those who reported no alopecia (relative risk = 2.74, 95% confidence interval: 1.23, 6.13). Furthermore, we observed a linear trend of increased risk of ALS with increasing level of balding at age 45 years (Ptrend = 0.02). In conclusion, men with early-onset alopecia seem to have a higher risk of ALS. The mechanisms underlying this association deserve further investigation.
    American journal of epidemiology 08/2013; DOI:10.1093/aje/kwt096 · 4.98 Impact Factor
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    ABSTRACT: Although individual nutrients have been investigated in relation to depression risk, little is known about the overall role of diet in depression. We examined whether long-term dietary patterns derived from a food-frequency questionnaire (FFQ) predict the development of depression in middle-aged and older women. We conducted a prospective study in 50,605 participants (age range: 50-77 y) without depression in the Nurses' Health Study at baseline (1996) who were followed until 2008. Long-term diet was assessed by using FFQs every 4 y since 1986. Prudent (high in vegetables) and Western (high in meats) patterns were identified by using a principal component analysis. We used 2 definitions for clinical depression as follows: a strict definition that required both a reported clinical diagnosis and use of antidepressants (3002 incident cases) and a broad definition that further included women who reported either a clinical diagnosis or antidepressant use (7413 incident cases). After adjustment for age, body mass index, and other potential confounders, no significant association was shown between the diet patterns and depression risk under the strict definition. Under the broad definition, women with the highest scores for the Western pattern had 15% higher risk of depression (95% CI: 1.04, 1.27; P-trend = 0.01) than did women with the lowest scores, but after addition adjustment for psychological scores at baseline, results were no longer significant (RR: 1.09; 95% CI: 0.99, 1.21; P-trend = 0.08). Overall, results of this large prospective study do not support a clear association between dietary patterns from factor analysis and depression risk.
    American Journal of Clinical Nutrition 07/2013; 98(3). DOI:10.3945/ajcn.112.052761 · 6.92 Impact Factor
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    ABSTRACT: Our goal in this study was to determine whether maternal fat intake before or during pregnancy was associated with risk of autism spectrum disorder (ASD) in the offspring. Our primary analysis included 317 mothers who reported a child with ASD and 17,728 comparison mothers from the Nurses' Health Study II (index births in 1991-2007). Dietary information was collected prospectively through a validated food frequency questionnaire. Binomial regression was used to estimate crude and adjusted risk ratios. Maternal intake of linoleic acid was significantly inversely associated with ASD risk in offspring, corresponding to a 34% reduction in risk in the highest versus lowest quartiles of intake. Mothers in the lowest 5% of ω-3 fatty acid intake had a significant increase in offspring ASD risk as compared with the remaining distribution (risk ratio = 1.53, 95% confidence interval: 1.00, 2.32); this association was also seen in the subgroup of women (86 cases and 5,798 noncases) for whom dietary information during pregnancy was available (risk ratio = 2.42, 95% confidence interval: 1.19, 4.91). Thus, variations in intake of polyunsaturated fats within the range commonly observed among US women could affect fetal brain development and ASD risk. Because the number of women with diet assessed during pregnancy was small, however, these results should be interpreted cautiously.
    American journal of epidemiology 06/2013; 178(2). DOI:10.1093/aje/kws433 · 4.98 Impact Factor
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    ABSTRACT: A low magnesium intake has been suggested to be associated with amyotrophic lateral sclerosis (ALS) in pathological and case-control studies, but prospective studies in humans are lacking. The relation between dietary intake of magnesium and ALS risk was explored in five large prospective cohort studies (the Nurses' Health Study, the Health Professionals Follow-up Study, the Cancer Prevention Study II Nutrition Cohort, the Multiethnic Cohort Study, and the National Institutes of Health - AARP Diet and Health Study), comprising over 1,050,000 males and females contributing 1093 cases of ALS during a mean of 15 years of follow-up. Cox proportional hazards models were used within each cohort, and cohort-specific estimates were subsequently pooled using a random-effects model. Results demonstrated that dietary magnesium intake was not associated with ALS risk, relative risk 1.07, 95% confidence interval 0.88 - 1.31 comparing the highest quintile of intake with the lowest. This finding does not support a protective effect of magnesium intake on ALS risk. Further analyses should explore magnesium intake in combination with heavy metal exposure and genetic variants affecting magnesium absorption.
    06/2013; 14(5-6). DOI:10.3109/21678421.2013.803577
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    ABSTRACT: OBJECTIVE: Prior research has suggested the possible role of oxidative stress in the pathogenesis of amyotrophic lateral sclerosis (ALS). Prospective data examining dietary antioxidants such carotenoids and vitamin C are limited. METHODS: Risk of ALS associated with carotenoid and vitamin C intake was investigated in 5 prospective cohorts: the National Institutes of Health-Association of American Retired Persons Diet and Health Study, the Cancer Prevention Study II Nutrition Cohort, the Multiethnic Cohort, the Health Professionals Follow-up Study (HPFS), and the Nurses Health Study (NHS). ALS deaths were documented using the National Death Index, and confirmed nonfatal ALS cases were included from HPFS and NHS. A total of 1,153 ALS deaths occurred among 1,100,910 participants (562,942 men; 537,968 women). Participants were categorized into cohort-specific quintiles of intake for dietary variables. We applied Cox proportional hazards regression to calculate cohort-specific risk ratios (RRs), and pooled results using random-effects methods. RESULTS: A greater total major carotenoids intake was associated with a reduced risk of ALS (pooled, multivariate-adjusted RR for the highest to the lowest quintile = 0.75, 95% confidence interval [CI] = 0.61-0.91, p for trend = 0.004). Individually, higher dietary intakes of β-carotene and lutein were inversely associated with ALS risk. The pooled multivariate RRs comparing the highest to the lowest quintile for β-carotene and lutein were 0.85 (95% CI = 0.64-1.13, p for trend = 0.03) and 0.79 (95% CI = 0.64-0.96, p for trend = 0.01), respectively. Lycopene, β-cryptoxanthin, and vitamin C were not associated with reduced risk of ALS. INTERPRETATION: Consumption of foods high in carotenoids may help prevent or delay onset of ALS. ANN NEUROL 2012.
    Annals of Neurology 02/2013; 73(2). DOI:10.1002/ana.23820 · 11.91 Impact Factor
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    ABSTRACT: Evidence suggests possible Parkinson's disease (PD)-relevant neural effects of exposure to polychlorinated biphenyls. Limited epidemiological evidence suggests that polychlorinated biphenyl exposure may increase PD risk, but no studies have involved biomarkers of polychlorinated biphenyl exposure before PD onset. We examined the prospective association between serum polychlorinated biphenyls and PD. We conducted a nested case-control study within the Finnish Mobile Clinic Health Examination Survey with serum samples collected during 1968-1972 and analyzed in 2005-2007 for polychlorinated biphenyls. Incident PD cases were identified through the Social Insurance Institution's registry and were confirmed by medical record review (n = 101). Controls (n = 349) were matched on age, sex, municipality, and vital status. We used logistic regression to estimate adjusted odds ratios. There was no evidence of increasing risk of PD with increasing polychlorinated biphenyl exposure in adjusted analyses. Instead, there was a trend toward lower odds of PD with increasing serum polychlorinated biphenyl concentrations, which was most pronounced for the sum of all measured polychlorinated biphenyl congeners and the sum of dioxin-like congeners. Compared with that of those in the lowest quintile, the odds ratio of PD among those in the highest quintile of total polychlorinated biphenyls was 0.29 (95% confidence interval, 0.12-0.70; P trend = .02) and for dioxin-like congeners was 0.34 (95% confidence interval, 0.13-0.90; P trend = .05). These results do not support an increased risk of PD from polychlorinated biphenyl exposure and instead suggest a possible protective effect of polychlorinated biphenyl exposure. © 2012 Movement Disorder Society.
    Movement Disorders 11/2012; 27(13). DOI:10.1002/mds.25217 · 5.63 Impact Factor
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    ABSTRACT: Our objective was to determine if amyotrophic lateral sclerosis (ALS) risk varies according to body mass index (BMI) captured up to three decades earlier. At baseline 537,968 females and 562,942 males in five ongoing cohorts reported height, current weight and weight at age 18/21 years. During 14-28 years of follow-up, 1153 participants developed ALS. Cohort-specific Cox proportional hazards models were used to estimate rates that were then pooled with random-effects models. Results showed that lower BMI at baseline was associated with ALS; for each 5-unit increase in BMI, ALS rates were 21% lower (95% CI 14% 27%). Compared to individuals with healthy BMI, ALS rates were significantly lower among the overweight (RR = 0.76 (95% CI 0.62-0.93)) and obese (RR = 0.73 (95% CI 0.55-0.96)). Among never smokers the association persisted: RR = 0.75 (95% CI 0.65-0.85) for each 5-unit increase. Excluding the first seven years of follow-up, the associations were materially unchanged suggesting that weight loss from undiagnosed disease does not fully explain the findings. Overall, 75% of males and females had a healthy BMI at age 18/21 years, 15% of males and 8% of females were overweight or obese; there was no association with ALS although numbers with an unhealthy weight were small. In conclusion, these findings support an association between lower premorbid BMI and ALS.
    Amyotrophic Lateral Sclerosis 10/2012; 14(3). DOI:10.3109/21678421.2012.735240 · 2.37 Impact Factor
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    ABSTRACT: Animal and pathological studies suggest that inflammation may contribute to amyotrophic lateral sclerosis (ALS) pathology and that non-steroidal anti-inflammatory drugs (NSAIDs) might be protective. However, there are no prospective data on the relation between NSAID use and ALS risk in humans. The relation between NSAID use and ALS risk was explored in five large prospective cohort studies (the Nurses' Health Study, the Health Professionals Follow-up Study, the Cancer Prevention Study II Nutrition Cohort, the Multiethnic Cohort Study, and the National Institutes of Health - AARP Diet and Health Study). Detailed NSAID information was sought from 780,000 participants, 708 of whom developed ALS during follow-up. Cox proportional hazards models were used within each cohort and cohort-specific estimates were pooled with random effects models. Results showed that neither non-aspirin NSAID use, nor aspirin use was associated with ALS risk overall. The multivariable, pooled relative risk was 0.96 (95% CI 0.76-1.22) among non-aspirin NSAID users compared with non-users. Duration of NSAID use in years and frequency of NSAID use were not associated with ALS risk overall. In conclusion, the results do not support an overall effect of NSAIDs on ALS risk, but because NSAIDs have heterogeneous effects, a role of individual compounds cannot be excluded.
    Amyotrophic Lateral Sclerosis 08/2012; 13(6):573-9. DOI:10.3109/17482968.2012.703209 · 2.37 Impact Factor
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    ABSTRACT: Most research on the association between restless legs syndrome (RLS) and depression has involved cross-sectional data. The objective of the present study was to evaluate this issue prospectively among Nurses' Health Study participants. A total of 56,399 women (mean age = 68 years) who were free of depression symptoms at baseline (2002) were followed until 2008. Physician-diagnosed RLS was self-reported. During 300,155 person-years of follow-up, the authors identified 1,268 incident cases of clinical depression (regular use of antidepressant medication and physician-diagnosed depression). Women with RLS at baseline were more likely to develop clinical depression (multivariate-adjusted relative risk (RR) = 1.5, 95% confidence interval (CI): 1.1, 2.1; P = 0.02) than those without RLS. The presence of RLS at baseline was also associated with higher scores on the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10) and the 15-item Geriatric Depression Scale (GDS-15) thereafter. Multivariable-adjusted mean differences were 1.00 (standard error, 0.12) for CESD-10 score and 0.47 (standard error, 0.07) for GDS-15 score between women with RLS and those without RLS (P < 0.0001). In conclusion, women with physician-diagnosed RLS had an increased risk of developing clinical depression and clinically relevant depression symptoms. Further prospective studies using refined approaches to ascertainment of RLS and depression are warranted.
    American journal of epidemiology 07/2012; 176(4):279-88. DOI:10.1093/aje/kws016 · 4.98 Impact Factor
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    ABSTRACT: BACKGROUND: Obesity in childhood and adolescence has important health consequences, but its relation to risk of adult depression remains uncertain. OBJECTIVE: To examine the effect of perceived and actual obesity during childhood and adolescence on prevalence and incidence of adult depression risk. METHODS: Cohort study of 91 798 female registered nurses followed longitudinally for 12 years. RESULTS: As compared with lean women of the same age, women in the two highest categories of body shape at age 10 had both higher prevalence (OR=2.59, 95% CI 1.46 to 4.61) and incidence (OR=2.01, 95% CI 1.08 to 3.71) of depression. Similar results were obtained for body shape at age 20 (OR=3.43 for prevalence and OR=2.03 for incidence) and for body mass index (BMI) at age 18 (OR=2.92 for BMI ≥40 kg/m(2)). These associations remained significant after adjustment for multiple confounders. CONCLUSION: These results indicate that childhood-adolescence obesity is a strong and independent risk factor for adult depression.
    Journal of epidemiology and community health 07/2012; 67(1). DOI:10.1136/jech-2012-201435 · 3.29 Impact Factor
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    ABSTRACT: Addictive behaviors, such as cigarette smoking and coffee drinking, have been associated with a reduced risk of Parkinson's disease (PD). Whether alcohol consumption is also associated with PD risk is less certain. We prospectively followed 132,403 participants in the Cancer Prevention Study II Nutrition Cohort from 1992 to 2005. Alcohol intake was assessed at baseline. Incident cases of PD (n = 605; 389 male and 216 female) were confirmed by treating physicians and medical record review. Relative risks (RRs) were estimated using proportional hazards models, adjusting for age, smoking, and other risk factors. Alcohol consumption was not significantly associated with PD risk. After adjustment for age, smoking, and other risk factors, the RR comparing men consuming 30 or more grams of alcohol per day (highest category) to nondrinker men was 1.29 (95% confidence interval [CI]: 0.90, 1.86; P trend: 0.40), and the RR comparing women consuming 15 or more grams of alcohol (highest category) per day to nondrinker women was 0.77 (95% CI: 0.41, 1.45; P trend: 0.87). Consumption of beer, wine, or liquor was also not associated with PD risk. The results of this large, prospective study do not support an association between alcohol intake and risk of PD.
    Movement Disorders 07/2012; 27(8):980-7. DOI:10.1002/mds.25050 · 5.63 Impact Factor
  • K. Lyall, E. O'Reilly
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    ABSTRACT: Background: Polyunsaturated fats, including omega-3 fatty acids, are essential for fetal brain development. While prior work has examined potential associations between maternal fish intake and child developmental outcomes, it is not known how maternal fat and fatty acid intake from other sources may influence risk of autism spectrum disorder (ASD). Objectives: To determine whether maternal intake of fats and fatty acids influences risk of ASD using prospectively collected dietary information. Methods: We utilized data from the Nurses’ Health Study II (NHS II), a large prospective cohort with questionnaires mailed every 2 years since 1989 to over 116,000 nurses in the United States. Dietary information was collected in 1991, 1995, 1999, and 2003 from a validated 131-item Food Frequency Questionnaire. 27,516 NHS II participants had a child born between 1991-2007; for the primary analysis, women who did not return at least one of two NHS II questionnaires with information on ASD, and those who did not have an FFQ completed before the child’s birth were excluded. Major types of fats and fatty acids were categorized into quartiles. We further explored risk in individuals with the top and bottom 10% of intake, as well as those in the lowest 5% of the distribution of intake. Intake of fish and use of fish oil supplements was also assessed. Binomial regression was used to obtain crude and multivariate adjusted risk ratios for the association between maternal dietary fat and ASD. Results: 18,045 women, including 317 who reported a child with ASD, were included in primary analyses. In adjusted analyses, risk of having a child with ASD decreased with increasing polyunsaturated fat intake (RR for the highest vs. the lowest quartile =0.67, 95% CI 0.49, 0.92; p for trend = 0.008); nearly identical protective associations were seen for the top quartiles of omega-6 and linoleic fatty acid intake. Overall, intake of omega-3 fatty acids was not associated with risk of ASD, although the results of exploratory analyses suggested a possible increase in risk among women with the lowest 5% of intake of omega-3 fatty acid (RR= 1.53, 95% CI 1.00, 2.32), and for those with the lowest 10% of intake of alpha-linoleic acid (ALA) in particular (RR=1.42, 95% CI 1.04, 1.95). These associations appeared to strengthen when assessed in women for whom dietary information referred to pregnancy (n=5,884, including only 86 cases; RR for omega-3=2.42, 95% CI 1.19, 4.91; RR for ALA=2.23, 95% CI 1.30, 3.84). Neither fish intake nor intakes of total fat, monounsaturated, trans, or saturated fat, or fat from animal, vegetable, and dairy sources, or other fatty acids, were significantly associated with ASD. In a secondary analysis, results were similar when including women with FFQs collected during lactation. Conclusions: The preliminary results of this large longitudinal investigation suggest that maternal intake of polyunsaturated fatty acids may influence risk of having a child with ASD. In particular, low intakes of essential fatty acids linoleic and alpha-linolenic may increase risk. Further work should assess maternal intake of these fats during pregnancy.
    2012 International Meeting for Autism Research; 05/2012

Publication Stats

3k Citations
442.92 Total Impact Points

Institutions

  • 2013–2014
    • Harvard Medical School
      • Division of Nutrition
      Boston, Massachusetts, United States
  • 2008–2014
    • Harvard University
      • Department of Nutrition
      Cambridge, Massachusetts, United States
  • 2010
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, MA, United States
  • 2005
    • National Public Health Institute
      Helsinki, Southern Finland Province, Finland
  • 2004
    • Umeå University
      Umeå, Västerbotten, Sweden