scholarly journals Polyunsaturated fatty acids and the risk of multiple sclerosis

2017 ◽  
Vol 23 (14) ◽  
pp. 1830-1838 ◽  
Author(s):  
Kjetil Bjørnevik ◽  
Tanuja Chitnis ◽  
Alberto Ascherio ◽  
Kassandra L Munger

Background: Results from previous studies on polyunsaturated fatty acid (PUFA) intake and multiple sclerosis (MS) risk are conflicting. Objective: To prospectively investigate the association between dietary intake of PUFA and MS risk. Methods: We followed 80,920 women from Nurses’ Health Study (1984–2004) and 94,511 women from Nurses’ Health Study II (1991–2009) who reported on diet using a validated food frequency questionnaire every 4 years and identified 479 incident MS cases during follow-up. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), for the effect of PUFA intake on MS risk adjusting for age, latitude of residence at age 15, ancestry, cigarette smoking, supplemental vitamin D intake, body mass index, and total energy intake. Results: Higher intake of total PUFA at baseline was associated with a lower risk of MS (HR top vs bottom quintile: 0.67, 95% CI: 0.49–0.90, p trend = 0.01). Among the specific types of PUFA, only α-linolenic acid (ALA) was inversely associated with MS risk (HR top vs bottom quintile: 0.61, 95% CI: 0.45–0.83, p trend = 0.001). The long-chain fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were not associated with MS risk. Conclusion: Low dietary PUFA intake may be another modifiable risk factor for MS.

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Luc Djousse ◽  
Andrew Petrone ◽  
John M Gaziano

Background: While previous studies have reported a positive relation of fried food consumption with type 2 diabetes, hypertension, and obesity, no previous study has examined the relation of total fried food intake with risk of heart failure (HF) in a prospective cohort. Objective: To test the hypothesis that fried food consumption is positively associated with risk of HF in male physicians. Methods: A prospective cohort of 19,968 participants from the Physicians’ Health Study. Frequency of fried food consumption was assessed between 1999 and 2002 using a food frequency questionnaire and HF was ascertained through annual follow-up questionnaires with validation in a subsample. We used Cox regression to estimate multivariable adjusted hazard ratios of HF. Results: During a median follow-up of 10.6 years, 862 cases of HF occurred. The mean age at baseline was 66.4 ± 9.2 years. Median frequency of fried food consumption was <1 time per week. Multivariable adjusted hazard ratios (95% CI) were: 1.0 (ref), 1.18 (1.01-1.37), 1.25 (1.02-1.54), and 1.68 (1.19-2.36) for fried food consumption of <1/week, 1-3/week, 4-6/week, and 7+/week, respectively (p for linear trend: 0.0004), after adjustment for age, alcohol use, smoking, exercise, and history of myocardial infarction, coronary artery bypass graph or angioplasty (Fig). Additional adjustment of total trans fats did not alter the findings. In a secondary analysis, body mass index did not modify the relation of fried foods with HF risk. Conclusions: Our data show a positive association between fried food intake and risk of HF in US male physicians.


Cephalalgia ◽  
2013 ◽  
Vol 34 (5) ◽  
pp. 327-335 ◽  
Author(s):  
Knut Hagen ◽  
Eystein Stordal ◽  
Mattias Linde ◽  
Timothy J Steiner ◽  
John-Anker Zwart ◽  
...  

Background Headache has not been established as a risk factor for dementia. The aim of this study was to determine whether any headache was associated with subsequent development of vascular dementia (VaD), Alzheimer’s disease (AD) or other types of dementia. Methods This prospective population-based cohort study used baseline data from the Nord-Trøndelag Health Study (HUNT 2) performed during 1995–1997 and, from the same Norwegian county, a register of cases diagnosed with dementia during 1997–2010. Participants aged ≥20 years who responded to headache questions in HUNT 2 were categorized (headache free; with any headache; with migraine; with nonmigrainous headache). Hazard ratios (HRs) for later inclusion in the dementia register were estimated using Cox regression analysis. Results Of 51,383 participants providing headache data in HUNT 2, 378 appeared in the dementia register during the follow-up period. Compared to those who were headache free, participants with any headache had increased risk of VaD ( n = 63) (multivariate-adjusted HR = 2.3, 95% CI 1.4–3.8, p = 0.002) and of mixed dementia (VaD and AD ( n = 52)) (adjusted HR = 2.0, 95% CI 1.1–3.5, p = 0.018). There was no association between any headache and later development of AD ( n = 180). Conclusion In this prospective population-based cohort study, any headache was a risk factor for development of VaD.


2019 ◽  
Vol 119 (12) ◽  
pp. 2053-2063 ◽  
Author(s):  
Trond Isaksen ◽  
Line H. Evensen ◽  
Sigrid K. Brækkan ◽  
John-Bjarne Hansen

Abstract Background Limited knowledge exists on the association between intake of long-chained n-3 polyunsaturated fatty acids (n-3 PUFAs) and risk of recurrence and all-cause mortality in patients with venous thromboembolism (VTE). Objectives This article investigates whether intake of marine n-3 PUFAs was associated with risk of recurrence and mortality in patients with incident VTE. Methods A total of 595 patients with incident VTE and available data on n-3 PUFA intake were derived from the Tromsø Study surveys 4 (1994–1995) and 6 (2007–2008). Weekly intake of n-3 PUFAs was categorized as low, medium, and high based on tertiles. Recurrent VTEs and all-cause mortality were registered up to December 31, 2016. Hazard ratios (HRs) were calculated using Cox regression models with the low intake category as reference. Results There were 98 recurrent VTEs and 227 deaths during follow-up. Overall, we found no association between intake of n-3 PUFAs and risk of recurrent VTE. However, inverse associations were found for high intakes in patients with unprovoked VTE (HR 0.45, 95% confidence interval [CI]: 0.20–1.01), cancer-free patients (HR 0.51, 95% CI: 0.27–0.95), and deep vein thrombosis (DVT) patients (HR 0.49, 95% CI: 0.24–0.97). The inverse associations were more evident when follow-up was restricted to the time after discontinuation of anticoagulant therapy. No association was observed between intake of n-3 PUFAs and mortality after incident VTE. Conclusion A high dietary intake of marine n-3 PUFAs was associated with lower risk of recurrent VTE after unprovoked index events, DVT, and in cancer-free patients.


Cardiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Luc Djousse ◽  
Mary L. Biggs ◽  
Nirupa R. Matthan ◽  
Joachim H. Ix ◽  
Annette L. Fitzpatrick ◽  
...  

Background: Heart failure (HF) is highly prevalent among older adults and is associated with high costs. Although serum total nonesterified fatty acids (NEFAs) have been positively associated with HF risk, the contribution of each individual NEFA to HF risk has not been examined. Objective: The aim of this study was to examine the association of individual fasting NEFAs with HF risk in older adults. Methods: In this prospective cohort study of older adults, we measured 35 individual NEFAs in 2,140 participants of the Cardiovascular Health Study using gas chromatography. HF was ascertained using review of medical records by an endpoint committee. Results: The mean age was 77.7 ± 4.4 years, and 38.8% were male. During a median follow-up of 9.7 (maximum 19.0) years, 655 new cases of HF occurred. In a multivariable Cox regression model controlling for demographic and anthropometric variables, field center, education, serum albumin, glomerular filtration rate, physical activity, alcohol consumption, smoking, hormone replacement therapy, unintentional weight loss, and all other measured NEFAs, we observed inverse associations (HR [95% CI] per standard deviation) of nonesterified pentadecanoic (15:0) (0.73 [0.57–0.94]), γ-linolenic acid (GLA) (0.87 [0.75–1.00]), and docosahexaenoic acid (DHA) (0.73 [0.61–0.88]) acids with HF, and positive associations of nonesterified stearic (18:0) (1.30 [1.04–1.63]) and nervonic (24:1n-9) (1.17 [1.06–1.29]) acids with HF. Conclusion: Our data are consistent with a higher risk of HF with nonesterified stearic and nervonic acids and a lower risk with nonesterified 15:0, GLA, and DHA in older adults. If confirmed in other studies, specific NEFAs may provide new targets for HF prevention.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Andrew B Petrone ◽  
J. Michael Gaziano ◽  
Luc Djousse

Background: Previous studies have suggested that dark chocolate consumption may lower blood pressure, a major risk factor for heart failure. However, limited and inconsistent data are available on the association of chocolate consumption with the incidence rate of heart failure. Objective: To test the hypothesis that chocolate consumption is associated with a lower risk of heart failure. Methods: We prospectively studied 20,278 men from the Physicians’ Health Study. Chocolate consumption was assessed between 1999 and 2002 via a food frequency questionnaire and heart failure was ascertained through annual follow-up questionnaires with validation in a subsample. We used Cox regression to estimate multivariable adjusted relative risk of heart failure. Results: During a median follow-up of 9.3 years, there were 876 new cases of heart failure. The mean age at baseline was 66.4 ± 9.2 years. Median chocolate consumption was 1-3 times per month. Hazard ratios (95% CI) for heart failure were 1.0 (ref), 0.87 (0.73-1.04), 0.80 (0.66-0.98), and 0.87 (0.72-1.04), for chocolate consumption of less than 1/month, 1-3/month, 1/week, and 2+/week, respectively, after adjusting for age, body mass index (BMI), smoking, alcohol intake, exercise, and history of atrial fibrillation. In a secondary analysis, chocolate consumption was inversely associated with risk of heart failure in men whose BMI was <25 kg/m 2 but not in those with BMI of 25+ kg/m 2 ( Figure 1 ), p for interaction=0.0895. Conclusions: Our data suggest that moderate consumption of chocolate might be associated with a lower risk of heart failure, especially in lean individuals.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2699
Author(s):  
Xiaoran Liu ◽  
Marta Guasch-Ferré ◽  
Deirdre K. Tobias ◽  
Yanping Li

Walnut consumption is associated with health benefits. We aimed to (1) examine the association between walnut consumption and mortality and (2) estimate life expectancy in relation to walnut consumption in U.S. adults. We included 67,014 women of the Nurses’ Health Study (1998–2018) and 26,326 men of the Health Professionals Follow-up Study (1998–2018) who were free of cancer, heart disease, and stroke at baseline. We used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During up to 20 years of follow-up, we documented 30,263 deaths. The hazard ratios for total mortality across categories of walnut intake (servings/week), as compared to non-consumers, were 0.95 (95% confidence interval (CI), 0.91, 0.98) for <1 serving/week, 0.94 (95% CI, 0.89, 0.99) for 1 serving/week, 0.87 (95% CI, 0.82, 0.93) for 2–4 servings/week, and 0.86 (95% CI, 0.79, 0.93) for >=5 servings/week (p for trend <0.0001). A greater life expectancy at age 60 (1.30 years in women and 1.26 years in men) was observed among those who consumed walnuts more than 5 servings/week compared to non-consumers. Higher walnut consumption was associated with a lower risk of total and CVD mortality and a greater gained life expectancy among U.S. elder adults.


2021 ◽  
pp. 1-24
Author(s):  
Bushra Hoque ◽  
Zumin Shi

Abstract Selenium (Se) is a trace mineral that has antioxidant and anti-inflammatory properties. This study aimed to investigate the association between Se intake, diabetes, all-cause and cause-specific mortality in a representative sample of US adults. Data from 18,932 adults who attended the 2003-2014 National Health and Nutrition Examination Survey (NHANES) were analysed. Information on mortality was obtained from the US mortality registry updated to 2015. Multivariable logistic regression and Cox regression were used. Cross-sectionally, Se intake was positively associated with diabetes. Comparing extreme quartiles of Se intake, the odds ratio (OR) for diabetes was 1.44 (95% CI: 1.09–1.89). During a mean of 6.6 years follow-up, there were 1627 death (312 CVD, 386 cancer). High intake of Se was associated with a lower risk of all-cause mortality. When comparing the highest with the lowest quartiles of Se intake, the hazard ratios (HRs) for all-cause, CVD mortality, cancer mortality and other mortality were: 0.77 (95% CI 0.59-1.01), 0.62 (95% CI, 0.35-1.13), 1.42 (95% CI, 0.78-2.58) and 0.60 (95% CI,0.40-0.80), respectively. The inverse association between Se intake and all-cause mortality was only found among white participants. In conclusion, Se intake was positively associated with diabetes but inversely associated with all-cause mortality. There was no interaction between Se intake and diabetes in relation to all-cause mortality.


2021 ◽  
Vol 79 (4) ◽  
pp. 1601-1612
Author(s):  
Johan Frederik Håkonsen Arendt ◽  
Erzsébet Horváth-Puhó ◽  
Henrik Toft Sørensen ◽  
Ebba Nexø ◽  
Lars Pedersen ◽  
...  

Background: It is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia. Objective: To assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer’s disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes). Methods: We conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000–2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200–600 pmol/L). We used multivariable Cox regression to compute 0–15-year hazard ratios for dementia. Results: For low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia. Conclusion: We found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.


Author(s):  
Gianfranco Umeres-Francia1 ◽  
María Rojas-Fernández ◽  
Percy Herrera Añazco ◽  
Vicente Benites-Zapata

Objective: To assess the association between NLR and PLR with all-cause mortality in Peruvian patients with CKD Methods: We conducted a retrospective cohort study in adults with CKD in stages 1 to 5. The outcome variable was mortality and as variables of exposure to NLR and PLR. Both ratios were categorized as high with a cut-off point of 3.5 and 232.5; respectively. We carried out a Cox regression model and calculated crude and adjusted hazard ratios (HR) with their 95% confidence interval (95%CI). Results: We analyzed 343 participants with a median follow-up time of 2.45 years (2.08-3.08). The frequency of deaths was 17.5% (n=60). In the crude analysis, the high NLR and PLR were significantly associated with all-cause mortality (HR=2.01; 95% CI:1.11-3.66) and (HR=2.58; 95% CI:1.31-5.20). In the multivariate model, after adjusting for age, sex, serum creatinine, CKD stage, albumin and hemoglobin, the high NLR and PLR remained as an independent risk factor for all-cause mortality, (HR=2.10; 95% CI:1.11-3.95) and (HR=2.71; 95% CI:1.28-5.72). Conclusion: Our study suggests the relationship between high NLR and PLR with all-cause mortality in patients with CKD.


2014 ◽  
Vol 112 (6) ◽  
pp. 984-991 ◽  
Author(s):  
Carmen Sayon-Orea ◽  
Maira Bes-Rastrollo ◽  
Alfredo Gea ◽  
Itziar Zazpe ◽  
Francisco J. Basterra-Gortari ◽  
...  

Reported associations between the consumption of fried foods and the incidence of obesity or weight gain make it likely that fried food consumption might also be associated with the development of hypertension. However, evidence from long-term prospective studies is scarce. Therefore, the aim of the present study was to longitudinally evaluate this association in a prospective cohort. The SUN (Seguimiento Universidad de Navarra) project is a Mediterranean cohort study of university graduates conducted in Spain, which started in December 1999 and is still ongoing. In the present study, we included 13 679 participants (5059 men and 8620 women), free of hypertension at baseline with a mean age of 36·5 (sd 10·8) years. Total fried food consumption was estimated at baseline. The outcome was the incidence of a medical diagnosis of self-reported hypertension during the follow-up period. To assess the association between the consumption of fried foods and the subsequent risk of developing incident hypertension during the follow-up period, Cox regression models were used. During a median follow-up period of 6·3 years, 1232 incident cases of hypertension were identified. After adjusting for potential confounders, the adjusted hazard ratios for developing hypertension were 1·18 (95 % CI 1·03, 1·36) and 1·21 (95 % CI 1·04, 1·41) for those consuming fried foods 2–4 and >4 times/week, respectively, compared with those consuming fried foods < 2 times/week (P for trend = 0·009). In conclusion, frequent consumption of fried foods at baseline was found to be associated with a higher risk of hypertension during the follow-up period in a Mediterranean cohort of university graduates.


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