Dietary ω-3 Polyunsaturated Fatty Acid Intake and Risk for Amyotrophic Lateral Sclerosis

Abstract

myotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder with few effective treatments and a disease pathogenesis that is poorly understood. [1][2][3] Diet-derived polyunsaturated fatty acids (PUFAs) in brain neural plasma membranes can modulate oxidative stress, excitotoxicity, and inflammation, 4-6 mechanisms that have been implicated in the etiology of ALS and other neurodegenerative conditions. [1][2][3] In particular, ω-3 PUFAs have been found to have neuroprotective effects in animal models of aging 6 and brain ischemia. 7 Unexpectedly, however, pretreatment with high doses of eicosapentaenoic acid, a long-chain ω-3 PUFA, accelerated disease progression in a mouse model of ALS. 8 However, it is unclear to what extent this experimental result applies to human disease.Data on the relation between PUFA intake and ALS risk are sparse. The results of 2 previous case-control studies 9,10 suggested lower ALS risk among individuals with high PUFA intake; however, to our knowledge, there are no prospective studies relating overall PUFA intake or ω-3 PUFA intake to ALS risk. Therefore, we conducted a pooled analysis of nearly 1000 cases of ALS occurring in 5 large prospective cohort studies, including the Health Professionals Follow-up Study (HPFS), the Nurses' Health Study (NHS), the Cancer Prevention Study II Nutrition Cohort (CPS-II Nutrition), the Multiethnic Cohort Study (MEC), and the National Institutes 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 ω-6 and ω-3 PUFA consumption and ALS risk.

Intakes of caffeine, coffee and tea and risk of amyotrophic lateral sclerosis: Results from five cohort studies

“…We evaluated potential confounders correlated with ALS or coffee intake, and adjusted for smoking (never smoked, pack-years: <10, 10-<20, 20-<30, 30-<40, 40+), education level (<high school, high school, >high school), body mass index (<23, 23-<25, 25-<30, ≥30), physical activity level (low, medium, high), total energy intake, vitamin E from food and supplements (in quartiles), and dietary carotenoid intake (in quartiles). The association with ALS and smoking (25), vitamin E (26), omega-3 fatty acids (27), and carotenoids (28) in these cohorts have previously been reported. In the main analyses, baseline caffeine, coffee and tea intakes were used in all cohorts.…”

Environmental Risk Factors and Amyotrophic Lateral Sclerosis: An Umbrella Review and Critical Assessment of Current Evidence from Systematic Reviews and Meta-Analyses of Observational Studies

“…Five were significant at p < 0.001 under the randomeffects model ( table 1 ): farming [32] , lead [33] , n-3 fatty acids [34] , pesticides [32] and serum uric acid [35] . The heterogeneity was large (I 2 ≥ 50 and ≤ 75%) in 5 metaanalyses and very large (I 2 >75%) in 3 meta-analyses.…”

Effect of Presymptomatic Body Mass Index and Consumption of Fat and Alcohol on Amyotrophic Lateral Sclerosis

“…[1][2][3][4][5][6][7] Oxidative stress, mitochondrial dysfunction, excitotoxicity, cortical hyperexcitability, disrupted axonal transport, and inflammation are mechanisms that are potentially involved in ALS pathogenesis. [8][9][10][11] Some of these mechanisms may be influenced by dietary nutrients.…”