Each year in the United States, ~800,000 people experience a stroke [1
]. Poststroke declines in metabolic control (i.e., development of proinflammatory conditions, including hyperlipidemia, obesity, and insulin resistance) are common and contribute to strokes being a leading cause of long-term disability. Although sedentary activity is often implicated in these declines, less attention has been given to the role of dietary factors.
Current guidelines suggest that the dietary intakes of omega-3 and omega-6 long-chain polyunsaturated fatty acids (LC-PUFA) are important substitutes for saturated fatty acids, since their intake is associated with beneficial effects on cardiovascular risk [2
]. Studies to date implicate higher dietary and systemic omega-6/omega-3 ratios in association with reduced physical functioning and elevated proinflammatory states in older adults [3
] and neurological deterioration following acute stroke [4
]. Despite being at elevated risk, the consumption and metabolic status of omega-6 and omega-3 fatty acids by chronic stroke survivors is not well documented. Though an optimal ratio has yet to be defined, the identification of omega-6/omega-3 as a clinical biomarker may have important implications for stroke recovery. Therefore, the purpose of this study was to examine the relationship between dietary and systemic omega-6/omega-3 and physical function and cardiovascular and diabetes risk in a cohort of chronic adult stroke survivors.
Though an optional serum omega-6/omega-3 has yet to be defined, a dietary intake ratio of (4–5)/1 is associated with a 70% decrease in total mortality and lower inflammation [10
]. We find that, on average, this ratio is approximately three times higher in our sample of stroke survivors, which is twice as high as that observed in other older, but generally healthy, adult populations [11
]. Further, this study provides novel preliminary evidence that greater dietary and serum omega-6/omega-3, signifying excess omega-6 LC-PUFAs intake and blood values relative to omega-3s, may adversely influence physical and metabolic health in chronic stroke survivors. While we are the first to examine these relationships in a cohort of chronic stroke survivors, this study supports data from non-stroke populations suggesting that higher dietary and systemic concentrations of omega-3 LC-PUFAs, compared to omega-6s, protect against accelerated age- and disease-associated decline of physical and psychosocial functioning and development of insulin resistance and chronic inflammation [12
Despite studies identifying an association between acute poststroke plasma fatty acid profiles and stroke recurrence, dietary omega-3 supplementation trials in stroke survivors have been unsuccessful at reducing cardiovascular risk [15
]. However, in stroke survivors receiving 250 mg/d of DHA and 250 mg/d of EPA orally for one year, a trend in greater improvements in functional status (i.e., activities of daily living and mobility disability) was observed [16
]. Further, associations between reduction in serum omega-6/omega-3 and cholesterol-lowering and improvements in insulin sensitivity are observed in patients with cardiovascular disease following statin treatment [17
]. These data suggest the need for further evaluation of dietary and systemic LC-PUFA modification on clinical outcomes beyond secondary prevention.
Consumption of omega-3 LC-PUFAs in the diet partially replaces the omega-6s in the membranes of most cells, including platelets, erythrocytes, neutrophils, monocytes, and hepatic cells [18
]. Although our data are limited in this regard, a higher omega-3 membrane concentration may explain the associations between higher omega-6/omega-3 LC-PUFA profiles and physical and metabolic dysfunction in stroke survivors by altering cell membrane fluidity, enhancing nitric-oxide-mediated vasodilation, and attenuating platelet aggregation [19
]. Further, there is some suggestion that the neuroprotective mechanism of action of omega-3s may occur through their effects on inflammation and oxidative stress; omega-6s produce eicosanoid products, which are more potent mediators of thrombosis and inflammation than similar products derived from omega-3s [20
]. Although the exact mechanisms are unclear, these findings suggest that dietary and serum omega-3s might be important indicators to help attenuate and monitor the progression of stroke disability.
Although a larger study is needed to confirm our results, the use of both dietary and systemic LC-PUFA assessments in this pilot study strengthens the comprehensive evaluation of the relationships between habitual dietary omega-6 and omega-3 intake and their serum concentrations. Further, recent studies in stroke survivors identified systemic EPA and DHA concentrations similar to the current assessment, which were lower than in non-stroke controls [21
], suggesting that these data may be generalizable to the larger U.S. stroke survivor population. However, the cross-sectional nature of the current study, with small sample size, limits the interpretation of the potential importance of covariates, including the latency of stroke and other comorbidities.