Depression after minor stroke: prevalence and predictors.

BACKGROUND AND PURPOSE: Post-stroke depression (PSD) is one of the most frequent complications of stroke, with a prevalence ranging 20-60%. As PSD seems to be related to stroke severity, we hypothesized that the prevalence of PSD would be lower in patients with minor stroke. METHODS: We investigated the prevalence and predictors of PSD over a 30-month follow-up period in a cohort of patients with minor ischaemic stroke (NIHSS≤5). RESULTS: We enrolled 105 patients (mean age 64.38±11.2years, M/F 69/36). PSD was diagnosed in 43 (41%) patients, 40 (93%) of whom had dysthymia; 22% of patients were already depressed at 1month. The most frequent depressive symptoms (DSs) were working inhibition, indecisiveness, and fatigability. Patients who developed PSD were less educated (P=0.044) and diabetic (P=0.006). After excluding patients that were already depressed at 1month, we performed a logistic regression model to detect predictors of PSD. Crying (P=0.012, OR 1.067, CI 0.269-4.553) and guilt (P=0.007, OR 0.037, CI 0.02ì03-0.401) at baseline were two DSs found to be significantly correlated with PSD. Higher educational level (P=0.022, OR 0.084, CI 0.010-0.698) and diabetes (P=0.007, OR 14.361, CI 2.040-101.108) were the risk factors significantly correlated with PSD. CONCLUSION: Post-stroke depression is frequent even in patients with minor stroke. Early detection of DSs might help to predict long-term development of PSD. No correlation was observed between lesion site or side and the development of PSD.

n-3 fatty acids induce oxidative modifications in human erythrocytes depending on dose and duration of dietary supplementation.

The present work was performed to study an optimal dose and duration of dietary n-3 polyunsaturated fatty acid (PUFA) supplementation that would not result in harmful modifications of oxidative cell metabolism. Forty healthy subjects were divided into four groups that received 2.5 g/d eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), 5.1 g EPA + DHA/d, 7.7 g EPA + DHA/d, or placebo. Fatty acid composition, tocopherol status, and susceptibility to lipid peroxidation induced in vitro by 2,2'-azobis-(2-amidinopropane) (AAPH) were evaluated in human red blood cell (RBC) membranes on days 30 and 180. n-3 PUFA treatment increased EPA and DHA concentrations in RBC membranes in a time-dependent manner in all of the n-3 PUFA groups. These modifications occurred with concomitant dose- and time-dependent increases in the membrane unsaturation index. After 30 d of treatment with n-3 PUFAs, alpha-to-copherol significantly increased in RBC membranes of the intermediate- and high-dose groups. Because of the higher concentration of this antioxidant in these groups, the susceptibility of RBC membranes to peroxidation was decreased. However, after 180 d of treatment, alpha-tocopherol decreased to baseline values and AAPH-induced lipid peroxidation increased in a dose-dependent manner. These results show that high doses of dietary n-3 PUFAs, as well as long-time treatments, affect human RBC susceptibility to lipid peroxidation by changes in fatty acid composition and tocopherol content.

Effect of beta-carotene and canthaxanthin on tert-butyl hydroperoxide-induced lipid peroxidation in murine normal and tumor thymocytes.

It has been reported that the anticarcinogenic effect of carotenoids could be related to an antioxidant mechanism. The antioxidant efficiency of beta-carotene and canthaxanthin was evaluated in murine normal and tumor thymocytes. Normal and tumor cells were exposed under air to tert-butyl hydroperoxide (t-BOOH) and lipid peroxidation was measured in the absence or in the presence of the two carotenoids. Our results show that: (a) Both carotenoids, added at effective and comparable concentrations (from 1 to 50 microM), were able to inhibit t-BOOH-induced malondialdehyde formation in a dose-dependent manner. (b) Canthaxanthin was a more potent antioxidant that beta-carotene. (c) The inhibition of lipid peroxidation was greater in tumor thymocytes. (d) Carotenoids were consumed differentially during the incubation with the prooxidant. beta-Carotene was consumed faster than canthaxanthin and in a larger amount in tumor than in normal thymocytes. The addition of the iron chelator deferoxamine or the SH group reducing agent dithiothreitol reduced t-BOOH-induced beta-carotene consumption in tumor cells but not in normal ones. (e) The loss of endogeneous alpha-tocopherol induced by t-BOOH was enhanced by the addition of beta-carotene, suggesting the possibility of oxidative interactions between the two antioxidants. These results confirmed the antioxidant effectiveness of carotenoids in normal and tumor cells, although differences depending on the kind of cells and carotenoids used were found.

n-3 PUFA and alpha-tocopherol control of tumor cell proliferation.

Subjects at high risk for colon cancer received different doses of fish oil on a 30-day randomized double-blind trial to evaluate the chemopreventive effect of n-3 fatty acids against colorectal cancer. Using rectal mucosal proliferation, assessed with 3H-thymidine autoradiography, fish oil induced in the treated groups but not in the placebo group a change in the proliferative pattern, which resulted similar to that observed in low risk population; in the same groups rectal mucosal n-3 fatty acid content increased, where arachidonic acid level decreased. Moreover, n-3 PUFA treatment induced modifications of Vitamin E status. The results suggest that n-3 PUFA could protect high-risk subjects from colon cancer by a mechanism involving a modulation of Vitamin E.