Background and Purpose-The role of serum fatty acids as a risk factor for stroke and stroke subtypes is largely unknown. Methods-A prospective nested case-control study of Japanese 40 to 85 years of age was conducted through the use of frozen serum samples from 7450 participants in cardiovascular risk surveys collected from 1984 to 1989 for 1 community and 1989 to 1992 for the other 2 communities. By the end of 1998, we identified 197 incident strokes whose subtypes were confirmed by imaging studies. Three controls per case were selected by matching for sex, age, community, year of serum storage, and fasting status. Results-Compared with controls, total (nϭ197), hemorrhagic (nϭ75), and ischemic (nϭ122) strokes had similar proportions of n3 polyunsaturated fatty acids, lower proportions of linoleic and arachidonic acids, and higher proportions of saturated and monosaturated acids, determined by gas chromatography. The multivariate odds ratios associated with a 1-SD increase in linoleic acid (5%) after adjustment for hypertension, diabetes, serum total cholesterol, and other cardiovascular risk factors were 0.72 [95% confidence interval (CI), 0.59 to 0.89] for total stroke, 0.66 (95% CI, 0.49 to 0.88) for ischemic stroke, 0.63 (95% CI, 0.46 to 0.88) for lacunar infarction, and 0.81 (95% CI, 0.59 to 1.12) for hemorrhagic stroke. The respective odds ratios for saturated fatty acids (4%) were 1.13 (95% CI, 1.05 to 1.65), 1.35 (95% CI, 1.01 to 1.79), 1.44 (95% CI, 1.03 to 2.01), and 1.21 (95% CI, 0.82 to 1.80). Further adjustment for other fatty acids attenuated these relations, but the relation between linoleic acid and risk of ischemic stroke remained statistically significant. Conclusions-A higher intake of linoleic acid may protect against ischemic stroke, possibly through potential mechanisms of decreased blood pressure, reduced platelet aggregation, and enhanced deformability of erythrocyte cells. (Stroke.

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Oxidative stress is a strong contributor to the progression from simple fatty liver to nonalcoholic steatohepatitis (NASH). Molecular hydrogen is an effective antioxidant that reduces cytotoxic reactive oxygen species. In this study, we investigated the effects of hydrogen-rich water and the drug pioglitazone on the progression of NASH in mouse models. A methionine-choline-deficient (MCD) diet mouse model was prepared. Mice were divided into three experimental groups and fed for 8 weeks as follows: (1) MCD diet 1 control water (CW group); (2) MCD diet 1 hydrogen-rich water (HW group); and (3) MCD diet mixed with pioglitazone (PGZ group). Plasma alanine aminotransferase levels, hepatic expression of tumor necrosis factor-a, interleukin-6, fatty acid synthesis-related genes, oxidative stress biomarker 8-hydroxydeoxyguanosine (8-OHdG), and apoptosis marker terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nickend labeling (TUNEL)-positive cells in the liver were decreased in the HW and PGZ groups. The HW group showed a smaller decrease in hepatic cholesterol; however, stronger antioxidative effects in serum and lower peroxisome proliferator-activated receptor-a expression in the liver were seen in comparison with the PGZ group. We then investigated the effects of hydrogen in the prevention of hepatocarcinogenesis in STAM mice, known as the NASH-related hepatocarcinogenesis model. Eight-week-old male STAM mice were divided into three experimental groups as follows: (1) control water (CW-STAM); (2) hydrogen-rich water (HW-STAM); and (3) pioglitazone (PGZ-STAM). After 8 weeks, hepatic tumors were evaluated. The number of tumors was significantly lower in the HW-STAM and PGZ-STAM groups than in the CW-STAM group. The maximum tumor size was smaller in the HW-STAM group than in the other groups. Conclusion: Consumption of hydrogen-rich water may be an effective treatment for NASH by reducing hepatic oxidative stress, apoptosis, inflammation, and hepatocarcinogenesis. (HEPATOLOGY 2012;56:912-921)

Abstract-We sought to examine effects of habitual alcohol intake on ambulatory blood pressure (BP), heart rate (HR), and HR variability among Japanese men. Subjects were 539 men aged 35 to 65 years from rural and urban communities. Ambulatory BP and HR were monitored with an automated, portable, noninvasive multibiomedical recorder. Power spectral analysis of the RR intervals on the ECG was performed every 5 minutes. Compared with nondrinkers, moderate drinkers (alcohol intake 23 to 45 g/d) and heavy drinkers (alcohol intake Ն46 g/d) showed higher age-and field-adjusted mean values of systolic and diastolic BPs during the morning and while awake, but there were no differences in BPs over 24-hour periods and while asleep among the alcohol intake categories. Alcohol intake was positively associated with mean values of sleep-morning differences and daytime variability in BPs, HRs while awake and asleep, and low frequency:high frequency ratio while asleep. The results were virtually unchanged after adjustment for body mass index, smoking, and diabetes mellitus. Compared with the nondrinkers, age-and field-adjusted odds ratios of the morning BP surge (excess elevation of BP in the morning: morning systolic BP minus sleep systolic BP Ն37 mm Hg) for light (alcohol intake 0 to 22 g/d), moderate, and heavy drinkers were 0.96 (95% CI: 0.34 to 2.78), 1.68 (95% CI: 0.64 to 4.38), and 2.73 (95% CI: 1.12 to 6.67), respectively. Habitual alcohol intake was associated with increased BP in the morning, HR while awake and asleep, and sympathetic activity while asleep, which may explain some of the mechanisms of the relationship between heavy alcohol intake and risk of cardiovascular diseases. Key Words: alcohol intake Ⅲ ambulatory blood pressure monitoring Ⅲ autonomic nerve function Ⅲ heart rate variability Ⅲ population-based .S everal prospective studies have reported that heavy alcohol intake increases the risk of stroke, 1-5 especially hemorrhagic stroke. 1-3 Because daily alcohol intake is positively associated with blood pressure (BP) levels, high BP is thought to be an important mediator between alcohol intake and the risk of stroke. However, although the associations of daily alcohol intake with casual BP are well documented, 6,7 the associations with 24-hour ambulatory BP are not, 7 because the effect of daily alcohol intake on BP depends on the time elapsed after alcohol intake. 8,9 Recent studies have indicated that morning BP surge, the excessive elevation of BP in the morning, could be associated with risk of stroke. 10,11 Kario et al showed that, in 519 Japanese older hypertensives, a higher morning BP surge was associated with a higher incidence of stroke independent of mean values of 24-hour systolic BP. 10 Another prospective study of 1430 Japanese men and women aged Ն40 years also found a positive association of morning BP surge with the incidence of hemorrhagic stroke after adjustment for 24-hour systolic BP and antihypertensive medication use but no association between morning BP surge and risk of ischemic stro...