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Background: Cognitive impairment is projected to affect a preponderant proportion of the aging population. Lifelong dietary habits have been hypothesized to play a role in preventing cognitive decline. Among the most studied dietary components, fish consumptionhas been extensively studied for its potential effects on the human brain. Aims: To perform a meta-analysis of observational studies exploring the association between fish intake and cognitive impairment/decline and all types of dementia. Methods: A systematic search of electronic databases was performed to identify observational studies providing quantitative data on fish consumption and outcomes of interest. Random effects models for meta-analyses using only extreme exposure categories, subgroup analyses, and dose-response analyses were performed to estimate cumulative risk ratios (RRs) and 95% confidence intervals (CIs). Results: The meta-analysis comprised 35 studies. Individuals reporting the highest vs. the lowest fish consumption were associated with a lower likelihood of cognitive impairment/decline (RR = 0.82, 95% CI: 0.75, 0.90, I2= 61.1%), dementia (RR = 0.82, 95% CI: 0.73, 0.93, I2= 38.7%), and Alzheimer’s disease (RR = 0.80, 95% CI: 0.67, 0.96, I2= 20.3%). The dose-response relation revealed a significantly decreased risk of cognitive impairment/decline and all cognitive outcomes across higher levels of fish intake up to 30% for 150 g/d (RR = 0.70, 95% CI: 0.52, 0.95). The results of this relation based on APOE ε4 allele status was mixed based on the outcome investigated. Conclusions: Current findings suggest fish consumption is associated with a lower risk of cognitive impairment/decline in a dose-response manner, while for dementia and Alzheimer’s disease there is a need for further studies to improve the strength of evidence.

Because elevated copeptin, a marker of vasopressin, is linked to low water intake and high diabetes risk, we tested the effect of water supplementation on copeptin and fasting glucose.

Unaccustomed strenuous physical exertion in hot environments can result in heat stroke and acute kidney injury (AKI). Both exercise-induced muscle damage and AKI are associated with the release of interleukin-6, but whether muscle damage causes AKI in the heat is unknown. We hypothesized that muscle-damaging exercise, before exercise in the heat, would increase kidney stress. Ten healthy euhydrated men underwent a randomized, crossover trial involving both a 60-min downhill muscle-damaging run (exercise-induced muscle damage; EIMD), and an exercise intensity-matched non-muscle-damaging flat run (CON), in random order separated by 2 wk. Both treatments were followed by heat stress elicited by a 40-min run at 33°C. Urine and blood were sampled at baseline, after treatment, and after subjects ran in the heat. By design, EIMD induced higher plasma creatine kinase and interleukin-6 than CON. EIMD elevated kidney injury biomarkers (e.g., urinary neutrophil gelatinase-associated lipocalin (NGAL) after a run in the heat: EIMD-CON, mean difference [95% CI]: 12 [5, 19] ng/ml) and reduced kidney function (e.g., plasma creatinine after a run in the heat: EIMD-CON, mean difference [95% CI]: 0.2 [0.1, 0.3] mg/dl), where CI is the confidence interval. Plasma interleukin-6 was positively correlated with plasma NGAL (r= 0.9, P= 0.001). Moreover, following EIMD, 5 of 10 participants met AKIN criteria for AKI. Thus for the first time we demonstrate that muscle-damaging exercise before running in the heat results in a greater inflammatory state and kidney stress compared with non-muscle-damaging exercise. Muscle damage should therefore be considered a risk factor for AKI when performing exercise in hot environments.

OBJECTIVE: To evaluate if the perioperative administration of a supplemented enteral formula modulates selective inflammatory and immune variables and gut function after surgery. DESIGN: Prospective, randomized, double-blind, clinical trial. SETTING: Department of surgery, university hospital. PATIENTS: Forty patients with neoplasm of the colorectum or stomach. INTERVENTION: Seven days before surgery, the patients drank I L/d of a control enteral formula (n=20) or the same formula enriched with arginine, RNA, and ω-3 fatty acids (n=20). Jejunal infusion with the same formulas was started 6 hours after operation and continued until day 7. MAIN OUTCOME MEASURES: Immune response was determined by phagocytosis ability and respiratory burst of polymorphonuclear cells, and inflammatory response by plasma levels of C-reactive protein. Operative intestinal microperfusion, postoperative intestinal mucosa oxygen metabolism, and plasma intestinal isoenzyme of alkaline phosphatase were used as indicators of gut function. Plasma nitric oxide also was determined. RESULTS: In the enriched group, phagocytosis ability and respiratory burst after surgery was higher (P<.01) and C-reactive protein level was lower (P<.05) than in the control group. The enriched group had higher mean (±SD) intestinal microperfusion (180±46 vs 146 ± 59 perfusion units, P<.05), intestinal mucosa oxygen metabolism (pHi 7.39±0.2 vs pHi 7.33±0.1, P<.05), and 5-fold lower levels of intestinal isoenzyme of alkaline phosphatase (P<.05). Postoperative levels of nitric oxide were higher in the enriched group (P<.05, analysis of variance). CONCLUSION: The perioperative administration of an enriched enteral formula significantly improved gut function and positively modulated postsurgical immunosuppressive and inflammatory responses.Arch Surg. 1996;131:1257-1265