To determine the impact of ω3 fatty acids on post-ischemic expression of pro- and anti-apoptotic proteins in hippocampus, male rats were received 10 or 100 mg/kg [Docosahexaenoic acid (DHA) + Ecosapentaenoic acid (EPA); gavage; 21 days before ischemia to 2-10 days after ischemia]. Global cerebral ischemia reperfusion (IR) was performed using the four-vessel occlusion model; ischemia 8 min and reperfusion 6, 48 h and 10 days. IR increased Bcl-2 and Bax expression after 48 h (p < 0.05 and p < 0.01 vs. sham) and 10 days (only Bax; p < 0.05), without significant difference with DHA + EPA groups after 6 h. But after 48 h expression of Bcl-2 increased (p < 0.05 vs. IR) and Bax decreased (p < 0.05). At day 10 after ischemia expression of Bax in DHA + EPA acid groups was less than IR (p < 0.05) and in 100 mg/kg DHA + EPA group Bcl-2 expression was more than IR (p < 0.05). These data suggested that long-term gavage with DHA + EPA increase hippocampal neurons survival for days after ischemia, revealed by increased Bcl-2 and decreased Bax expressions.

Background: Given the impact of high intake sugar sweetened beverages on type2 diabetes, intervention to reduce their consumption can be a top priority for any health system. Thus, the purpose of the present study is to simulate the impact of policy options related to reduce consumption of sugar-sweetened beverages on the prevalence and mortality of type 2 diabetes in Iranian men and women.Methods: A Markov micro-simulation (MM) model was used to predict the effect of several policy options on the incidence and death from type 2 diabetes in Azar Cohort Databases. Population age-and sex-specific prevalence and incidence rate of diagnosed diabetes were derived from the national health data. The PRIME model was used for coding the input parameters of simulation using R and Python software.Results: The prevalence and mortality rate of type 2 diabetes under the scenario of reduced consumption of sugar sweetened beverages indicated that the highest and lowest prevalence and mortality rates of type 2 diabetes for men and women were related to no policy condition and replacing sugar-sweetened beverages with healthy drinks such as water, respectively. Also, the maximum number of death postponed/prevented from type 2 diabetes was related to replacing sugar-sweetened beverages with water and levying 10% tax on sugar sweetened beverages, respectively. Conclusion: Regarding the effect of simulating different policy options on reducing the consumption of sugar sweetened beverages, the most effective policy options were replacing sugar-sweetened beverages with water.

Background: Deficiencies or imbalances in dietary fat intake may influence on mental and neurological functions of children with Autism Spectrum Disorders (ASD). This study aimed to compare the amount of fatty acids intake in the autistic cases with the healthy controls.Methods: This case-control was carried out on 200 randomly selected children (100 autistic cases and 100 healthy controls) in Tehran, Iran. The food frequency questionnaire (FFQ) was used to assess the intake of calorie, macronutrients, and dietary fatty acids including saturated fatty acids (SFA), monounsaturated fatty acids (MUFAs), poly unsaturated fatty acids (PUFAs), linoleic acid (LA), α-Linolenic acid (ALA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and trans fatty acids.Results: No significant difference was found in the amount of dietary calorie, protein, carbohydrate, and total fat intake between two groups. In terms of the type of dietary fatty acids, the amount of MUFAs (OR: 3.18(1.13-4.56); p=0.04), PUFAs (OR: 4.12(2.01-6.25); p=0.01), and LA (4.76(1.34-14.32); p=0.01) were significantly higher in ASD children compared to the control group. The amounts of ALA, EPA, DHA, SFA, and trans fatty acid were not significantly different between two groups. Conclusions: The autistic children had higher unsaturated fatty acids intake except for omega-3 fatty acids. Future longitudinal studies are needed to confirm these findings and to determine the underlying mechanisms of possible associations between unsaturated fatty acids intake and ASD.

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