RESUMEN
â¢Is the Index of Nutritional Quality (INQ) associated with colon cancer? â¢This study compared the INQ of various dietary components between colorectal cancer patients and healthy controls. A total of 480 participants were enrolled in the study (160 patients with colorectal cancer as a case group and 320 healthy control). The results showed that CRC is significantly associated with INQ for some micronutrients. INQ can be considered as an indicator to assess clinical nutritional problems. Background - The nutritional quality of diet may influence the risk of colorectal cancer (CRC). This study compared the Index of Nutritional Quality (INQ) of various dietary components between colorectal cancer patients and healthy controls. Methods - A total of 480 participants were enrolled in the study (160 patients with colorectal cancer as a case group and 320 healthy control). An analysis was conducted on the general characteristics of the participants, their medical histories, anthropometric indicators, physical activity, alcohol consumption, reproductive history, smoking and food intake. A valid food frequency questionnaire was used to assess nutrient intake and INQ was calculated from daily nutrient intake. Results - A Significant inverse association was found between CRC and INQ for vitamins A (OR=0.01, CI: 0.01-0.01), K (OR=0.04, CI: 0.01-0.15), and B12 (OR=0.71, CI: 0.51-0.98), B5 (OR=0.43, CI: 0.00-0.01), zinc (OR=0.35, CI: 0.13-0.95), and phosphorus (OR=0.17, 0.19-0.94). The association between the INQ of vitamin B12 and zinc with colorectal cancer was disappeared after age adjustment. There was a significant negative association between CRC with the INQ of vitamins A, K, B5, phosphorus, and calcium after further adjustments for gender, BMI, menopausal status, and total energy intake. Conclusion -CRC is significantly associated with INQ for some micronutrients. INQ can be considered as an indicator to assess clinical nutritional problems.
Asunto(s)
Neoplasias Colorrectales , Dieta , Femenino , Humanos , Estudios de Casos y Controles , Vitaminas , Micronutrientes , Valor Nutritivo , Neoplasias Colorrectales/etiología , Zinc , FósforoRESUMEN
Background & objectives: Fatty acids may affect the expression of genes, and this process is influenced by sex hormones. Cytokines are involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), so this study was aimed to assess the association of erythrocyte membrane fatty acids with three cytokines and markers of hepatic injury in NAFLD patients and to explore whether these associations were the same in both sexes. Methods: In this cross-sectional study, 62 consecutive patients (32 men and 30 women) with NAFLD during the study period. Tumour necrosis factor-α (TNF-α), interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), aspartate aminotransferase and alanine aminotransferase were measured in a fasting serum sample, and Fibroscan was conducted for each individual. Gas chromatography was used to measure erythrocyte membrane fatty acids. Univariate and multiple linear regressions were used to analyze data. Results: In men, IL-6 had a significant (P <0.05) positive association with total ω-3 polyunsaturated fatty acids (PUFAs). In women, TNF-α had a significant positive association with total ω-3 (P <0.05) and ω-6 (P <0.01) PUFAs, IL-6 had a significant (P <0.05) positive association with total monounsaturated fatty acids and MCP-1 had a significant positive association with total trans-fatty acids (P <0.05). No significant associations were observed between erythrocyte membrane fatty acids and liver enzymes or Fibroscan report in both sexes. In this study, women were significantly older than men [51 (42.75-55) vs 35.5 (29-52), P <0.01], so the associations were adjusted for age and other confounders. Interpretation & conclusions: Erythrocyte membrane fatty acid profile was not associated with serum liver enzymes or Fibroscan reports in NAFLD patients, but it had significant associations with serum TNF-α, IL-6 and MCP-1 and these associations were probably sex dependent.
Asunto(s)
Membrana Eritrocítica/química , Ácidos Grasos/metabolismo , Enfermedad del Hígado Graso no Alcohólico , Estudios Transversales , Citocinas , Ácidos Grasos Omega-3 , Femenino , Humanos , Irán , Hígado , MasculinoRESUMEN
BACKGROUND AND OBJECTIVES: Nephrotic syndrome is a chronic disease especially common in the childhood and adolescence. Reactive oxygen species (ROS) and free radicals have significant role in the pathogenesis of nephrotic syndrome. The aim of this study was to evaluate the effect of soy protein and genistein (main isoflavone of soybean) on renal antioxidant status of nephrotic rats. METHODS: This study was done for 8 weeks on 40 adult male Sprague-Dawley rats divided into four groups of 10 rats each. Study groups included: 1-Control, 2-Nephrotic syndrome, 3-Nephrotic syndrome+soy protein diet and 4-Nephrotic syndrome+soy protein diet+genistein. Urine protein and urine creatinine were measured. After homogenization of kidney, total antioxidant capacities (TAC), activities of catalase enzyme, the concentration of malondialdehydes (MDA) and carbolynated proteins were determined spectrophotometrically. Pathological examination was done on kidneys with light microscope. Cell viability was evaluated with MTT assay on WEHI-164 fibro sarcoma cell line. The MMP2 enzyme activity was evaluated in different concentrations of genistein. RESULTS: Total antioxidant capacity was significantly increased in soy genistein. Catalase activity was significantly increased in soy and soy genistein groups. Protein carbonyl and MDA were significantly lower in soy and soy genistein groups. The scores of pathological examination showed significant improvement in soy and soy genistein groups. Genistein decreased the proliferation of the WEHI-164 fibrosarcoma cell line. CONCLUSION: It seems that soy protein decreases kidney damages in nephrotic syndrome. Adding genistein to soy protein causes improvements in antioxidant status of kidney tissue. Genistein decreases proliferation of cell.
Asunto(s)
Antioxidantes/metabolismo , Genisteína/farmacología , Genisteína/uso terapéutico , Riñón/metabolismo , Síndrome Nefrótico/tratamiento farmacológico , Síndrome Nefrótico/metabolismo , Proteínas de Soja/farmacología , Proteínas de Soja/uso terapéutico , Animales , Línea Celular Tumoral , Masculino , Síndrome Nefrótico/patología , Ratas , Ratas Sprague-DawleyRESUMEN
OBJECTIVE: It is postulated that ritalin may adversely affect sleep, appetite, weight and growth of some children with ADHD. Therefore, we aimed to evaluate melatonin supplementation effects on dietary intake, growth and development of children with ADHD treated with ritalin through circadian cycle modification and appetite mechanisms. METHOD: After obtaining consent from parents, 50 children aged 7-12 with combined form of AD/HD were randomly divided into two groups based on gender blocks: one received melatonin (3 or 6 mg based on weight) combined with ritalin (1mg/kg) and the other took placebo combined with ritalin (1mg/kg) in a double blind randomized clinical trial. Three-day food record, and standard weight and height of children were evaluated prior to the treatment and 8 weeks after the treatment. Children's appetite and sleep were evaluated in weeks 0, 2, 4 and 8. Hypotheses were then analyzed using SPSS17. RESULTS: Paired sample t-test showed significant changes in sleep latency (23.15±15.25 vs. 17.96±11.66; p=0.047) and total sleep disturbance score (48.84±13.42 vs. 41.30±9.67; p=0.000) before and after melatonin administration, respectively. However, appetite and food intake did not change significantly during the study. Sleep duration and appetite were significantly correlated in melatonin group (Pearson r=0.971, p=0.029). Mean height (138.28±16.24 vs. 141.35±16.78; P=0.000) and weight (36.73±17.82 vs. 38.97±17.93; P=0.005) were significantly increased in melatonin treated children before and after the trial. CONCLUSION: Administration of melatonin along with ritalin improves height and weight growth of children. These effects may be attributed to circadian cycle modification, increasing sleep duration and the consequent more growth hormone release during sleep.