ABSTRACT
AIM: Highlighting the impact of obesity on mental and cognitive functions using serum ceramide kinase enzyme concentration as a biomarker for cognitive evaluation in the middle aged females, and also targeting to control the obesity and simultaneously postponing the deterioration of the cognitive functions, by implementing two slimming dietary therapies each incorporating different functional ingredients known to boost cognition. SUBJECTS AND METHODS: Ninety six obese middle aged females, divided into two groups volunteered to follow a low caloric balanced diet combined with two bread supplements composed essentially of barley flour and wheat germ mixed with either 5% turmeric, group (A); or with 5% ginger, group (B) for 4 weeks, phase (1); to be followed by the hypocaloric diet alone for another 4 weeks, phase (2). RESULTS: By the end of phase (1), the biochemical analysis showed a positive response of the levels of C-peptide and modified homeostatic model assessment of insulin resistance; also increased levels of the serum ceramide kinase enzyme, coupled with improved cognitive functions tests. Improvement of the relevant metabolic profile, fasting blood glucose, blood pressure and the anthropometric measurements was detected. CONCLUSION: Using dietary therapy supported by special formulas which contain active ingredients succeeded in reducing weight and improving both the metabolic profile and the cognitive functions.
ABSTRACT
AIM: To study the interaction between sleep deprivation, obesity and cognitive functions, and the effect of following a balanced low caloric diet and increasing sleep duration on those variables. SUBJECTS AND METHODS: Ninety two obese females with mean age 47.00 ± 2.00 years and body mass index (BMI) 36.14 ± 3.00 kg/m² were divided into 3 groups according to their sleeping hours. They followed balanced low-caloric diet and were instructed to increase sleeping hours. Full clinical examination, 24 hours dietary intake recall, anthropometric measurements, mini mental state test, questionnaire for subjective sleep and life style evaluation were performed at baseline and after 2 months. Serum visfatin, fasting blood glucose and C-peptide were assessed; Modified homeostatic model assessment of insulin resistance was calculated. RESULTS: About one third of our sample slept less than 6 hours daily, group (1), all patients had elevated visfatin serum level (33.87 ± 2.8 ng/ml) with the highest level in group (1). At base line, group (1) showed the highest BMI, lowest cognitive functions, highest visfatin level and highest insulin resistance (P < 0.05). After 2 months of intervention, improvement was recorded in all variables, with the best improvement in group (1) after extending sleep duration (P < 0.05). CONCLUSION: Sleep deprivation may be a modifiable risk factor for obesity, cognitive impairment and visfatin elevation.
