***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: High blood pressure increases the risks of stroke , dementia , and neurocognitive dysfunction . Although aerobic exercise and dietary modifications have been shown to reduce blood pressure , no r and omized trials have examined the effects of aerobic exercise combined with dietary modification on neurocognitive functioning in individuals with high blood pressure ( ie , prehypertension and stage 1 hypertension ) . As part of a larger investigation , 124 participants with elevated blood pressure ( systolic blood pressure 130 to 159 mm Hg or diastolic blood pressure 85 to 99 mm Hg ) who were sedentary and overweight or obese ( body mass index : 25 to 40 kg/m2 ) were r and omized to the Dietary Approaches to Stop Hypertension ( DASH ) diet alone , DASH combined with a behavioral weight management program including exercise and caloric restriction , or a usual diet control group . Participants completed a battery of neurocognitive tests of executive function-memory-learning and psychomotor speed at baseline and again after the 4-month intervention . Participants on the DASH diet combined with a behavioral weight management program exhibited greater improvements in executive function-memory-learning ( Cohen 's D=0.562 ; P=0.008 ) and psychomotor speed ( Cohen 's D=0.480 ; P=0.023 ) , and DASH diet alone participants exhibited better psychomotor speed ( Cohen 's D=0.440 ; P=0.036 ) compared with the usual diet control . Neurocognitive improvements appeared to be mediated by increased aerobic fitness and weight loss . Also , participants with greater intima-medial thickness and higher systolic blood pressure showed greater improvements in executive function-memory-learning in the group on the DASH diet combined with a behavioral weight management program . In conclusion , combining aerobic exercise with the DASH diet and caloric restriction improves neurocognitive function among sedentary and overweight/obese individuals with prehypertension and hypertension BACKGROUND While high adiposity in middle age appears to be related to greater dementia risk , studies exploring this association in the elderly are conflicting . OBJECTIVE To evaluate associations between midlife and late-life obesity and risk of dementia . DESIGN Prospect i ve study with mean follow-up of 5.4 years ( 1992 - 1994 through 1999 ) . SETTING Community-dwelling sample in 4 US sites recruited from Medicare eligibility files . PARTICIPANTS A total of 2798 adults without dementia ( mean age , 74.7 years ; 59.1 % women ) participating in the Cardiovascular Health Study who underwent magnetic resonance imaging were measured for height and weight at baseline at age 65 years or older ( late life ) , and self-reported weight at age 50 years ( midlife ) . Body mass index ( BMI ) ( calculated as weight in kilograms divided by height in meters squared ) was calculated at both times . MAIN OUTCOME MEASURES Dementia , Alzheimer disease , and vascular dementia classified by a multidisciplinary committee using st and ardized criteria . RESULTS Classification result ed in 480 persons with incident dementia , 245 with Alzheimer disease ( no vascular dementia ) , and 213 with vascular dementia ( with or without Alzheimer disease ) . In evaluations of midlife obesity , an increased risk of dementia was found for obese ( BMI > 30 ) vs normal-weight ( BMI 20 - 25 ) persons , adjusted for demographics ( hazard ratio [ HR ] , 1.39 ; 95 % confidence interval [ CI ] , 1.03 - 1.87 ) and for cardiovascular risk factors ( 1.36 ; 0.94 - 1.95 ) . The risk estimates were reversed in assessment s of late-life BMI . Underweight persons ( BMI < 20 ) had an increased risk of dementia ( 1.62 ; 1.02 - 2.64 ) , whereas being overweight ( BMI > 25 - 30 ) was not associated ( 0.92 ; 0.72 - 1.18 ) and being obese reduced the risk of dementia ( 0.63 ; 0.44 - 0.91 ) compared with those with normal BMI . CONCLUSION These results help explain the " obesity paradox " as differences in dementia risk across time are consistent with physical changes in the trajectory toward disability The early stages of dieting to lose weight have been associated with neuro-psychological impairments . Previous work has not eluci date d whether these impairments are a function solely of unsupported or supported dieting . Raised cortico-steroid levels have been implicated as a possible causal mechanism . Healthy , overweight , pre-menopausal women were r and omised to one of three conditions in which they dieted either as part of a commercially available weight loss group , dieted without any group support or acted as non-dieting controls for 8 weeks . Testing occurred at baseline and at 1 , 4 and 8 weeks post baseline . During each session , participants completed measures of simple reaction time , motor speed , vigilance , immediate verbal recall , visuo-spatial processing and ( at Week 1 only ) executive function . Cortisol levels were gathered at the beginning and 30 min into each test session , via saliva sample s. Also , food intake was self-recorded prior to each session and fasting body weight and percentage body fat were measured at each session . Participants in the unsupported diet condition displayed poorer vigilance performance ( p = 0.001 ) and impaired executive planning function ( p = 0.013 ) ( along with a marginally significant trend for poorer visual recall ( p = 0.089 ) ) after 1 week of dieting . No such impairments were observed in the other two groups . In addition , the unsupported dieters experienced a significant rise in salivary cortisol levels after 1 week of dieting ( p < 0.001 ) . Both dieting groups lost roughly the same amount of body mass ( p = 0.011 ) over the course of the 8 weeks of dieting , although only the unsupported dieters experienced a significant drop in percentage body fat over the course of dieting ( p = 0.016 ) . The precise causal nature of the relationship between stress , cortisol ,  unsupported dieting  and cognitive function is , however , uncertain and should be the focus of further research BACKGROUND Low-carbohydrate diets are often used to promote weight loss , but their effects on psychological function are largely unknown . OBJECTIVE We compared the effects of a low-carbohydrate , high-fat ( LCHF ) diet with a conventional high-carbohydrate , low-fat ( HCLF ) diet on mood and cognitive function . DESIGN Ninety-three overweight or obese participants [ x + /- SEM age : 50.2 + /- 0.8 y ; body mass index ( in kg/m2 ) : 33.6 + /- 0.4 ] were r and omly assigned to an energy-restricted ( approximately 6 - 7 MJ , 30 % deficit ) , planned isocaloric LCHF diet or an HCLF diet for 8 wk . Body weight and psychological well-being were measured by using the Profile of Mood States , Beck Depression Inventory , and Spielberger State Anxiety Inventory instruments at baseline and fortnightly . Cognitive functioning ( working memory and speed of processing ) was assessed at baseline and week 8 . RESULTS The LCHF diet result ed in significantly greater weight loss than did the HCLF diet ( 7.8 + /- 0.4 and 6.4 + /- 0.4 kg , respectively ; P = 0.04 ) . Both groups showed improvements in psychological well-being ( P < 0.01 for time ) , with the greatest effect occurring during the first 2 wk , but there was no significant difference between groups . There were no significant between-group differences in working memory ( P = 0.68 ) , but there was a significant time x diet interaction for speed of processing ( P = 0.04 ) , so that this measure improved less in the LCHF than in the HCLF diet group . CONCLUSIONS Both dietary patterns significantly reduced body weight and were associated with improvements in mood . There was some evidence for a smaller improvement in cognitive functioning with the LCHF diet with respect to speed of processing , but further studies are required to determine the replicability of this finding Background Caloric restriction without malnutrition extends life span in a range of organisms including insects and mammals and lowers free radical production by the mitochondria . However , the mechanism responsible for this adaptation are poorly understood . Methods and Findings The current study was undertaken to examine muscle mitochondrial bioenergetics in response to caloric restriction alone or in combination with exercise in 36 young ( 36.8 ± 1.0 y ) , overweight ( body mass index , 27.8 ± 0.7 kg/m2 ) individuals r and omized into one of three groups for a 6-mo intervention : Control , 100 % of energy requirements ; CR , 25 % caloric restriction ; and CREX , caloric restriction with exercise ( CREX ) , 12.5 % CR + 12.5 % increased energy expenditure ( EE ) . In the controls , 24-h EE was unchanged , but in CR and CREX it was significantly reduced from baseline even after adjustment for the loss of metabolic mass ( CR , −135 ± 42 kcal/d , p = 0.002 and CREX , −117 ± 52 kcal/d , p = 0.008 ) . Participants in the CR and CREX groups had increased expression of genes encoding proteins involved in mitochondrial function such as PPARGC1A , TFAM , eNOS , SIRT1 , and PARL ( all , p < 0.05 ) . In parallel , mitochondrial DNA content increased by 35 % ± 5 % in the CR group ( p = 0.005 ) and 21 % ± 4 % in the CREX group ( p < 0.004 ) , with no change in the control group ( 2 % ± 2 % ) . However , the activity of key mitochondrial enzymes of the TCA ( tricarboxylic acid ) cycle ( citrate synthase ) , beta-oxidation ( beta-hydroxyacyl-CoA dehydrogenase ) , and electron transport chain ( cytochrome C oxidase II ) was unchanged . DNA damage was reduced from baseline in the CR ( −0.56 ± 0.11 arbitrary units , p = 0.003 ) and CREX ( −0.45 ± 0.12 arbitrary units , p = 0.011 ) , but not in the controls . In primary cultures of human myotubes , a nitric oxide donor ( mimicking eNOS signaling ) induced mitochondrial biogenesis but failed to induce SIRT1 protein expression , suggesting that additional factors may regulate SIRT1 content during CR . Conclusions The observed increase in muscle mitochondrial DNA in association with a decrease in whole body oxygen consumption and DNA damage suggests that caloric restriction improves mitochondrial function in young non-obese adults This study examined the effects of the Dietary Approaches to Stop Hypertension ( DASH ) diet on insulin sensitivity and lipids . In a r and omized control trial , 144 overweight ( body mass index : 25 to 40 ) men ( n=47 ) and women ( n=97 ) with high blood pressure ( 130 to 159/85 to 99 mm Hg ) were r and omly assigned to one of the following groups : ( 1 ) DASH diet alone ; ( 2 ) DASH diet with aerobic exercise and caloric restriction ; or ( 3 ) usual diet controls ( UC )  . Body composition , fitness , insulin sensitivity , and fasting lipids were measured before and after 4 months of treatment . Insulin sensitivity was estimated on the basis of glucose and insulin levels in the fasting state and after an oral glucose load . Participants in the DASH diet with aerobic exercise and caloric restriction condition lost weight ( −8.7 kg [ 95 % CI : −2.0 to −9.7 kg ] ) and exhibited a significant increase in aerobic capacity , whereas the DASH diet alone and UC participants maintained their weight ( −0.3 kg [ 95 % CI : −1.2 to 0.5 kg ] and + 0.9 kg [ 95 % CI : 0.0 to 1.7 kg ] , respectively ) and had no improvement in exercise capacity . DASH diet with aerobic exercise and caloric restriction demonstrated lower glucose levels after the oral glucose load , improved insulin sensitivity , and lower total cholesterol and triglycerides compared with both DASH diet alone and UC , as well as lower fasting glucose and low-density lipoprotein cholesterol compared with UC . DASH diet alone participants generally did not differ from UC in these measures . Combining the DASH diet with exercise and weight loss result ed in significant improvements in insulin sensitivity and lipids . Despite clinical ly significant reductions in blood pressure , the DASH diet alone , without caloric restriction or exercise , result ed in minimal improvements in insulin sensitivity or lipids Abstract Objective To evaluate any association between obesity in middle age , measured by body mass index and skinfold thickness , and risk of dementia later in life . Design Analysis of prospect i ve data from a multiethnic population based cohort . Setting Kaiser Permanente Northern California Medical Group , a healthcare delivery organisation . Participants 10 276 men and women who underwent detailed health evaluations from 1964 to 1973 when they were aged 40 - 45 and who were still members of the health plan 
    Output:
    
Weight loss appears to be associated with low-order improvements in executive/attention functioning and memory in obese but not in overweight individuals