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Nutrition et maladie d’Alzheimer

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Abstract

Deterioration of memory function and ultimately establishment of Alzheimer's disease (AD) severely debilitates the affected individual, uncompromisingly decreasing the quality of life of both patients and their caregivers. The global prevalence of cognitive impairment and dementia including Alzheimer's disease is expected to rise significantly in proportion to increased life expectancy. Weight loss is a common problem among patients with AD and is associated with mortality, morbidity, disease progression, and poor quality of life. The aim of this article is: (1) to emphasize the importance of malnutrition in Alzheimer's disease and (2) to review published evidences for the role of nutrition as a risk factor of the disease.

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... Les personnes en EHPAD sont particulièrement exposées à ce risque d'insuffisance alimentaire compte tenu de leur âge avancé et/ou de leur pathologie [12,13]. C'est notamment le cas des personnes ayant une maladie d'Alzheimer [14]. Les conséquences de cette sous-nutrition sont sévères puisqu'elle contribue au syndrome de fragilité [15], conduisant à un risque accru de chutes, d'infections et de co-morbidité [16]. ...
Article
La sous-nutrition est la cause principale de la dénutrition chez les personnes âgées. Une solution culinaire, délices du soir (DDS®), appétente et nourrissante sous forme d’un velouté de 330 mL élaboré à partir d’une recette cuisinée traditionnellement a été proposée en EHPAD le soir en remplacement du repas classique. Le but de cette étude était d’en étudier l’impact sur la prise alimentaire et sur la consommation de compléments nutritionnels oraux (CNO).
... In the context of Alzheimer's disease, primary dementia, research has identified protective dietary factors (fruits, polyunsaturated fatty acids and flavonoids) and factors that increase risk (alcohol consumption, saturated fatty acids) (4)(5)(6)(7)(8)(9). Furthermore, weight loss must be prevented in patients with dementia because it is responsible for a decrease in quality of life and a worsening of cognitive impairment (10). In Western countries, 30-50% of people with dementia lose weight through mechanisms that may be central, such as atrophy of the medial temporal cortex or decreased secretion of neuropeptide Y (orexigenic hypothalamic neuropeptide), or because of the appearance of apraxia or oppositional behavior when taking meals (11)(12)(13)(14)(15)(16). ...
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To determine the nutritional status of elderly African people and to investigate the association between undernutrition and dementia. Door-to-door cross-sectional surveys in the general population. Representative districts of Bangui (Central African Republic) and Brazzaville (Republic of Congo). Population aged over 65 years. Undernutrition was defined as a body mass index <18.5. Anthropometric parameters (arm circumference, waist circumference and triceps skinfold thickness) were measured, and information was gathered on nutritional habits. PARTICIPANTS underwent cognitive screening using the Community Screening Interview for Dementia (CSI-D) and the Five-Word Test. After further neuropsychological testing and neurological examination, the diagnosis of dementia was confirmed according to DSM-IV criteria. Multivariate logistic regression models were applied in order to identify factors associated with undernutrition in populations with or without dementia. 1016 people were included. In the general population, the prevalence of undernutrition was 19.2%. Dementia was found in 7.4% of elderly people. Compared with healthy people, patients with dementia had an increased prevalence of undernutrition (32.0% vs. 17.7%; p=0.002), lower weight (49.3±10.5 kg vs. 58.4±13.5 kg ; p<0.001), and lower BMI (20.8±4.1 vs. 22.9±4.8 ; p<0.001); they were less likely to eat their fill (38.9% vs. 45.9% ; p=0.001), had more dietary restrictions (36.1% vs. 24.3% ; p=0.03) and ate less often with their family (66.7% vs. 90.6% ; p<0.0001). Eating only one meal per day was the sole factor associated with undernutrition in dementia (OR: 7.23 [CI: 1.65-31.7]; p=0.03). The prevalence of undernutrition is high in the older population. The nutritional status of patients with dementia is more impaired than that of healthy patients. However, they are less often malnourished than in French home care settings. This study is the first to look at the nutritional status of at-home patients with dementia in Africa. These comparative data will eventually be used in the development of new nutritional intervention strategies.
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Alzheimer’s disease (AD) is often associated with feeding difficulties and changes in eating behavior with may lead to malnutrition. In French nursing homes, AD patients may live in special care units that better meet dementia residents' needs. However, meals are often delivered to AD patients by using meal trays coming from central kitchens. This led to the disappearance of cues that could help residents to foresee mealtime, such as the smell of food odors. The aim of the present study was to assess the impact of odorizing the dining room of AD Units with a meat odor before lunch on subsequent food intake and eating behavior. Thirty-two residents (> 75 yo) from three AD Units were included in the study. They participated in two control lunches and two primed lunches, for which a meat odor was diffused in the dining room 15 minutes before the arrival of the meal tray (olfactory priming). Results of the first replication showed a significant effect of olfactory priming, with a 25% increase in meat and vegetable consumption compared to the control condition. Behavioral measurements also showed a significant increase of resident’s interest toward the meal in the primed lunch. However, this effect was no longer observed when the priming session was replicated two weeks later with the same priming odor and the same menu. Despite further researches are needed to understand why this priming effect cannot be replicated, our experiment is one of the very first to investigate the effect of food odor priming on subsequent food intake in Alzheimer patients in a real life setting.
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Antioxidant properties of some vitamins and trace elements may help to prevent cognitive decline. The aim of the current study was to estimate the long-term effects of antioxidant nutrient supplementation on the cognitive performance of participants in the Supplementation in Vitamins and Mineral Antioxidants (SU.VI.MAX) study 6 y after the end of the trial. This study included 4447 French participants aged 45-60 y who were enrolled in the SU.VI.MAX study (1994-2002), which was a double-blind, placebo-controlled, randomized trial. From 1994 to 2002, participants received daily vitamin C (120 mg), β-carotene (6 mg), vitamin E (30 mg), selenium (100 μg), and zinc (20 mg) in combination or as a placebo. In 2007-2009, the cognitive performance of participants was assessed with 4 neuropsychological tests (6 tasks). Principal components analysis (PCA) was performed to identify cognitive-function summary scores. Associations between antioxidant supplementation and cognitive functions, in the full sample and by subgroups, were estimated through ANOVA and expressed as mean differences and 95% CIs. Subgroup analyses were performed according to baseline characteristics. Subjects receiving active antioxidant supplementation had better episodic memory scores (mean difference: 0.61; 95% CI: 0.02, 1.20). PCA indicated 2 factors that were interpreted as showing verbal memory and executive functioning. Verbal memory was improved by antioxidant supplementation only in subjects who were nonsmokers or who had low serum vitamin C concentrations at baseline. This study supports the role of an adequate antioxidant nutrient status in the preservation of verbal memory under certain conditions. This trial was registered at clinicaltrials.gov as NCT00272428.
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Higher adherence to a Mediterranean diet (MeDi) and n-3 PUFA may both contribute to decreased dementia risk, but the association between MeDi adherence and lipid status is unclear. The aim of the present study was to analyse the relationship between plasma fatty acids and MeDi adherence in French elderly community dwellers. The study population (mean age 75·9 years) consisted of 1050 subjects from Bordeaux (France) included in the Three-City cohort. Adherence to the MeDi (scored as 0-9) was computed from a FFQ and 24 h recall. The proportion of each plasma fatty acid was determined. Cross-sectional analysis of the association between plasma fatty acids and MeDi adherence was performed by multi-linear regression. After adjusting for age, sex, energy intake, physical activity, smoking status, BMI, plasma TAG and apoE-ɛ4 genotype, plasma palmitoleic acid was significantly inversely associated with MeDi adherence, whereas plasma DHA, the EPA+DHA index and total n-3 PUFA were positively associated with MeDi adherence. The n-6:n-3 PUFA, arachidonic acid (AA):EPA, AA:DHA and AA:(EPA+DHA) ratios were significantly inversely associated with MeDi adherence. Plasma EPA was positively associated with MeDi adherence only in apoE-ɛ4 non-carriers. There was no association between MeDi adherence and SFA and total MUFA. The present results suggest that the protective effect of the MeDi on cognitive functions might be mediated by higher plasma DHA and lower n-6:n-3 PUFA ratios.
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An increased rate of brain atrophy is often observed in older subjects, in particular those who suffer from cognitive decline. Homocysteine is a risk factor for brain atrophy, cognitive impairment and dementia. Plasma concentrations of homocysteine can be lowered by dietary administration of B vitamins. To determine whether supplementation with B vitamins that lower levels of plasma total homocysteine can slow the rate of brain atrophy in subjects with mild cognitive impairment in a randomised controlled trial (VITACOG, ISRCTN 94410159). Single-center, randomized, double-blind controlled trial of high-dose folic acid, vitamins B(6) and B(12) in 271 individuals (of 646 screened) over 70 y old with mild cognitive impairment. A subset (187) volunteered to have cranial MRI scans at the start and finish of the study. Participants were randomly assigned to two groups of equal size, one treated with folic acid (0.8 mg/d), vitamin B(12) (0.5 mg/d) and vitamin B(6) (20 mg/d), the other with placebo; treatment was for 24 months. The main outcome measure was the change in the rate of atrophy of the whole brain assessed by serial volumetric MRI scans. A total of 168 participants (85 in active treatment group; 83 receiving placebo) completed the MRI section of the trial. The mean rate of brain atrophy per year was 0.76% [95% CI, 0.63-0.90] in the active treatment group and 1.08% [0.94-1.22] in the placebo group (P =  0.001). The treatment response was related to baseline homocysteine levels: the rate of atrophy in participants with homocysteine >13 µmol/L was 53% lower in the active treatment group (P =  0.001). A greater rate of atrophy was associated with a lower final cognitive test scores. There was no difference in serious adverse events according to treatment category. The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine-lowering B vitamins. Sixteen percent of those over 70 y old have mild cognitive impairment and half of these develop Alzheimer's disease. Since accelerated brain atrophy is a characteristic of subjects with mild cognitive impairment who convert to Alzheimer's disease, trials are needed to see if the same treatment will delay the development of Alzheimer's disease. Controlled-Trials.com ISRCTN94410159.
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Docosahexaenoic acid (DHA) plays an important role in neural function. Decreases in plasma DHA are associated with cognitive decline in healthy elderly adults and in patients with Alzheimer's disease. Higher DHA intake is inversely correlated with relative risk of Alzheimer's disease. The potential benefits of DHA supplementation in age-related cognitive decline (ARCD) have not been fully examined. Determine effects of DHA administration on improving cognitive functions in healthy older adults with ARCD. Randomized, double-blind, placebo-controlled, clinical study was conducted at 19 U.S. clinical sites. A total of 485 healthy subjects, aged ≥55 with Mini-Mental State Examination >26 and a Logical Memory (Wechsler Memory Scale III) baseline score ≥1 standard deviation below younger adults, were randomly assigned to 900 mg/d of DHA orally or matching placebo for 24 weeks. The primary outcome was the CANTAB Paired Associate Learning (PAL), a visuospatial learning and episodic memory test. Intention-to-treat analysis demonstrated significantly fewer PAL six pattern errors with DHA versus placebo at 24 weeks (difference score, -1.63 ± 0.76 [-3.1, -0.14, 95% CI], P = .03). DHA supplementation was also associated with improved immediate and delayed Verbal Recognition Memory scores (P < .02), but not working memory or executive function tests. Plasma DHA levels doubled and correlated with improved PAL scores (P < .02) in the DHA group. DHA was well tolerated with no reported treatment-related serious adverse events. Twenty-four week supplementation with 900 mg/d DHA improved learning and memory function in ARCD and is a beneficial supplement that supports cognitive health with aging. Clinicaltrials.gov, Identifier: NCT0027813.
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Background: Very-long-chain n¿3 polyunsaturated fatty acids (n¿3 PUFAs) are suggested to be related to cognitive performance in older adults. However, limited data exist on the association between n¿3 PUFAs and performance in specific cognitive domains. Objective: We evaluated the association between plasma n¿3 PUFA proportions and cognitive performance in 5 cognitive domains and determined whether plasma n¿3 PUFA proportions predict cognitive change over 3 y. Design: We used data from the FACIT trial, in which participants received folic acid or placebo capsules for 3 y. Fatty acid proportions in plasma cholesteryl esters at baseline were measured in 807 men and women aged 50¿70 y. Cognitive performance for memory, sensorimotor speed, complex speed, information-processing speed, and word fluency was assessed at baseline and after 3 y. The cross-sectional analyses were based on all 807 participants; the longitudinal analyses were based only on 404 participants in the placebo group. Results: Higher plasma n¿3 PUFA proportions predicted less decline in sensorimotor speed (multiple linear regression coefficient, z score = 0.31; 95% CI: 0.06, 0.57) and complex speed (0.40; 95% CI: 0.10, 0.70) over 3 y. Plasma n¿3 PUFA proportions did not predict 3-y changes in memory, information-processing speed, or word fluency. The cross-sectional analyses showed no association between plasma n¿3 PUFA proportions and performance in any of the 5 cognitive domains. Conclusions: In this population, plasma n¿3 PUFA proportions were associated with less decline in the speed-related cognitive domains over 3 y. These results need to be confirmed in randomized controlled trials.
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High homocysteine concentrations may be neurotoxic and contribute to cognitive decline in older persons. The objective was to examine the effect of supplementation with folic acid, vitamin B-12, and vitamin B-6 on cognitive change in women with cardiovascular disease (CVD) or CVD risk factors. The Women's Antioxidant and Folic Acid Cardiovascular Study is a randomized placebo-controlled trial designed to test the effect of a combination of B vitamins (2.5 mg folic acid/d, 50 mg vitamin B-6/d, and 1 mg vitamin B-12/d) on secondary prevention of CVD. Female health professionals aged >or=40 y (n = 5442) with CVD or >or=3 coronary risk factors in 1998 (after folic acid fortification began in the United States) were randomly assigned to treatment. Shortly after randomization (mean: 1.2 y), a substudy of cognitive function was initiated among 2009 participants aged >or=65 y. Telephone cognitive function testing was administered up to 4 times over 5.4 y with 5 tests of general cognition, verbal memory, and category fluency. Repeated-measures analyses were conducted, and the primary outcome was a global composite score averaging all test results. Mean cognitive change from baseline did not differ between the B vitamin and placebo groups (difference in change in global score: 0.03; 95% CI: -0.03, 0.08; P = 0.30). However, supplementation appeared to preserve cognition among women with a low baseline dietary intake of B vitamins. Combined B vitamin supplementation did not delay cognitive decline among women with CVD or CVD risk factors. The possible cognitive benefits of supplementation among women with a low dietary intake of B vitamins warrant further study.
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Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline. To determine the efficacy and safety of B vitamin supplementation in the treatment of AD. A multicenter, randomized, double-blind controlled clinical trial of high-dose folate, vitamin B(6), and vitamin B(12) supplementation in 409 (of 601 screened) individuals with mild to moderate AD (Mini-Mental State Examination scores between 14 and 26, inclusive) and normal folic acid, vitamin B(12), and homocysteine levels. The study was conducted between February 20, 2003, and December 15, 2006, at clinical research sites of the Alzheimer Disease Cooperative Study located throughout the United States. Participants were randomly assigned to 2 groups of unequal size to increase enrollment (60% treated with high-dose supplements [5 mg/d of folate, 25 mg/d of vitamin B(6), 1 mg/d of vitamin B(12)] and 40% treated with identical placebo); duration of treatment was 18 months. Change in the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog). A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Although the vitamin supplement regimen was effective in reducing homocysteine levels (mean [SD], -2.42 [3.35] in active treatment group vs -0.86 [2.59] in placebo group; P < .001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-cog score during 18 months (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P = .52; 95% confidence interval of rate difference, -0.06 to 0.12; based on the intention-to-treat generalized estimating equations model), or on any secondary measures. A higher quantity of adverse events involving depression was observed in the group treated with vitamin supplements. This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD. clinicaltrials.gov Identifier: NCT00056225.
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Atherosclerosis and thrombosis may lead to cognitive impairment through cerebral infarcts or white matter hyperintensities. Oxidative stress is now seen as a major contributor to the process of atherogenesis. High intake of polyunsaturated fatty acids, e.g., linoleic acid, or low intake of antioxidants can increase oxidative stress. High intake of n-3 polyunsaturated fatty acids and its main source, fish, may reduce the risk of thrombosis. Little is known, however, about the relation between these dietary factors and cognitive function. The authors investigated this relation with data derived from a cohort of men, aged 69-89 years, who were participants in the Zutphen Elderly Study. The 30-point Mini-Mental State Examination was used to assess cognitive impairment in 1990 (score < or = 25 in 153/476 men, 32%) and cognitive decline from 1990 to 1993 (drop > 2 points in 51/342 men, 15%). Food intake was estimated in 1985 and 1990 by the cross-check dietary history method. High linoleic acid intake was associated with cognitive impairment after adjustment for age, education, cigarette smoking, alcohol consumption, and energy intake (odds ratio (OR) for highest vs. lowest tertile = 1.76, 95% confidence interval (CI) 1.04-3.01). Intake of n-3 polyunsaturated fatty acids was not associated with cognitive impairment, whereas high fish consumption tended to be inversely associated with cognitive impairment (OR = 0.63, 95% CI 0.33-1.21) and cognitive decline (OR = 0.45, 95% CI 0.17-1.16). Intakes of beta-carotene, vitamins C and E, and flavonoids were not inversely associated with cognitive impairment or decline. This study raises the possibility that high linoleic acid intake is positively associated with cognitive impairment and high fish consumption inversely associated with cognitive impairment.
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Objectives: To study the ictal phenomenology, aetiology, and outcome of convulsions occurring within seconds of impact in violent collision sport. Design: Retrospective identification of convulsions associated with concussive brain injury from case records from medical officers of football clubs over a 15 year period. Subjects: Elite Australian rules and rugby league footballers. Main outcome measures: Neuroimaging studies, electroencephalography, neuropsychological test data, and statistics on performance in matches to determine presence of structural or functional brain injury. Clinical follow up and electroencephalography for evidence of epilepsy. Results: Twenty two cases of concussive convulsions were identified with four events documented on television videotape. Convulsions began within 2 seconds of impact and comprised an initial period of tonic stiffening followed by myoclonic jerks of all limbs lasting up to 150 seconds. Some asymmetry in the convulsive manifestations was common, and recovery of consciousness was rapid. No structural or permanent brain injury was present on clinical assessment, neuropsychological testing, or neuroimaging studies. All players returned to elite competition within two weeks of the incident. Epilepsy did not develop in any player over a mean (range) follow up of 3.5 (1-13) years. Conclusions: These concussive or impact convulsions are probably a non-epileptic phenomenon, somewhat akin to convulsive syncope. The mechanism may be a transient traumatic functional decerebration. In concussive convulsions the outcome is universally good, antiepileptic treatment is not indicated, and prolonged absence from sport is unwarranted.
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Associations between dietary intake and cognitive performance were examined in 260 elderly people aged 65-90 y who were free of significant cognitive impairment. Dietary intake was monitored with a weighed-food record for 7 consecutive days. The subjects' cognitive capacity was tested by using Folstein et al's Mini-Mental State Examination (MMSE) and Pfeiffer's Mental Status Questionnaire (PMSQ). Subjects with adequate MMSE results (> or = 28 points) had lower intakes of monounsaturated fatty acids, saturated fatty acids, and cholesterol, and higher intakes of total food, fruit, carbohydrate, thiamine, folate, and vitamin C compared with those with less satisfactory results. Subjects who made no errors on the PMSQ had greater intakes of total food, vegetables, fruit, carbohydrate, fiber, folate, vitamin C, beta-carotene, iron, and zinc, and lower intakes of saturated fatty acids compared with those who made errors. Our results agree with those of other authors indicating that intakes of different nutrients or the consumption of a more satisfactory global diet is associated with better cognitive function in the elderly. However, more research is required to determine whether differences in intake of a particular nutrient are the result of or a conditioning factor for incipient impaired cognition. Unmeasured confounding factors may also affect both dietary intake and risk of cognitive impairment. A diet with less fat, saturated fat, and cholesterol, and more carbohydrate, fiber, vitamins (especially folate, vitamins C and E, and beta-carotenes), and minerals (iron and zinc) may be advisable not only to improve the general health of the elderly but also to improve cognitive function.
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Objective: To explore the associations of low serum levels of vitamin B(12) and folate with AD occurrence. Methods: A population-based longitudinal study in Sweden, the Kungsholmen Project: A random sample of 370 nondemented persons, aged 75 years and older and not treated with B(12) and folate, was followed for 3 years to detect incident AD cases. Two cut-off points were used to define low levels of vitamin B(12) (< or =150 and < or =250 pmol/L) and folate (< or =10 and < or =12 nmol/L), and all analyses were performed using both definitions. AD and other types of dementia were diagnosed by specialists according to DSM-III-R criteria. Results: When using B(12) < or =150 pmol/L and folate < or =10 nmol/L to define low levels, compared with people with normal levels of both vitamins, subjects with low levels of B(12) or folate had twice higher risks of developing AD (relative risk [RR] = 2.1, 95% CI = 1.2 to 3.5). These associations were even stronger in subjects with good baseline cognition (RR = 3.1, 95% CI = 1.1 to 8.4). Similar relative risks of AD were found in subjects with low levels of B(12) or folate and among those with both vitamins at low levels. A comparable pattern was detected when low vitamin levels were defined as B(12) < or =250 pmol/L and folate < or =12 nmol/L. Conclusions: This study suggests that vitamin B(12) and folate may be involved in the development of AD. A clear association was detected only when both vitamins were taken into account, especially among the cognitively intact subjects. No interaction was found between the two vitamins. Monitoring serum B(12) and folate concentration in the elderly may be relevant for prevention of AD.
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Sous l’égide de la Société Française de Gériatrie et Gérontologie, un groupe pluridisciplinaire de spécialistes en gériatrie, neurologie, épidémiologie, psychiatrie, neuroradiologie, pharmacologie, santé publique a entrepris une démarche de consensus sur les modalités d’évaluation, de suivi et de prise en charge globale de la démence de type Alzheimer au stade sévère. Cette réflexion, fondée sur l’état des connaissances en 2005, a permis de formuler 21 recommandations à destination des praticiens hospitaliers, médecins traitants, médecins coordonnateurs et spécialistes. Quel que soit le stade évolutif de la maladie, l’objectif de la prise en charge est d’améliorer la qualité de vie de la personne malade et de sa famille, en associant projet de soins et projet de vie et ce jusqu’en fin de vie. La prise en charge, pour être globale, doit être nécessairement pluridisciplinaire et coordonnée, en mobilisant les ressources sanitaires et médico-sociales de proximité pour optimiser leur utilisation. Le groupe a souligné également l’importance d’une recherche dynamique : recherche clinique visant à mieux connaître l’évolution des troubles, évaluation des stratégies de prise en soins.
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Self-reported, dietary intake and biochemical estimates of thiamine, riboflavin, folate, vitamin B-12, protein, and iron were compared in 22, free-living elders by individuals who had senile dementia of the Alzheimer's type (SDAT) and in 41 who were cognitively normal (CN). The two groups did not differ significantly in their intake of these nutrients or the number of deficiency states for intake (<67% RDA). Low serum transketolase (thiamin; p < 0.055), red blood cell (RBC) folate (p. < 0.06), and serum vitamin B-12 (p < 0.05) levels occurred more often in SDAT patients than in CN subjects. Individuals in both groups who used multivitamin supplements had significantly higher biochemical values for thiamine (p < 0.03), riboflavin (p < 0.01), and vitamin B-12 (p < 0.003) than nonsupplement users. Because of the differences in vitamin B-12 and RBC folate levels between groups, a retrospective analysis was performed on a larger group of subjects drawn from a geriatric assessment clinic. Patients with SDAT had significantly lower serum vitamin B-12 (p <0.01) and lower RBC folate (p <0.03) values than CN subjects. When mean values for vitamin B-12 and RBC folate were grouped by degree of impairment in SDAT subjects, vitamin B-12 was significantly lower in mildly and moderately impaired subjects than in those with normal cognition. Mean values for both nutrients did not differ significantly between severely impaired and CN subjects. There was a significant quadratic relationship between cognitive impairment and biochemical values for vitamin B-12. The authors concluded that the self-reported dietary intake of free-living SDAT patients is similar to that of cognitively normal elderly people, and multivitamin supplementation significantly increases biochemical measurements for nutritional status. Further studies are needed on the importance of low serum vitamin B-12 and RBC folate, particularly as they relate to the degree of cognitive impairment.
Article
The evolution of nutritional parameters was studied over 1 year in patients with Alzheimer's disease (AD). Seventy-six community dwelling patients with probable AD underwent a comprehensive nutritional assessment at entry into the study and 1 year later. The nutritional assessment included anthropometric and biological markers, as well as a complete dietary assessment. A comprehensive functional and neuropsychological evaluation was performed on each patient using a number of standardized and validated tools, as well as a scale to evaluate caregiver burden. Just over 44% of our subjects experienced a greater than 4% weight loss in 1 year. Over 13% of our subjects lost more than 10% body weight. Patients having lost weight resembled patients without weight loss, except that caregiver burden was perceived to be higher in the weight loosing group, they tended to lose independence in activities of daily living (ADL). This group also had a decrease in daily caloric intake (-400 kCal/day). In 1 year, a large number of AD patients lose weight. Given the seriousness of the problems associated with weight loss it seems to be prudent to recommend a regular monitoring of the nutritional status in AD patients, as soon as the diagnosis is suspected, and instituting a weight loss prevention program where caregiver burden is perceived as the greatest.
Article
On page 845 in the first paragraph of the “All Randomized Trials” subsection, the sentence that read “Heterogeneity was not significant (I²=18.6%, P=.10)” should have read “Heterogeneity was significant (I²=18.9%, P=.10).” In the following sentence that begins “Adjusted-rank correlation test (P=.08), but not the regression asymmetry test (P=.26), suggested the bias among trials,” the respective P values should have read “(P=.09)” and “(P=.24).” In the second paragraph of the same subsection, the portion of the sentence that begins on page 845: “Univariate meta-regression analyses revealed significant influences of dose of beta carotene (RR, 1.004; 95% CI, 1.001-1.007; P=.012),” the P value should have been equal to “.014.” In the latter part of the same sentence that falls on page 847, the P value for the dose of selenium that read “P=.002” should have read “P=.001.” In the following part of the sentence, the upper confidence limit that read “1.29” should have read “1.30.” In the third paragraph of the same subsection, on page 847, the P value for the “multivariate meta-regression” for dose of selenium that read “P=.005” should have read “P=.004,” the lower confidence limit for low-bias risk trials that read “1.05” should have read “1.04,” and the P value for the low-bias risk trials in the same sentence that read “P=.005” should have read “P=.006.” In Table 5 on page 853, the RR (95% CI) in the “Beta carotene given singly” row that read “1.06 (1.01-1.11)” should have read “1.05 (1.00-1.11)” and the I² value that read “5.4” should have read “11.8.” In the “Beta carotene given in combination with other antioxidant supplements” row, the I² value that read “55.6” should have read “55.5.” In the “Beta carotene given singly or in combination with other antioxidant supplements” row, the CI range that read “(0.96-1.08)” should have read “(0.95-1.07)” and the I2 value that read “52.2” should have read “52.5.” In the “Beta carotene given singly or in combination with other antioxidant supplements after exclusion of high-bias risk and selenium trials” row, the I² value that read 36.8” should have read “34.4” In the “Vitamin E given singly” row, the number of study participants that read “47 007” should have read “41 341.” In the “Vitamin E given in combination with other antioxidant supplements” row, the RR that read “1.01” should have read “1.00” and the I² value that read “17.2” should have read “16.9.” In the “Vitamin E given singly or in combination with other antioxidant supplements” row, the I²value that read “2.8” should have read “2.4.” In the “Vitamin E given singly or in combination with other antioxidant supplements after exclusion of high-bias risk and selenium trials” row, the list of references should have included reference 87 and excluded 95.
Article
Weight loss is commonly observed in patients with Alzheimer's disease and is an accepted symptom of the clinical diagnostic criteria in current use. It is, however, unclear as to whether disease or dietetic factors are responsible for the causation of weight loss. Difficulty also arises due to variability in clinical diagnostic criteria used in defining Alzheimer's disease and clinical heterogeneity with respect to weight loss. This review examines the evidence available for weight loss in Alzheimer's disease and the possible explanations for this.
Article
The physiologically active form of vitamin D, 1,25-dihydroxyvitamin D3, is a fat-soluble steroid hormone with a well established role in skeletal health. A growing body of evidence suggests low vitamin D levels also play a role in the pathogenesis of a wide range of non-skeletal, age-associated diseases including cancer, heart disease, type 2 diabetes mellitus and stroke. Low levels of serum 25-hydroxyvitamin D [25(OH)D], a stable marker of vitamin D status, are also associated with increased odds of prevalent cognitive dysfunction, Alzheimer’s disease and all-cause dementia in a number of studies, raising the possibility that vitamin D plays a role in the aetiology of cognitive dysfunction and dementia. To date, the majority of human studies reporting associations between vitamin D and cognition or dementia have been cross-sectional or case-control designs that do not permit us to exclude the possibility that such associations are a result of disease progression rather than being causal. Animal and in vitro experiments have identified a number of neuroprotective mechanisms that might link vitamin D status to cognitive dysfunction and dementia, including vasoprotection and amyloid phagocytosis and clearance, but the clinical relevance of these mechanisms in humans is not currently clear. Two recent, large, prospective studies go some way to establish the temporal relationship with cognitive decline. The relative risk of cognitive decline was 60% higher (relative risk = 1.6, 95% CI 1.2, 2.0) in elderly Italian adults with severely deficient 25(OH)D levels (
Article
Studies have shown less cognitive decline and lower risk of Alzheimer's disease in elderly individuals consuming either antioxidant vitamins or nonsteroidal anti-inflammatory drugs (NSAIDs). The potential of added benefit from their combined use has not been studied. We therefore analyzed data from 3,376 elderly participants of the Cache County Study who were given the Modified Mini-Mental State examination up to three times during a period of 8 years. Those who used a combination of vitamins E and C supplements and NSAIDs at baseline declined by an average 0.96 fewer points every 3 years than nonusers (P < .05). This apparent effect was attributable entirely to participants with the APOE epsilon4 allele, whose users declined by 2.25 fewer points than nonusers every 3 years (P < .05). These results suggest that among elderly individuals with an APOE epsilon4 allele, there is an association between using antioxidant supplements in combination with NSAIDs and less cognitive decline over time.
Article
This study examined the association of plasma DHA, dietary DHA, and fish intake with dementia and Alzheimer's Disease (AD) in older adults. Case-cohort study. Clinic visit in 1991-93. 266 community dwelling men and women aged 67-100 years (mean=80.2). Participants had neurological and neuropsychological evaluations for dementia in 1991-93. Plasma DHA was measured in blood samples obtained at that visit. Dietary intakes of DHA and fish were obtained from an earlier (1988-91) visit. Three DHA exposure variables were used in separate analyses; plasma DHA, dietary DHA, and consumption of cold-water fish. All-cause dementia included AD and other types of possible or probable dementia. Among these 266 participants, 42 had dementia and 30 had possible or probable AD. Plasma DHA in the highest tertile was associated with a 65% reduced odds of all-cause dementia (95% CI: 0.17, 0.92) and a 60% reduced odds of AD (95% CI: 0.15, 1.10). Dietary DHA in the highest tertile was associated with a 73% reduced odds of all-cause dementia (95% CI: 0.09, 0.79) and a 72% reduced odds of AD (95% CI: 0.09, 0.93). Fish intake had similar, though not significant, reduced odds of dementia (OR = 0.51; 95% CI: 0.20, 1.32) and AD (OR = 0.55; 95% CI: 0.20, 1.48). Plasma and dietary DHA appear to protect against dementia. Increasing DHA intake from marine sources may be recommended for reducing dementia risk.
Article
To determine if caregiver burden (CB) can be an independent predictive factor of weight loss at three months in older outpatients suffering from mild to moderate Alzheimer's disease (AD) and living at home. Prospective cohort study involving 105 subjects aged 70 years or more, affected by mild to moderate AD and living at home with the assistance of at least one informal caregiver, who consecutively underwent a multidimensional geriatric assessment. Body weight was re-evaluated at a three month follow-up, from December 2008 to April 2009. Those who experienced a weight loss greater than 3% of the baseline weight constituted the 'weight loss' group. Out of the 97 older participants attending follow-up, 22 (23%) had experienced a weight loss > 3%. At a multivariate logistic regression analysis, a greater CB at baseline, defined by a score of the caregiver burden inventory scale in the highest tertile (i.e. 36+ out of 96), turned out to predict weight loss at three months (odds ratio (OR) 13.93, 95% confidence interval (CI) 1.91-101.33, p = 0.009), independently of other factors associated with the 'weight loss' group such as age, functional dependence and the risk of malnutrition estimated by means of the Mini Nutritional Assessment Short Form (MNA-SF). For older outpatients affected by mild to moderate AD and living at home, CB constitutes a risk factor for weight loss even in the short-term, independently of other factors such as the risk of malnutrition assessed by means of the MNA-SF.
Article
The decision to place a feeding tube in a patient with advanced dementia is difficult for both family members and health care professionals. There is increasing evidence that the use of feeding tubes in these patients does not improve survival, prevent aspiration pneumonia, prevent or heal decubitus ulcers, or improve other clinical outcomes. Yet, despite this evidence, more than one third of nursing home residents with advanced dementia have feeding tubes, and many of these individuals have feeding tubes inserted on hospital admission for an acute care problem. Health care professionals need to examine the evidence carefully to identify practices that provide patients and families with information to make informed choices and respect their rights and dignity at end of life.
Article
Both higher adherence to a Mediterranean-type diet and more physical activity have been independently associated with lower Alzheimer disease (AD) risk but their combined association has not been investigated. To investigate the combined association of diet and physical activity with AD risk. Prospective cohort study of 2 cohorts comprising 1880 community-dwelling elders without dementia living in New York, New York, with both diet and physical activity information available. Standardized neurological and neuropsychological measures were administered approximately every 1.5 years from 1992 through 2006. Adherence to a Mediterranean-type diet (scale of 0-9; trichotomized into low, middle, or high; and dichotomized into low or high) and physical activity (sum of weekly participation in various physical activities, weighted by the type of physical activity [light, moderate, vigorous]; trichotomized into no physical activity, some, or much; and dichotomized into low or high), separately and combined, were the main predictors in Cox models. Models were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, body mass index, smoking status, depression, leisure activities, a comorbidity index, and baseline Clinical Dementia Rating score. Time to incident AD. A total of 282 incident AD cases occurred during a mean (SD) of 5.4 (3.3) years of follow-up. When considered simultaneously, both Mediterranean-type diet adherence (compared with low diet score, hazard ratio [HR] for middle diet score was 0.98 [95% confidence interval {CI}, 0.72-1.33]; the HR for high diet score was 0.60 [95% CI, 0.42-0.87]; P = .008 for trend) and physical activity (compared with no physical activity, the HR for some physical activity was 0.75 [95% CI, 0.54-1.04]; the HR for much physical activity was 0.67 [95% CI, 0.47-0.95]; P = .03 for trend) were associated with lower AD risk. Compared with individuals neither adhering to the diet nor participating in physical activity (low diet score and no physical activity; absolute AD risk of 19%), those both adhering to the diet and participating in physical activity (high diet score and high physical activity) had a lower risk of AD (absolute risk, 12%; HR, 0.65 [95% CI, 0.44-0.96]; P = .03 for trend). In this study, both higher Mediterranean-type diet adherence and higher physical activity were independently associated with reduced risk for AD.
Article
Cardiovascular factors are associated with cognitive decline. Antioxidants may be beneficial. The Women's Antioxidant Cardiovascular Study was a trial of vitamin E (402 mg every other day), beta carotene (50 mg every other day), and vitamin C (500 mg daily) for the secondary prevention of cardiovascular disease. From 1995 to 1996, women > or =40 years of age with cardiovascular disease or > or =3 coronary risk factors were randomized. From 1998 to 1999, a cognitive function substudy was initiated among 2824 participants > or =65 years of age. With 5 cognitive tests, cognition was assessed by telephone 4 times over 5.4 years. The primary outcome was a global composite score averaging all scores; repeated-measures analyses were used to examine cognitive change over time. Vitamin E supplementation and beta carotene supplementation were not associated with slower rates of cognitive change (mean difference in change for vitamin E versus placebo, -0.01; 95% confidence interval, -0.05 to 0.04; P=0.78; for beta carotene, 0.03; 95% confidence interval, -0.02 to 0.07; P=0.28). Although vitamin C supplementation was associated with better performance at the last assessment (mean difference, 0.13; 95% confidence interval, 0.06 to 0.20; P=0.0005), it was not associated with cognitive change over time (mean difference in change, 0.02; 95% confidence interval, -0.03 to 0.07; P=0.39). Vitamin C was more protective against cognitive change among those with new cardiovascular events during the trial (P for interaction=0.009). Antioxidant supplementation did not slow cognitive change among women with preexisting cardiovascular disease or cardiovascular disease risk factors. A possible late effect of vitamin C or beta carotene among those with low dietary intake on cognition warrants further study.
Article
Higher adherence to the Mediterranean diet (MeDi) may protect from Alzheimer disease (AD), but its association with mild cognitive impairment (MCI) has not been explored. To investigate the association between the MeDi and MCI. In a multiethnic community study in New York, we used Cox proportional hazards to investigate the association between adherence to the MeDi (0-9 scale; higher scores indicate higher adherence) and (1) the incidence of MCI and (2) the progression from MCI to AD. All of the models were adjusted for cohort, age, sex, ethnicity, education, APOE genotype, caloric intake, body mass index, and duration between baseline dietary assessment and baseline diagnosis. Incidence of MCI and progression from MCI to AD. There were 1393 cognitively normal participants, 275 of whom developed MCI during a mean (SD) follow-up of 4.5 (2.7) years (range, 0.9-16.4 years). Compared with subjects in the lowest MeDi adherence tertile, subjects in the middle tertile had 17% less risk (hazard ratio [HR] = 0.83; 95% confidence interval [CI], 0.62-1.12; P = .24) of developing MCI and those in the highest tertile had 28% less risk (HR = 0.72; 95% CI, 0.52-1.00; P = .05) of developing MCI (trend HR = 0.85; 95% CI, 0.72-1.00; P for trend = .05). There were 482 subjects with MCI, 106 of whom developed AD during a mean (SD) follow-up of 4.3 (2.7) years (range, 1.0-13.8 years). Compared with subjects in the lowest MeDi adherence tertile, subjects in the middle tertile had 45% less risk (HR = 0.55; 95% CI, 0.34-0.90; P = .01) of developing AD and those in the highest tertile had 48% less risk (HR = 0.52; 95% CI, 0.30-0.91; P = .02) of developing AD (trend HR = 0.71; 95% CI, 0.53-0.95; P for trend = .02). Higher adherence to the MeDi is associated with a trend for reduced risk of developing MCI and with reduced risk of MCI conversion to AD.
Article
High intake of n-3 polyunsaturated fatty acids may protect against age-related cognitive decline. However, results from epidemiologic studies are inconclusive, and results from randomized trials in elderly subjects without dementia are lacking. To investigate the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation on cognitive performance. Double-blind, placebo-controlled trial involving 302 cognitively healthy (Mini-Mental State Examination score > 21) individuals aged 65 years or older. Participants were randomly assigned to 1,800 mg/d EPA-DHA, 400 mg/d EPA-DHA, or placebo capsules for 26 weeks. Cognitive performance was assessed using an extensive neuropsychological test battery that included the cognitive domains of attention, sensorimotor speed, memory, and executive function. The mean age of the participants was 70 years, and 55% were male. Plasma concentrations of EPA-DHA increased by 238% in the high-dose and 51% in the low-dose fish oil group compared with placebo, reflecting excellent compliance. Baseline scores on the cognitive tests were comparable in the three groups. Overall, there were no significant differential changes in any of the cognitive domains for either low-dose or high-dose fish oil supplementation compared with placebo. In this randomized, double-blind, placebo-controlled trial, we observed no overall effect of 26 weeks of eicosapentaenoic acid and docosahexaenoic acid supplementation on cognitive performance.
Article
Synopsis Anthropometric and biochemical indices of nutritional status and weighed dietary intake have been studied in hospitalized patients with senile dementia, demented patients living in the community and age-matched control subjects who were not cognitively impaired. Demented patients were lighter than control subjects, and had a lower body mass index, skinfold thickness, mid-arm circumference and arm muscle bulk. The hospitalized patients were more seriously affected than those living in the community, and body weight was significantly negatively correlated with duration of hospitalization. Over a 6-month period the hospitalized patients showed a further weight loss, while those living in the community did not. Both groups of demented patients had higher intakes of energy, protein, vitamins and minerals than the control subjects. The diet of the hospitalized patients was slightly, but not significantly, superior to that of the patients living in the community. Biochemical evidence of specific vitamin inadequacy was equally prevalent in all three groups of subjects, and there were no significant correlations between the degree of cognitive impairment or behavioural disorder and any of the indices of nutritional state. Clinical signs suggestive of malnutrition were not correlated with either biochemical evidence of deficiency or cognitive impairment and behavioural disturbance.
Article
Many chronically ill mental patients show rapid and severe weight loss leading to severe nutritional debilitation. Excessive energy requirements secondary to hypermetabolism or hyperactivity have been proposed as the cause. This hypothesis was tested using the new doubly-labelled water (2H218O) technique to obtain accurate estimates of total energy expenditure (TEE) in 14 such patients. Mean TEE was very low (6.1 ±1.3 MJ/day). None of the subjects was in significant negative energy balance when studied. Mean resting metabolic rate (RMR) was lower than predicted from standard equations based on healthy elderly subjects. The energy cost of physical activity plus thermogenesis was also low (1.7 ± 0.9 MJ/day) in all except one subject. The data refute the initial hypothesis and suggest that negative energy balance may be episodic, perhaps during periods of infection and subsequent recovery.
Article
Self-reported, dietary intake and biochemical estimates of thiamine, riboflavin, folate, vitamin B-12, protein, and iron were compared in 22, free-living elders by individuals who had senile dementia of the Alzheimer's type (SDAT) and in 41 who were cognitively normal (CN). The two groups did not differ significantly in their intake of these nutrients or the number of deficiency states for intake (less than 67% RDA). Low serum transketolase (thiamin; p less than 0.055), red blood cell (RBC) folate (p less than 0.06), and serum vitamin B-12 (p less than 0.05) levels occurred more often in SDAT patients than in CN subjects. Individuals in both groups who used multivitamin supplements had significantly higher biochemical values for thiamine (p less than 0.03), riboflavin (p less than 0.01), and vitamin B-12 (p less than 0.003) than nonsupplement users. Because of the differences in vitamin B-12 and RBC folate levels between groups, a retrospective analysis was performed on a larger group of subjects drawn from a geriatric assessment clinic. Patients with SDAT had significantly lower serum vitamin B-12 (p less than 0.01) and lower RBC folate (p less than 0.03) values than CN subjects. Which mean values for vitamin B-12 and RBC folate were grouped by degree of impairment in SDAT subjects, vitamin B-12 was significantly lower in mildly and moderately impaired subjects than in those with normal cognition. Mean values for both nutrients did not differ significantly between severely impaired and CN subjects. There was a significant quadratic relationship between cognitive impairment and biochemical values for vitamin B-12.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
Nutritional status, dietary intake, weight change, and mortality were studied in a sample of severely demented, institutionalized patients. Dietary intake was registered during five days in two periods, five weeks apart. A weighing method was used. Nutritional status was assessed by anthropometric measurements (weight for height index, triceps skinfold thickness, arm muscle circumference) and determination of circulating proteins (albumin, transferrin, and prealbumin). Energy and/or protein malnutrition was found in 50% of the patients. The mean dietary intake was sufficient according to energy (2059 kcallday), proteins, vitamins, and minerals. A comparison of patients with or without malnutrition showed no differences in dietary intake, diagnoses, age, length of hospital stay, or duration of illness. However, malnourished patients had had four times as many infectious periods treated by antibiotics as patients with no malnutrition. Thirty‐nine of 44 patients lost weight during their hospital stay. There was no correlation between loss of weight, length of hospital stay, or duration of illness.
Article
Nutritional assessments were performed in three groups of hospitalized elderly women comparable in age and mobility: a group with Alzheimer's disease (ALZ), a multi-infarct demèntia group (MID) and a nondemented group (ND). We have shown that: ALZ patients lose weight and on average weigh 21% less than ND patients and 14% less than MID patients. This weight loss is not accounted for by any obvious deficit in food intake, or by malabsorption. Biochemical indices of nutrition are little different in the three groups. The reason for weight loss in ALZ remains uncertain.
Article
To describe the incidence, anthropometric parameters, and clinical significance of weight loss in older outpatients. Four-year prospective cohort study. University-affiliated Veterans Affairs Medical Center. Two hundred forty-seven community-dwelling male veterans 65 years of age or older. Anthropometrics (weight, height, skin-folds, and circumferences), health status measures (Sickness Impact Profile scores, health care utilization, self-reported ratings of health), and bloodwork (cholesterol, albumin, others) were obtained at baseline and followed annually for 2 years. Outcome measures (hospitalization, nursing home placement, and mortality rates) were followed for a minimum of 2 years after any identified weight change. The mean annual percentage weight change for the study population was -0.5% (SD: +/- 4.0%; range: -17% to +25%). Four percent annual weight loss was determined to be the optimal cutpoint for defining clinically important involuntary weight loss using ROC curve analysis. The annual incidence of this degree of involuntary weight loss was 13.1%. At baseline, involuntary weight losers were similar to nonweight losers in age (73.9 +/- 7.9 vs 73.3 +/- 6.7 years), body mass index (26.8 +/- 3.9 vs 26.9 +/- 4.1 kg/m2), and all other anthropometric, health status, and laboratory measures. Relative to nonweight losers, involuntary weight losers had significantly (P < or = .05) greater decrements in central skinfold and circumference measures (subscapular skinfolds, -2.9 vs -0.4 mm; suprailiac skinfolds, -4.2 vs -0.2 mm; and waist to hip ratio, -.01 vs + .00). Both groups had significant decreases in their triceps skinfolds (an estimate of peripheral subcutaneous fat), whereas arm muscle area and albumin levels did not decline significantly in either group. Over a 2-year follow-up period, mortality rates were substantially higher (RR = 2.43; 95% CI = 1.34-4.41) among involuntary weight losers (28%) than among nonweight losers (11%). Of interest, a similar increase in 2-year mortality (36%) was also observed among subjects with voluntary weight loss (by dieting). Survival analyses adjusting for differences between weight losers and nonweight losers in baseline age, BMI, tobacco use, and other health status and laboratory measures yielded similar results. These results indicate that involuntary weight loss occurred frequently (13.1% annual incidence) in this population of older veteran outpatients. When involuntary weight loss occurred, the predominant anthropometric changes were decrements in measures of centrally distributed fat (trunkal skinfolds and circumferences). Finally, involuntary weight loss greater than 4% of body weight appears to be clinically important as an independent predictor of increased mortality.
Article
The debilitating consequences of age-related brain deterioration are widespread and extremely costly in terms of quality of life and longevity. One of the potential major causes of age-related destruction of neuronal tissue is toxic free radicals that are a natural result of aerobic metabolism. The brain is particularly susceptible to free radical attack because it generates more of these toxicants per gram of tissue than does any other organ. The major defense mechanisms the brain uses to combat reducing equivalents is via their enzymatic metabolism. The vitamin antioxidants, vitamin E (alpha-tocopherol in particular) and vitamin C (ascorbate), also aid in protecting the brain from oxidative stress by directly scavenging toxic radicals. A newly discovered, potentially highly important antioxidant in the brain is the indole melatonin. The pineal hormone melatonin is rapidly taken up by the brain. In vitro melatonin is more effective than glutathione in scavenging the highly toxic hydroxyl radical and also more efficient than vitamin E in neutralizing the peroxyl radical. Furthermore, it stimulates the main antioxidant enzyme of the brain, glutathione peroxidase. In vivo melatonin is a potent antioxidant and it lacks prooxidant actions.
Article
Intracerebroventricular injection of neuropeptide Y (NPY) has two effects on energy metabolism in addition to increased feeding: decreased brown fat thermogenesis and increased white fat lipoprotein lipase (LPL) enzymatic activity. We hypothesized that the paraventricular nucleus (PVN) of the hypothalamus is the controlling neural site for these responses. We further hypothesized that NPY stimulation at PVN would reduce gene expression for the critical brown fat thermogenic protein, uncoupling protein (UCP), and increase gene expression for the key white fat storage enzyme, LPL. In the first experiment, three groups of rats received injections every 6 h for 24 h (5 injections total) into the PVN:1) NPY (1 micrograms/1 microliters injection) and ad libitum food; 2) NPY (1 micrograms/1 microliters injection) and food restricted to control intake; 3) saline injection (1 microliter) and ad libitum food. Both NPY-treated groups showed significant reductions (P < 0.05) in brown fat UCP mRNA levels and marked stimulation of LPL mRNA levels relative to controls. In the second experiment, four groups of seven rats had NPY injected into the PVN:0 (vehicle control); 0.1 microgram; 0.5 microgram; and 1 microgram. Injections were made every 6 h for 24 h. There was a dose-related reduction in UCP mRNA produced by the NPY treatment. NPY treatment increased LPL mRNA, but a smooth dosing effect was not evident. The observation that NPY in the PVN can coordinate more than one component of energy metabolism is significant when considered with many reports of responsiveness of NPY activity in the arcuate nucleus-PVN neural circuit to perturbations of energy balance such as fasting and feeding, diabetes, and genetic obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
To determine the natural history of weight change and the occurrence of clinically significant weight loss in subjects with Alzheimer's disease (AD). Subjects with AD and cognitively normal older controls were recruited from 21 U.S. university medical centers that were participating in the Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Annual assessments were performed. Subjects with AD (n = 362) and controls (n = 317) with two or more weight measurements taken a year or more apart were included in this analysis. The average period of follow-up was > 2 years for both subjects with AD and controls. Four variables describing different aspects of weight change were defined: >/= 5% weigh loss, percent weight change/year, maximum percent weight loss over 1 year, and standard deviation of measurements/subject. Nearly twice as many subjects with AD experienced a weight loss of 5% or more when compared with controls (men P = .003 women P = .001). Surprisingly, a weight gain of 5% or more was also more common among AD cases. Overall, there was a tendency toward weight loss for both subjects with AD and controls, as measured by percent weight change/year. When other possible causes of weight loss were controlled using a multivariate model, a diagnosis of AD remained a significant predictor of >/= 5% weigh loss (P < .001), maximum percent weight loss over 1 year (P < .001), and standard deviation of measurements/subject (P < .001). A trend toward significance was noted for percent weight change/year (P = .07). Other than AD, very few of the possible confounders of this association remained significant predictors of weight change. In bivariate analysis, the severity of AD at entry correlated with percent weight change/year and standard deviation of measurements/subject. Additionally, the functional status of subjects with AD correlated with all four measures of weight change. Clinically important weight loss occurs more frequently among patients with AD than among cognitively normal control subjects. Instances of weight gain, periods of acute weight loss, and greater fluctuations in weight suggest that the natural history of weight change in AD may be characterized by dysfunction in body weight regulation. Further analysis is warranted regarding the relationship of severity of dementia, functional status, and other specific aspects of AD to weight change.
Article
There are reports of weight loss and low body mass index (BMI) in patients with AD.The mesial temporal cortex (MTC) is involved in feeding behavior and memory and is preferentially involved in AD. We studied 74 subjects, including 58 AD patients and 16 control subjects, to determine whether BMI is associated with atrophy of the MTC or other brain regions. We used MRI morphometric analysis to provide measures of regional brain atrophy. AD patients had significant brain atrophy in all measured brain regions, except the white matter, compared with normal control subjects. The MTC was the only brain region significantly associated with BMI in AD patients (r = 0.39, p = 0.003). Multiple-regression analysis indicated that addition of brain regions other than the MTC to the model did not significantly add to the prediction of BMI. We conclude that low BMI correlates best and specifically with MTC atrophy. This finding supports a connection between limbic system damage and low body weight in AD. NEUROLOGY 1996;46: 1585-1591
Article
It has previously been suggested that Alzheimer's disease patients have higher resting energy requirements than healthy individuals, which may contribute to their unexplained weight loss. We examined whether resting metabolic rate, the largest component of daily energy expenditure, is elevated in Alzheimer's patients compared with healthy older controls. Cross-sectional. General Clinical Research Center and Baltimore VA Medical Center. Twenty-five noninstitutionalized demented patients (74 +/- 8 years; mean +/- SD) with a wide range of Mini-Mental Examination scores (1 to 20) and 73 healthy older individuals (69 +/- 7 years). Resting metabolic rate was measured by indirect calorimetry, fat-free mass and fat mass by dual energy X-ray absorptiometry, and daily energy intake by food diaries. No differences in fat-free mass and fat mass were noted between Alzheimer's disease patients and healthy older controls. Resting metabolic rate was similar in Alzheimer's disease patients (5446 +/- 962 kJ/day) and healthy older individuals (5647 +/- 887 kJ/day). These results persisted when resting metabolic rate was statistically adjusted for differences in body composition and age. These results provide no evidence for an elevation in resting energy requirements in noninstitutionalized demented patients.
Article
To determine whether the weight loss associated with Alzheimer's disease precedes or follows the dementia. Older community-dwelling men (n = 134) and women (n = 165) were followed for 20 years before they were diagnosed as cognitively intact or demented. A repeated measures analysis was used to compare weight change in those who developed Alzheimer's Disease (AD) with those who remained cognitively intact. Weight was measured at three clinic visits between 1972-74, 1984-87, and 1990-93. Participants were classified as having probable or possible AD or being cognitively intact at the 1990-93 evaluation. Diagnoses were made by two neurologists and a neuropsychometrist, based on neuropsychological tests and physical examination, using NINCDS-ADRDA criteria. There were 36 men and 24 women diagnosed with probable or possible AD; they were considered to have mild to moderate dementia based on their test scores and community-dwelling status. Those who developed dementia were older than those diagnosed as cognitively intact. In age-adjusted analyses, both men and women who were later diagnosed with AD had a significant decrease in weight after the baseline visit (P < .001 and P < .003, respectively), but there was no significant weight loss in the men and women who remained cognitively intact. These differences were not explained by lifestyle, depression, or other illness. Weight loss precedes mild to moderate dementia; early weight loss is, therefore, unlikely to be a consequence of AD patients being unable or unwilling to eat.
Article
The main object of this review is to describe the most significant alterations of neuropeptide patterns occurring in the brain and in the cerebral spinal fluid of demented patients and particularly of elderly patients with Alzheimer type dementia. The changes in concentration in the different brain areas are described along with their peripheral endocrine implications. Alterations in the synthesis and release of neuropeptides may play a significant role in the pathogenesis of dementia in elderly patients, in addition to the well known changes in classical neurotransmitter systems. Measurements of neuropeptide levels in cerebrospinal fluid or postmortem brain material as alleged biological markers for the diagnostic purpose, however, have produced controversial results. Neuropeptide changes in the demented brain show regional differences and are not specific and selective enough to differentiate between senile dementia, Alzheimer type dementia and other degenerative disorders.
Article
Associations between nutritional status and cognitive performance were examined in 137 elderly (aged 66-90 y) community residents. Participants were well-educated, adequately nourished, and free of significant cognitive impairment. Performance on cognitive tests in 1986 was related to both past (1980) and concurrent (1986) nutritional status. Several significant associations (P < 0.05) were observed between cognition and concurrent vitamin status, including better abstraction performance with higher biochemical status and dietary intake of thiamine, riboflavin, niacin, and folate (rs = 0.19-0.29) and better visuospatial performance with higher plasma ascorbate (r = 0.22). Concurrent dietary protein in 1986 correlated significantly (rs = 0.25-0.26) with memory scores, and serum albumin or transferrin with memory, visuospatial, or abstraction scores (rs = 0.18-0.22). Higher past intake of vitamins E, A, B-6, and B-12 was related to better performance on visuospatial recall and/or abstraction tests (rs = 0.19-0.28). Use of self-selected vitamin supplements was associated with better performance on a difficult visuospatial test and an abstraction test. Although associations were relatively weak in this well-nourished and cognitively intact sample, the pattern of outcomes suggests some direction for further research on cognition-nutrition associations in aging.
Article
Weight loss is common in Alzheimer's disease (AD), but its pathogenesis is poorly understood. It is unclear whether an elevated daily energy expenditure contributes to the weight loss. We tested the hypothesis that daily energy expenditure is higher in AD patients compared to healthy elderly. Thirty AD (73 +/- 8 years; Mini-Mental State Examination score: 16 +/- 8) and 103 healthy elderly (69 +/- 7 years) were characterized for daily energy expenditure and its components (resting and free-living physical activity energy expenditure) from doubly labeled water and indirect calorimetry. Fat-free mass and fat mass were measured from dual energy X-ray absorptiometry. Fat-free mass tended to be lower in AD patients (45 +/- 9 kg) versus healthy elderly (49 +/- 10 kg; p = 0.07), whereas no differences were noted in fat mass between groups. Daily energy expenditure was 14% lower in AD (1901 +/- 517 kcal/d) compared to healthy elderly (2213 +/- 513 kcal/d; p < 0.001), due to lower resting (1287 +/- 227 versus 1418 +/- 246 kcal/d; p < 0.01) and physical activity energy expenditures (425 +/- 317 versus 574 +/- 342 kcal/d; p < 0.05). No differences in energy expenditure were noted between groups after controlling for differences in body composition. Daily energy expenditure was examined in a subgroup (n = 11) of AD patients who lost significant body weight (5.6 +/- 2.3 kg) within the past year. There was a lower daily energy expenditure in cachectic AD patients (1799 +/- 474 kcal/d) versus non-cachectic patients (1960 +/- 544 kcal/d) and healthy elderly (2213 +/- 513 kcal/d; p < 0.01). Similarly, no differences in energy expenditure were noted between groups after controlling for differences in body composition. We conclude that absolute levels of daily energy expenditure are lower in AD patients due to their lower body mass. However, after taking into account differences in body composition, daily energy expenditure in AD patients is appropriate for their metabolic size. The hypothesis that elevated daily energy expenditure contributes to weight loss in AD is not supported by these findings.
Article
A high intake of saturated fat and cholesterol and a low intake of polyunsaturated fatty acids have been related to an increased risk of cardiovascular disease. Cardiovascular disease has been associated with dementia. We investigated the association between fat intake and incident dementia among participants, age 55 years or older, from the population-based prospective Rotterdam Study. Food intake of 5,386 nondemented participants was assessed at baseline with a semiquantitative food-frequency questionnaire. At baseline and after an average of 2.1 years of follow-up, we screened for dementia with a three-step protocol that included a clinical examination. The risk of dementia at follow-up (RR [95% CI]) was assessed with logistic regression. After adjustment for age, sex, education, and energy intake, high intakes of the following nutrients were associated with an increased risk of dementia: total fat (RR = 2.4 [1.1-5.2]), saturated fat (RR = 1.9 [0.9-4.0]), and cholesterol (RR = 1.7 [0.9-3.2]). Dementia with a vascular component was most strongly related to total fat and saturated fat. Fish consumption, an important source of n-3 polyunsaturated fatty acids, was inversely related to incident dementia (RR = 0.4 [0.2-0.91), and in particular to Alzheimer's disease (RR = 0.3 [0.1-0.9]). This study suggests that a high saturated fat and cholesterol intake increases the risk of dementia, whereas fish consumption may decrease this risk.
Article
The goal of this study was to project the future prevalence and incidence of Alzheimer's disease in the United States and the potential impact of interventions to delay disease onset. The numbers of individuals in the United States with Alzheimer's disease and the numbers of newly diagnosed cases that can be expected over the next 50 years were estimated from a model that used age-specific incidence rates summarized from several epidemiological studies, US mortality rates, and US Bureau of the Census projections. in 1997, the prevalence of Alzheimer's disease in the United States was 2.32 million (range: 1.09 to 4.58 million); of these individuals, 68% were female. It is projected that the prevalence will nearly quadruple in the next 50 years, by which time approximately 1 in 45 Americans will be afflicted with the disease. Currently, the annual number of new incident cases in 360,000. If interventions could delay onset of the disease by 2 years, after 50 years there would be nearly 2 million fewer cases than projected; if onset could be delayed by 1 year, there would be nearly 800,000 fewer prevalent cases. As the US population ages, Alzheimer's disease will become an enormous public health problem. interventions that could delay disease onset even modestly would have a major public health impact.
Article
To describe weight loss in relation to the severity of Alzheimer's disease (AD), to identify confounders that might account for weight loss, and to investigate the association of weight change with mortality. This study included 666 subjects with AD from the Consortium to Establish a Registry for Alzheimer's Disease, a longitudinal study of subjects with AD studied for < or = 6 years. Body weight was measured on entry and at annual follow-up examinations as part of standardized clinical assessments. Hierarchical linear models were used to estimate weight change per change in stage of AD, as measured by the Clinical Dementia Rating scale, and to assess the impact of possible confounders on the tendency for weight loss. Linear correlation of the trajectories of weight and CDR over time were used to determine the association between weight change and stage change. The association between weight change and mortality was modeled using the Cox proportional hazards model. Each change in stage of AD was associated with an estimated average weight loss of nearly 2 lb (P = .0001). The correlation between change in stage of AD and weight change was statistically significant (r = -0.09, P = .005), which indicates a greater tendency toward weight loss with progression of AD. Weight loss of > or = 5% in any year before death was a significant predictor of mortality. When weight loss in the year before death or censoring was analyzed as a continuous variable, it was a significant predictor of mortality. Additionally, the relative risk of death increased as weight loss increased. In contrast, weight gain decreased the risk of mortality. The risk of weight loss tends to increase with severity and progression of AD. Weight loss is a predictor of mortality among subjects with AD, whereas weight gain appears to have a protective effect.
Article
Patients with advanced dementia frequently develop eating difficulties and weight loss. Enteral feeding tubes are often used in this situation, yet benefits and risks of this therapy are unclear. We searched MEDLINE, 1966 through March 1999, to identify data about whether tube feeding in patients with advanced dementia can prevent aspiration pneumonia, prolong survival, reduce the risk of pressure sores or infections, improve function, or provide palliation. We found no published randomized trials that compare tube feeding with oral feeding. We found no data to suggest that tube feeding improves any of these clinically important outcomes and some data to suggest that it does not. Further, risks are substantial. The widespread practice of tube feeding should be carefully reconsidered, and we believe that for severely demented patients the practice should be discouraged on clinical grounds.