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ESPEN Guidelines on Nutrition in Dementia

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ESPEN Guidelines on Nutrition in Dementia YCLNU2644_proof ■ 28 September 2015 ■ 1/23 Clinical Nutrition xxx (2015) 1e23 55 Contents lists available at ScienceDirect 56 57 Clinical Nutrition 58 59 60 journal homepage: http://www.elsevier.com/locate/clnu 61 62 63 e-SPEN guideline 64 65 1 Q7 ESPEN guidelines on nutrition in dementia 66 2 67 3 a, * b c d 68 Q6 Dorothee Volkert , Michael Chourdakis , Gerd Faxen-Irving , Thomas Frühwald , 4 e f g a, h 69 5 Francesco Landi , Merja H. Suominen , Maurits Vandewoude , Rainer Wirth , i 70 6 Stephane M. Schneider 71 7 a Institute for Biomedicine of Aging (IBA), Friedrich-Alexander-Universitat€ (FAU) Erlangen-Nürnberg, Nuremberg, Germany 72 8 b Department of Medicine, Aristotle University of Thessaloniki (AUTH), Greece 73 9 c Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden 74 10 d Department of Geriatric Acute Care, Krankenhaus Hietzing, Vienna, Austria e 75 11 Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart, Rome, Italy f Unit of Primary Health Care, Helsinki University Central Hospital, Helsinki, Finland 76 12 g Department of Geriatrics, Medical School, University of Antwerp, Belgium 77 13 h St. Marien-Hospital Borken, Department for Internal Medicine and Geriatrics, Borken, Germany 78 i 14 Nutritional Support Unit, Centre Hospitalier Universitaire de Nice, Nice, France 79 15 80 16 81 17 article info summary 82 18 83 19 Article history: Background: Older people suffering from dementia are at increased risk of malnutrition due to various 84 20 Received 20 August 2015 nutritional problems, and the question arises which interventions are effective in maintaining adequate Accepted 10 September 2015 85 21 nutritional intake and nutritional status in the course of the disease. It is of further interest whether fi 86 22 supplementation of energy and/or speci c nutrients is able to prevent further cognitive decline or even Keywords: fi fi 87 23 correct cognitive impairment, and in which situations arti cial nutritional support is justi ed. Guideline Objective: It is the purpose of these guidelines to cover these issues with evidence-based 88 24 Dementia recommendations. 89 25 Malnutrition 90 Nutritional support Methods: The guidelines were developed by an international multidisciplinary working group in 26 fi Nutritional interventions accordance with of cially accepted standards. The GRADE system was used for assigning strength of 91 27 evidence. Recommendations were discussed, submitted to Delphi rounds and accepted in an online 92 28 survey among ESPEN members. 93 29 Results: 26 recommendations for nutritional care of older persons with dementia are given. In every 94 30 person with dementia, screening for malnutrition and close monitoring of body weight are recom- 95 31 mended. In all stages of the disease, oral nutrition may be supported by provision of adequate, attractive 96 food in a pleasant environment, by adequate support and elimination of potential causes of malnutrition. 32 97 Supplementation of single nutrients is not recommended unless there is a sign of deficiency. Oral 33 98 34 nutritional supplements are recommended to improve nutritional status but not to correct cognitive impairment or prevent cognitive decline. Artificial nutrition is suggested in patients with mild or 99 35 moderate dementia for a limited period of time to overcome a crisis situation with markedly insufficient 100 36 oral intake, if low nutritional intake is predominantly caused by a potentially reversible condition, but 101 37 not in patients with severe dementia or in the terminal phase of life. 102 38 Conclusion: Nutritional care and support should be an integral part of dementia management. In all 103 39 stages of the disease, the decision for or against nutritional interventions should be made on an indi- 104 40 vidual basis after carefully balancing expected benefit and potential burden, taking the (assumed) patient 105 41 will and general prognosis into account. 106 © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. 42 107 43 108 44 109 45 110 46 111 47 112 48 Abbreviations: AD, Alzheimer's disease; APOE, apolipoprotein E-e4 allele; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; MCI, mild cognitive impairment; MNA, 113 49 mini nutritional assessment; MNA-SF, mini nutritional assessment short form; MMSE, mini mental state examination; RCT, randomized controlled trial. 114 50 * Corresponding author. Institute for Biomedicine of Aging (IBA), Friedrich-Alexander-Universitat€ (FAU) Erlangen-Nürnberg, Kobergerstraße 60, 90408 Nürnberg, Germany. 115 þ 51 Tel.: 49 911 5302 96150. 116 E-mail address: [email protected] (D. Volkert). 52 117 53 http://dx.doi.org/10.1016/j.clnu.2015.09.004 118 54 0261-5614/© 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. 119 Please cite this article in press as: Volkert D, et al., ESPEN guidelines on nutrition in dementia, Clinical Nutrition (2015), http://dx.doi.org/ 10.1016/j.clnu.2015.09.004 YCLNU2644_proof ■ 28 September 2015 ■ 2/23 2 D. Volkert et al. / Clinical Nutrition xxx (2015) 1e23 1 1. Development of guidelines on nutrition in dementia Table 2 66 2 Strength of recommendation. 67 3 Q1 The European Society for Clinical Nutrition and Metabolism Strength of recommendation 68 4 69 (ESPEN) launched a process of developing guidelines on nutrition Strong We recommend/do not recommend 5 care for patients with dementia. The group included physicians, Weak We suggest/do not suggest 70 6 nutritionists and dietitians with a background in geriatrics, nutri- 71 7 tion and/or ethics, all experienced in treatment and nutritional 72 8 therapy of persons with dementia, as well as the guidelines coor- more common, but it is not normal healthy aging and it is not 73 9 dinator (SMS); all are authors of this guideline document. benign. It is a malignant and devastating condition leading invari- 74 10 The experts followed the GRADE method, which was based on ably to dependence and finally death [4]. As a clinical syndrome, it 75 11 determinations of grade of evidence and strength of recommenda- is characterized by global cognitive impairment with a decline in 76 12 tion; the methodology is described elsewhere [1]. A two-day live memory and at least in one other cognitive domain, such as lan- 77 13 meeting was organized in Biedenkopf, Germany, in April of 2014, guage, visuospatial, or executive function. It represents a decline 78 14 and three phone conferences were held. from the previous level of cognitive functioning, and is associated 79 15 Descriptive findings that did not lead to specific recommenda- with impairment in functional abilities and, in many cases, 80 16 tions are grouped in a first part (general considerations), whereas behavioral and psychiatric disturbances [5,6]. Many diseases can 81 17 all questions that led to comparisons of interventions and to rec- cause a dementia syndrome; Alzheimer's disease and cerebrovas- 82 18 ommendations are grouped in a second part (recommendations). cular dementia are the two most common causes, and many cases 83 19 A systematic literature search was conducted in PubMed and the of dementia involve both these disorders. Lewy body disorders 84 20 Cochrane Library. The grade of evidence (GOE) was determined by a (Parkinson's disease and dementia with Lewy bodies) and fronto- 85 21 number of factors, starting with the number and type of research temporal dementia are less common but still make up 8% of peo- 86 22 studies [2]. Grading from High to Very Low was used to rate the ple referred to a memory clinic [5]. Although some potentially 87 23 quality of the underlying evidence and the level of certainty for reversible conditions, such as hypothyroidism or vitamin B12 defi- 88 24 effect (Table 1) [3]. Highest quality evidence resulted from consis- ciency, are often thought to cause dementia, no more than 1.5% of 89 25 tent results or meta-analysis of multiple randomized controlled cases of mild to moderate dementia are fully reversible. Age is the 90 26 trials, with the next highest level defined by at least one well- best-studied and strongest risk factor for dementia, which explains 91 27 designed randomized controlled trial. Moderate and low-level ev- the increasing burden of cognitive disorders in the years to come 92 28 idence came from controlled trials that were not randomized, from [7]. Other risk factors for Alzheimer's disease include genetic risk 93 29 cohort- or case-controlled studies, or from multiple time series factors such as having a first-degree relative with a history of Alz- 94 30 trials. Very low-level evidence was from expert clinical experience heimer's disease, having the apolipoprotein ε4 genotype or 95 31 or from descriptive studies. The grade was then decreased if there suffering from the Down syndrome. Cardiovascular risk factors 96 32 were limitations to study quality, inconsistencies in findings, such as hypertension are associated with an increased risk for both 97 33 imprecise or sparse data, or high likelihood of reporting bias. The Alzheimer's disease and vascular dementia. Also lifestyle factors 98 34 grade was increased if there was high consistency of findings or such as low educational level or head trauma may play an impor- 99 35 strong evidence of association (Table 1). tant role [7]. 100 36 The strength of recommendation was based on a consensus dis- Dementia causes a high burden of suffering for patients, their 101 37 cussion, which included expression and deliberation of expert families, and society [8]. For patients, it leads to increased anxiety, 102 38 opinions, risk-benefit ratio of recommendation, costs, and a review depression and dependency and complicates other comorbid con- 103 39 of supportive evidence, followed by Delphi rounds and votes until ditions.
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