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Evidence-based prevention of Alzheimer's disease: systematic review and meta-analysis of 243 observational prospective studies and 153 randomised controlled trials
- http://orcid.org/0000-0002-7686-0547Jin-Tai Yu1,
- http://orcid.org/0000-0002-3310-5875Wei Xu2,
- Chen-Chen Tan2,
- Sandrine Andrieu3,
- John Suckling4,
- Evangelos Evangelou5,
- An Pan6,
- Can Zhang7,
- Jianping Jia8,
- Lei Feng9,
- Ee-Heok Kua9,
- Yan-Jiang Wang10,
- Hui-Fu Wang2,
- Meng-Shan Tan2,
- Jie-Qiong Li2,
- Xiao-He Hou2,
- Yu Wan2,
- Lin Tan2,
- Vincent Mok11,
- Lan Tan2,
- Qiang Dong1,
- Jacques Touchon12,
- Serge Gauthier13,
- Paul S Aisen14,
- Bruno Vellas15
- Correspondence to Professor Jin-Tai Yu, Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai 200040, China; jintai_yu@fudan.edu.cn
Abstract
Background Evidence on preventing Alzheimer’s disease (AD) is challenging to interpret due to varying study designs with heterogeneous endpoints and credibility. We completed a systematic review and meta-analysis of current evidence with prospective designs to propose evidence-based suggestions on AD prevention.
Methods Electronic databases and relevant websites were searched from inception to 1 March 2019. Both observational prospective studies (OPSs) and randomised controlled trials (RCTs) were included. The multivariable-adjusted effect estimates were pooled by random-effects models, with credibility assessment according to its risk of bias, inconsistency and imprecision. Levels of evidence and classes of suggestions were summarised.
Results A total of 44 676 reports were identified, and 243 OPSs and 153 RCTs were eligible for analysis after exclusion based on pre-decided criteria, from which 104 modifiable factors and 11 interventions were included in the meta-analyses. Twenty-one suggestions are proposed based on the consolidated evidence, with Class I suggestions targeting 19 factors: 10 with Level A strong evidence (education, cognitive activity, high body mass index in latelife, hyperhomocysteinaemia, depression, stress, diabetes, head trauma, hypertension in midlife and orthostatic hypotension) and 9 with Level B weaker evidence (obesity in midlife, weight loss in late life, physical exercise, smoking, sleep, cerebrovascular disease, frailty, atrial fibrillation and vitamin C). In contrast, two interventions are not recommended: oestrogen replacement therapy (Level A2) and acetylcholinesterase inhibitors (Level B).
Interpretation Evidence-based suggestions are proposed, offering clinicians and stakeholders current guidance for the prevention of AD.
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Introduction
An unequivocal downtrend in the prevalence and incidence of dementia was recently reported and associated with earlier population-level investment (eg, improved education and vascular health),1–3 strengthening the necessity for primary prevention.4 The past few decades have witnessed great global efforts in updating and upgrading the evidence on how to prevent Alzheimer’s disease (AD),5 6 accounting for approximately two-thirds of all cases of dementia and affecting up to 20% of individuals older than 80 years.7 8 Nevertheless, key issues in the field are the inconsistency among conclusions and variable levels of credibility arising from the wide variety of study designs.9 Two types of studies are generally regarded as having the greatest impact on the extant literature: (1) observational prospective studies (OPSs), which describe temporal relationships with potential causal links and often use large samples recruited from community dwellers; and (2) randomised controlled trials (RCTs), which possess strong internal validity to infer causality by testing the effects of specific interventions on the incidence of AD. Although both approaches are useful, the major concerns in OPSs are usually the elusive sources of bias when interpreting the identified wide-ranging factors, and current RCTs are often compromised by short follow-up durations, subjective endpoints, small sample sizes and specific recruitment criteria with uncertain generalisability.5
Considerable evidence has been generated regarding AD through OPSs and RCTs. Because it is almost impossible to conduct RCTs that evaluate all risk factors of AD, a quantitative depiction of AD’s prevention 'profile' based on these two complementary study types is urgently needed for prevention guidelines that weigh the benefits against the risks. Deconstructing the bias sources from OPSs will facilitate the interpretation of credibility ratings and also guide future research directions. In this study we consolidated the extant evidence from both OPSs and RCTs to formulate the levels of evidence and classes of clinical suggestions for AD prevention.
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