Obesity and Alzheimer's Disease

By Chang, C. L. | Hong Kong Journal of Psychiatry, March 2008 | Go to article overview

Obesity and Alzheimer's Disease


Chang, C. L., Hong Kong Journal of Psychiatry


Abstract

Objectives: To review existing literature on obesity and Alzheimer's disease and evaluate evidence of an association between them.

Methods: A selected review of the epidemiologic studies published from 1987 to June 2007 from MEDLINE, EMBASE, PsychoINFO, and Cochrane Database about the relationship between obesity and Alzheimer's disease.

Results: There was some evidence that obesity may increase the risk of Alzheimer's disease; the association was stronger for midlife than late-life obesity.

Conclusions: Preliminary evidence indicates that obesity is a risk factor of Alzheimer's disease. Further large-scale, lifetime assessments are suggested to confirm the association and formulate effective measures to delay the onset of Alzheimer's disease.

Key words: Alzheimer disease; Dementia; Epidemiologic studies; Obesity; Risk factors

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Introduction

In November 1906, Alois Alzheimer described the classical case of dementia as exhibiting typical clinical features with severe cognitive disturbances, delusions, and unpredictable behaviour. Neuropathological findings included military bodies (amyloid plaques) and dense bundles of fibrils (neurofibrillary tangles). In 1910, Kraepelin named this dementia as Alzheimer's disease (AD). (1) According to the Global Burden of Disease estimates for the 2003 World Health Report, (2) dementia contributed 11.2% of years lived with disability in people aged 60 years and older. Alzheimer's disease accounts for 50-60% of all patients with dementia, responsible for increasingly significant morbidity and mortality and ranked as the eighth leading cause of death among the elderly in the USA. (3)

Over the last century, we have gained more understanding about AD. The amyloid plaques and neurofibrillary tangles were found to develop as early as in the third decade. (4) The need for a life course approach to understanding the causes of AD was recognised because the consequences and timing of AD are relevant throughout life. There is increasing evidence that vascular risk factors, such as hypertension, (5-7) high cholesterol levels, (7,8) and diabetes mellitus (9,10) are also relevant, which often occur together with obesity. However, to date, there is no agreement on the association between obesity and AD. (11,12) Postulated explanations for an association include the coincidence of these common disorders in the elderly, vascular and cerebrovascular diseases precipitating AD, an additive or synergistic pathogenesis of dementia, and misdiagnosis of vascular dementia and AD.

Obesity is a potentially remediable risk factor for many diseases, through lifestyle interventions. (13) Moreover, numerous pharmacological and surgical treatments are also available. (14-17) If obesity is a risk factor for AD, potentially it is modifiable. In this review, we examine the current literature and discuss the relationships between obesity and AD.

Obesity is a complex, multifactorial chronic health condition, characteristically giving rise to increased morbidity and mortality. The discovery of leptin and other hormones affecting fat has led to the concept that adipose tissue is an endocrine organ and not merely an energy storage depot. Body mass index (BMI) is currently the most common measure of general obesity, calculated as the body weight in kilograms divided by the square of body height in metres. In 1993, a WHO (World Health Organization) expert committee proposed BMI cut-off points of 25.0-29.9 kg/[m.sup.2] for overweight grade 1, 30.0 to 39.9 kg/[m.sup.2] for grade 2, and 40.0 kg/[m.sup.2] or higher for grade 3. (18) Body mass index also reflects the risk for type 2 diabetes and cardiovascular disease. However, the cut-off points are affected by age and ethnicity. Body mass index is less useful in bodybuilders who have high BMI due to their muscular builds rather than fat. …

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