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Neurotoxic chemicals in adipose tissue: A role in puzzling findings on obesity and dementia
Kyungpook Natl Univ, Sch Med, Dept Prevent Med, Daegu, South Korea.
Univ Autonoma Barcelona, Sch Med, Hosp del Mar, Inst Med Res IMIM, Barcelona, Spain.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.ORCID iD: 0000-0003-2335-8542
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.ORCID iD: 0000-0002-8949-3555
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2018 (English)In: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 90, no 4, p. 176-182Article in journal (Refereed) Published
Abstract [en]

Midlife obesity is associated with increased risk of dementia, whereas late-life obesity is commonly associated with a lower risk of dementia. Although methodologic issues are often discussed in this apparent risk reversal, chronic exposure to low-dose organochlorine pesticides (OCPs), an emerging risk factor for dementia in general populations, may contribute to a direct explanation for these differences. OCPs are strong lipophilic chemicals with very long half-lives (several years), primarily stored in adipose tissue and very slowly released and metabolized over years. As serum concentrations of neurotoxic OCPs strongly correlate with brain OCPs (r = 0.95), any condition enhancing the release of OCPs from the adipose tissue into circulation would increase the risk of dementia. Increased release of OCPs from adipose tissue typically occurs in (1) dysfunctional adipocytes accompanied by uncontrolled lipolysis and (2) weight loss. Weight gain may help sequester circulating OCPs in adipose tissue. As obesity is the most common reason that adipocytes become dysfunctional, midlife obesity can increase dementia risk through the chronic release of OCPs into circulation. However, late-life obesity potentially decreases dementia risk because weight loss after midlife will increase the release of OCPs while weight gain may actually decrease the release. These countervailing forces may underlie paradoxical associations with dementia of obesity in midlife vs late life which is influenced by weight change after midlife. This hypothesis should be tested in future experimental and human studies on obesity and dementia.

Place, publisher, year, edition, pages
2018. Vol. 90, no 4, p. 176-182
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Occupational Health and Environmental Health Neurosciences
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URN: urn:nbn:se:uu:diva-348561DOI: 10.1212/WNL.0000000000004851ISI: 000427799500018PubMedID: 29358509OAI: oai:DiVA.org:uu-348561DiVA, id: diva2:1197941
Available from: 2018-04-16 Created: 2018-04-16 Last updated: 2018-05-31Bibliographically approved

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