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      Biomarker assessment of tobacco smoking exposure and risk of dementia death: pooling of individual participant data from 14 cohort studies

      , , , ,   , ,  
      Journal of Epidemiology and Community Health
      BMJ
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          Abstract

          Background

          While there is a suggestion that self-reported tobacco smoking may be a risk factor for dementia, to date, it has not been possible to explore the thresholds at which this exposure elevates risk. Accordingly, our aim was to relate cotinine, a biomarker of tobacco smoking, to risk of dementia death.

          Methods

          We pooled 14 prospective cohort studies that held data on cotinine (plasma or saliva), covariates and death records.

          Results

          In the 33 032 study members (17 107 women) with salivary cotinine data, a mean duration of 8.3 years of follow-up gave rise to 135 deaths ascribed to dementia; while in 15 130 study members (7995 women) with plasma cotinine data, there were 119 dementia deaths during 14.3 years of mortality surveillance. After multiple adjustment, both plasma cotinine (per 1 SD higher cotinine; 95% CI 1.29; (1.05 to 1.59)) and salivary cotinine (1.10 (0.89 to 1.36)) were positively related to dementia risk, with stronger effects apparent for plasma.

          Conclusion

          Our finding that plasma cotinine was related to an elevated risk of dementia death warrants testing in studies with measures of disease onset as opposed to just mortality.

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          Most cited references9

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          Cardiovascular effects of secondhand smoke: nearly as large as smoking.

          Secondhand smoke increases the risk of coronary heart disease by approximately 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system--platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size--is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
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            Risk factors and preventive interventions for Alzheimer disease: state of the science.

            Numerous studies have investigated risk factors for Alzheimer disease (AD). However, at a recent National Institutes of Health State-of-the-Science Conference, an independent panel found insufficient evidence to support the association of any modifiable factor with risk of cognitive decline or AD. To present key findings for selected factors and AD risk that led the panel to their conclusion. An evidence report was commissioned by the Agency for Healthcare Research and Quality. It included English-language publications in MEDLINE and the Cochrane Database of Systematic Reviews from 1984 through October 27, 2009. Expert presentations and public discussions were considered. Study inclusion criteria for the evidence report were participants aged 50 years and older from general populations in developed countries; minimum sample sizes of 300 for cohort studies and 50 for randomized controlled trials; at least 2 years between exposure and outcome assessment; and use of well-accepted diagnostic criteria for AD. Included studies were evaluated for eligibility and data were abstracted. Quality of overall evidence for each factor was summarized as low, moderate, or high. Diabetes mellitus, hyperlipidemia in midlife, and current tobacco use were associated with increased risk of AD, and Mediterranean-type diet, folic acid intake, low or moderate alcohol intake, cognitive activities, and physical activity were associated with decreased risk. The quality of evidence was low for all of these associations. Currently, insufficient evidence exists to draw firm conclusions on the association of any modifiable factors with risk of AD.
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              Socioeconomic status as a risk factor for dementia death: individual participant meta-analysis of 86 508 men and women from the UK.

              Life-course socioeconomic factors may have a role in dementia aetiology but there is a current paucity of studies. Meta-analyses of individual participant data would considerably strengthen this evidence base. To examine the association between socioeconomic status in early life and adulthood with later dementia death. Individual participant meta-analysis of 11 prospective cohort studies (1994-2004, n = 86 508). Leaving full-time education at an earlier age was associated with an increased risk of dementia death in women (fully adjusted hazard ratio (HR) for age ≤14 v. age ≥16: HR = 1.76, 95% CI 1.23-2.53) but not men. Occupational social class was not statistically significantly associated with dementia death in men or women. Lower educational attainment in women was associated with an increased risk of dementia-related death independently of common risk behaviours and comorbidities.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Journal of Epidemiology and Community Health
                J Epidemiol Community Health
                BMJ
                0143-005X
                1470-2738
                May 10 2018
                June 2018
                June 2018
                January 24 2018
                : 72
                : 6
                : 513-515
                Article
                10.1136/jech-2017-209922
                29367284
                72da30b0-aff4-4f34-b721-c7f31540aefe
                © 2018
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