Smoking is a possible risk factor for dementia, although its impact may have been underestimated in elderly populations because of the shorter life span of smokers.
To examine the association between smoking history and cognitive decline in the transition from midlife to old age.
The Whitehall II study. The first cognitive assessment was in 1997 to 1999, repeated over 2002 to 2004 and 2007 to 2009.
Data are from 5099 men and 2137 women in the Whitehall II study, mean age 56 years (range, 44-69 years) at the first cognitive assessment.
The cognitive test battery was composed of tests of memory, vocabulary, executive function (composed of 1 reasoning and 2 fluency tests), and a global cognitive score summarizing performance across all 5 tests. Smoking status was assessed over the entire study period. Linear mixed models were used to assess the association between smoking history and 10-year cognitive decline, expressed as z scores.
In men, 10-year cognitive decline in all tests except vocabulary among never smokers ranged from a quarter to a third of the baseline standard deviation. Faster cognitive decline was observed among current smokers compared with never smokers in men (mean difference in 10-year decline in global cognition=-0.09 [95% CI, -0.15 to -0.03] and executive function=-0.11 [95% CI, -0.17 to -0.05]). Recent ex-smokers had greater decline in executive function (-0.08 [95% CI, -0.14 to -0.02]), while the decline in long-term ex-smokers was similar to that among never smokers. In analyses that additionally took dropout and death into account, these differences were 1.2 to 1.5 times larger. In women, cognitive decline did not vary as a function of smoking status.
Compared with never smokers, middle-aged male smokers experienced faster cognitive decline in global cognition and executive function. In ex-smokers with at least a 10-year cessation, there were no adverse effects on cognitive decline.
"Correspondingly , CNS OxS and inflammation tend to occur in tandem in many diseases/disorders, including AD, atherosclerosis, alcohol/substance use disorders, and cigarette smoking (Butterfield et al., 2013; Crews and Nixon, 2009; Durazzo et al., 2010; Enciu et al., 2013; Gill et al., 2010; Khandelwal et al., 2011; Khanna et al., 2013). Animal models and human post-mortem studies indicate that cigarette smoking-induced OxS promotes brain tissue damage via lipid peroxidation and proteolysis (Anbarasi et al., 2005, 2006; Ho et al., 2012; Khanna et al., 2013; Rueff-Barroso et al., 2012; Sonnen et al., 2009; Tyas et al., 2003). Since smoking is a risk factor for AD, it is possible that smoking-induced OxS increases the risk for ADlike neuropathological changes; however, there are no published in vivo studies that have specifically compared human smokers and non-smokers on CNS-derived biomarkers of cerebral OxS. "
[Show abstract][Hide abstract] ABSTRACT: Background
Cigarette smoking in adults is associated with abnormalities in brain neurobiology. Smoking-induced central nervous system oxidative stress (OxS) is a potential mechanism associated with these abnormalities. The goal of this study was to compare cognitively-normal elders on cerebrospinal fluid (CSF) levels of F2-isoprostane biomarkers of OxS.
Elders with a lifetime history of smoking (smokers; n = 50; 75 ± 5 years of age; 34 ± 28 pack-years; approximately 12% were actively smoking at the time of study) were compared to never-smokers (n = 61; 76 ± 6 years of age) on CSF iPF2α-III and 8,12, iso-iPF2α-VI F2-isoprostanes levels. F2-isoprostanes levels were quantitated with HPLC-atmospheric pressure chemical ionization-tandem mass spectrometry. Associations between F2-isoprostanes levels, hippocampal volumes, and cigarette exposure measures were also evaluated.
Smokers showed higher iPF2α-III level than never-smokers. An age x smoking status interaction was observed for 8,12, iso-iPF2α-VI, where smokers demonstrate a significantly greater concentration with increasing age than non-smokers. In smokers only, higher 8,12, iso-iPF2α-VI concentration was associated with smaller hippocampal volume, and greater iPF2α-III level was related to greater pack years.
This is the first study to demonstrate that a history of cigarette smoking in cognitively-normal elders was associated with significantly elevated CSF F2-isoprostane levels and greater age-related increases in F2-isoprostane levels, and that higher F2-isoprostane levels in smokers were related to smaller hippocampal volume. These findings provide additional novel evidence that a history of chronic smoking during adulthood is associated with adverse effects on the human brain that are potentially persistent even with extended smoking cessation.
Drug and Alcohol Dependence 09/2014; 142. DOI:10.1016/j.drugalcdep.2014.06.030 · 3.42 Impact Factor
"Even non - deprived smokers showed poorer cognitive performance compared to never - smokers ( see introduction ) . Furthermore , Kalmijn and colleagues ( Kalmijn et al , 2002 ) showed that smoking is negatively correlated with cognitive performance and more recent , the Whitehall II study provides evidence that at least in males , smoking leads to faster cognitive declines ( Sabia et al , 2012 ) . For the first time we identified significant structural deficits in the olfactory gyrus of current - smokers . "
[Show abstract][Hide abstract] ABSTRACT: Nicotine modulates prefrontal processing when tested with functional imaging. Previous studies on changes in regional brain volumes in small samples, reporting different life-time exposure to nicotine, identified reduced volume in smokers in prefrontal areas, but reported controversial results for other areas. We investigated the association of cigarette smoking and regional gray and white matter volume by using voxel based morphometry (VBM) for T1-weighted high resolution magnetic resonance imaging in 315 current-smokers and 659 never-smokers from the representative Study of Health in Pomerania (SHIP). Our study showed that in current-smokers smoking is significantly associated with gray matter volume loss in the prefrontal cortex, the anterior cingulate cortex, the insula and the olfactory gyrus. White matter volumes were not relevantly reduced in current-smokers. In current-smokers, we found associations of gray matter loss and smoking exposure (pack-years) in the prefrontal cortex, the anterior and middle cingulate cortex and the superior temporal and angular gyrus, which however did not stand corrections for multiple testing. We confirmed associations between smoking and gray matter differences in the anterior cingulate cortex and the insula in the general population of Pomerania (Germany). For the first time, we identified differences in brain volumes in the olfactory gyrus. Other cerebral regions did not show significant differences when correcting for multiple comparisons within the whole brain. The regions of structural deficits might be involved in addictive behavior and withdrawal symptoms, whereas further investigations have to show if the observed atrophies were caused by smoking itself or are preexisting differences between smoking and non-smoking individuals.Neuropsychopharmacology accepted article preview online, 16 May 2014; doi:10.1038/npp.2014.112.
Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 05/2014; 39(11). DOI:10.1038/npp.2014.112 · 7.05 Impact Factor
"In addition to conflicting results between men and women, many of the studies assessing cognitive function and lifestyle have not assessed the independent effects of all three lifestyle factors together   , or have not adjusted for important confounders including socio-demographic status , measures of health such as obesity and metabolic abnormalities , or potential effect modifiers, such as the genetic risk of dementia determined by apolipoproteinE-4 allele (ApoE-4) presence which may  or may not  have negative effects for drinking and protective effects for smoking . Additionally, most studies have been either cross-sectional  or had relatively short follow-up periods   . "
[Show abstract][Hide abstract] ABSTRACT: Background: Smoking, excessive drinking, and physical inactivity are associated with reduced cognitive function but the independence, domain specific cognitive effects, and trajectories of these associations are not firmly established. Objective: Our aim was to examine these lifestyle-cognitive function associations in middle-to-older aged women across time. Methods: Cohort study design with repeat surveys (2001, 2005, and 2008). Participants were volunteers from a random sample of Australian women on the Brisbane electoral roll; mean (±SD) age 60 ± 11 years in 2001. Outcome measures were the Mini-Mental State Examination (MMSE), Auditory Delayed Index (ADI), Visual Delayed Index (VDI), Working Memory Index (WMI), and Processing Speed Index (PSI). Results: 489 women completed cognitive testing in 2001, 451 in 2005, and 376 in 2008. Mean (±SD) cognitive scores in 2001 were MMSE: 29.1 ± 1.2, ADI: 104.6 ± 13.4, VDI: 107.2 ± 14.0, WMI: 104.1 ± 12.3, and PSI: 102.7 ± 11.8. Multivariate adjusted mean scores (95% CI) over the 7-year study period were higher for moderate drinkers than non-drinkers for the MMSE (β = 0.32; 0.04, 0.61), the VDI (β = 4.33; 0.96, 7.70), and the WMI (β = 3.21; 0.34,6.07). Current smokers performed worse than never-smokers for the MMSE (β = -0.35; 0.64, -0.06), the VDI (β = -3.91; -7.57, -0.26), the WMI (β = -3.42; -6.67, -0.18), and the PSI (β = -5.89; -8.91, -2.87). PSI was higher in women performing strenuous physical activity compared to inactive women (β = 2.14; 0.37, 3.90). None of the three lifestyle parameters influenced the changes in cognition across time. Conclusions: Alcohol and exercise were associated with selective protective effects and tobacco with selective harmful effects on cognitive function in middle-to-older aged women. Associations remained consistent across time.
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