scholarly journals Cigarette smoking and cerebral blood flow in a cohort of middle-aged adults

2018 ◽  
Vol 39 (7) ◽  
pp. 1247-1257 ◽  
Author(s):  
Martine Elbejjani ◽  
Reto Auer ◽  
Sudipto Dolui ◽  
David R Jacobs ◽  
Thaddeus Haight ◽  
...  

Cigarette smoking is often associated with dementia. This association is thought to be mediated by hypoperfusion; however, how smoking behavior relates to cerebral blood flow (CBF) remains unclear. Using data from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort (mean age = 50; n = 522), we examined the association between smoking behavior (status, cumulative pack-years, age at smoking initiation, and years since cessation) and CBF (arterial spin labeling) in brain lobes and regions linked to dementia. We used adjusted linear regression models and tested whether associations differed between current and former-smokers. Compared to never-smokers, former-smokers had lower CBF in the parietal and occipital lobes, cuneus, precuneus, putamen, and insula; in contrast, current-smokers did not have lower CBF. The relationship between pack-years and CBF was different between current and former-smokers ( p for interaction < 0.05): Among current-smokers, higher pack-years were associated with higher occipital, temporal, cuneus, putamen, insula, hippocampus, and caudate CBF; former-smokers had lower caudate CBF with increasing pack-years. Results show links between smoking and CBF at middle-age in regions implicated in cognitive and compulsive/addictive processes. Differences between current and former smoking suggest that distinct pathological and/or compensatory mechanisms may be involved depending on the timing and history of smoking exposure.

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Douglas Levy ◽  
Sydney L Goldberg ◽  
Emily P Hyle ◽  
Krishna P Reddy

Background: The AHA’s 2030 Impact Goals seek to increase population health-adjusted life expectancy (LE) by 2y. Tobacco is a top contributor to all-cause mortality and cardiovascular disease (CVD). We estimated the potential contribution of improved tobacco control to achieve the 2030 Impact Goals in the US. Methods: We used the validated STOP microsimulation model with NHIS estimates of age- and sex-stratified mortality and CVD incidence to project changes in LE, as well as 10y, 20y, and lifetime CVD cumulative incidence, if cigarette smoking declined among the current US population. We assessed the impact of preventing initiation (current v never smokers) or increasing cessation (current v former smokers) at different ages. To examine the maximum impact of population-wide cessation, we projected changes in population LE and CVD incidence if smoking prevalence among those ≥20yo went immediately to 0%. Results: Preventing smoking initiation increases LE by 10.2y (men [M]) and 9.1y (women [W]) and reduces lifetime CVD incidence by 16.8% (M) and 26.2% (W) compared to lifetime smoking. Even cessation at age 60 extends LE by 3.7y (M) and 2.5y (W) and reduces 10y CVD incidence by 39.1% (M) and 59.4% (W) (Table). Total elimination of cigarette smoking in the 2020 US population aged ≥20y (e.g. by outlawing cigarettes) would increase the cohort LE by 0.4 (M) and 0.2 (W) years and reduce 20y CVD incidence by 6.0% (M) and 7.0% (W). Conclusion: Preventing smoking initiation offers the greatest benefit, but cessation at any age substantially improves LE and reduces CVD risk. The modest potential contribution of tobacco elimination to achieving the 2030 Impact Goals is due to already low smoking prevalence: <14% (projected) in 2020.


2020 ◽  
Vol 40 (4) ◽  
pp. 904-905
Author(s):  
Olaf B Paulson ◽  
Ida Vigdis

Cigarette smoking increases cerebral blood flow. Both nicotine and carbon monoxide contribute to the flow increase. Due to carbon monoxide’s high affinity to hemoglobin and slow clearance from the blood, the effect lasts for hours. Nicotine also stays in the organism for some hours. This immediate effect of smoking may explain a recently observed higher cerebral blood flow in current-smokers as compared to former-smokers.


2019 ◽  
Vol 22 (8) ◽  
pp. 1404-1408 ◽  
Author(s):  
Andrea H Weinberger ◽  
Cristine D Delnevo ◽  
Katarzyna Wyka ◽  
Misato Gbedemah ◽  
Joun Lee ◽  
...  

Abstract Introduction Despite increasing use of cannabis, it is unclear how cannabis use is related to cigarette transitions. This study examined cannabis use and smoking initiation, persistence, and relapse over 1 year among a nationally representative sample of US adults. Methods Data were from US adults (≥18 years) who completed two waves of longitudinal data from the Population Assessment of Tobacco and Health Study (Wave 1, 2013–2014; Wave 2, 2014–2015; n = 26 341). Logistic regression models were used to calculate the risk of Wave 2 incident smoking among Wave 1 never-smokers, smoking cessation among Wave 1 smokers, and smoking relapse among Wave 1 former smokers by Wave 1 cannabis use. Analyses were adjusted for age, gender, race/ethnicity, income, and education. Results Among Wave 1 never-smokers, cannabis use was associated with increased odds of initiation of nondaily (adjusted odds ratio [AOR] = 5.50, 95% confidence limits [CL] = 4.02–7.55) and daily cigarette smoking (AOR = 6.70, 95% CL = 4.75–9.46) 1 year later. Among Wave 1 daily smokers, cannabis use was associated with reduced odds of smoking cessation (AOR = 0.36, 95% CL = 0.20–0.65). Among Wave 1 former smokers, cannabis use was associated with increased odds of relapse to daily and nondaily cigarette smoking (daily AOR = 1.90, 95% CL = 1.11–3.26; nondaily AOR = 2.33, 95% CL = 1.61–3.39). Conclusions Cannabis use was associated with increased cigarette smoking initiation, decreased smoking cessation, and increased smoking relapse among adults in the United States. Increased public education about the relationship between cannabis use and cigarette smoking transitions may be needed as cannabis use becomes more common among US adults. Implications As cannabis use increases in the United States and other countries, an evaluation of the relationships of cannabis use to other health-related behaviors (eg, cigarette smoking) is needed to understand the population-level impact of legalization. Little is known about associations between cannabis use and cigarette smoking transitions (1) using recent longitudinal data, (2) among adults, and (3) examining transitions other than smoking initiation (eg, smoking relapse). Our results suggest that among US adults, cannabis use was associated with increased cigarette smoking initiation among never-smokers, decreased cigarette smoking cessation among current smokers, and increased cigarette smoking relapse among former smokers.


2007 ◽  
Vol 28 (2) ◽  
pp. 412-419 ◽  
Author(s):  
Meike W Vernooij ◽  
Aad van der Lugt ◽  
Mohammad Arfan Ikram ◽  
Piotr A Wielopolski ◽  
Henri A Vrooman ◽  
...  

Reduced cerebral perfusion may contribute to the development of cerebrovascular and neurodegenerative diseases. Little is known on cerebral perfusion in the general population, as most measurement techniques are too invasive for application in large groups of healthy individuals. Total cerebral blood flow (tCBF) can be noninvasively measured by magnetic resonance imaging (MRI) but is highly correlated with brain volume. We calculated total brain perfusion by dividing tCBF by brain volume, and we investigated determinants of total brain perfusion in comparison with tCBF. Secondly, we studied whether persons with a low tCBF or low total brain perfusion have a larger volume of white matter lesions (WML). This study is based on 892 persons aged 60 to 91 years from the Rotterdam Study, a population-based cohort study. We performed two-dimensional (2D) phase-contrast MRI for tCBF measurement. Brain volume and WML volume were quantitatively assessed. Cardiovascular determinants were assessed by interview and physical examination. We assessed associations between cardiovascular determinants and flow measures with linear regression models, adjusted for age and sex. Associations between tCBF or total brain perfusion and WML volume were assessed using general linear models. We found that determinants of tCBF and total brain perfusion differed largely due to the large influence of brain volume on tCBF values. Persons with low total brain perfusion had a significantly larger WML volume compared with those with high total brain perfusion. Prospective studies are required to unravel whether hypoperfusion contributes to WML formation or that tissue damage, manifested by WML, leads to brain hypoperfusion.


2001 ◽  
Vol 280 (6) ◽  
pp. H2591-H2597 ◽  
Author(s):  
A. Rebel ◽  
C. Lenz ◽  
H. Krieter ◽  
K. F. Waschke ◽  
K. Van Ackern ◽  
...  

We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity (Bvis) arterial oxygen content (CaO2 ) is gradually decreased. CaO2 was decreased by hemodilution to hematocrits (Hct) of 30, 22, 19, and 15% in two groups. One group received blood replacement (BR) only and served as the control. The second group received an additional high viscosity solution of polyvinylpyrrolidone (BR/PVP). Bvis was reduced in the BR group and was doubled in the BR/PVP. Despite different Bvis, CBF did not differ between BR and BR/PVP rats at Hct values of 30 and 22%, indicating a complete vascular compensation of the increased Bvis at decreased CaO2 . At an Hct of 19%, local cerebral blood flow (LCBF) in some brain structures was lower in BR/PVP rats than in BR rats. At the lowest Hct of 15%, LCBF of 15 brain structures and mean CBF were reduced in BR/PVP. The resulting decrease in cerebral oxygen delivery in the BR/PVP group indicates a global loss of vascular compensation. We concluded that vasodilating mechanisms compensated for Bvis increases thereby maintaining constant cerebral oxygen delivery. Compensatory mechanisms were exhausted at a Hct of 19% and lower as indicated by the reduction of CBF and cerebral oxygen delivery.


2005 ◽  
Vol 77 (2) ◽  
pp. P67-P67
Author(s):  
T SHINOHARA ◽  
K NAGATA ◽  
E YOKOYAMA ◽  
M SATO ◽  
S MATSUOKA ◽  
...  

2015 ◽  
Vol 35 (11) ◽  
pp. 1882-1887 ◽  
Author(s):  
Hazel I Zonneveld ◽  
Elizabeth A Loehrer ◽  
Albert Hofman ◽  
Wiro J Niessen ◽  
Aad van der Lugt ◽  
...  

The question remains whether reduced cerebral blood flow (CBF) leads to brain atrophy or vice versa. We studied the longitudinal relation between CBF and brain volume in a community-dwelling population. In the Rotterdam Study, 3011 participants (mean age 59.6 years (s.d. 8.0)) underwent repeat brain magnetic resonance imaging to quantify brain volume and CBF at two time points. Adjusted linear regression models were used to investigate the bidirectional relation between CBF and brain volume. We found that smaller brain volume at baseline was associated with a steeper decrease in CBF in the whole population (standardized change per s.d. increase of total brain volume (TBV) = 0.296 (95% confidence interval (CI) 0.200; 0.393)). Only in persons aged ≥ 65 years, a lower CBF at baseline was associated with steeper decline of TBV (standardized change per s.d. increase of CBF = 0.003 (95% CI −0.004; 0.010) in the whole population and 0.020 (95% CI 0.004; 0.036) in those aged ≥65 years of age). Our results indicate that brain atrophy causes CBF to decrease over time, rather than vice versa. Only in persons aged >65 years of age did we find lower CBF to also relate to brain atrophy.


2018 ◽  
Vol 46 (10) ◽  
pp. 4214-4225 ◽  
Author(s):  
Antonio P. Mansur ◽  
Glaura Souza Alvarenga ◽  
Liliane Kopel ◽  
Marco Antonio Gutierrez ◽  
Fernanda Marciano Consolim-Colombo ◽  
...  

Objective Heart failure (HF) is associated with intermittent hypoxia, and the effects of this hypoxia on the cardiovascular system are not well understood. This study was performed to compare the effects of acute hypoxia (10% oxygen) between patients with and without HF. Methods Fourteen patients with chronic HF and 17 matched control subjects were enrolled. Carotid artery changes were examined during the first period of hypoxia, and brachial artery changes were examined during the second period of hypoxia. Data were collected at baseline and after 2 and 4 minutes of hypoxia. Norepinephrine, epinephrine, dopamine, and renin were measured at baseline and after 4 minutes hypoxia. Results The carotid blood flow, carotid systolic diameter, and carotid diastolic diameter increased and the carotid resistance decreased in patients with HF. Hypoxia did not change the carotid compliance, distensibility, brachial artery blood flow and diameter, or concentrations of sympathomimetic amines in patients with HF, but hypoxia increased the norepinephrine level in the control group. Hypoxia increased minute ventilation and decreased the oxygen saturation and end-tidal carbon dioxide concentration in both groups. Conclusion Hypoxia-induced changes in the carotid artery suggest an intensification of compensatory mechanisms for preservation of cerebral blood flow in patients with HF.


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