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Smoking and cognitive abilities

Smoking and cognitive abilities


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How does smoking affect cognitive abilities?

Could it have a positive impact on alertness (like coffee)? Could it reduce our ability to concentrate? Could it lead to less oxygen in the brain, and some 'sluggishness' in thoughts?

I'm specially interested in the long term effect, present even when there's no nicotine in the body.


Smoking is associated with reduced memory and with decline in cognitive function over the long term. Compared to people who continue smoking, people who stop smoking sooner have less decline.

From Sabia et al 2008:

smokers compared with those who never smoked were more likely to be in the lowest quintile of cognitive performance. After adjustment for multiple covariates, this risk remained for memory (OR, 1.37; 95% CI, 1.10-1.73)

and

From Sabia et al 2012:

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 the second study, the effect was observed in men but not women.

Because these are not randomized studies (and indeed, randomizing people to smoke or not smoke over decades is not an ethical study that will ever be conducted), causality is difficult to infer, but they are strongly suggestive.

Because these are long-term studies, they say little about the acute effects of nicotine. Acutely, like other stimulants, nicotine can cause cognitive enhancement. However, long-term users become sensitive to being deprived of nicotine and require nicotine to get back to baseline. Smoking more and more and more to get a benefit is probably not a great idea, so there is no potential for nicotine to be used for long-term cognitive enhancement.

From Myers et al 2008:

Overnight tobacco deprivation resulted in impaired functioning on all cognitive tests and increased self-reports of tobacco craving and negative mood; nicotine normalized these deficits. In the nondeprived condition, nicotine enhanced performance on the continuous performance test (CPT) and an arithmetic test in a dose-related manner, but had no effect on working memory.


Myers, C. S., Taylor, R. C., Moolchan, E. T., & Heishman, S. J. (2008). Dose-related enhancement of mood and cognition in smokers administered nicotine nasal spray. Neuropsychopharmacology, 33(3), 588.

Sabia, S., Elbaz, A., Dugravot, A., Head, J., Shipley, M., Hagger-Johnson, G.,… & Singh-Manoux, A. (2012). Impact of smoking on cognitive decline in early old age: the Whitehall II cohort study. Archives of general psychiatry, 69(6), 627-635.

Sabia, S., Marmot, M., Dufouil, C., & Singh-Manoux, A. (2008). Smoking history and cognitive function in middle age from the Whitehall II study. Archives of internal medicine, 168(11), 1165-1173.


Cigarette Smoking, Cognitive Performance, and Severe Mental Illness: Quitting Smoking Really Does Seem to Matter

Cigarette smoking is commonly associated with severe mental illness. As noted in an article by Vermeulen et al. in this issue (1), as many as two-thirds of community-dwelling people with severe mental illness are current smokers, and the likelihood that their relatives will smoke is elevated as well, compared with the general population. Smoking appears to be associated with severe mental illness across the entire lifetime course of the illnesses, and at the time of their first diagnosis, people who develop severe mental illness are much more likely than the population as a whole to be smokers (2). There are many reasons for this elevated rate of smoking, which have been examined in previous research.

Among the potential influences on smoking are genomic alterations in the alpha-7 nicotinic receptor gene complex, and these alterations are shared with first-degree relatives and are closely related to susceptibility to schizophrenia (3). Other nicotinic receptor genes have also been linked to schizophrenia (4). Moreover, nicotine normalizes, at least temporarily, the sensory gating abnormalities that are commonly seen in schizophrenia (5), possibly leading to a subjective sense of reduced stress and greater control over the strength and valance of environmental stimuli. In addition, nicotine has been shown to temporarily enhance cognition in a variety of nonsmoking populations, including people with schizophrenia (6). Treatment with agents that directly target nicotinic receptors has been shown in proof-of-concept studies to enhance cognitive performance in schizophrenia populations (7), but large-scale trials have not yet found any treatments that separate from placebo in phase 3 clinical trials (8).

Smoking prevalence, normalization of critical elements of neurobiological processing, potential cognition-enhancing effects, and genomic alterations all point to the reasons for smoking in severe mental illness. Many studies, such as those cited above, suggest a potentially beneficial role for nicotine. Why, then, do the results of the Vermeulen et al. study strongly suggest the opposite conclusion? Being a smoker is clearly bad for your cognitive performance the more you smoke, the worse your performance and quitting or reducing smoking leads to improved cognitive functioning.

The Vermeulen et al. study had a very large sample and was longitudinal, with relatives and healthy control subjects also examined, and the researchers were able to examine the effects of quitting smoking on cognition. Their findings fit into the bigger picture of smoking and cognition, in that in the general population, the longer you smoke and the more you smoke, the greater your risk for late-life cognitive decline. The findings also fit into the picture of severe mental illness, in that current smoking in both schizophrenia and bipolar disorder is associated not only with poorer cognition but also with greater real-world disability and challenges in the ability to perform everyday living tasks, as reported in a previous study by a different research group (9). In that study, the effects of smoking on cognition and everyday functioning did not differ by diagnosis across schizophrenia and bipolar illness. Notably, former smokers were found to perform equivalently to never-smokers and to outperform current smokers by 0.4 standard deviations on composite measures of cognitive performance. Time since quitting was not correlated with cognitive performance, suggesting that effects on cognition could be rapid, as suggested in the Vermeulen et al. study.

Multiple critical take-home points may be drawn from the data in the Vermeulen et al. study. First, stopping smoking leads to a relatively rapid recovery of cognitive performance, consistent with previous cross-sectional studies. Second, the number of cigarettes smoked per day was inversely correlated with cognitive performance. Third, the smoking-related adverse effects on processing speed were seen in both patients and healthy control subjects, indicating that the adverse effects of cigarette smoking on processing speed were not diagnosis specific.

There are some questions that cannot be answered with these data as they are presented. The first is why smokers who continue smoking experience more adverse cognitive effects over time instead of fewer. It is possible that these smokers are noticing changes associated with improvements in sensory gating after each cigarette and feel more comfortable immediately after nicotine use. The paradox of initial, short-term pleasurable effects, including cognitive enhancement, driving addiction and then subsequent dysphoria with adverse cognitive effects in chronic users is well known in the nicotine literature. Nicotine is an extremely effective agonist at nicotinic cholinergic receptors, and, at the same time, chronic exposure leads to desensitization and inactivation of these very receptors. Smokers, including those with mental illness, continue to smoke to recapture the short-term effects, all the while increasing the chronic levels of nicotine that then block their receptors (10).

The second question is why some people with schizophrenia are able to quit smoking while others continue. The authors do not present analyses of the cognitive performance, while smoking, of those who subsequently quit. It would be of interest to see if they had less cognitive impairment beforehand or smoked fewer cigarettes. The third question is why some people with schizophrenia never start smoking. If there is shared vulnerability to psychosis and smoking (or at least abnormalities in the nicotinic system), then we might expect that the minority of patients with severe mental illness who never smoked would look fundamentally different in some ways from those who do or did smoke. Comparisons of never smokers and quitters (e.g., 9) have found minimal differences in symptoms or cognition between them, even in the context of substantial lifetime smoking on the part of quitters.

The data from Vermeulen et al. make a powerful argument for interventions aimed at smoking cessation in individuals with severe mental illness. The rapid return of cognitive performance in quitters with severe mental illness, particularly in a domain with considerable functional relevance, is a strong argument for rapid benefits. The previously demonstrated extension of smoking-related cognitive deficits to everyday functioning and functional capacity suggest considerable morbidity reduction with smoking cessation as well. Finally, it is not just patients with schizophrenia who experience smoking-related adverse effects these treatment efforts should be extended to people with bipolar disorder and major depression as well.

Dr. Harvey has received research grant support from Takeda and the Stanley Medical Research Foundation he has received consulting fees or travel reimbursements from Akili, Allergan, Biogen, Boehringer Ingelheim, Forum Pharma, Genentech (Roche), Intra-Cellular Therapies, Jazz Pharmaceuticals, Lundbeck, Minerva, Otsuka America (Otsuka Digital Health), Sanofi, Sunovion, Takeda, and Teva and he receives royalties for the Brief Assessment of Cognition in Schizophrenia. Dr. Freedman has reviewed this editorial and found no evidence of influence from these relationships.

1 Vermeulen JM, Schirmbeck F, Blankers M, et al. : Association between smoking behavior and cognitive functioning in patients with psychosis, siblings, and healthy control subjects: results from a prospective 6-year follow-up study . Am J Psychiatry 2018 175:1121–1128Link , Google Scholar

2 Wade D, Harrigan S, Edwards J, et al. : Course of substance misuse and daily tobacco use in first-episode psychosis . Schizophr Res 2006 81:145–150Crossref, Medline , Google Scholar

3 Mexal S, Berger R, Logel J, et al. : Differential regulation of α7 nicotinic receptor gene (CHRNA7) expression in schizophrenic smokers . J Mol Neurosci 2010 40:185–195Crossref, Medline , Google Scholar

4 Jackson KJ, Fanous AH, Chen J, et al. : Variants in the 15q25 gene cluster are associated with risk for schizophrenia and bipolar disorder . Psychiatr Genet 2013 23:20–28Crossref , Google Scholar

5 Adler LE, Hoffer LD, Wiser A, et al. : Normalization of auditory physiology by cigarette smoking in schizophrenic patients . Am J Psychiatry 1993 150:1856–1861Link , Google Scholar

6 Jubelt LE, Barr RS, Goff DC, et al. : Effects of transdermal nicotine on episodic memory in non-smokers with and without schizophrenia . Psychopharmacology (Berl) 2008 199:89–98Crossref , Google Scholar

7 Keefe RS, Meltzer HA, Dgetluck N, et al. : Randomized, double-blind, placebo-controlled study of encenicline, an α7 nicotinic acetylcholine receptor agonist, as a treatment for cognitive impairment in schizophrenia . Neuropsychopharmacology 2015 40:3053–3060Crossref, Medline , Google Scholar

8 Haig GM, Bain EE, Robieson WZ, et al. : A randomized trial to assess the efficacy and safety of ABT-126, a selective α7 nicotinic acetylcholine receptor agonist, in the treatment of cognitive impairment in schizophrenia . Am J Psychiatry 2016 173:827–835Link , Google Scholar

9 Depp CA, Bowie CR, Mausbach BT, et al. : Current smoking is associated with worse cognitive and adaptive functioning in serious mental illness . Acta Psychiatr Scand 2015 131:333–341Crossref, Medline , Google Scholar

10 Harris JG, Kongs S, Allensworth D, et al. : Effects of nicotine on cognitive deficits in schizophrenia . Neuropsychopharmacology 2004 29:1378–1385Crossref, Medline , Google Scholar


Psychological Perspectives of Smoking

Psychological perspectives of smoking This essay will consider how each of the 5 psychological perspectives explain smoking. I will cover the psychodynamic, the behaviouristic, the biological, the cognitive and the humanistic approach. Psychodynamic approach The psychodynamic approach views behaviour in terms of past childhood experiences, and the influence of unconscious processes. There are five psychosexual stages in Freud’s theory, the first being the oral stage during which the infant focuses on satisfying hunger orally.

Sigmund Freud believed that during this stage of development the person can become fixated in the oral stage of development.

An infant’s pleasure and comfort centres on having things in the mouth during this psychodynamic stage. If the mother weaned too early, it may fail to be resolved later in life which can then lead to oral fixation. The action of putting something in their mouth (a cigarette) is what fulfils this oral fixation. Freud’s evidence for this was through his studies on ‘Little Hans’.

Hans’ father would exchange letters between him and Freud about little Hans’ dreams and fears and was able to place him into one of the five psychosexual stages. This study was flawed in the way that all of the material Freud used for the study was second hand. One of the strengths of the approach is that it provides a valuable insight into how early experiences or relationships can affect our adult personality, having said this the approach is too focused on sex and is biased. The behaviourist approach The behaviourist approach explains human behaviour as being learned from peers and the environment.

The approach suggests that smoking may be explained through learning through classical conditioning. Smoking may be acquired from their peers which results in acceptance and happiness, therefore smoking alone results in the conditioned response of pleasure. Young people may have observed others smoking and them being popular or getting praise, either their peers or through popular films and see those as successful or popular therefore may imitate this behaviour. Ivan Pavlov conducted an experiment where he had surgically implanted tubes into the cheeks of dogs to monitor the secretion of saliva whilst the dog was eating. Pavlov, 1902)

He noticed that the dog started to salivate before the food was put in its mouth. He then presented to food to the dog whilst playing the sound of a metronome, eventually the dog started to salivate when just hearing the metronome alone. This can be related to smoking using the following model: Conditioning diagram Peer groupsbefore conditioningacceptance and happiness Peer groups + Smokingduring conditioningacceptance and happiness Smokingafter conditioningacceptance and happiness One of the main strengths of the behaviourist approach is that it focuses only on behaviour that can be observed and manipulated.

Therefore, this approach has proved very useful in experiments under laboratory conditions. On the other hand this has been criticized for suggesting that most human behaviour is mechanical, and that human behaviour is simply the product of stimulus-response behaviours. The biological approach The biological approach looks at our genetics to construct a reason why we act the way we do and why we develop abnormal behaviours. This approach suggests that the reason people smoke is a biological addiction from a chemical in cigarettes called nicotine.

Nicotine is a chemical that alters the brains behaviour by creating an addiction to nicotine which causes smokers to crave a cigarette as it gives them the nicotine they need to fulfil this addiction. When smokers try to stop, the loss of nicotine changes the levels of dopamine and noradrenaline. This can make them feel anxious, depressed and irritable. Evidence for this has been given by the NHS. On average 20% of adults in the UK have an addiction to smoking. (NHS, 2012) As this approach is solely based on empirical evidence from a biological perspective it relies on hard evidence giving a clear analysis.

The approach however, doesn’t take into consideration, thoughts feelings and the effect of the environment. The cognitive approach The cognitive approach focuses on mental processes, perception, and language as a way of explaining and understanding human behaviour. The approach focuses on the importance of mental processes such as beliefs, desires and motivation in determining behaviour. People who smoke may see smoking as doing something that is considered a taboo thing to do giving them a certain enjoyment by ‘staring the face of danger’.

Evidence can be shown for this in the suspension bridge ‘Love on a suspension bridge’ experiment conducted by Dutton & Aron in 1974 . (Billingham, 2008) In this study, an attractive female experimenter approached men as they crossed either a high, rickety suspension bridge or a low safe bridge and asked them to answer some questions and write a brief story in relation to a picture and to call the experimenter for the results. Men who walked across the high bridge were more likely to write a more sexual story and were more likely to call the experimenter.

This suggests that when the subjects heart rate was raised they were more likely to have an attraction to something. This approach is good because it uses lab experiments rather than speculation but is also considered as being too basic and deterministic I. E. one input, a decision is made and then an output created and doesn’t take in to consideration any other effects. The humanistic approachCongruence diagram The humanistic approach emphasises the study of the whole person rather than studying individual components. It views every individual as being unique. The main concept of the humanistic approach is to reach congruence.

This is a state of consistency between the ‘real self’ and the ‘ideal self. This can be explained in the following diagram. The closer you are to reaching your idea l self, the more over lapped the two circles become. Smokers smoke to feel good. According to Maslow’s hierarchy of needs this is part of the self-actualisation process. (Billingham, 2008) This is their unique desire to achieve their highest potential as individuals. The approach is effective as it is based on free will and the individuals own experiences. On the other hand the approach is too subjective and lacks scientific research to support its ideas.


Recent Advances – Smoking and Cognitive Functioning: The Dilemma

Understanding the effect of cigarette smoke on the brain is a global imperative since smoking continues to rise in developing countries at a rate of more than 3% per year. While tobacco smoking rates in the United States have gone down overall, the highest use is among those with lower education and income. The World Health Organization (WHO) predicts that 1.5 to 1.9 billion people worldwide will be smokers in 2025.

Cigarette smoke consists of thousands of compounds, including nicotine. Many of these compounds have known toxicity to the brain, cardiovascular, and pulmonary systems. Nicotine, in contrast, has positive effects on certain cognitive domains. Nicotine is structurally similar to acetylcholine and has been shown to improve cognitive functioning, possibly through stimulation of both &alpha4&beta2 and &alpha7 nicotinic receptors, which are essential for memory functioning. Decreased nicotinic activity in the hippocampus and amygdala may impair memory function. Additionally, a number of studies have found that nicotine can improve attention following both chronic and acute administration. The improvement may be attributed to a number of factors including nicotine stimulation of dopamine in the striatum or stimulation of nicotinic neurons in the thalamus or other brain regions associated with attention or arousal, such as anterior cingulate cortex. Clinically, nicotinic treatments (e.g. nicotine patch) are being evaluated as therapeutic treatment for cognitive impairment. Several initial studies have reported positive therapeutic effects on cognitive disorders, such as Alzheimer&rsquos disease and age-related memory deficits.

On the other hand, there is growing evidence that cognitive impairment and dementia is associated with cigarette smoking. In a recent meta-analysis of 19 prospective studies, each with 12 months or more of follow-up, current smokers had an increased risk of dementia including Alzheimer&rsquos disease, vascular dementia, and any dementia and had greater declines in mental state testing compared to subjects who have never smoked. These findings suggest that cigarette smoke has neurotoxic effects and is associated with an increased risk of dementia. To date, however, there are relatively few studies assessing the association between secondhand smoke and cognitive dysfunction.

Secondhand smoke, defined as tobacco smoke inhaled by individuals who do not smoke, contains a greater concentration of toxic and carcinogenic chemicals than the smoke inhaled by tobacco smokers. The U.S. Centers for Disease Control and Prevention reported that almost 50,000 deaths per year can be ascribed to secondhand smoke. The mechanisms by which active smoking and secondhand tobacco smoke exposure induce their ill effects may include systemic inflammation, pro-inflammatory cytokine induction, and endothelial dysfunction. Each of these mechanisms has been independently associated with cognitive impairment and dementia.

A cross-sectional analysis of 4,809 non-smoking adults aged 50 years or more from the English Longitudinal Study of Aging (Llewellyn et al.) was carried out to examine the relationship between secondhand smoke exposure and cognitive functioning. The study used levels of salivary cotinine (ng/ml) as a biomarker for recent secondhand smoke exposure. The results showed that participants with high levels of salivary cotinine (0.8-13.5 ng/ml) were more likely to perform in the lowest 10% of scores on a battery of neuropsychological tests than those with low levels of salivary cotinine (0.0-0.1 ng/ml). The authors, therefore, suggested that high levels of secondhand smoke exposure might be related to increased odds of cognitive impairment. Similarly, using the Geriatric Mental State Examination as an assessment of dementia syndromes, a research team in China interviewed 5,921 individuals aged 60 or above and characterized their secondhand smoke exposure. The researchers found that dementia syndromes were significantly associated with exposure to secondhand smoke. It was reported that the more severe the dementia syndrome, the stronger the relationship with secondhand smoke exposure. Another study by Orsitto et al., conducted in Paradiso Hospital, Italy, found that patients with a diagnosis of mild cognitive impairment reported a significantly higher frequency of secondhand smoke compared to those with normal cognition.

While the cardiovascular and cancer risks associated with tobacco smoking are clear, the cognitive risks are complicated. Nicotinic stimulation may improve cognition but the effects of smoking may be toxic to the brain and cognitive function. Further, the effects may be experienced by those who never smoked due to second hand exposure. Other forms of nicotine delivery, including trans-dermal patch, are under investigation for cognitive benefits and indeed are worthy of study given how few agents are available to improve cognitive performance. Further studies are also needed to investigate the relationship between secondhand tobacco smoke and increased risk of cognitive disorders. Establishing that exposure to cigarette smoke may contribute to cognitive loss and dementia could provide additional motivation for smoking cessation and improve compliance with withdrawal and abstention.

References:
1. Anstey, K.J., von Sanden, C., Salim, A., O&rsquoKearney, R. Smoking as a risk factor for dementia and cognitive decline: a meta-analysis of prospective studies. American Journal of Epidemiology 2007 Aug 15 166: 367-78.
2. Barnes, D.E., Haight, T.J., Mehta, K.M., Carlson, M.C., Kuller, L.H., Tager, I.B. Secondhand smoke, vascular disease, and dementia incidence: findings from the cardiovascular health cognition study. American Journal of Epidemiology 2010 Feb 1 171(3): 292-302.
3. Chen, R., Wilson, K., Chen, Y., Zhang, D., Qin, X., He, M., Hu, Z., Ma, Y., Copeland, J.R. Association between environmental tobacco smoke exposure and dementia syndromes. Occupational and Environmental Medicine 2013 Jan 70(1): 63-9.
4. Levin, E.D., McClernon, F.J., Rezvani, A.H. Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization. Psychopharmacology (Berl) 2006 Mar 184(3-4): 523-39.
5. Llewellyn, D.J., Lang, I.A., Langa, K.M., Naughton, F., Matthews, F.E. Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement. British Medical Journal 2009 Feb 12 338: b462.
6. Orsitto, G., Turi, V., Venezia, A., Fulvio, F., Manca, C. Relation of secondhand smoking to mild cognitive impairment in older inpatients. Scientific World Journal 2012 2012: 726948.
7. http://www.who.int/mediacentre/factsheets/fs339/en/

Excerpted article as reprinted from IPA&rsquos newsletter, the IPA Bulletin , Volume 30, Number 6


Cigarette smoking and cognitive performance

Requests for reprints should be addressed to: George J. Spilich, PhD, Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA.Search for more papers by this author

Department of Psychology, Delaware State College, Dover, DE 19901, USA

Allegheny County Law Department, 445 Fort Pitt Boulevard Suite 300, Pittsburgh, PA 15219, USA

Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA

Requests for reprints should be addressed to: George J. Spilich, PhD, Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA.Search for more papers by this author

Department of Psychology, Delaware State College, Dover, DE 19901, USA

Allegheny County Law Department, 445 Fort Pitt Boulevard Suite 300, Pittsburgh, PA 15219, USA

Abstract

While some investigations into the relationship between smoking and cognitive performance have reported that smoking facilitates performance, other research has come to the opposite conclusion. A review of the literature suggests that this variance in results may be due to differences among studies in design (comparing smokers only with deprived smokers rather than with non-smokers) and also to differences in task demands. Therefore, performance of smokers having just smoked, matched smokers deprived for a brief period, and also non-smokers was contrasted on a series of tasks which ranged from repetitive and perceptually-bound tasks to complex, dynamic tasks dependent upon long-term memory. It was found that while cigarette smoking had no negative effect upon performance for simple perceptual tasks, smoking was found to exert measurable negative effects upon performance for more complex information processing tasks.


Cigarette smoking and cognitive decline in midlife: evidence from a prospective birth cohort study

Objectives: The authors investigated the effects of cigarette smoking on midlife cognitive performance.

Methods: Multiple regression was used to test the association between cigarette smoking and changes in cognitive test scores among male and female members of the British 1946 birth cohort aged between 43 and 53 years.

Results: Smoking was associated with faster declines in verbal memory and with slower visual search speeds. These effects were largely accounted for by individuals who smoked more than 20 cigarettes per day and were independent of sex, socioeconomic status, previous (adolescent) cognitive ability, and a range of health indicators.

Conclusions: The present results show that heavy smoking is associated with cognitive impairment and decline in midlife. Smokers who survive into later life may be at risk of clinically significant cognitive declines.


Quitting Smoking Improves Memory

Former smokers have a better-functioning memory than those who still light up, a new study finds. On a practical test of their recollection ability, people who on average had quit smoking for 2.5 years performed 25 percent better than current smokers did. People who had never smoked scored 37 percent better than the smokers. "We already know that giving up smoking has huge health benefits for the body, but this study also shows how stopping smoking can have knock-on benefits for cognitive function, too," said study researcher Tom Heffernan, a psychology professor at Northumbria University in England. Lighting up, or learning? The researchers aimed to measure "real world" memory abilities by sending 69 study participants on a tour of a university campus. Twenty-seven were smokers, 18 were former smokers, and 24 never smoked. The participants were given a list of 15 locations around campus and an action to perform at each location. For example, upon reaching the library, participants were supposed to remember to check for messages on their cell phones upon reaching the sports center, they were supposed to remember to ask about the cost of membership. On average, the smokers performed 8.9 tasks correctly. The participants who had quit smoking averaged 11 correctly performed tasks, and those who had never smoked averaged 12.1. There were no differences between the groups in terms of their IQs, the study said. Previous studies showed that quitting smoking improves "retrospective memory," which is the ability to learn information and retrieve it later. The new study instead measured participants' "prospective memory," which is the ability to remember to carry out a particular action at some future point in time. For example, remembering to take medication at a certain time of day requires prospective memory. Previous research on the effect of smoking on prospective memory yielded mixed results, with some results showing smokers were worse off, and others showing no effect from smoking, the study noted. How does it work? Although it is unclear exactly how smoking may interfere with memory, research has shown that chronic smoking is linked to a breakdown, or atrophy, of parts of the brain. The researchers hypothesized that smoking could damage brain areas such as the prefrontal cortex, hippocampus or thalamus all of those regions have been linked in brain imaging studies to prospective memory, they said. Heffernan also has studied the effects of alcohol and marijuana on memory. He and the other researchers acknowledged that their new study was small and relied on self-reports of smoking, which would be subject to inaccuracy and dishonesty on the part of participants. Future work should follow a cohort of smokers and former smokers over time, they said. The study will be published in an upcoming issue of the journal Drug and Alcohol Dependence. Pass it on: Quitting smoking could improve people's memory abilities to rival those of people who have never smoked.

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Smoking tied to declines in memory, cognitive abilities

As adults age, they're more likely to experience declines in memory and cognitive abilities. New research suggests that smoking might significantly speed up those declines.

For the study, researchers analyzed data from an ongoing study of aging that involved nearly 8,800 participants who were an average of 66 years old, a majority of whom were females.

They was given tests that measured blood pressure, cholesterol levels and body mass index (BMI), and were also asked about their smoking habits. Participants were also tested for their risks for stroke and heart disease, and were given tasks that helped measure their memory and cognitive abilities after four and eight-year follow-up periods.

The researchers found those at the highest risk for stroke had lower scores in cognition, memory and executive processing as measured by the tasks. High blood pressure specifically was associated with lower cognitive and memory scores after the eight years, while high BMI -- used to measure if a person is overweight or obese -- was also tied to lower memory scores.

However across the board, smoking was associated with lower performance on all cognitive measures studied at four and eight-year intervals.

"Smoking emerged as the most consistent predictor of cognitive decline," wrote the study's authors, lead by Dr. Alex Dregan, a public health sciences researcher at Kings College London. The study appears in the Nov. 25 issue of Age and Aging.

The authors say their study shows that the most promising preventive approach to reduce cognitive declines should consider the potential multiple causes, such as smoking and cardiovascular risks.

Trending News

"Specifically, interventions to limit cognitive decline should consider the combined effect of multiple vascular risk factors rather than focusing on the management of individual-risk factors as routinely performed in the past," they wrote.

Alzheimer's disease is the most common form of dementia, affecting 5.4 million Americans according to the U.S. Alzheimer's Association. The disease, which typically occurs in people 65 and older, starts with mild memory loss and progresses to the inability to carry a conversation or to recognize one's environment. It is the sixth-leading cause of death in the United States.

Other risk factors for cognitive decline include diabetes and lack of physical exercise.


Methods

Participants

This study used data from ELSA, a panel study designed to be representative of individuals aged 50 years and older living in England.19 A total of 11 391 participants took part in Wave 1 in 2002–2003. Wave 1 participants were individuals who had previously taken part in the Health Survey for England, were born before 1 March 1952 and were living in a private household in England at the first wave.19 These participants have been followed up every 2 years, and the sample has been refreshed at subsequent waves to maintain a representative sample of participants aged over 50 years. More information on this cohort is provided elsewhere.19 The current sample consists of participants who completed the Wave 2 (2004–2005) interview (n=8780) this is the first wave in which health literacy was assessed. Ethical approval was granted. This study conformed to the principles embodied in the Declaration of Helsinki.

Measures

ELSA interviews were carried out using computer-assisted interviewing in the participants’ own home.

Smoking

Two aspects of smoking status (ever vs never smoker and current vs former smoker) were the outcome variables in these analyses. Participants were asked ‘Have you ever smoked cigarettes?’. Participants were categorised as ever smokers if they answered ‘yes’ and never smokers if they answered ‘no’ at either Wave 1 or 2. Ever smokers were additionally asked ‘Do you smoke cigarettes at all nowadays?’. Ever smokers who answered ‘yes’ to smoking cigarettes nowadays at Wave 2 were categorised as current smokers, whereas ever smokers who answered ‘no’ were categorised as former smokers.

Health literacy

Health literacy was assessed at Wave 2 using a four-item comprehension test previously used in the International Adult Literacy Survey.20 Participants were presented with a piece of paper containing instructions similar to those that would be found on a packet of over-the-counter medication. Participants were instructed to read the medicine label and were then asked four questions about the information on this label (eg, ‘what is the maximum number of days you may take this medicine?’). The label was available to the participant to refer to at any time. This task was designed to measure the skills thought to be required to understand and use health materials correctly, such as the ability to read and use numbers in a health context.21 One point was awarded for each correctly answered question (range 0–4). As has been done in previous ELSA studies,22 23 health literacy scores were categorised as ‘adequate’ (4/4 correct) or ‘limited’ (≤3 correct).

Cognitive function

Four tests of cognitive function that were administered at Wave 2 of the ELSA study were used here. These tests are thought to assess episodic memory, executive function and processing speed these are cognitive domains which tend to decline on average with increasing age.24 25 In the word list recall test, participants heard a list of 10 words which they had to recall immediately (immediate recall test) and again after a short delay (delayed recall test). The score on each occasion was the number of words remembered (range 0–10). Executive function was assessed using categorical verbal fluency (number of animals named in 60 s). The letter cancellation test, in which participants were to scan rows of letters and score out all Ps and Ws, was used to measure processing speed. The score is the number of Ps and Ws scored out in 60 s. Exploratory factor analysis (EFA) using principal axis factoring was used to derive a composite measure of general cognitive ability. Scores on the four cognitive tests were entered into the EFA. Prior to this, individuals who scored 0 or greater than 4 SD above the mean on the animal fluency test and the letter cancellation test were removed. Scores of 0 indicate that the participant did not understand the task, and scores 4 SD above the mean were seen as dubiously high given the 1 min time limit for these tests. One unrotated factor was extracted which accounted for 44% of the total variance in the four cognitive tests. The loadings of the tests were: immediate word recall=0.78 delayed word recall=0.83 animal naming=0.53 letter cancellation=0.42. This factor score was converted to a z-score (mean=0.00, SD=1.00) and was used as a measure of general cognitive ability.

Covariates

Age in years, sex, age of leaving full-time education and occupational social class were used as covariates. For confidential reasons, owing to there being few of them, participants aged over 90 years have had their age set to 90. Participants were asked at what age they left continuous full-time education (recorded as not yet finished, never went to school, 14 or under, at 15, at 16, at 17, at 18, and 19 or over). For the purpose of this study, age of leaving full-time education was categorised as 14 years or under, 15–16 years, 17–18 years and 19 years or over. Occupational social class was categorised using the National Statistics Socio-economic Classification 3 categories: managerial and professional, intermediate and routine and manual.26

Patient and public involvement

Participants were not involved in the development of any part of this study.

Statistical analysis

Two sets of analyses were carried out. First, ever smokers were compared with never smokers second, current smokers were compared with former smokers. To determine whether ever versus never smokers and current versus former smokers differ on health literacy, general cognitive ability and sociodemographic variables, t-tests were used for normally distributed continuous variables, Mann-Whitney U tests were used for non-normal continuous variables and χ 2 tests were used for categorical variables. Rank-order correlations were calculated between the predictor variables to examine any bivariate associations between these variables. Binary logistic regression was used to examine the independent associations of health literacy and general cognitive ability on smoking status. Age and sex were entered in all models. Health literacy and general cognitive ability were entered individually in models 1 and 2, respectively. To determine whether both health literacy and general cognitive ability are independently associated with smoking, both predictors were included in model 3. Model 4 additionally adjusted for age of finishing full-time education and occupational social class to determine whether any associations between health literacy, cognitive function and smoking remained after controlling for these sociodemographic variables.


Footnotes

Statement 2: Contributors Qian Guo was the Project Manager of China Seven Cities Study (CSCS). She conducted the present smoking attribution study and wrote the manuscript. Carl Anderson Johnson was the Principal Investigator of CSCS and Principal Investigator of TTAURC. He worked closely with Qian Guo on this study and provided instructive and mentor assistance throughout the process. Jennifer B. Unger, Stanley P. Azen, and David P. MacKinnon provided input on statistical analysis and interpretation. All authors contributed to and have approved the final manuscript.

Statement 3: Conflict of Interest All authors declare that they have no conflicts of interest.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.


Recent Advances – Smoking and Cognitive Functioning: The Dilemma

Understanding the effect of cigarette smoke on the brain is a global imperative since smoking continues to rise in developing countries at a rate of more than 3% per year. While tobacco smoking rates in the United States have gone down overall, the highest use is among those with lower education and income. The World Health Organization (WHO) predicts that 1.5 to 1.9 billion people worldwide will be smokers in 2025.

Cigarette smoke consists of thousands of compounds, including nicotine. Many of these compounds have known toxicity to the brain, cardiovascular, and pulmonary systems. Nicotine, in contrast, has positive effects on certain cognitive domains. Nicotine is structurally similar to acetylcholine and has been shown to improve cognitive functioning, possibly through stimulation of both &alpha4&beta2 and &alpha7 nicotinic receptors, which are essential for memory functioning. Decreased nicotinic activity in the hippocampus and amygdala may impair memory function. Additionally, a number of studies have found that nicotine can improve attention following both chronic and acute administration. The improvement may be attributed to a number of factors including nicotine stimulation of dopamine in the striatum or stimulation of nicotinic neurons in the thalamus or other brain regions associated with attention or arousal, such as anterior cingulate cortex. Clinically, nicotinic treatments (e.g. nicotine patch) are being evaluated as therapeutic treatment for cognitive impairment. Several initial studies have reported positive therapeutic effects on cognitive disorders, such as Alzheimer&rsquos disease and age-related memory deficits.

On the other hand, there is growing evidence that cognitive impairment and dementia is associated with cigarette smoking. In a recent meta-analysis of 19 prospective studies, each with 12 months or more of follow-up, current smokers had an increased risk of dementia including Alzheimer&rsquos disease, vascular dementia, and any dementia and had greater declines in mental state testing compared to subjects who have never smoked. These findings suggest that cigarette smoke has neurotoxic effects and is associated with an increased risk of dementia. To date, however, there are relatively few studies assessing the association between secondhand smoke and cognitive dysfunction.

Secondhand smoke, defined as tobacco smoke inhaled by individuals who do not smoke, contains a greater concentration of toxic and carcinogenic chemicals than the smoke inhaled by tobacco smokers. The U.S. Centers for Disease Control and Prevention reported that almost 50,000 deaths per year can be ascribed to secondhand smoke. The mechanisms by which active smoking and secondhand tobacco smoke exposure induce their ill effects may include systemic inflammation, pro-inflammatory cytokine induction, and endothelial dysfunction. Each of these mechanisms has been independently associated with cognitive impairment and dementia.

A cross-sectional analysis of 4,809 non-smoking adults aged 50 years or more from the English Longitudinal Study of Aging (Llewellyn et al.) was carried out to examine the relationship between secondhand smoke exposure and cognitive functioning. The study used levels of salivary cotinine (ng/ml) as a biomarker for recent secondhand smoke exposure. The results showed that participants with high levels of salivary cotinine (0.8-13.5 ng/ml) were more likely to perform in the lowest 10% of scores on a battery of neuropsychological tests than those with low levels of salivary cotinine (0.0-0.1 ng/ml). The authors, therefore, suggested that high levels of secondhand smoke exposure might be related to increased odds of cognitive impairment. Similarly, using the Geriatric Mental State Examination as an assessment of dementia syndromes, a research team in China interviewed 5,921 individuals aged 60 or above and characterized their secondhand smoke exposure. The researchers found that dementia syndromes were significantly associated with exposure to secondhand smoke. It was reported that the more severe the dementia syndrome, the stronger the relationship with secondhand smoke exposure. Another study by Orsitto et al., conducted in Paradiso Hospital, Italy, found that patients with a diagnosis of mild cognitive impairment reported a significantly higher frequency of secondhand smoke compared to those with normal cognition.

While the cardiovascular and cancer risks associated with tobacco smoking are clear, the cognitive risks are complicated. Nicotinic stimulation may improve cognition but the effects of smoking may be toxic to the brain and cognitive function. Further, the effects may be experienced by those who never smoked due to second hand exposure. Other forms of nicotine delivery, including trans-dermal patch, are under investigation for cognitive benefits and indeed are worthy of study given how few agents are available to improve cognitive performance. Further studies are also needed to investigate the relationship between secondhand tobacco smoke and increased risk of cognitive disorders. Establishing that exposure to cigarette smoke may contribute to cognitive loss and dementia could provide additional motivation for smoking cessation and improve compliance with withdrawal and abstention.

References:
1. Anstey, K.J., von Sanden, C., Salim, A., O&rsquoKearney, R. Smoking as a risk factor for dementia and cognitive decline: a meta-analysis of prospective studies. American Journal of Epidemiology 2007 Aug 15 166: 367-78.
2. Barnes, D.E., Haight, T.J., Mehta, K.M., Carlson, M.C., Kuller, L.H., Tager, I.B. Secondhand smoke, vascular disease, and dementia incidence: findings from the cardiovascular health cognition study. American Journal of Epidemiology 2010 Feb 1 171(3): 292-302.
3. Chen, R., Wilson, K., Chen, Y., Zhang, D., Qin, X., He, M., Hu, Z., Ma, Y., Copeland, J.R. Association between environmental tobacco smoke exposure and dementia syndromes. Occupational and Environmental Medicine 2013 Jan 70(1): 63-9.
4. Levin, E.D., McClernon, F.J., Rezvani, A.H. Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization. Psychopharmacology (Berl) 2006 Mar 184(3-4): 523-39.
5. Llewellyn, D.J., Lang, I.A., Langa, K.M., Naughton, F., Matthews, F.E. Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement. British Medical Journal 2009 Feb 12 338: b462.
6. Orsitto, G., Turi, V., Venezia, A., Fulvio, F., Manca, C. Relation of secondhand smoking to mild cognitive impairment in older inpatients. Scientific World Journal 2012 2012: 726948.
7. http://www.who.int/mediacentre/factsheets/fs339/en/

Excerpted article as reprinted from IPA&rsquos newsletter, the IPA Bulletin , Volume 30, Number 6


Cigarette smoking and cognitive decline in midlife: evidence from a prospective birth cohort study

Objectives: The authors investigated the effects of cigarette smoking on midlife cognitive performance.

Methods: Multiple regression was used to test the association between cigarette smoking and changes in cognitive test scores among male and female members of the British 1946 birth cohort aged between 43 and 53 years.

Results: Smoking was associated with faster declines in verbal memory and with slower visual search speeds. These effects were largely accounted for by individuals who smoked more than 20 cigarettes per day and were independent of sex, socioeconomic status, previous (adolescent) cognitive ability, and a range of health indicators.

Conclusions: The present results show that heavy smoking is associated with cognitive impairment and decline in midlife. Smokers who survive into later life may be at risk of clinically significant cognitive declines.


Quitting Smoking Improves Memory

Former smokers have a better-functioning memory than those who still light up, a new study finds. On a practical test of their recollection ability, people who on average had quit smoking for 2.5 years performed 25 percent better than current smokers did. People who had never smoked scored 37 percent better than the smokers. "We already know that giving up smoking has huge health benefits for the body, but this study also shows how stopping smoking can have knock-on benefits for cognitive function, too," said study researcher Tom Heffernan, a psychology professor at Northumbria University in England. Lighting up, or learning? The researchers aimed to measure "real world" memory abilities by sending 69 study participants on a tour of a university campus. Twenty-seven were smokers, 18 were former smokers, and 24 never smoked. The participants were given a list of 15 locations around campus and an action to perform at each location. For example, upon reaching the library, participants were supposed to remember to check for messages on their cell phones upon reaching the sports center, they were supposed to remember to ask about the cost of membership. On average, the smokers performed 8.9 tasks correctly. The participants who had quit smoking averaged 11 correctly performed tasks, and those who had never smoked averaged 12.1. There were no differences between the groups in terms of their IQs, the study said. Previous studies showed that quitting smoking improves "retrospective memory," which is the ability to learn information and retrieve it later. The new study instead measured participants' "prospective memory," which is the ability to remember to carry out a particular action at some future point in time. For example, remembering to take medication at a certain time of day requires prospective memory. Previous research on the effect of smoking on prospective memory yielded mixed results, with some results showing smokers were worse off, and others showing no effect from smoking, the study noted. How does it work? Although it is unclear exactly how smoking may interfere with memory, research has shown that chronic smoking is linked to a breakdown, or atrophy, of parts of the brain. The researchers hypothesized that smoking could damage brain areas such as the prefrontal cortex, hippocampus or thalamus all of those regions have been linked in brain imaging studies to prospective memory, they said. Heffernan also has studied the effects of alcohol and marijuana on memory. He and the other researchers acknowledged that their new study was small and relied on self-reports of smoking, which would be subject to inaccuracy and dishonesty on the part of participants. Future work should follow a cohort of smokers and former smokers over time, they said. The study will be published in an upcoming issue of the journal Drug and Alcohol Dependence. Pass it on: Quitting smoking could improve people's memory abilities to rival those of people who have never smoked.

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Cigarette Smoking, Cognitive Performance, and Severe Mental Illness: Quitting Smoking Really Does Seem to Matter

Cigarette smoking is commonly associated with severe mental illness. As noted in an article by Vermeulen et al. in this issue (1), as many as two-thirds of community-dwelling people with severe mental illness are current smokers, and the likelihood that their relatives will smoke is elevated as well, compared with the general population. Smoking appears to be associated with severe mental illness across the entire lifetime course of the illnesses, and at the time of their first diagnosis, people who develop severe mental illness are much more likely than the population as a whole to be smokers (2). There are many reasons for this elevated rate of smoking, which have been examined in previous research.

Among the potential influences on smoking are genomic alterations in the alpha-7 nicotinic receptor gene complex, and these alterations are shared with first-degree relatives and are closely related to susceptibility to schizophrenia (3). Other nicotinic receptor genes have also been linked to schizophrenia (4). Moreover, nicotine normalizes, at least temporarily, the sensory gating abnormalities that are commonly seen in schizophrenia (5), possibly leading to a subjective sense of reduced stress and greater control over the strength and valance of environmental stimuli. In addition, nicotine has been shown to temporarily enhance cognition in a variety of nonsmoking populations, including people with schizophrenia (6). Treatment with agents that directly target nicotinic receptors has been shown in proof-of-concept studies to enhance cognitive performance in schizophrenia populations (7), but large-scale trials have not yet found any treatments that separate from placebo in phase 3 clinical trials (8).

Smoking prevalence, normalization of critical elements of neurobiological processing, potential cognition-enhancing effects, and genomic alterations all point to the reasons for smoking in severe mental illness. Many studies, such as those cited above, suggest a potentially beneficial role for nicotine. Why, then, do the results of the Vermeulen et al. study strongly suggest the opposite conclusion? Being a smoker is clearly bad for your cognitive performance the more you smoke, the worse your performance and quitting or reducing smoking leads to improved cognitive functioning.

The Vermeulen et al. study had a very large sample and was longitudinal, with relatives and healthy control subjects also examined, and the researchers were able to examine the effects of quitting smoking on cognition. Their findings fit into the bigger picture of smoking and cognition, in that in the general population, the longer you smoke and the more you smoke, the greater your risk for late-life cognitive decline. The findings also fit into the picture of severe mental illness, in that current smoking in both schizophrenia and bipolar disorder is associated not only with poorer cognition but also with greater real-world disability and challenges in the ability to perform everyday living tasks, as reported in a previous study by a different research group (9). In that study, the effects of smoking on cognition and everyday functioning did not differ by diagnosis across schizophrenia and bipolar illness. Notably, former smokers were found to perform equivalently to never-smokers and to outperform current smokers by 0.4 standard deviations on composite measures of cognitive performance. Time since quitting was not correlated with cognitive performance, suggesting that effects on cognition could be rapid, as suggested in the Vermeulen et al. study.

Multiple critical take-home points may be drawn from the data in the Vermeulen et al. study. First, stopping smoking leads to a relatively rapid recovery of cognitive performance, consistent with previous cross-sectional studies. Second, the number of cigarettes smoked per day was inversely correlated with cognitive performance. Third, the smoking-related adverse effects on processing speed were seen in both patients and healthy control subjects, indicating that the adverse effects of cigarette smoking on processing speed were not diagnosis specific.

There are some questions that cannot be answered with these data as they are presented. The first is why smokers who continue smoking experience more adverse cognitive effects over time instead of fewer. It is possible that these smokers are noticing changes associated with improvements in sensory gating after each cigarette and feel more comfortable immediately after nicotine use. The paradox of initial, short-term pleasurable effects, including cognitive enhancement, driving addiction and then subsequent dysphoria with adverse cognitive effects in chronic users is well known in the nicotine literature. Nicotine is an extremely effective agonist at nicotinic cholinergic receptors, and, at the same time, chronic exposure leads to desensitization and inactivation of these very receptors. Smokers, including those with mental illness, continue to smoke to recapture the short-term effects, all the while increasing the chronic levels of nicotine that then block their receptors (10).

The second question is why some people with schizophrenia are able to quit smoking while others continue. The authors do not present analyses of the cognitive performance, while smoking, of those who subsequently quit. It would be of interest to see if they had less cognitive impairment beforehand or smoked fewer cigarettes. The third question is why some people with schizophrenia never start smoking. If there is shared vulnerability to psychosis and smoking (or at least abnormalities in the nicotinic system), then we might expect that the minority of patients with severe mental illness who never smoked would look fundamentally different in some ways from those who do or did smoke. Comparisons of never smokers and quitters (e.g., 9) have found minimal differences in symptoms or cognition between them, even in the context of substantial lifetime smoking on the part of quitters.

The data from Vermeulen et al. make a powerful argument for interventions aimed at smoking cessation in individuals with severe mental illness. The rapid return of cognitive performance in quitters with severe mental illness, particularly in a domain with considerable functional relevance, is a strong argument for rapid benefits. The previously demonstrated extension of smoking-related cognitive deficits to everyday functioning and functional capacity suggest considerable morbidity reduction with smoking cessation as well. Finally, it is not just patients with schizophrenia who experience smoking-related adverse effects these treatment efforts should be extended to people with bipolar disorder and major depression as well.

Dr. Harvey has received research grant support from Takeda and the Stanley Medical Research Foundation he has received consulting fees or travel reimbursements from Akili, Allergan, Biogen, Boehringer Ingelheim, Forum Pharma, Genentech (Roche), Intra-Cellular Therapies, Jazz Pharmaceuticals, Lundbeck, Minerva, Otsuka America (Otsuka Digital Health), Sanofi, Sunovion, Takeda, and Teva and he receives royalties for the Brief Assessment of Cognition in Schizophrenia. Dr. Freedman has reviewed this editorial and found no evidence of influence from these relationships.

1 Vermeulen JM, Schirmbeck F, Blankers M, et al. : Association between smoking behavior and cognitive functioning in patients with psychosis, siblings, and healthy control subjects: results from a prospective 6-year follow-up study . Am J Psychiatry 2018 175:1121–1128Link , Google Scholar

2 Wade D, Harrigan S, Edwards J, et al. : Course of substance misuse and daily tobacco use in first-episode psychosis . Schizophr Res 2006 81:145–150Crossref, Medline , Google Scholar

3 Mexal S, Berger R, Logel J, et al. : Differential regulation of α7 nicotinic receptor gene (CHRNA7) expression in schizophrenic smokers . J Mol Neurosci 2010 40:185–195Crossref, Medline , Google Scholar

4 Jackson KJ, Fanous AH, Chen J, et al. : Variants in the 15q25 gene cluster are associated with risk for schizophrenia and bipolar disorder . Psychiatr Genet 2013 23:20–28Crossref , Google Scholar

5 Adler LE, Hoffer LD, Wiser A, et al. : Normalization of auditory physiology by cigarette smoking in schizophrenic patients . Am J Psychiatry 1993 150:1856–1861Link , Google Scholar

6 Jubelt LE, Barr RS, Goff DC, et al. : Effects of transdermal nicotine on episodic memory in non-smokers with and without schizophrenia . Psychopharmacology (Berl) 2008 199:89–98Crossref , Google Scholar

7 Keefe RS, Meltzer HA, Dgetluck N, et al. : Randomized, double-blind, placebo-controlled study of encenicline, an α7 nicotinic acetylcholine receptor agonist, as a treatment for cognitive impairment in schizophrenia . Neuropsychopharmacology 2015 40:3053–3060Crossref, Medline , Google Scholar

8 Haig GM, Bain EE, Robieson WZ, et al. : A randomized trial to assess the efficacy and safety of ABT-126, a selective α7 nicotinic acetylcholine receptor agonist, in the treatment of cognitive impairment in schizophrenia . Am J Psychiatry 2016 173:827–835Link , Google Scholar

9 Depp CA, Bowie CR, Mausbach BT, et al. : Current smoking is associated with worse cognitive and adaptive functioning in serious mental illness . Acta Psychiatr Scand 2015 131:333–341Crossref, Medline , Google Scholar

10 Harris JG, Kongs S, Allensworth D, et al. : Effects of nicotine on cognitive deficits in schizophrenia . Neuropsychopharmacology 2004 29:1378–1385Crossref, Medline , Google Scholar


Cigarette smoking and cognitive performance

Requests for reprints should be addressed to: George J. Spilich, PhD, Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA.Search for more papers by this author

Department of Psychology, Delaware State College, Dover, DE 19901, USA

Allegheny County Law Department, 445 Fort Pitt Boulevard Suite 300, Pittsburgh, PA 15219, USA

Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA

Requests for reprints should be addressed to: George J. Spilich, PhD, Department of Psychology, Dunning Science Center, Washington College, Chestertown, MD 21620, USA.Search for more papers by this author

Department of Psychology, Delaware State College, Dover, DE 19901, USA

Allegheny County Law Department, 445 Fort Pitt Boulevard Suite 300, Pittsburgh, PA 15219, USA

Abstract

While some investigations into the relationship between smoking and cognitive performance have reported that smoking facilitates performance, other research has come to the opposite conclusion. A review of the literature suggests that this variance in results may be due to differences among studies in design (comparing smokers only with deprived smokers rather than with non-smokers) and also to differences in task demands. Therefore, performance of smokers having just smoked, matched smokers deprived for a brief period, and also non-smokers was contrasted on a series of tasks which ranged from repetitive and perceptually-bound tasks to complex, dynamic tasks dependent upon long-term memory. It was found that while cigarette smoking had no negative effect upon performance for simple perceptual tasks, smoking was found to exert measurable negative effects upon performance for more complex information processing tasks.


Footnotes

Statement 2: Contributors Qian Guo was the Project Manager of China Seven Cities Study (CSCS). She conducted the present smoking attribution study and wrote the manuscript. Carl Anderson Johnson was the Principal Investigator of CSCS and Principal Investigator of TTAURC. He worked closely with Qian Guo on this study and provided instructive and mentor assistance throughout the process. Jennifer B. Unger, Stanley P. Azen, and David P. MacKinnon provided input on statistical analysis and interpretation. All authors contributed to and have approved the final manuscript.

Statement 3: Conflict of Interest All authors declare that they have no conflicts of interest.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.


Methods

Participants

This study used data from ELSA, a panel study designed to be representative of individuals aged 50 years and older living in England.19 A total of 11 391 participants took part in Wave 1 in 2002–2003. Wave 1 participants were individuals who had previously taken part in the Health Survey for England, were born before 1 March 1952 and were living in a private household in England at the first wave.19 These participants have been followed up every 2 years, and the sample has been refreshed at subsequent waves to maintain a representative sample of participants aged over 50 years. More information on this cohort is provided elsewhere.19 The current sample consists of participants who completed the Wave 2 (2004–2005) interview (n=8780) this is the first wave in which health literacy was assessed. Ethical approval was granted. This study conformed to the principles embodied in the Declaration of Helsinki.

Measures

ELSA interviews were carried out using computer-assisted interviewing in the participants’ own home.

Smoking

Two aspects of smoking status (ever vs never smoker and current vs former smoker) were the outcome variables in these analyses. Participants were asked ‘Have you ever smoked cigarettes?’. Participants were categorised as ever smokers if they answered ‘yes’ and never smokers if they answered ‘no’ at either Wave 1 or 2. Ever smokers were additionally asked ‘Do you smoke cigarettes at all nowadays?’. Ever smokers who answered ‘yes’ to smoking cigarettes nowadays at Wave 2 were categorised as current smokers, whereas ever smokers who answered ‘no’ were categorised as former smokers.

Health literacy

Health literacy was assessed at Wave 2 using a four-item comprehension test previously used in the International Adult Literacy Survey.20 Participants were presented with a piece of paper containing instructions similar to those that would be found on a packet of over-the-counter medication. Participants were instructed to read the medicine label and were then asked four questions about the information on this label (eg, ‘what is the maximum number of days you may take this medicine?’). The label was available to the participant to refer to at any time. This task was designed to measure the skills thought to be required to understand and use health materials correctly, such as the ability to read and use numbers in a health context.21 One point was awarded for each correctly answered question (range 0–4). As has been done in previous ELSA studies,22 23 health literacy scores were categorised as ‘adequate’ (4/4 correct) or ‘limited’ (≤3 correct).

Cognitive function

Four tests of cognitive function that were administered at Wave 2 of the ELSA study were used here. These tests are thought to assess episodic memory, executive function and processing speed these are cognitive domains which tend to decline on average with increasing age.24 25 In the word list recall test, participants heard a list of 10 words which they had to recall immediately (immediate recall test) and again after a short delay (delayed recall test). The score on each occasion was the number of words remembered (range 0–10). Executive function was assessed using categorical verbal fluency (number of animals named in 60 s). The letter cancellation test, in which participants were to scan rows of letters and score out all Ps and Ws, was used to measure processing speed. The score is the number of Ps and Ws scored out in 60 s. Exploratory factor analysis (EFA) using principal axis factoring was used to derive a composite measure of general cognitive ability. Scores on the four cognitive tests were entered into the EFA. Prior to this, individuals who scored 0 or greater than 4 SD above the mean on the animal fluency test and the letter cancellation test were removed. Scores of 0 indicate that the participant did not understand the task, and scores 4 SD above the mean were seen as dubiously high given the 1 min time limit for these tests. One unrotated factor was extracted which accounted for 44% of the total variance in the four cognitive tests. The loadings of the tests were: immediate word recall=0.78 delayed word recall=0.83 animal naming=0.53 letter cancellation=0.42. This factor score was converted to a z-score (mean=0.00, SD=1.00) and was used as a measure of general cognitive ability.

Covariates

Age in years, sex, age of leaving full-time education and occupational social class were used as covariates. For confidential reasons, owing to there being few of them, participants aged over 90 years have had their age set to 90. Participants were asked at what age they left continuous full-time education (recorded as not yet finished, never went to school, 14 or under, at 15, at 16, at 17, at 18, and 19 or over). For the purpose of this study, age of leaving full-time education was categorised as 14 years or under, 15–16 years, 17–18 years and 19 years or over. Occupational social class was categorised using the National Statistics Socio-economic Classification 3 categories: managerial and professional, intermediate and routine and manual.26

Patient and public involvement

Participants were not involved in the development of any part of this study.

Statistical analysis

Two sets of analyses were carried out. First, ever smokers were compared with never smokers second, current smokers were compared with former smokers. To determine whether ever versus never smokers and current versus former smokers differ on health literacy, general cognitive ability and sociodemographic variables, t-tests were used for normally distributed continuous variables, Mann-Whitney U tests were used for non-normal continuous variables and χ 2 tests were used for categorical variables. Rank-order correlations were calculated between the predictor variables to examine any bivariate associations between these variables. Binary logistic regression was used to examine the independent associations of health literacy and general cognitive ability on smoking status. Age and sex were entered in all models. Health literacy and general cognitive ability were entered individually in models 1 and 2, respectively. To determine whether both health literacy and general cognitive ability are independently associated with smoking, both predictors were included in model 3. Model 4 additionally adjusted for age of finishing full-time education and occupational social class to determine whether any associations between health literacy, cognitive function and smoking remained after controlling for these sociodemographic variables.


Smoking tied to declines in memory, cognitive abilities

As adults age, they're more likely to experience declines in memory and cognitive abilities. New research suggests that smoking might significantly speed up those declines.

For the study, researchers analyzed data from an ongoing study of aging that involved nearly 8,800 participants who were an average of 66 years old, a majority of whom were females.

They was given tests that measured blood pressure, cholesterol levels and body mass index (BMI), and were also asked about their smoking habits. Participants were also tested for their risks for stroke and heart disease, and were given tasks that helped measure their memory and cognitive abilities after four and eight-year follow-up periods.

The researchers found those at the highest risk for stroke had lower scores in cognition, memory and executive processing as measured by the tasks. High blood pressure specifically was associated with lower cognitive and memory scores after the eight years, while high BMI -- used to measure if a person is overweight or obese -- was also tied to lower memory scores.

However across the board, smoking was associated with lower performance on all cognitive measures studied at four and eight-year intervals.

"Smoking emerged as the most consistent predictor of cognitive decline," wrote the study's authors, lead by Dr. Alex Dregan, a public health sciences researcher at Kings College London. The study appears in the Nov. 25 issue of Age and Aging.

The authors say their study shows that the most promising preventive approach to reduce cognitive declines should consider the potential multiple causes, such as smoking and cardiovascular risks.

Trending News

"Specifically, interventions to limit cognitive decline should consider the combined effect of multiple vascular risk factors rather than focusing on the management of individual-risk factors as routinely performed in the past," they wrote.

Alzheimer's disease is the most common form of dementia, affecting 5.4 million Americans according to the U.S. Alzheimer's Association. The disease, which typically occurs in people 65 and older, starts with mild memory loss and progresses to the inability to carry a conversation or to recognize one's environment. It is the sixth-leading cause of death in the United States.

Other risk factors for cognitive decline include diabetes and lack of physical exercise.


Psychological Perspectives of Smoking

Psychological perspectives of smoking This essay will consider how each of the 5 psychological perspectives explain smoking. I will cover the psychodynamic, the behaviouristic, the biological, the cognitive and the humanistic approach. Psychodynamic approach The psychodynamic approach views behaviour in terms of past childhood experiences, and the influence of unconscious processes. There are five psychosexual stages in Freud’s theory, the first being the oral stage during which the infant focuses on satisfying hunger orally.

Sigmund Freud believed that during this stage of development the person can become fixated in the oral stage of development.

An infant’s pleasure and comfort centres on having things in the mouth during this psychodynamic stage. If the mother weaned too early, it may fail to be resolved later in life which can then lead to oral fixation. The action of putting something in their mouth (a cigarette) is what fulfils this oral fixation. Freud’s evidence for this was through his studies on ‘Little Hans’.

Hans’ father would exchange letters between him and Freud about little Hans’ dreams and fears and was able to place him into one of the five psychosexual stages. This study was flawed in the way that all of the material Freud used for the study was second hand. One of the strengths of the approach is that it provides a valuable insight into how early experiences or relationships can affect our adult personality, having said this the approach is too focused on sex and is biased. The behaviourist approach The behaviourist approach explains human behaviour as being learned from peers and the environment.

The approach suggests that smoking may be explained through learning through classical conditioning. Smoking may be acquired from their peers which results in acceptance and happiness, therefore smoking alone results in the conditioned response of pleasure. Young people may have observed others smoking and them being popular or getting praise, either their peers or through popular films and see those as successful or popular therefore may imitate this behaviour. Ivan Pavlov conducted an experiment where he had surgically implanted tubes into the cheeks of dogs to monitor the secretion of saliva whilst the dog was eating. Pavlov, 1902)

He noticed that the dog started to salivate before the food was put in its mouth. He then presented to food to the dog whilst playing the sound of a metronome, eventually the dog started to salivate when just hearing the metronome alone. This can be related to smoking using the following model: Conditioning diagram Peer groupsbefore conditioningacceptance and happiness Peer groups + Smokingduring conditioningacceptance and happiness Smokingafter conditioningacceptance and happiness One of the main strengths of the behaviourist approach is that it focuses only on behaviour that can be observed and manipulated.

Therefore, this approach has proved very useful in experiments under laboratory conditions. On the other hand this has been criticized for suggesting that most human behaviour is mechanical, and that human behaviour is simply the product of stimulus-response behaviours. The biological approach The biological approach looks at our genetics to construct a reason why we act the way we do and why we develop abnormal behaviours. This approach suggests that the reason people smoke is a biological addiction from a chemical in cigarettes called nicotine.

Nicotine is a chemical that alters the brains behaviour by creating an addiction to nicotine which causes smokers to crave a cigarette as it gives them the nicotine they need to fulfil this addiction. When smokers try to stop, the loss of nicotine changes the levels of dopamine and noradrenaline. This can make them feel anxious, depressed and irritable. Evidence for this has been given by the NHS. On average 20% of adults in the UK have an addiction to smoking. (NHS, 2012) As this approach is solely based on empirical evidence from a biological perspective it relies on hard evidence giving a clear analysis.

The approach however, doesn’t take into consideration, thoughts feelings and the effect of the environment. The cognitive approach The cognitive approach focuses on mental processes, perception, and language as a way of explaining and understanding human behaviour. The approach focuses on the importance of mental processes such as beliefs, desires and motivation in determining behaviour. People who smoke may see smoking as doing something that is considered a taboo thing to do giving them a certain enjoyment by ‘staring the face of danger’.

Evidence can be shown for this in the suspension bridge ‘Love on a suspension bridge’ experiment conducted by Dutton & Aron in 1974 . (Billingham, 2008) In this study, an attractive female experimenter approached men as they crossed either a high, rickety suspension bridge or a low safe bridge and asked them to answer some questions and write a brief story in relation to a picture and to call the experimenter for the results. Men who walked across the high bridge were more likely to write a more sexual story and were more likely to call the experimenter.

This suggests that when the subjects heart rate was raised they were more likely to have an attraction to something. This approach is good because it uses lab experiments rather than speculation but is also considered as being too basic and deterministic I. E. one input, a decision is made and then an output created and doesn’t take in to consideration any other effects. The humanistic approachCongruence diagram The humanistic approach emphasises the study of the whole person rather than studying individual components. It views every individual as being unique. The main concept of the humanistic approach is to reach congruence.

This is a state of consistency between the ‘real self’ and the ‘ideal self. This can be explained in the following diagram. The closer you are to reaching your idea l self, the more over lapped the two circles become. Smokers smoke to feel good. According to Maslow’s hierarchy of needs this is part of the self-actualisation process. (Billingham, 2008) This is their unique desire to achieve their highest potential as individuals. The approach is effective as it is based on free will and the individuals own experiences. On the other hand the approach is too subjective and lacks scientific research to support its ideas.


Watch the video: 31 Μαΐου 2019: Παγκόσμια Μέρα Κατά του Καπνίσματος, Κάπνισμα και Υγεία των Πνευμόνων (June 2022).


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