Smoking sex samples-Cigarette Smoking | JNCI: Journal of the National Cancer Institute | Oxford Academic

Andrew W. Cigarette smoking is the largest preventable risk factor for morbidity and mortality in developed countries. Dramatic changes in the prevalence of cigarette smoking in the second half of this century in the United States i. Current smoking in the United States is positively associated with younger age, lower income, reduced educational achievement, and disadvantaged neighborhood environment. Daily smokers smoke cigarettes to maintain nicotine levels in the brain, primarily to avoid the negative effects of nicotine withdrawal, but also to modulate mood.

Smoking sex samples

Smoking sex samples

Smoking sex samples

Smoking sex samples

Smoking sex samples

In the Journals. Racial and ethnic differences in serum cotinine levels of Smoking sex samples smokers: Third National Health and Nutrition Examination Survey, Pomerleau CS. Genetics of nicotine response in four inbred strains of mice. Nicotine dependence is a model for drug dependence, where tobacco smoking fulfills the physiologic, behavioral, and social characteristics of a dependence syndrome, but it also acts as a gateway drug for other drugs of abuse EBioMedicine 2129—36 We optimized the feature spaces that were used to train the models for age prediction first excluding smoking status using a multifactorial adaptive statistical arbitrage model 13 for subsets of samples with Smokinf numbers of measured markers.

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AIM: To evaluate the prevalence, socio-demographic patterns and behavioural characteristics of tobacco smoking in a pilot group of PONS respondents.

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Smoking used to be seen as glamorous and seductive. You know the scene: a couple lies naked in bed, sheets tangled, basking in the afterglow of lovemaking.

A cigarette is lit, shared and savoured. Eroticised smokers have shown up in countless advertisements and cinematic frames, looking sophisticated, glamorous and seductive. There is nothing like sharing a post-coital drag on a cigarette with your lover. At least, that's the message pushed in countless sex scenes. In reality, cigarettes are far from erotic. Aside from the obvious cosmetic turn-offs like bad breath, cigarette chemicals irritate blood vessels, causing cholesterol to get stuck to artery walls.

This gunk can stiffen into plaque, constricting blood flow and can make it hard to get stiff elsewhere. Vasoconstriction may also reduce circulation to lady parts, plus cigarettes are linked with increased risk of vaginal bacterial infections. Smoking is a vascular cock block and many smokers are now switching to e-cigarettes to avoid the unsexy effects of cigarettes.

Studies show that quitting cigarettes boosts sexual arousal and satisfaction. So butt out for the love of the almighty smash. But the trope sidelines an inconvenient truth - cigarettes are far from sexy. In reality, that idealised couple sharing a cigarette in bed would face more obstacles to great sex than non-smoking lovebirds. As a result, non-smokers are now about three times more attractive to prospective partners compared to people who smoke. Beyond these skin-deep ways that cigarettes mess with sex lives, smokers are also more likely to develop chronic medical conditions that get in the way of getting off.

Smoking has particularly deleterious consequences for male sexual performance. Men who smoke are twice as likely as non-smokers to develop erectile dysfunction and impotence.

When a man is aroused, his brain sends a signal to widen the arteries in order to boost blood flow to the penis, which requires about eight times as much fluid to maintain an erection compared to its flaccid state.

Chemicals in tobacco irritate the linings of blood vessels, causing arterial walls to accumulate cholesterol and other molecules that stiffen into plaque over time.

The good news is that smokers affected by erectile dysfunction may start to get their mojo back just weeks after they butt out for good. Not only does this make it easier to maintain an erection, in time it decreases your risk of smoking-related heart disease, so men can play hard in bed without worrying as much about cardiac risk factors like stroke or heart attack.

The link between smoking and sexual performance in women is not so straightforward, in part because arousal is, broadly speaking, less understood in women than in men.

We do know that female sexual pleasure, including orgasms, are facilitated by increased blood flow to the genitals. When a woman gets turned on, the neurovascular system sends about three times as much blood to the vagina, boosting oxygenation and lubrication of vaginal tissues. This has led to speculation that female smokers may experience less sexual sensitivity compared to non-smokers, for the same reasons that male smokers are more at risk of erectile dysfunction.

More research needs to be done before that connection is made explicit. It is clear, however, that smoking raises the risk of contracting certain vaginal infections. Vaginas are home to diverse communities of microbes, called the vaginal flora, which normally keep the genital tract healthy and free from infection.

Chemicals in cigarettes have been found in the cervical mucus and vaginal flora of female smokers, which heightens the odds of contracting conditions like bacterial vaginosis, genital herpes, and chlamydia.

Smoking is also a risk factor for developing cervical cancer. Pain during sex is a major symptom of this disease, which is yet another way that cigarettes can disrupt female sexual satisfaction. Generally, both male and female smokers are more likely to be exhausted by physical exercise relative to their nonsmoking peers, because smoking reduces. One of the big upsides to kicking the habit is a sense of renewed vitality, and that can translate into more satisfaction and endurance in the bedroom, too.

Some smokers have switched to e-cigarettes with the hope of dodging the unsexy side effects of cigarettes. In fact, there even appears to be interest in vape liquids as aphrodisiacs. But most vape liquids still contain nicotine, which can put a damper on your love life — these effects of nicotine might be transient, but it could well be enough to kill off your night of passion.

If you separate nicotine from all the other gross stuff in a cigarette, it still acts as a vasoconstrictor, meaning that it narrows and hardens blood vessels regardless of whether it is smoked or vaped with other chemicals.

Nicotine is also linked with lower libidos in both men and women. Studies have found that isolated nicotine intake from chewing gum inhibits female sexual arousal by about 30 percent and male sexual arousal by 23 percent. There are still plenty of people out there who fetishise smoking and some people still do find the habit sexy. But in nations that have launched anti-smoking campaigns, which often rely on unflattering portraits of smokers, the link between sex and the cigarette has, well, gone up in smoke.

Smoking makes it much more difficult to men to maintain an erection, and may also reduce sexual arousal in women Smoking has particularly deleterious consequences for male sexual performance. Smoking throws off the delicate ecological balance of the vagina, which can lead to infections and diseases that make sex painful It is clear, however, that smoking raises the risk of contracting certain vaginal infections. Generally, both male and female smokers are more likely to be exhausted by physical exercise relative to their nonsmoking peers, because smoking reduces lung capacity and blood flow.

Vaping is Less Harmful Compared to Smoking. Nicotine is a solo boner-kill.

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Smoking sex samples

Smoking sex samples

Smoking sex samples

Smoking sex samples

Smoking sex samples. Categories

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Andrew W. Cigarette smoking is the largest preventable risk factor for morbidity and mortality in developed countries. Dramatic changes in the prevalence of cigarette smoking in the second half of this century in the United States i. Current smoking in the United States is positively associated with younger age, lower income, reduced educational achievement, and disadvantaged neighborhood environment.

Daily smokers smoke cigarettes to maintain nicotine levels in the brain, primarily to avoid the negative effects of nicotine withdrawal, but also to modulate mood. Regular smokers exhibit higher and lower levels of stress and arousal, respectively, than nonsmokers, as well as higher impulsivity and neuroticism trait values. Nicotine dependence is the single most common psychiatric diagnosis in the United States, and substance abuse, major depression, and anxiety disorders are the most prevalent psychiatric comorbid conditions associated with nicotine dependence.

Studies in twins have implicated genetic factors that explain most of the variability in vulnerability to smoking and in persistence of the smoking phenotype. Future research into the causes of smoking must take into account these associated demographics, social factors, comorbid psychiatric conditions, and genetic factors to understand this complex human behavior.

Lung cancer is the largest single cause of cancer-associated mortality 3 and is the most common cause of smoking-related mortality in the United States 4. The attributable risk from smoking for oral, pharyngeal, and esophageal cancers is substantial, although less than that for lung cancer 5 , 6. The attributable risk from both smoking and alcohol consumption accounts for the majority of both oral and pharyngeal cancers 5 and of esophageal cancer 7.

Morbidity and mortality attributable to smoking would decline in the future if reductions in smoking prevalence were to be observed. However, despite dramatic declines in adult male smoking prevalence in the United States observed from the s through the s 8 , the decline in current adult smoking prevalence slowed by about 9 , and recent surveys of current smoking in youth, defined as cigarette use on at least one of the last 30 days preceding the survey, show a statistically significant increase from Projected demographic and smoking prevalence trends suggest that the absolute number of current smokers in the United States, about 47 million individuals in , will continue to increase, especially in those below the poverty threshold, in those with less than 13 years of education, and in those greater than or equal to 65 years of age 9, Smoking prevalence in men worldwide is higher than it is in the United States, while smoking prevalence among women worldwide is usually less than the prevalence in men, although it has equaled or exceeded that in men in some northern European countries 19 , Because of the delayed health effects of smoking, morbidity and mortality in developing countries attributable to smoking have not yet surpassed those in developed countries but are likely to do so in the next century 20 , The study of biomarkers in smoking-attributable cancer has concentrated on measures of exposure i.

The investigation of such biomarkers is predicated on the assumption that an enhanced understanding of metabolic mechanisms will help to identify susceptible groups or individuals and direct future research or prevention efforts.

Another group of risk factors for lung cancer and other smoking-related cancers are those that are associated with smoking, its initiation, and its persistence. We will review factors associated with current and persistent smoking that have been studied by use of pharmacologic, epidemiologic, behavior genetic, psychologic, and psychiatric perspectives.

The identification of those factors consistently and statistically significantly associated with smoking will provide biologic and social variables with which to investigate mechanisms that contribute to the persistence of this behavioral phenotype. Improved understanding of these mechanisms may enable improved cancer prevention and control efforts. The purpose of this review is to describe and evaluate demographic, psychosocial, and biologic factors found to show statistically significant associations with current and persistent cigarette smoking in order to make research recommendations concerning which covariates are important in the study of the human phenotype of cigarette smoking.

Reports from the Surgeon General, monographs, and internet sites were also searched for relevant studies and evaluated for inclusion in this review. The purpose of the search was to gather studies on the cigarette smoking phenotype from the epidemiologic, pharmacologic, psychiatric, and psychologic literature.

Studies evaluated for associated factors included the following: case-control and case-case studies of demographic, genetic, psychiatric, and psychologic variables; factor analyses of case series; twin studies; and animal model studies.

To distinguish between studies included or excluded, the criteria of sample size, validated or controlled measures of phenotype, established analytic approaches, and reasonable interpretation were used for evaluation. The narrative method was used to provide examples of the evidence presented in the studies reviewed.

The method used to make research recommendations was to identify those phenotypes that were consistently and statistically significantly associated with current cigarette smoking.

Addiction to nicotine has been established as the psychopharmacologic mechanism that maintains cigarette smoking behavior Nicotine activates the brain's mesolimbic dopaminergic reward system 24 , 25 and produces dependence resulting in physical and neurobiologic withdrawal symptoms on abrupt cessation 26 , In rodent and primate animal models of drug addiction, once study subjects are trained in a controlled schedule paradigm to avoid the aversive effects of high concentrations of nicotine, nicotine is self-administered 28 - The increased numbers of nAChRs upon chronic nicotine treatment is associated with the development of behavioral tolerance to nicotine in animal models and is statistically significantly related to intensity and duration of smoking history in human postmortem brain 34 , Nicotine also acts as an antagonist, not because the increased numbers of nAChRs are associated with an increase in nAChR messenger RNA 39 , 40 or a change in binding parameters of nicotine to the receptor 33 - 35 but rather because of a reduction in nAChR turnover and accumulation of nAChR at the cell surface Smokers of cigarettes increase smoking intensity, smoking rate, or inhalation to maintain levels of nicotine, as measured by plasma levels of nicotine in both ad libitum and laboratory smoking settings 43 - Nicotine absorption per cigarette has been measured both by graphical methods from nicotine concentration curves obtained from plasma blood measurements 46 and by parametric calculation by use of stable isotope studies of nicotine to cotinine conversion and nicotine and cotinine clearance values obtained in inpatient-infusion studies These studies suggest that smokers are extracting approximately mg of nicotine per cigarette.

The total amount of nicotine per cigarette measured by smoking machines by use of human smoking parameters of puff volume, duration, and frequency is about mg per cigarette 50 , 51 , suggesting that smokers absorb more than half of the inhaled nicotine. However, none of these methods measures the peak brain concentration of nicotine, which is presumed to be the major pharmacologic factor that mediates reward, dependence, and the development of tolerance. Studies of dosing kinetics in animal models demonstrate the development of higher levels of tolerance with higher peak concentrations 31 , One behavioral mechanism responsible for differences in nicotine consumption may be related to variation in nicotine and cotinine metabolism 53 - Nicotine from tobacco smoke is absorbed quickly in seconds throughout the body on initial dosing 46 , 48 and then is eliminated with a half-life of hours The typical smoker experiences a nicotine concentration nadir in the morning after overnight abstinence and then smokes to increase nicotine levels over the first few hours of the day and to maintain a plateau throughout the remainder of the day Clearance of nicotine in humans is primarily diurnal, peaking at midday, with spikes of increased clearance after meals, which is concordant with increased human smoking rates early in the day, lowest smoking rates in the evening, and increased smoking after meals P 2A6 activity varies approximately fold in humans as measured by analysis of protein levels and in kinetic experiments with liver samples 58,62, The basis for constitutive differences in activity has been associated with variant CYP2A6 alleles encoding inactive enzyme 62, A statistically significantly reduced frequency of two CYP2A6 null alleles in nicotine and alcohol -dependent smoking-clinic patients versus never nicotine-dependent individuals and a statistically significant negative association with the numbers of cigarettes smoked per week have been reported This study needs to be replicated in additional samples to confirm the possible role of inherited variation at the CYP2A6 locus in smoking behavior.

Plasma and urinary nicotine and cotinine concentrations have repeatedly been found to be associated with the number of cigarettes smoked per day 69 - Since cotinine has a half-life an order of magnitude greater than that of nicotine, it is useful as a biomarker in smoking surveys, smoking cessation trials, and the assessment of exposure to environmental cigarette smoke 72 , Interindividual variation in the conversion of nicotine to cotinine and in the clearance of cotinine may have effects on nicotine consumption and dependence For example, cotinine levels were found to be higher in African-Americans than in Caucasian-Americans or Mexican-Americans, after adjustment was made for reported cigarette smoking While nicotine metabolism was not found to be statistically significantly different in African-Americans and Caucasian-Americans, mean nonrenal and total metabolism clearance of cotinine was shown to be significantly lower in African-Americans than in Caucasian-Americans 74 , Calculation of nicotine intake per cigarette on the basis of the inpatient infusion studies also indicates that African-Americans absorb statistically significantly more nicotine per cigarette smoked than do Caucasian-Americans This suggests that differences in the numbers of cigarettes smoked among African-American and Caucasian-American smokers 76 , 77 may be influenced by metabolic differences between the groups.

Evidence for genetic determinants affecting the smoking phenotype has steadily accumulated both from studies of substance abuse in animals and from analysis of the contributions of genetics and personality to substance abuse in humans 78 , Two recent linkage studies in humans 80 , 81 have indicated regions of the genome in which loci affecting nicotine dependence and ever smoking may be found with further work.

However, an appreciation of the neurotransmitter-related mechanisms involved in reward circuits in the human brain has suggested many candidate loci potentially associated with nicotine dependence The first genetic association studies in humans at dopaminergic loci 82 - 88 have reported statistically significant differences in the allele frequencies between smokers and nonsmokers at markers linked to the genes coding for the D1, D2, and D4 dopamine receptors and at the dopamine transporter, consistent with the dopaminergic reward hypothesis of nicotine dependence As in some previous studies of the D2 dopamine receptor in case-control studies of substance abuse 90 , the less frequent allele A1 at a genetic marker flanking the dopamine receptor D2 coding sequence DRD2 was found to be at a higher frequency in the collections of smokers versus nonsmokers 82 , In a sample of smokers undergoing a limited smoking cessation intervention, a protective association with a particular allele allele 9 at the dopamine transporter SLC6A3 was observed with smoking status, age at smoking initiation, and history of quitting, and the protective association with smoking status was stronger in those individuals with DRD2 A2 genotypes Since the DRD2 A1 allele has been found previously to be associated with lower D2 receptor densities 91 and the SLC6A3 allele 9 has been associated with excess dopamine after cocaine abuse 92 , this suggests that the protective association with smoking status observed may be due to normal densities of DRD2 receptors and increased synaptic dopamine that may provide some resistance to nicotine dependence At the D4 dopamine receptor locus, allele DRD4.

In Caucasian-Americans, a statistically significant association of allele 4 of the DRD4 receptor not associated with novelty seeking with smoking for the regulation of mood in depressed smokers was observed 87 , suggesting that the DRD4 locus may affect smoking behavior in depressed individuals as well as increase vulnerability to nicotine dependence in some populations These preliminary candidate gene studies need to be repeated in larger samples, in samples with similar and different ethnic origins, and in family-based samples to confirm the effect of these alleles on vulnerability to nicotine dependence, to explore the effect in samples that differ in allele frequency and smoking prevalence, and to control for potential confounding in case-control samples.

Future studies involving neurobiologic candidate loci that potentially affect smoking behavior should also emphasize the analysis of functional genetic polymorphisms or of linkage disequilibrium structure to identify haplotypes potentially carrying functional polymorphisms Genetic epidemiologic studies using the twin-study design 95 , where multiple genetic and environmental risk factors and a threshold disease model are modeled by use of concordance data in monozygotic and dizygotic twins, have estimated the effects of genetic and environmental factors on current smoking, smoking initiation, and smoking persistence From the same studies, the mean additive genetic effect on the liability to smoking initiation i.

Thus, twin studies estimate that the majority of the liability to become and to remain a smoker is explained by additive genetic factors. A variable remaining portion of the risk is estimated to be related to specific environmental effects, but there is no consistent, statistically significant evidence for a shared or common environment effect.

To assess whether the decline in smoking initiation in men and the increase in smoking initiation in women have led to a change in the interaction of genetic and environmental effects with birth cohort, three large twin studies were reanalyzed that covered birth cohorts from the early s to the mids Researchers tested heterogeneity of twin tetrachoric correlations across samples and across sex and found increased genetic effects in men in two of the samples compared with the third sample; however, there was no genetic heterogeneity by age cohort The modeling of age-related changes in the effects of genetic and environmental factors in smoking initiation in adolescent twin pairs showed that genetic effects increased with age; however, shared environmental effects, which explain the majority of variation in risk at early ages years , were not statistically significant in early adulthood Family studies of the relatives of substance-dependent individuals ascertained in treatment settings, with control subjects located via a random-digit-dialing protocol, suggest that there are both general factors increasing vulnerability to substance abuse and specific factors increasing vulnerability to specific drugs, including habitual smoking Only habitual smoking in the proband, but not other substance abuse, was a statistically significant predictor of habitual smoking in siblings, suggesting a specific risk factor for nicotine dependence.

Personality and behavioral studies have suggested why some people are more likely to smoke and what smokers perceive that they derive from smoking tobacco. Research in motives for smoking posits a limited number of factors based on responses to questions concerning hypothesized reasons for smoking - These factors have been constructed from psychosocial models of various motives for smoking, such as smoking to modify affect, smoking to relax, food substitution smoking, etc. Investigation of the correlation structure among these hypothesized motives for smoking provided consistent and statistically significant support for six of these factors: addiction, automatic, stimulation, psychosocial, indulgent, and sensorimotor manipulation , Interfactor correlation analysis suggested that the first three factors loaded onto a second-order pharmacologic factor and the last three loaded onto a nonpharmacologic factor Smokers experience self-reported increases in arousal and decreases in stress after smoking cigarettes, with absolute levels of arousal and stress peaking in midday and in the morning, respectively Smokers experience stimulation and sedation simultaneously from each cigarette; however, they also experience lower equilibrium levels of arousal and higher equilibrium levels of stress than nonsmokers.

After smoking cessation, mean arousal and stress levels are increased and reduced, respectively, suggesting that smoking cigarettes may contribute to the increased stress observed in smokers Personality and temperament constructs that use questionnaires to measure heritable personality dimensions quantitatively, e.

Novelty seeking, extraversion, impulsivity, and neuroticism have been identified as the personality factors found at higher levels among smokers than among nonsmokers - That both dependent and nondependent smokers exhibit similarly increased sensation-seeking scores relative to nonsmokers suggests that, while increased sensation-seeking may increase liability to smoking initiation, it may not be related to differences in nicotine dependence among smokers.

FTQ and FTND scores have been found to show statistically significant associations with biochemical measures related to the quantity of cigarettes smoked plasma nicotine, plasma or urinary cotinine, and expired CO and are also associated with cessation outcome in trials without nicotine replacement therapy , FTND scores from population-based samples of smokers are statistically significantly lower than scores from smokers seeking cessation help A small fraction of active cigarette smokers are known as chippers or nondependent smokers, defined as smoking five or fewer cigarettes per day Compared with regular smokers, chippers were found to extract similar amounts of nicotine per cigarette and to exhibit similar elimination half-lives of nicotine but to be statistically significantly less nicotine dependent and to have begun their smoking careers significantly more slowly - Regular smokers scored higher on pharmacologic smoking motive factors, and chippers scored higher on nonpharmacologic smoking motive factors Chippers and regular smokers both appear to smoke for affect management; however, unlike regular smokers, chippers do not crave cigarettes and exhibit lower levels of smoking for stimulation and smoking to relieve negative affect.

The establishment of nicotine dependence in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders DSM , third edition, represented the nosologic and diagnostic recognition of this drug dependency Specifically, nicotine is not considered to produce intoxication, and a diagnosis other than nicotine dependence would not be appropriate for maladaptive use of the substance Nicotine dependence is a model for drug dependence, where tobacco smoking fulfills the physiologic, behavioral, and social characteristics of a dependence syndrome, but it also acts as a gateway drug for other drugs of abuse However, the morbidity and mortality due to the direct effects of tobacco smoking exceed the direct or indirect effects of other drugs of abuse or, indeed, of any other single behavior on a population level 2 , While consumption and dependence are statistically significantly associated for all drugs of abuse, tobacco is similar to cocaine and the opiates in terms of its addiction liability; i.

Statistically significant associations have been found in different young adult and adult samples between smoking and depression, anxiety, and alcohol dependence.

Smoking sex samples

Smoking sex samples

Smoking sex samples