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Pharmacologic aspects of cigarette smoking and nicotine addiction
... [9,10] Slower nicotine metabolism may allow longer nicotine exposure and maintain longer nicotine concentration in the blood, leading to a lesser frequency of cigarette smoking. [11] CYP2A6 polymorphism was reported to be existed in Indonesian population, [12] however the allele frequency and variations remains unclear. This study aimed to investigate the correlation between the CYP2A6 gene variants and coronary atherosclerosis severity in Indonesian male smokers. ...
... Nicotine also promotes the sympathetic nervous system continuously for 24 hours, affecting vasoconstriction and coronary spasms, atherogenic for lipid profiles, as well as increasing platelet aggregation and hypercoagulation. [11] Categorical data were presented as N (%), while continuous data as mean ± SD. Comparisons between groups were analyzed using Pearson Chi-square for categorical and independent t test for numerical variables. ...
... [13] CYP2A6*4,*7,*8,*9, and *10 were mutant allele variants with a single amino acid mutation that led to an inactive catalytic enzyme. [11] CYP2A6*4 is a form of entire deleted types, and hence, this ultimately has no enzyme activity. [13] CYP2A6*9 allele contains a mutation on 5ʹ-region in TATA box (TAGA), which changed 48T→G and decreased enzyme activity. ...
Nicotine is a toxic alkaloid known to be responsible for the addictive feature of cigarettes. CYP2A6 genetic polymorphism among individuals was suspected to explain the relationship between cigarette smoking and related diseases. CYP2A6 works to slow nicotine metabolism and thus maintain a more prolonged nicotine concentration and increase nicotine exposure to the blood. We aimed to investigate the correlation between the CYP2A6 gene with the severity of coronary atherosclerosis. This cross-sectional study was conducted from April to July 2010 in Makassar Cardiac Centre, Dr Wahidin Sudirohusodo Hospital, Indonesia. Sixty-four male active smokers at the age of ≥45 years, diagnosed with coronary artery disease (CAD), were recruited and asked to smoke the usual number of cigarettes in the last 1 month prior to blood collection for CYP2A6 genotyping. Spearman correlation was performed to analyze the association between the allele variants and coronary stenosis degree, adjusted for CAD risk factors. Furthermore, we estimated the risk ratio to quantify the correlation. Of the 64 male smokers with CAD, the mean duration of smoking was 36.9 ± 8.6 years, and 49 (76.6%) were heavy smokers with >20 cigarettes per day. All 128 alleles were observed. Our results showed that all participants with CYP2A6 variants had a significant correlation with severe coronary artery stenosis (P = .006). Thus, this study suggests that the mutant CYP2A6 gene allele significantly increased the risk of having severe coronary stenosis 1.2 times higher compared to the wild type. This pilot study showed that CYP2A6 gene has an influential role in atherosclerotic development in male smokers. However, our findings should be confirmed with further more extensive studies.
... It is well known that nicotine is classified as narcotic medication and as a psycho-stimulant drug. Such effects are known to produce nicotine induced "kick", causing stimulation of the adrenal glands and as a result which stimulate release of adrenaline (apinephrine) [1][2][3][4]. Nicotine induced hormonal stimulation are reported to boost energy causing increased release of blood glucose and activate various metabolic process at the cellular levels. The chemical reactive nature of nicotine indicated that it forms salts with acids. ...
... Thus adequate measure should be taken by India and International authority to make dentrifices free from tobacco/nicotine. Thus from the ten sample materials taken to perform the experimentation resulted indicating the presence of nicotine in 4 samples namely Closeup M [2], Colgate M [5], Pepsodent [6], Himalayas [8]. ...
Nicotine is a nitrogen-containing alkaloid produced by a small number of plants, including the tobacco plant. Although the use of tobacco products as dentifrices is still popular in some parts of India, Indian law prohibits the use of nicotine in dentifrices. Nicotiana tobacco, the type of nicotine found in tobacco plants, is a nightshade family member and has a potential to cause oral lesions and other oral hazard in a few individuals. In the present study, we focussed to find the quantitative limits of Nicotine in toothpaste varieties. Ten brands for ordinarily utilized toothpaste were assessed by Agarwal and Rajagopal method for extraction and seclusion of nicotine from toothpowder. Another most proposed method for the practical and reliable detection of alkaloids belong to pyrrolidine group -test by Wagner reagent (iodine-potassium-iodide solution). Our results demonstrated the presence of nicotine content in a few commercial brands tested like Closeup, Pepsodent, Colgate and Himalaya. Our approach involved in demonstrating a simplified method to analyse nicotine compounds in tooth pastes by expressing titrations values using aqueous solutions using Wagner reagent. Further safety studies need to be focussed in validating a simplistic and rapid method in monitoring and expressing the permissible limits of nicotine in commonly available tooth paste varieties.
... pneumococcal disease, tuberculosis). 1,2 Thousands of compounds comprise complex matrices for tobacco and tobacco smoke, and more than 3000 chemicals, heavy metals, and other constituents have been isolated from tobacco. 3 However, most of the undesirable effects of cigarette smoking have been attributed to nicotine, the major constituent of the particulate phase of tobacco smoke, 4,5 to which people are addicted and subject themselves to frequent and high doses, often throughout their life. The targets of nicotine in the central nervous system have been identified as nicotinic acetylcholine receptors. ...
... This study also showed that the severity of attachment loss was highly correlated with the number of pack-years. The odds for more severe attachment loss in smokers compared with nonsmokers ranged from 2.05% for light smokers to 4.75% for heavy smokers. ...
Tobacco smoking has been implicated in periodontal pathology through various mechanisms, including perturbations of the inflammatory and host responses to putative periodontal pathogens, alterations in the subgingival microbial communities, and a compromised healing potential of the tissues leading to imbalance of tissue homeostasis. This review provides the evidence for the relationship between cigarette smoking and periodontal disease in an attempt to explain possible mechanisms of how tobacco smoking may exert its negative effects on the periodontal tissues via systemic and localized pathways. Early and more recent studies explore cigarette smoking–induced changes in periodontal clinical indices; in subgingival microbial flora by employing traditional detection methods for selected microorganisms, in addition to modern techniques such as deep sequencing and bioinformatics analyses that are able to fully characterize the microbial communities; and in inflammatory and immune responses critically appraising study limitations and differences in study protocol designs. Periodontal treatment outcomes and implant therapy outcomes are reviewed in an attempt to shed light on possible mechanisms for the inferior treatment outcome noted in smokers. The potential harmful effects of passive smoking are also reviewed, providing evidence for the advantages of smoking cessation. Quitting cigarette smoking should be recommended by the dentist, and effort should be made to inform smokers about the negative effects of smoking on the periodontal status and implant therapy outcomes.
... However, only 11-24% of smokers will develop lung cancer, and for the same reported lifetime quantity of cigarettes lung cancer risk differs by racial/ethnic group (6,7). Nicotine, the primary psychoactive compound present in tobacco, is responsible for maintaining smoking behaviors (8), and individual variation in nicotine metabolism is an important contributor to racial/ethnic and individual differences in lung cancer risk (6). ...
... These investigations began with microsomal studies in the 1970s and 80s (19)(20)(21)(22). Also, in the 1980s, the addictive nature of nicotine became well recognized (8). This knowledge, combined with the realization that most smokers metabolize more than 80% of the nicotine they consume to cotinine, led to the hypothesis that the activity of the enzyme responsible for nicotine 5'-oxidation would influence smoking behaviors (23). ...
Nicotine is the key addictive constituent of tobacco. It is not a carcinogen, but it drives smoking and the continued exposure to the many carcinogens present in tobacco. The investigation into nicotine biotransformation has been ongoing for more than 60 years. The dominant pathway of nicotine metabolism in humans is the formation of cotinine, which occurs in two steps. The first is cytochrome P450 (P450, CYP) 2A6-catalyzed 5'-oxidation to an iminium ion, the second is oxidation of the iminium ion to cotinine. The half-life of nicotine is longer in individuals with low P450 2A6 activity, and smokers with low activity often decrease either the intensity of their smoking or the number of cigarettes they use compared to those with “normal” activity. The effect of P450 2A6 activity on smoking may influence one's tobacco-related disease risk. This review provides an overview of nicotine metabolism and a summary of the use of nicotine metabolite biomarkers to define smoking dose. Some more recent findings, for example the identification of UDP-glucuronosyltransferase (UGT) 2B10 as the catalyst of nicotine N-glucuronidation, are discussed. We also describe epidemiology studies that establish the contribution of nicotine metabolism and CYP2A6 genotype to lung cancer risk, particularly with respect to specific racial/ethnic groups, such as those with Japanese, African or European ancestry. We conclude that a model of nicotine metabolism and smoking dose could be combined with other lung cancer risk variables to more accurately identify ex-smokers at the highest risk of lung cancer, and to intervene accordingly.
... As the baseline 6 Journal of Interventional Cardiology medication analysis showed, antiplatelet drugs were highly prescribed in the two groups, showing no significant differences. Other pathological mechanisms shown in previous studies include an unfavorable modulation of autonomic cardiac control, leading to a shift towards sympathetic predominance accompanied by increased levels of catecholamines, lower arrhythmogenic threshold, increased vasoconstriction, and increased myocardial oxygen consumption [26][27][28][29][30]. The corresponding drug solutions involve appropriate -blockers and calcium antagonists. ...
... How to interpret the results for clinical practice. Maybe we should be conscious of the complicated clinical situation that smoking possibly plays more important role in initial triggering mechanisms in ACS, due to vasoconstriction, hypercoagulability, platelet aggregation, and endothelial dysfunction [13][14][15][23][24][25][26][27][28][29][30]. However, the progression of atherosclerosis can be influenced by multifactors, including genetic mechanisms and secondary medication [34,35]. ...
Objectives:
This study analyzed a large sample to explain the association of baseline smoking state with long-term prognosis of coronary artery disease (CAD) patients who underwent percutaneous coronary intervention (PCI).
Background:
Data is limited up to now regarding whether smoker's paradox exists in Chinese population.
Methods:
A total of 10724 consecutive cases were enrolled from January to December 2013. 2-year clinical outcomes were evaluated among current smokers and nonsmokers. Major adverse coronary event (MACCE) included all-cause death, revascularization, myocardial infarction (MI), and stroke.
Results:
Current smokers and nonsmokers accounted for 57.1% and 42.9%, respectively. Current smokers were presented with predominant male sex, lower age, and less comorbidities. The rates of 2-year all-cause death were not significantly different among two groups. But the rate of stroke and bleeding was significantly higher in nonsmokers than in current smokers (1.6% and 1.1%, P=0.031; 7.2% and 6.1%, P=0.019). The rate of revascularization was significantly higher in current smokers than in nonsmokers (9.1% and 8.0%, P=0.037). Multivariable Cox regression indicated that, compared with nonsmokers, current smokers were not independently associated with all endpoints (all P>0.05).
Conclusions:
2-year all-cause death, MACCE, MI, revascularization, stroke, ST, and bleeding risk were similar between current smokers and nonsmokers in CAD patients undergoing PCI.
... The nicotine content of Nicotiana rustica L. has been reported to be 6-10 times higher than the nicotine content of Nicotiana tabacum used for cigarettes (17). One study revealed that blood nicotine levels were 15 times higher when tobacco was consumed orally, compared to smoking (18). A limiting factor in the evaluation of the results of our study was that we did not measure nicotine levels of participants. ...
... Smoking is an important public health problem because it is legal to use and is easily available, and nicotine can become habit-forming in a short time and harm not only the individual who uses it but also other people around it. Today, the relationship between many diseases and smoking has been proven, and extensive campaigns have been initiated to avoid smoking all over the world (1) . Smoking has negative effects on many systems, including the cardiovascular system. ...
Background: Considering the concept of controlled hypotension, it is known that it creates a bloodless surgical field by keeping the mean arterial pressure (MAP) between 50-70 mmHg in patients without hypertension or by reducing the basal MAP by 30% in patients with hypertension. Thus, it will be demonstrated that it is necessary for anesthetic blood transfusion, which increases the success of the operation and reduces the need. This method is frequently used in otorhinolaryngology and all other surgical procedures with a high bleeding potential.
Objective: To investigate whether smoking has an effect on controlled hypotension administered with nitroglycerin in otolaryngological surgical procedures.
Methods: In our prospective and observational study, septoplasty was performed in 50 (Group 1) and 50 non-smoker patients by applying total intravenous anesthesia (TIVA) and controlled hypotension with nitroglycerin. Ethics committee approval was obtained for the study. The study was conducted with a total of 100 patients, 1 of whom was also a smoker (Group 2). Intravenous propofol infusion was also used as part of the maintenance of anesthesia, and nitroglycerin was titrated at a dose range of 0.25-1 µg/kg/min to provide controlled hypotension.
Results: There was no significant difference between the groups in demographic data, BMI (Body Mass Index) values, ASA (American Society of Anesthesiologists) classifications, operation times, controlled hypotension times, total propofol and nitroglycerin amounts used. However, Fromme scale values were found to be statistically significantly higher in smokers (Group 2) than in non-smoker patients (Group 1) (P<0.05).
Conclusion: It has been observed that nitroglycerin, which is preferred for controlled hypotension applied to reduce bleeding in the surgical field in nasal surgery, causes more pronounced hypotension and reflex tachycardia in smokers due to nicotine-induced endothelial dysfunction.
... [14] It is thought that the kidney concentrates cotinine, increasing the concentration in urine to levels 5-6 times higher than the concentration in plasma and saliva. [15] Various foods (such as cauliflower, eggplant, tomato, tea) contain low amounts of nicotine; however, dietary nicotine intake may be ignored in studies since it has been determined that daily intake does not cause a significant difference in cotinine levels. [14] Since urine cotinine is completely specific to cigarettes and a product of internal metabolism, the possibility of changes in cotinine levels with external environmental conditions during the collection of samples is also low. ...
Bacground: Our study was planned to reveal the objective relation between urine cotinine level and tobacco smoke exposure in children suffering from chronic cough. Methods: Between ages 5-18 years, 58 patients with chronic cough with no underlying specific cause and 54 healthy individuals were included in the study. Results: There was a statistically significant difference between urine cotinine levels of cases those who exposed and unexposed (based on the declaration of parents) to tobacco smoke (p
... Especialmente para pessoas geneticamente suscetíveis, a nicotina é uma droga altamente viciante (BENOWITZ, 1988; U.S. SURGEON GENERAL 'S REPORT, 1988 ...
... Nicotine has been found to stimulate the catecholamines which results in lipolysis and release of free fatty acids. This also leads to enhanced secretion of hepatic free fatty acids (FFAs) and triglycerides & VLDL in blood (17)(18)(19) . Hyperinsulinemia in smokers decreases the lipoprotein lipase activity & results in increased cholesterol, triglycerides & LDL-cholesterol. ...
ntroduction: Cigarette smoking is known to cause damage to many organs in the body. Nicotine may cause alterations in the exocrine and endocrine function of pancreas. This study aims to assess the effect of smoking on amylase, insulin levels and lipid profile in healthy smokers. Materials and Methods: 27 healthy smokers and 27 non- smokers were recruited as cases and controls. Fasting blood samples were collected for estimating the glucose, lipid profile, amylase, lipase and insulin levels. Results: There is a significant dyslipidemia, higher insulin levels and HOMA-IR and decrease in amylase and lipase levels in smokers compared to non- smokers. Conclusion: Smoking is associated with risk of development of diabetes mellitus and cardiovascular disease.
... Cigarettes have a widespread use and their smoke contains more than 4000 very toxic compounds, mainly nicotine (10). Various clinical and pathological investigations revealed that cigarette smoking gave rise to cardiovascular (11)(12)(13)(14), respiratory, endocrine, urogenital and immune system disorders, and demonstrated that it increased morbidity and mortality (15)(16)(17). Moreover, as the number of cigarettes smoked increases, cardiovascular mortality increases by 1.5-2 times, the rate of coronary artery disease and overall mortality increases by 2-2.5 times (18). ...
Objective: A plant powder called "Marafl Powder" has been used widely instead of cigarette in the SouthEastern region of Turkey. It was confirmed that this powder has been made of tobacco N. rustica L. Our aim was to investigate whether the use of Marafl Powder is as harmful as cigarette smoking or not. Methods: Forty-five Marafl Powder users (Group I), 32 persons who smoked cigarette (control-Group II) and 30 healthy persons neither smoking nor using Marafl Powder (Group III) were included into the study. Laboratory investigations, electrocardiography and echocardiography were performed in all participants of the study. For evaluation of the ventri-cular repolarization parameters, 50 mm/sec ECG recordings were used. Echocardiographic investigation was performed for assessment systolic and diastolic function. Results: No differences were found by means of ventricular repolarization parameters among the three groups (p>0.05). Echocardiographic investigation revealed similar systolic function results in all of the three groups. There was reduced early filling velocity of the left ventricle (p=0.03, p=0.02) and increased filling velocity of the atrial component (p=0.02, p=0.02) in group I and group II. When they were compared to group III, deceleration time was also increased (p<0.01, p<0.01). Isovolumetric relaxation time was higher in group I and group II than that of group III (p=0.02, p=0.03). In group I and group II, total cholesterol (p=0.03, p=0.02), LDL-cholesterol (p<0.01, p<0.01) and triglyceride levels (p<0.01, p<0.01) were found to be higher than those of group III, whereas HDL levels were lower (p=0.02, p<0.01). Conclusion: As a result, we thought that Marafl Powder is as harmful as cigarette smoking and it has similar negative effects on cardiovascular system. In our opinion, "Marafl Powder" is a smokeless tobacco use. (Anadolu Kardiyol Derg 2003; 3: 230-5)
... Tobacco-related morbidity and mortality remain a significant public health burden in the U.S., driven primarily by use of cigarettes and other combustible products (United States Department of Health and Human Services, 2014; Wang et al., 2017). Nicotine is the addictive tobacco constituent that promotes repeated use of cigarettes upon smoking initiation, and reduction of nicotine content in cigarettes should reduce use and dependence risk (Benowitz, 1988(Benowitz, , 2010. The 2009 Family Smoking Prevention and Tobacco Control Act (Tobacco Control Act) gave the U.S. Food and Drug Administration (FDA) authority to regulate tobacco products in the interest of public health (Family Smoking Prevention and Tobacco Control Act, 2009) including broad regulatory authority over the manufacturing, sale, and distribution of tobacco products (U.S. Food and Drug Administration, 2020). ...
A national nicotine reduction policy has the potential to reduce cigarette smoking and associated adverse health impacts among vulnerable populations. However, possible unanticipated adverse effects of reducing nicotine content in cigarettes, such as increasing the use of alcohol or other abused substances, must be examined. The purpose of this study was to evaluate the effects of exposure to varying doses of nicotine in cigarettes on use of other substances. This was a secondary analysis (n = 753) of three simultaneous, multisite, double-blind, randomized-controlled trials examining 12 weeks of exposure to study cigarettes varying in nicotine content (0.4, 2.4, 15.8 mg nicotine/g tobacco) among daily smokers from three vulnerable populations: individuals with affective disorders (n = 251), individuals with opioid use disorder (n = 256), and socioeconomically-disadvantaged women of reproductive age (n = 246). Effect of study cigarette assignment on urine toxicology screens (performed weekly) and responses to drug and alcohol use questionnaires (completed at study weeks 6 and 12) were examined using negative binomial regression, logistic regression, or repeated measures analysis of variance, controlling for sex, age, and menthol status. The most common substances identified using urine toxicology included tetrahydrocannabinol (THC; 44.8%), cocaine (9.2%), benzodiazepine (8.6%), and amphetamines (8.0%), with 57.2% of participants testing positive at least once for substance use (27.3% if excluding THC). No significant main effects of nicotine dose were found on any of the examined outcomes. These results suggest that reducing nicotine content does not systematically increase use of other substances, even among individuals at increased risk of substance use.
ClinicalTrials.gov Identifiers: NCT02232737, NCT2250664, NCT2250534.
... As a result of the inhibition of the cyclooxygenase enzyme and increased thromboxane synthesis, platelets' adhesion and aggregation properties increase [32]. Although an increase in platelet activity is observed in chronic smokers, their life span is shortened [33]. ...
Smoking is the leading cause of preventable death. Epicardial adipose tissue (EAT) surrounds the heart surface and creates local and systemic effects secreting the hormones, cytokines, inflammatory mediators. Previous studies demonstrated that both smoking and EAT have a strong association with inflammation and atherosclerosis.Our study aimed to determine the relationship of smoking with EAT thickness and inflammation by evaluating smokers and non-smokers. A total of 259 healthy male and female participants between the ages of 18-65, without a history of chronic disease and with a body mass index within normal limits, were included in a study. EAT thickness measurements were made by transthoracic echocardiography and EAT thicknesses of smokers and non-smokers were compared. In addition, the effects of smoking and EAT thickness on different inflammatory parameters were evaluated. When the EAT thicknesses were compared between smokers and non-smokers (2.60±1.2), a statistically significant difference was found in favor of smokers (3.84±1.84) (p<0.001). A moderate positive correlation was found among age, body mass index, smoking duration in years, pack/year and EAT thickness. The difference among waist circumference, the number of cigarettes smoked daily, diastolic blood pressure, fasting blood glucose, ALT, AST, total cholesterol, triglyceride, LDL-cholesterol, CRP, uric acid, platelet count, MPV values, platelet/lymphocyte ratio and EAT thickness were found meaningful, but the weak correlation in different ratios were determined. Smoking was found to be the most important determinant of EAT thickness. Other determinants of EAT thickness were age, body mass index, CRP and female gender. The significant statistical relationship between smoking and EAT thickness suggests that smoking increases EAT thickness and inflammatory parameters. Co-assessment of the EAT and blood inflammatory parameters in smokers may guide the initiation of medical treatment in primary prevention or other therapies.
... lung cancer. Moreover, it has been shown that cigarette smoking may accelerate the progression of renal, pulmonary, and cardiac fibrosis [1,2,3,4]. The detrimental effects of smoking have been extensively investigated by studies regarding the direct administration of nicotine, a major pharmacologically active component of tobacco smoke in a variety of cell systems [5,6,7]. ...
Nicotine is the most abundant component in cigarette smoking and is involved in the pathogenesis of lung cancer and increases the risk of developing hepatocellular carcinoma and liver cirrhosis. Prevention of nicotine-induced lung cancer and liver damage may be achieved via decreasing nicotine-induced pathological effects. Nicotine is metabolized in the liver. Natural diet contains a variety of compounds e.g. apple cider vinegar (ACV) that exhibits protective effects against different toxins. This study aims to investigate the effects of nicotine on the liver using morphometrical, histopathological and biochemical parameters and study the protective effect of ACV against toxicity of nicotine. Three groups of the male albino rat were used: untreated control group, nicotine treated group (4 mg/kg/day) while the third group received both ACV (2ml/kg/day) and nicotine (4 mg/kg/day). Treatment was given for 30 days. There was a significant increase in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) together with a damage and degeneration in the liver tissues of the nicotine treated groups. ACV administration to nicotine-treated rats showed near normal liver biochemical markers with reduction in the tissue damage associated with the nicotine administration. ACV administration to nicotine-treated rat ameliorated the decrease in the size of the hepatocytes nuclei. These results, along with previous observations, suggest that ACV may be useful in combating tissue injury resulting from nicotine toxicity. In prophetic medicine, Prophet Muhammad peace be upon him strongly recommended eating vinegar in the prophetic hadeeth: "vinegar is the best edible". Conclusion: These finding confirm that chronic nicotine administration causes harmful effects to the liver and suggest that ACV may be useful in combating tissue injury resulting from nicotine toxicity. Hence, the intake of ACV might suppress the toxicity and mutagenic activity of nicotine. ACV may protect against nicotine-induced carcinogenesis.
... The NCC commonly used is a quantitative marker of smoking, related to the pack-year indicator corresponding to the frequency of exposition of specific molecules as hydrocarbons and nitrosamines which can induce over time carcinogenesis [19]. By contrast, the FTND represents a qualitative marker of smoking, with a questionnaire linked to the smoking behavior and the nicotine dependence [20,21]. Therefore, the instant of the day or the general condition can modulate the way of patient smokes, indeed the impact the level of dependence [8], perceptible thanks to the FTND [22,23]. ...
INTRODUCTION
Smoking is considered as a risk factor for the poor outcomes after periodontitis non-surgical treatment (PNST). The aim of this short communication is to predict probing depth reduction after periodontal non-surgical treatment in smokers according to the nicotine dependence (FTND) and the number of cigarette consumed (NCC).
METHODS
This work is a post-hoc study of a prospective controlled study on the effect of oral hygiene instructions and PNST on periodontal outcomes. This short communication focused only on the current conventional smokers (N=34), based on specific smoking indicators, and on probing depth (PD) parameter that were recorded at baseline (time 0), after oral hygiene instuction (time 1) and 3 months after PNST (time 2) .
RESULTS
The 34 smokers had a mean age 46.5 ± 11.5 years. The NCC- and FTND- based predictions allowed to show in a specific nomogram the PD values 3 months after PNST for each NCC and FTND category.
CONCLUSION
Two nomograms are proposed for prognostic purposes and allow patients to understand the impact of smoking on periodontitis according to the number of cigarette consumed and the level of nicotine dependence. These nomograms might be also used for supporting smoking cessation.
Clinical Significance
In smoker patients with periodontitis, there is a need to predict, for both patient and clinicians , the impact of the number of cigarettes consumed and the level of nicotine dependence on probing depth after oral hygiene instructions and debridement. Two nomograms are proposed for prognostic purposes.
... In chronic pain patients who smoke, they have reported that smoking was a method to cope with the pain [18,31]. The analgesic effect of nicotine is believed to act via activation of endogenous opioid, serotonergic, hypothalamic-pituitary-adrenocortical, and sympatho-adrenomedullary systems [29,[32][33][34]. Additionally, animal models suggest nicotine alters pain sensitivity via altering the expression of glutamate decarboxylase 67, GAD65, μ-opioid receptors, endorphins, and γ-aminobutyric acid which could explain the hyperalgesia and increase in opioid use in smokers in the perioperative period [35•]. ...
Purpose of Review
The purpose of this review is to examine the impact of smoking and its role on the development of chronic pain and provide a critical review of recent literature.
Recent Findings
Recent studies demonstrate the bidirectional and dependent relationship between smoking and chronic pain. Those who are in pain have a more difficult time in the cessation of smoking as well as an increased sensitivity to pain during abstinence, lower confidence, and higher relapse rates. The fear of pain and the anxiety and depression that abstinence causes results in a grim outcome for long-term cessation.
Summary
The dependent nature between chronic pain and smoking is affected by numerous variables. Providers should consider a multiprong approach to treating chronic pain and targeting smoking cessation treatment by providing motivational therapy, nicotine replacement, and medication therapies to prevent relapse, and providing those who are more likely to relapse with a higher level of care.
... ng/ mL (Table 2). In some older publications, mean plasma Nic levels in the range of 8.5-40 ng/mL were obtained under similar conditions (blood sample drawn in the late afternoon of a smoking day) were reported (Oates et al., 1988;Benowitz et al., 1987;Gupta et al., 1995;Russell et al., 1976;Russell et al., 1975). Despite the mentioned uncertainties, there is a good agreement between literature data and our results. ...
Today various tobacco and nicotine products are available, many of them can be regarded as potentially risk-reduced products when compared to the most frequently used product, combustible cigarettes (CCs). A commonality of these products is that they deliver nicotine, although in quite different amounts and uptake routes, the most common of which are inhalation through the lung and absorption through the oral mucosa. Product-specific nicotine delivery as well as the subject-related use patterns are important factors which determine the pharmacokinetics and achieved internal dose levels of the alkaloid. The latter two parameters are highly relevant for the long-term product loyalty and, consequently, for the implicated health risks, since the risk-reduced products will replace CCs in the long-term only when users will experience a similar level of satisfaction. We measured nicotine and its major metabolites in plasma, saliva and urine samples collected in a controlled clinical study with habitual users (10 per group) of CCs, electronic cigarettes (ECs), heated tobacco products (HTP), oral tobacco (OT), and nicotine replacement therapy (NRT). Non-users (NU) of any tobacco/nicotine products served as (negative) control group. Moderate to strong correlations were observed between the daily consumption and the urinary nicotine equivalents (comprising nicotine and its 10 major metabolites, Nic+10) or plasma and saliva cotinine concentrations. The average daily nicotine dose as measured by the urinary excretion of Nic+10 (reflecting approximately 95 % of the absorbed nicotine) amounted to 17 and 22 mg/24 h for smokers (CC) and OT users, respectively, while it was in the range of 6 – 12 mg/24h for users of ECs, HTP and NRT products, with high inter-individual variations in each user group. The individual daily nicotine intake, which was calculated by applying product-specific models, showed none to good agreement with the corresponding internal nicotine dose measured by Nic+10 excretion. Possible reasons for the observed deviations between calculated and objectively measured nicotine doses are discussed.
... Cigarette smoking, the leading preventable cause of death, is associated with a myriad of negative health consequences including cancer and death. 1 Annual US costs associated with cigarette smoking are estimated at over $300 billion. 1 Nicotine is one of the primary addictive constituents in combustible cigarettes. 2 Some have proposed that limiting the amount of nicotine in combustible cigarettes could benefit individuals and society, including decreased dependence and a lower likelihood of initiation among new smokers. [3][4][5] In 2009, the Food and Drug Administration (FDA) was granted authority to regulate the amount of nicotine in combustible cigarettes. ...
Background
Cigarette smoking continues to be a major health concern and remains the leading preventable cause of death in the U.S. Recent efforts have been made to determine the potential health and policy benefits of reducing nicotine in combustible cigarettes. The degree to which changes in blood nicotine relate to measures of the abuse liability of reduced-nicotine cigarettes is unknown. The current study examined the relation between blood nicotine and behavioral economic demand measures of cigarettes differing in nicotine content.
Methods
Using a within-subject design, participants smoked a single cigarette during each experimental session. Cigarettes included the participant’s usual-brand cigarette and SPECTRUM investigational cigarette differing in nicotine level (mg of nicotine to g of tobacco; 15.8mg/g, 5.2mg/g, 2.4mg/g, 1.3mg/g, and 0.4mg/g). During each session, blood was collected at multiple timepoints and behavioral economic demand was assessed. Nonlinear mixed-effects models were used to estimate differences derived intensity (Q0) and change in elasticity (α).
Results
Measures related to blood nicotine decreased in an orderly fashion related to nicotine level and significantly predicted change in elasticity (α), but not derived intensity. No differences in demand parameters between the usual brand and 15.8mg/g cigarettes were observed. However, αwas significantly higher (lower valuation) for 0.4mg/g than 15.8mg/g cigarettes.
Conclusions
The lowest nicotine level (0.4mg/g) corresponded with the lowest abuse liability (α) compared to the full-strength control (15.8mg/g), with the 1.3mg/g level also resulting in low abuse liability.
Implications
This is the first study examining the relative contributions of nicotine content in cigarettes and blood nicotine levels on the behavioral economic demand abuse liability of cigarettes ranging in nicotine content. Our results suggest blood nicotine and nicotine content both predict behavioral economic demand abuse liability. In addition, our results suggest a nicotine content of 1.3mg/g or lower may be effective at reducing cigarette uptake among first-time (naïve) smokers. Our results largely conform to previous findings suggesting a very low nicotine content cigarette maintains lower abuse liability than full-strength cigarettes.
... Besides, many previous studies have revealed that smoking is highly correlated to back pain, and tobacco users may display IVD degenerative characteristics 6,7 . Of tobacco products, nicotine is well-known to be a major addictive component which may contribute to various pathophysiologies including IVD degeneration 8,9 , possibly through vasoconstriction, arteriosclerotic, carboxyhemoglobin production, changes in blood flow, and impaired fibrinolytic activity [10][11][12] . Besides, passive cigarette smoking has also been implicated in exerting histologic changes in intervertebral disc 13 , indicating that nicotine exposure may contribute to degeneration of IVD; however, the underlying mechanism still remain unclear. ...
Apart from aging process, adult intervertebral disc (IVD) undergoes various degenerative processes. However, the nicotine has not been well identified as a contributing etiology. According to a few studies, nicotine ingestion through smoking, air or clothing may significantly accumulate in active as well as passive smokers. Since nicotine has been demonstrated to adversely impact various physiological processes, such as sympathetic nervous system, leading to impaired vasculature and cellular apoptosis, we aimed to investigate whether nicotine could induce IVD degeneration. In particular, we evaluated dose-dependent impact of nicotine in vitro to simulate its chronic accumulation, which was later treated by platelet-derived biomaterials (PDB). Further, during in vivo studies, mice were subcutaneously administered with nicotine to examine IVD-associated pathologic changes. The results revealed that nicotine could significantly reduce chondrocytes and chondrogenic indicators (Sox, Col II and aggrecan). Mice with nicotine treatment also exhibited malformed IVD structure with decreased Col II as well as proteoglycans, which was significantly increased after PDB administration for 4 weeks. Mechanistically, PDB significantly restored the levels of IGF-1 signaling proteins, particularly pIGF-1 R, pAKT, and IRS-1, modulating ECM synthesis by chondrocytes. Conclusively, the PDB impart reparative and tissue regenerative processes by inhibiting nicotine-initiated IVD degeneration, through regulating IGF-1/AKT/IRS-1 signaling axis.
... The advantage of this method is it's easy application and regular release of nicotine. The doses are decreased over time and whole therapy lasts for complete duration of three months [5] . ...
... It is eminent that smoking deranges serum lipid profile and it increases TC, TG, ApoB, and LDL-c level in the blood, while it decreases HDL-c. 36,37 The linking between smoking and dyslipidemia is multifaceted, but a supposed association might be due to the stimulation of the sympathetic adrenal system by nicotine to secrete catecholamines 38 and these catecholamines may potentiate lipolysis and increases the concentration of lipids in plasma. ...
Background
Dyslipidemia is one of the adverse metabolic outcomes associated with psychotropic medications and the nature of the mental illness itself. Therefore, this study aimed to assess magnitude of dyslipidemia and associated factors among patients with severe mental illness on antipsychotic treatments.
Methods
A cross-sectional study was conducted among 245 patients with severe mental illness in Hawassa University Comprehensive Specialized Hospital, Sidama Regional state, Southern Ethiopia. Socio-demographic and other important data were collected using a structured questionnaire through a systematic random sampling technique. Individual dyslipidemia was characterized by the National Cholesterol Education Program Adult Treatment Panel-III (NCEP ATP-III) guideline.
Results
Mean total cholesterol (TC) was significantly higher in males when compared to females (162.2 mg/dl vs 121 mg/dl, P = .023). While, mean LDL-cholesterol was significantly higher in females when compared to males (100.9 mg/dl vs 93.6 mg/dl, P = .028). Overall 58.4% (95% CI: 52.2-64.8) of participants had at least 1 dyslipidemia. The prevalence of TC ⩾200 mg/dl, HDL-cholesterol <40 mg/dl, triglyceride (TG) and LDL-cholesterol were 61 (24.9%), 75 (30.6%), 66 (26.9%), and 47 (19.2%), respectively. Female sex and smoking were significantly and positively associated with LDL-c dyslipidemia, the aOR (95% CI) were 2.1 (1.0-4.2) for female sex and 3.4 (1.1-10.5) for smoking. Also, Age >40 years was significantly associated with TC dyslipidemia, the aOR (95% CI) was 2.0 (1.1-3.7).
Conclusion
More than half of psychiatric patients are at risk of developing cardiovascular and other related health problems. Therefore, periodic screening of lipid profiles during healthcare follow-up is mandatory to limit risks of cardiovascular-related comorbidities among patients with severe mental illness.
... Most of these deaths occur in smokers, but smokeless tobacco use [2] and exposure to secondhand smoke in non-smokers also poses a signi icant health risk [3,4]. Most smokers in the say they want to quit, but the majority of them are unable to do so, in large part because of nicotine addiction [5]. ...
Background: Epidemiological studies in smokers indicate a dose-response relationship between the number of cigarettes smoked per day and the risk of developing certain smoking related diseases. The alkaloid nicotine is the major pharmacologically active substance in tobacco. Objective: To estimate the cotinine level excretion in urine among smoked and smokeless tobacco users and nonsmokers among the Indian population. Materials and methods: The study sample consisted of 250 subjects who were apparently healthy, asymptomatic and not using any drug. The study sample was divided into smoked tobacco users (bidi and cigarette), smokeless tobacco users, both smoked and smokeless tobacco users and controls (non-users of tobacco in the past or present). Results: The mean Cotinine level in urine was significantly (p – value < 0.05) more among smoked tobacco users in comparison to smokeless tobacco users and non-users of tobacco. Whereas, the mean Cotinine level in urine was significantly (p – value < 0.05) more among smokeless tobacco users in comparison to non-users of tobacco. Conclusion: The mean cotinine levels among smokers and both smokeless and smoked tobacco users were found to be higher than only smokeless tobacco users and non-users of tobacco.
... Along with the stimulation of the androgen signaling pathway, upregulation of the receptors also correlated with the central regulators' overexpression (HDAC6, CTNNB1, and SMARCA4) of the androgen pathways [83]. Increased TPMRSS4 expression in lung epithelial cells of smokers may be due to prolonged exposure to several compounds in tobacco smoke, including nicotine [107], acetaldehyde [108], and tar [109], resulting in oxidative stress and bronchial inflammation [110][111][112]. On the contrary, Cai et al. [74] did not find any correlation between smoking and TMPRSS2 expression. ...
Susceptibility to severe illness from COVID-19 is anticipated to be associated with cigarette smoking as it aggravates the risk of cardiovascular and respiratory illness, including infections. This is particularly important with the advent of a new strain of coronaviruses, the severe acute respiratory syndrome coronavirus (SARS-CoV-2) that has led to the present pandemic, coronavirus disease 2019 (COVID-19). Although, the effects of smoking on COVID-19 are less described and controversial, we presume a link between smoking and COVID-19. Smoking has been shown to enhance the expression of the angiotensin-converting enzyme-2 (ACE-2) and transmembrane serine protease 2 (TMPRSS2) key entry genes utilized by SARS-CoV-2 to infect cells and induce a ‘cytokine storm’, which further increases the severity of COVID-19 clinical course. Nevertheless, the impact of smoking on ACE-2 and TMPRSS2 receptors expression remains paradoxical. Thus, further research is necessary to unravel the association between smoking and COVID-19 and to pursue the development of potential novel therapies that are able to constrain the morbidity and mortality provoked by this infectious disease. Herein we present a brief overview of the current knowledge on the correlation between smoking and the expression of SARS-CoV-2 key entry genes, clinical manifestations, and disease progression.
... It is well known that passive smoking is associated with cardiovascular disease (CVD) (1)(2)(3), which can be explained by the effect of passive smoking on low-density lipoprotein (LDL) and high-density lipoprotein (HDL). That is, smoking increases catecholamine levels, which leads to free fatty acid release resulting from lipolysis, an increase in very low-density lipoprotein (VLDL) and LDL levels, and a decrease in HDL cholesterol (HDL-C) levels (4). Smoking also reduces lecithin cholesterol acyltransferase and hepatic lipase (5,6), and increases cholesterol ester transfer protein (7). ...
Background
Passive smoking in childhood has been reported to be associated with dyslipidemia in Western countries. However, this association in Asian countries remains unclear. Further, no study has investigated the sex difference of the association. This study aimed to elucidate the association between passive smoking and dyslipidemia in boys and girls during adolescence in Japan.
Method
We used a cross-sectional data of junior high school students in the Adachi Child Health Impact of Living Difficulty (A-CHILD) study in Adachi City, Tokyo, Japan in 2016 and 2018. Of the 1,431 available students, 1,166 students and their parents responded to the survey, including frequency of passive smoking (response rate 81.5%). We assessed dyslipidemia using total cholesterol (TC) levels, low-density lipoprotein cholesterol (LDL-C) levels and high-density lipoprotein cholesterol (HDL-C) levels. The association between passive smoking and dyslipidemia was evaluated by using multivariate regression analyses adjusted for socioeconomic status and lifestyle factors stratified by boys (N=564) and girls (N=602).
Result
Among boys, HDL-C levels were significantly lower if exposed to passive smoking frequently, compared to those not exposed to passive smoking (β=−3.19, 95% CI −5.84 to −0.55). However, this trend does not hold true among girls. Passive smoking was not associated with TC levels and LDL-C levels in both boys and girls.
Conclusion
We found exposure to passive smoking was associated with HDL-C level among boys in Japan, but not in girls. Further longitudinal study is needed to confirm the association between passive smoking and dyslipidemia among boys in Japan.
... Chronic use is linked with adverse effects like cerebrovascular accidents, seizures, psychosis, and these complications mostly occur in the body with pre-existing risk factors. Nicotine, a stimulant is available as a medicinal agent in chewing gum form to overcome the withdrawal symptoms 8 . Alcohol use & indulgence in drugs by students have become a global concern. ...
Objective: To track the trends and patterns of psychoactive substance abuse among medical students.
Study Design: Cross-sectional questionnaire based study.
Place and Duration of Study: Medical Colleges and Universities of Lahore, from Aug to Sep 2019.
Methodology: Total 200 medical students from Medical Colleges and Universities were included. The data were analyzed and computed using SPSS-21. Frequencies and percentages related to all the factors were computed.
Results: Among study participants, 96 (48%) of males and 104 (52%) of females with 154 (77%) of these students belong to 21-25 years of age group. The observed prevalence of substance abuse among students was 42 (21%). Joy seeking and a friend's offer was the initiation of psychoactive substance use among these students. Tobacco was the most highly consumed substance among students, followed by marijuana. Besides, the results also revealed that students also consumed cocaine and methamphetamine. Among 21% abusers, 4 (9%) and 5 (11%) of the students experienced side effects and withdrawal symptoms respectively.
Conclusion: The increasing consumption of tobacco and indulgence in psychoactive drugs are concerning issues because of uncontrolled consumption can cause serious brain damage. Academic burden and stress are the mediators of drug abuse among students. Therefore, stress management training and workshops should be conducted in institutes.
... Tobacco contains a package of harmful and addictive compounds [2] that its all forms rise the health problems in humans [47]. Long-term is speaking of lung cancer, heart disease, stroke and other fatal and non-fatal diseases [7,23,33]. ...
In this research, quantitative structure–activity relationship (QSAR) studies were carried out on the inhibitory activities of a set of nicotine derivatives against the cytochrome-p450 2A6 (CYP2A6) enzyme. Two-dimensional quantitative structure–activity relationship (2D-QSAR) models were developed using multiple linear regression (MLR) and linear square-support vector machine (LS-SVM) methods. The result of statistical parameters of the MLR method show that the correlation coefficient (R2) and standard error (SE) for the training set respectively are R2 = 0.702, SE = 0.49 and for the test set R2 = 0.689, SE = 0.52 and the results of statistical parameters of the LS-SVM method for the training set R2 = 0.993, SE = 0.10 and for the test set R2 = 0.977, SE = 0.20. The obtained results reveal the superiority of LS-SVM over MLR model. Then three-dimensional quantitative structure–activity relationship (3D-QSAR) model was developed using comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA) on the same dataset of nicotine derivatives. The acquired statistical parameters of the CoMFA model for the training set are R2 = 0.884, SE = 0.316 and for the test set R2 = 0.847, SE = 0.33, F = 41.27, Q2 = 0.581, while the statistical values of CoMSIA model for the training set are R2 = 0.889, SE = 0.31 and for the test set R2 = 0.670, SE = 0.54, F = 39.049, Q2 = 0.554. The results of this study revealed that the CoMFA model was more predictive and could be helpful in designing novel potent nicotine derivatives with enhanced inhibitory activity.
... Although nicotine has been recognized as an addictive substance for many years (Benowitz, 1988;Robinson and Pritchard, 1992;Stolerman and Jarvis, 1995), little progress has been made in developing successful pharmacotherapies for oral tobacco cessation, and even for smoking cessation rates of abstinence are modest at best. Existing smoking cessation therapies, including nicotine replacements and partial agonists like varenicline and cytisine, have at best a 20% success rate (Picciotto and Kenny, 2013;Picciotto and Mineur, 2014). ...
... 4 Smoking, another risk factor for the development of AF, 26-30 causes a worsening of endothelial function and arteriosclerosis through the combined effects of nicotine, carbon monoxide and aromatic hydrocarbons. Smoking also negatively changes myocardial substrate and action potential threshold leading to more frequent AF. 31 It has been found that 15-30% of all cases of AF can be related to alcohol consumption. 32 Alcohol intake affects the normal heart rate by developing a hyperadrenergic state, decreased vagal tone, an effect on the myocardial structure and various electrophysiological changes in the arterial cells. ...
Background
Risk factors of atrial fibrillation include diabetes, obesity and physical inactivity. Positive effects such as decreased atrial fibrillation burden have been reported for atrial fibrillation patients who have participated in lifestyle changing interventions after atrial fibrillation ablation treatment.
Aim
The aim of this study was to assess the evidence on the benefits and harms of lifestyle and risk factor management interventions in patients undergoing atrial fibrillation ablation.
Method
Our systematic review searched MEDLINE, EMBASE, CINAHL, Psychinfo, Web of Science and CENTRAL using key terms related to atrial fibrillation and lifestyle, including interventional trials. The primary outcomes were mortality and serious adverse events. Random effects meta-analyses of outcomes were conducted when appropriate.
Results
Two randomised controlled trials and two non-randomised interventional trials with a total of 498 patients were included. Six primary events were reported for the intervention groups and five events for the control groups (relative risk of 1.03, 95% confidence interval (CI) 0.3 to 3.1, I ² 0%, P = 0.537). Effects in favour of the intervention groups were found for atrial fibrillation frequency (0.82 points, 95% CI –1.60 to –0.03, I ² 87.3%, P = 0.005), atrial fibrillation duration (–0.76 points, 95% CI –1.64 to 0.12, I ² 89.1%, P = 0.002) and body mass index (–5.40 kg/m ² , 95% CI 6.22 to –2.57, I ² 83.9%, P = 0.013). Risk of bias in the four studies was judged to be low to moderate.
Conclusion
Lifestyle changing interventions seem to have a positive effect on outcomes relevant to patients undergoing atrial fibrillation ablation, but the included studies were small, interventions were inhomogeneous, and the quality of evidence was low to moderate. More studies are warranted.
... The cells were maintained in 5% CO2 and 95% air at 37°C. Average serum nicotine level in moderate smokers is 220 nmol/L and the level can reach 440 nmol/L after consumption of a single cigarette [28]. Therefore, HAECs were incubated with 50 or 500 nM nicotine for 48 h in our experiments. ...
Rationale: Nicotine exposure via cigarette smoking is strongly associated with atherosclerosis. However, the underlying mechanisms remain poorly understood. The current study aimed to identify whether endothelial to mesenchymal transition (EndMT) contributes to nicotine-induced atherosclerosis.
Methods: ApoE-/- mice were administered nicotine in their drinking water for 12 weeks. The effects of nicotine on EndMT were determined by immunostaining on aortic root and RNA analysis in aortic intima. In vitro nicotine-treated cell model was established on human aortic endothelial cells (HAECs). The effects of nicotine on the expression of EndMT-related markers, ERK1/2 and Snail were quantified by real-time PCR, western blot and immunofluorescent staining.
Results: Nicotine treatment resulted in larger atherosclerotic plaques in ApoE-/- mice. The vascular endothelial cells from nicotine-treated mice showed mesenchymal phenotype, indicating EndMT. Moreover, nicotine-induced EndMT process was accompanied by cytoskeleton reorganization and impaired barrier function. The α7 nicotine acetylcholine receptor (α7nAChR) was highly expressed in HAECs and its antagonist could effectively relieve nicotine-induced EndMT and atherosclerotic lesions in mice. Further experiments revealed that ERK1/2 signaling was activated by nicotine, which led to the upregulation of Snail. Blocking ERK1/2 with inhibitor or silencing Snail by small interfering RNA efficiently preserved endothelial phenotype upon nicotine stimulation.
Conclusion: Our study provides evidence that EndMT contributes to the pro-atherosclerotic property of nicotine. Nicotine induces EndMT through α7nAChR-ERK1/2-Snail signaling in endothelial cells. EndMT may be a therapeutic target for smoking-related endothelial dysfunction and cardiovascular disease.
... Smoking is other risk factors for CHD increases the risk of cardiovascular diseases include systemic haemostatic and coagulatory disturbances, lipid abnormalities, increase in oxidative stress, and vasc increase in the concentration of serum total cholesterol, LDL anti-atherogenic HDL-c [21]. It is presumed that nicotine stimulates sympathetic increased secretion of catecholamine fatty acids, which further results in increased synthesis of hepatic triglycerides, along with VLDL stream [22]. High levels of LDL-c, VLDL coronary artery disease, while a low level of HDL artery disease [23]. ...
Introduction: The major independent risk factors for the development of atherosclerosis are the plasma cholesterol concentration, triglyceride, cigarette smoking, hypertension and diabetes, which are by them self’s risk factor for coronary heart disease. Cardiovascular disease (CVD) threatens to cripple India’s workforce and stunt India’s growth if timely and appropriate public health measures are not instituted. Hyperglycemia, hypertension and cigarette smoking depletes natural antioxidants and facilitates the production of reactive oxygen species (ROS) which has the ability to react with all biological molecules and exert cytotoxic effects on cellular components that promotes and accelerate atherosclerosis. Hence the present study was aimed to find out collective effect of NIDDM, hypertension and cigarette smoking on lipid profile and oxidative stress in progression of CHD events. Materials and methods: We studied 50 healthy and 50 diabetes with hypertension and or smokers patients (i. e. had two or more CHD risk factors) patients with matched for age and body mass index. Blood samples were drawn after an overnight fast. W e estimated serum triglycerides,total cholesterol, HDL-c and LDL-c and VLDL- c values were calculated by Friedwald’s equation. We also estimated the total serum lipid peroxides by reaction with thiobarbituric acid. Results: In the control group I mean values of total cholesterol were 180.21 ± 18.13 mg %, LDL-c 106.60 ±18.2 mg%, serum triglycerides were 99.90 ± 16.14 mg %, HDL-c were 53.83 ± 16.42mg% and in the group II serum triglycerides 217.9 ± 19.1 mg% and were significantly increased as compared to group I. The serum HDL-c group II 29.6 ± 8.07mg % were significantly decreased as compared to group I (P is<0.05). The serum lipid peroxides in the group 2nd (296.9.±60.10) were significantly increased as compared to group 1st (180.96±35.16). Conclusion: It can be concluded that patients of NIDDM with hypertension, smoking have higher total serum cholesterol, serum triglycerides, serum lipid peroxides (MDA), LDL- c and VLDL-c with lower HDL- c. These can be corrected, treated by dietary and life style modification before the development of end organ damage. For realization of exact role of lipid profile and oxidative stress further higher level studies should be done.
... Varenicline is a full agonist at the α7-, and a partial agonist at the α4β2-containing nicotinic cholinergic receptors (Coe et al., 2005;Rollema et al., 2007a,b), which mediate the primary reinforcement properties of nicotine, the major psychoactive compound of tobacco (Benowitz, 1992). However, the relatively weak primary reinforcement of nicotine cannot explain the pervasiveness of tobacco abuse alone ( Caggiula et al., 2001;Rose, 2006). ...
Nicotine is acknowledged as the key addictive compound of tobacco. Varenicline (Champix or Chantix), mainly acting as a partial agonist at the α4β2 nicotinic receptor, is an approved smoking cessation pharmacotherapy, although with efficacy limited to a portion of smokers. Smokers differ in the motives that drive their drug seeking and Varenicline might be more efficient in some groups more than others. Studies in rodents revealed that nicotine-seeking is strongly supported by complex interactions between nicotine and environmental cues, and notably the ability of nicotine to enhance the reinforcing properties of salient environmental stimuli. It is not yet understood whether the decrease of nicotine-seeking by acute Varenicline in rats results from antagonism of the primary reinforcing effects of nicotine, of the reinforcement-enhancing effect of nicotine on cues, or of a combination of both. Thanks to a protocol that allows assessment of the reinforcement-enhancing effect of nicotine on cues during self-administration in rats, we showed that Varenicline targets both nicotine reinforcing effects and reinforcement-enhancing effect of nicotine on cues. Importantly, individual variations in the latter determined the amplitude of acute Varenicline-induced decrease in seeking. These results suggest that Varenicline might be more beneficial in smokers who are more sensitive to nicotine effects on surrounding stimuli.
... Early addiction research focused on drugs of abuse such as alcohol, morphine and nicotine. This has since been extended to include gambling, eating and more recently, sugar consumption (Comings et al., 2001;Weeks, 1962;Jellinek, 1952;Benowitz, 1988;Gearhardt et al., 2009;Klenowski et al., 2016;Benton, 2010). Addiction to substances of (NAc). ...
In 2016 the World Health Organization reported 39% of the world's adult population (over 18 y) was overweight, with western countries such as Australia and the United States of America at 64.5% and 67.9% respectively. Overconsumption of high fat/sugar containing food and beverages contribute to the development of obesity. Neural plasticity that occurs as a result of long term sugar consumption has been shown to reduce impulse control and therefore lower the ability to resist the high fat/sugar foods contributing to the obesity epidemic. There is significant overlap between the neural pathways involved in emotions that guide behavioural responses to survival situations with those regulating overconsumption of highly palatable food. This suggests that having a clearer understanding of the role of stress and emotions in the development of obesity will lead to the development of novel therapeutic strategies. Sucrose consumption activates the mesocorticolimbic system in a manner synonymous with substances of abuse. There is overwhelming evidence to support the hypothesis that sucrose consumption results in pathophysiological consequences such as morphological neuronal changes, altered emotional processing and modified behaviour in rodent and human models. In this comprehensive review, we examined >300 studies investigating the interaction between sugar consumption, stress and emotions. Preclinical and clinical trials investigating highly palatable foods and stress, anxiety, depression and fear are reviewed. Importantly, the synergy between sugar consumption and neurobiology is addressed. This review summarizes the neurochemical changes and neural adaptations ö including changes in the dopaminergic system ö that influence emotion and behaviour following sugar consumption.
... C igarette smoking is the leading preventable cause of death in the United States (US) 1 and incurs more than $300 billion in healthcare costs annually. 2 Understanding the variables that maintain cigarette use, especially the role of nicotine, 3 is an important avenue of inquiry that informs tobacco/nicotine control policies aimed at reducing smoking. 4 Research shows that substantial reductions in nicotine content in tobacco cigarettes can result in lower exposure to toxins and reduce dependence. ...
Objectives: Lowering the nicotine content in combustible cigarettes may be a viable strategy for reducing dependence and toxin exposure. Understanding how marketing and education may affect initial uptake is an important avenue of inquiry prior to any policy change. There has yet to be an investigation of how framing reductions in nicotine may affect intentions to purchase and consume these cigarettes using the behavioral economic framework. Methods: Participants from Amazon Mechanical Turk completed several tasks, including the Cigarette Purchase Task and Experimental Tobacco Marketplace, under conditions in which a new, reduced-nicotine cigarette alternative is the only cigarette available. Results: Cigarette purchasing was largely unaffected by stated nicotine concentration, but lower concentrations suggested the potential of small estimated compensatory purchasing. Exposure to a narrative detailing how others have perceived the negative subjective effects of lower nicotine cigarettes (eg, less satisfaction) significantly reduced the perceived value of cigarettes. Conclusions: These results suggest information about nicotine content alone is unlikely to reduce initial uptake without accompanying narratives about the effects of this reduced-nicotine content.
... In addition, smoking may be under-reported in Korean women because of the traditional Korean cultural background, which stigmatizes smoking in women 11 . Several biomarkers for tobacco smoking (nicotine, cotinine, and exhaled carbon monoxide) have been used to validate the smoking status 31,32 . Plasma nicotine is the most accurate method for validating smoking status; however, it is difficult to use in the national survey research due to its short half-life (2-3 hr). ...
Cigarette smoking is believed to affect thyroid function and autoimmune thyroid disease. However, there is little information to analyze their association using objective biomarkers. The aim of this study was to investigate the dose-related effect of smoking on thyroid hormones and thyroid peroxidase antibody (TPO Ab) using urinary cotinine levels and a population-based cohort. The present study used the thyroid hormone and urinary cotinine dataset from sixth Korean National Health and Nutrition Examination Survey in 2014 and 2015, and a total of 4249 participants were included. Dose-response relationships between thyroid hormone (free T4, TSH, and TPO Ab) and urinary cotinine levels were estimated using ANCOVA after adjustment for all variables (age, height, weight, alcohol, exercise, and log- transformed iodine in urine). Urinary cotinine level was negatively correlated with TSH. The estimated coefficients were −0.0711 in males and −0.0941 in females (p < 0.0001). TPO Ab titer was positively correlated with cotinine levels in males (p < 0.0001). Our findings indicated a significant dose-related effect of urinary cotinine level on thyroid function, and thyroid autoimmunity.
... Despite the development of effective voluntary oral NIC self-administration models (Hauser et al. 2012b;Deehan et al. 2015), i.v. NIC is commonly employed in an attempt to parallel rapid increases in blood NIC levels produced by smoking, which is not observed during the use of chewing tobacco (Benowitz 1988). However, oral tobacco products, such as snus, produce the same rapid increase in blood NIC levels as observed in smokers. ...
Rationale and objectives
Simultaneous alcohol and nicotine consumption occurs in the majority of individuals with alcohol use disorder (AUD) and nicotine dependence. Varenicline (Var) is used to assist in the cessation of nicotine use, while naltrexone (Nal) is the standard treatment for AUD. Despite evidence that ethanol (EtOH) and nicotine (NIC) co-use produces unique neuroadaptations, preclinical research has focused on the effects of pharmacotherapeutics on a single reinforcer. The current experiments examined the effects of Var and Nal on EtOH, NIC, or EtOH+NIC intake.
Methods
Animals were randomly assigned to one of four drinking conditions of 24-h access to a three-bottle choice paradigm, one of which always contained water. Drinking conditions were water only, 0.07 and 0.14 mg/mL NIC (NIC only), 15% and 30% EtOH (EtOH only), or 15% and 30% EtOH with 0.14 mg/mL NIC (EtOH+NIC). The effects of Var (0, 1, or 2 mg/kg) or Nal (0, 1, or 10 mg/kg) injections on maintenance and relapse consumption were determined during four consecutive days.
Results
Var reduced maintenance and relapse NIC intake but had no effect on EtOH or EtOH+NIC drinking. Conversely, Nal reduced EtOH maintenance and relapse drinking, but had no effect on NIC or EtOH+NIC drinking.
Discussion
The results indicate the standard pharmacological treatments for nicotine dependence and AUD were effective at reducing consumption of the targeted reinforcer but neither reduced EtOH+NIC co-use/abuse. These findings suggest that co-abuse may promote unique neuroadaptations that require models of polysubstance abuse to develop pharmacotherapeutics to treat AUD and nicotine dependence.
... Nicotine poses an international health threat because of its carcinogenic properties. In humans, it promotes a host of interoceptive changes ("subjective effects") including alertness, increased mood, and a subtle "high" (Benowitz, 1988). Nicotine also modulates responsiveness to exteroceptive stimuli predictive of drug-reward (see Hogarth and Troisi, 2015;Troisi, 2003a,b;Troisi, 2014). ...
Nicotine promotes interoceptive changes in the nervous system. Such interoceptive stimuli play important roles in modulating addictive behavior. Operant and Pavlovian stimulus control modulate responsiveness to environmental stimuli related to drug-seeking and self-administration. Nicotine functions as a discriminative stimulus in modulating operant behavior as well as Pavlovian feature stimuli in modulating the conditional responding (CR) to exteroceptive CS→US contingencies. Elucidation of the interaction of these interoceptive stimulus control functions is vital for a comprehensive understanding of nicotine use/abuse, which might lead to better behavioral treatment strategies. This experiment evaluated the interaction among Pavlovian feature positive (FP) and feature negative (FN) effects of nicotine on concurrently occurring operant SD and SΔ effects. Sixteen rats were trained in a Pavlovian and operant bidirectional contingency paradigm, using nicotine (0.3 mg/kg) and non-drug (saline) states as interoceptive cues for operant discriminative stimulus conditions (SD and SΔ) as well as Pavlovian FP and FN for a light-CS, either leading to a shared food pellet outcome or non-outcome. Nicotine and saline sessions were intermixed. For one group of rats (n = 8), nicotine served as an SD for lever pressing (variable interval 60 s) and simultaneously functioned as an FN for CS-light→noUS relation on the same sessions. On intermixed sessions, saline served as the SΔ for lever pressing (non-reinforced) and FP, during which the 8-sec light preceded delivery of the food pellet (variable time ITI = 60 s). For the other group (n = 8) nicotine served as the SΔ (lever pressing non-reinforced) and FP for the CS, with saline serving in the reverse roles. Consecutive brief non-reinforcement tests revealed that: A) rates of lever pressing were significantly greater in SD than SΔ with nicotine and saline suggesting strong operant discriminative stimulus control; B) FP responding to the light CS with nicotine and saline was evident; and C) FN suppression of the CR with nicotine was not evident but weak under saline. These data suggest that nicotine can function as an interoceptive context that hierarchically can enter into concurrently opposing modulatory relations in Pavlovian and operant drug discrimination procedures.
... We speculate that sub-toxic clinical concentration of nicotine might affect fracture healing in other mechanisms. According to clinical epidemiological investigation, the blood levels of nicotine obtained from habitual cigarette smokers range from 0.06 to 1.2 mM and, the level of nicotine in the saliva has been reported to be 0.6-9.6 mM [32]. In the present study, nicotine concentrations, ranging from 1 μM to 10 mM, were carefully selected to correspond to the levels in blood and saliva of smokers. ...
Wound and fracture healing are affected by exposure to nicotine and other compounds in cigarettes. This study examined the effects of exposure to low-dose nicotine at sub-toxic concentrations on the proliferation, differentiation and migration of bone marrow stem cells (BMSCs) in vitro and their homing to fracture site in C57BL/6 mice. BMSCs were investigated in cells treated with or without nicotine (1 μM to 1 mM). Different concentrations of nicotine exhibited varied effects on BMSCs growth regulation and bone differentiation. CCK8 test significantly increased at a high nicotine concentration of 1 mM while calcium nodule staining with Alizarin red decreased at the same concentration. In vitro scratch test, Transwell tests and in vivo BMSCs homing tests showed negative effects on BMSCs migration at 10 μM to 1 mM nicotine test. Real-time PCR analysis revealed the down-regulation of SDF-1, CXCR4 and CXCR7, which were members of the potent chemotactic signaling system. Western blot analysis indicated the down-regulated expression levels of periostin expressed by nicotine-treated osteoblasts (1 μM to 100 μM). Micro CT results showed that nicotine delayed the fracture healing in mice. Our data suggest that exposure to low-dose nicotine concentrations may affect bone formation by inhibiting the migration and homing of BMSCs, which may be an important risk factor for bone healing delay in smoking patients.
... In a previous paper, we reported, using easily administered tasks, which impose few cognitive demands and thus not substantially affected by performance confounds (20,21) that a behavioral addiction, pathological gambling (22), was characterized by constructional apraxia along with impairments in filtrating visual signal from noise and orienting in space (20). Notably, the Copy Figure Test (CFT) for constructional apraxia that is "almost pathognomonic" for brain damage in the presence of grossly abnormal performance on even one out of seven figures (23), was validated across behavioral (20)-and chemical (21) types of addictive behaviors, which also encompass overeating (1) and smoking (24). ...
Neurological soft signs (NSSs) are highly prevalent among patients with schizophrenia, but their pathophysiological significance remains unclear. The present study employed perceptual-motor and visuospatial processing tests that have not yet been attempted in this patient population. Patients with schizophrenia or schizoaffective disorder (n = 42) and mentally healthy subjects (n = 10) were administered Copy Figure Test, Detection and Recognition of an Object Test and Road Map Test. As compared to controls, schizophrenic and schizoaffective patients displayed significantly poorer ability to copy three-dimensional figures (namely, Necker- and hidden line elimination cubes) and to orient in space on a road-map test; group differences in copying two-dimensional figures and on objects' recognition against a background noise were not apparent. In the schizophrenia/schizoaffective group, more mistakes on the hidden line elimination cube was associated with greater body mass index and greater severity of nicotine dependence measured via the Fagerstrom Test of Nicotine Dependence. The above findings replicate those of prior reports and extend them to the tasks that do not involve motivational and attentional confounds. Furthermore, the present data support the hypothesis that subtle cerebral cortical abnormalities detected with specific NSSs tests may be related to some aspects of metabolic and motivational function in patients with schizophrenia/schizoaffective disorder.
Nicotine is highly addictive plant derived alkaloid and the most important species in human use today is Nicotiana tabacum. There are direct health effects of chronic nicotine exposure. Even in low doses, nicotine causes vasoconstriction and other cardiovascular effects related to catecholamine release and promote angiogenesis, neuroteratogenicity, and possibly some cancers¹. Periodontal disease and dental cavities and have up to 48 times the risk of oropharyngeal cancers compared with people who do not use tobacco products². Low doses exposure produces fine tremor, cutaneous vasoconstriction, increased GI motility, and increase in heart rate, respiratory rate and blood pressure³. Low dose nicotine also increases mental alertness and produces euphoria and desired psychoactive effects³. Metabolism is via the hepatic cytochrome oxidase system. The half life of nicotine in the body is 1 to 4 hours and decreases with repeated nicotine exposure4.
A BSTRACT
Background and Aim
In this study, the aim was to research the effects of smoking habits on controlled hypotension administered with nitroglycerin during ear-nose-throat surgery.
Materials and Methods
This study administered controlled hypotension with nitroglycerin and total intravenous anesthesia to a total of 80 patients undergoing septoplasty operations. The patients were divided into two groups of 40 non-smokers (Group 1) and 40 smokers (Group 2). Intravenous propofol infusion was used for anesthesia maintenance. Nitroglycerin with 0.25–1 μg/kg/min dose was titrated to provide controlled hypotension. During this process, the hemodynamic parameters of patients, total propofol and nitroglycerin amounts used, operation duration, and duration of controlled hypotension were recorded at the end of the operation. At the end of the operation, the surgeon assessed the lack of blood in the surgical field with Fromme Scale.
Results
Fromme scale values were significantly higher in Group 2 compared to Group 1. The MAP values at 10, 20, 30 min, and end of operation were lower, while 10- and 20-min heart rate values were higher in Group 2 compared to Group 1.
Conclusion
Nitroglycerin, chosen for controlled hypotension to reduce hemorrhage in the surgical field during nasal surgery, was shown to cause more pronounced hypotension and reflex tachycardia due to endothelial dysfunction linked to nicotine in patients who smoke. Despite lower pressure values in the smoking group, the negative effects of nicotine on platelet functions combined with similar effects of nitroglycerin to increase bleeding amounts.
Cigarette smoke consists of a mix of chemical substances in the form of gases and dispersed particles. Recently, more than 4000 compounds presented incigarette smoke have been isolated. Most of these compounds are toxic to our body’s cells. Toxic gases including carbon monoxide (CO), hydrogen cyanide(HCN), nitrogen oxides, and volatile chemicals such as nitrosamines, formaldehyde are found in in cigarette smoke. besides toxic compounds, cigarettesmoke also containsfree radicalsincluding peroxynitrite, hydrogen peroxide, and superoxide. These free radicals may accelerate cellular damage due tooxidative stress. Targets od free radical attacks include DNA, protein and lipids. The harmful chemicals in form of gases and volatile substances in cigarettescause multiple genetic mutations. the combination of genetic mutations and DNA damage lead to genetic instability and it may cause cancer. OxidativeDNA damage caused by cigarette smoke can be identified with the presence of 8-oxoguanosine used as one of the biomarkers for oxidative DNA damage.Increased concentration of 8-oxoguanosine in DNA has an important role in carcinogenesis and triggers tumor cells. both active and passive smokers havebeen reported to have an elevated concentration of 8-oxoguanosine in their lung tissue and peripheral leukocytes as well as for passive smokers. This paperprovide informations and understanding of the effects of smoking on the genetic stability, especially in the DNA molecule.
Com o intuito de aproximar os gestores estaduais e municipais de
saúde com a gestão da Coordenação-Geral de Assistência Farmacêutica
e Medicamentos Estratégicos (CGAFME), no sentido de qualificar a
Assistência Farmacêutica, foi idealizado a realização do Seminário
Nacional do Componente Estratégico.
O primeiro “Seminário Nacional do Componente Estratégico da
Assistência Farmacêutica”, que ocorreu em 2014, teve por objetivo discutir
os principais desafios e perspectivas no âmbito do Componente Estratégico
da Assistência Farmacêutica (Cesaf) e possibilitar a troca de experiências
entre os gestores na busca da integralidade na assistência à saúde.
Devido à importância da contribuição dos estados e dos municípios para
a gestão participativa da CGAFME, em agosto de 2015 ocorreu a segunda
edição do Seminário, que teve como objetivo contribuir com o avanço do
processo de qualificação do Cesaf nas suas dimensões, oferecer garantia
do acesso e da qualidade de medicamentos, assim como organizar os
serviços farmacêuticos, com a atualização e a elaboração de Diretrizes
Clínicas e Terapêuticas para o Cuidado Farmacêutico nas doenças e
agravos que são de responsabilidade do Cesaf.
O II Seminário foi constituído de mesas de debate com a participação dos
gestores municipais, estaduais e federais. Além disso, foram apresentadas
a experiência do planejamento da CGAFME e a organização da gestão do
Cesaf por meio de relatos de experiência estaduais e municipais.
O Seminário possibilitou o aprofundamento do debate para a qualificação
do cuidado farmacêutico e do uso racional de medicamentos. Os avanços
alcançados foram destacados e os desafios a serem superados, tais
como o fortalecimento da relação interfederativa e a organização dos
serviços farmacêuticos.
Before visiting a doctor, using the internet & search engines regarding health-related issues became more common practice nowadays. E-cigarettes help in smoking cessation but caused switching to a new smoking habit. In teenagers’ e-cigarettes have a detrimental effect on their health and they are a threat of switching to other drugs. The United States Food and Drug Administration (FDA) cautioned the public about serious lung diseases and deaths associated with vaping. Non-nicotine e-cigarettes may pump toxic chemicals & carcinogens directly into the lungs. Nicotine replacement therapy (NRT) may not give a feeling of active smoking so, people are switching to e-cigarettes. Nicotine causes addiction and may affect brain development. The approved NRT may have side effects but one should not forget that safety & efficacy has been evaluated and approved by the FDA for smoking cessation. It is strictly cautioned to stay away from adulterated vaping products.
This study was designed to identify the effects of nicotine on the skeletal and internal organ abnormalities of mice prenatally. Seventy two female mice strain Balb/C were used. Pregnant mice on gestation days (GD) 8, 10, and 12 was injected intraperitoneally with 3, 6, and 12 mg/kg BW nicotine respectively. Control nice was injected by aguabidestylata. On GD 18, and all of pregnant mice were sacrificed, and a half of living fetuses were immersed in Bouin’s solution to observe their internal organs, while another half were immersed in 95 percent ethanol to observed sekeletal malformation using alizarin red S staining. Results were analyzed using SPSS program version 11 for personal computer. The results showed that nicotine caused Skeletal malformation, especially in the sternum when administered on GD 8 and 10, in doses of 3 and 6 mg/kg BW, delayed of ossification was observed in the supraoccipital and sacrocaudal bones on GD 10 and 12 and doses of 12 mg/kg BW, while in the extremitas the malformation was observed in the proximal and medial phalanx both in the fore and hind limb especially on GD 10 and 12, and doses of 6 and 12 mg/kg BW. Nicotine was effects on the brain development especially hydrocephalus was observed on GD 8 and doses 10 and 12 mg/kg BW. Another internal malformation such as ectopic renalis was observed on GD 8 and doses of 3 and 6 mg/kg BW. These finding suggested that nicotine has caused skeletal malformation, brain malformatin and ectopic renalis, when administered in mice prenatally.
Summary: Cigarette smoking is the single most important risk factor contributing to premature mortality and to development of many diseases. Smoking has and epidemic character in all population groups. The aim of this paper was to point out the importance of quitting smoking and the prevention of many diseases and to bring out the fact which contribute to the understanding to the nicotine addiction, nicotine pharmacology, and to emphasize the imperative that health care workers improve own education in this field in their everyday work with every patient, without missing any single appointment of the patient, to get repetitive counseling about quitting smoking with final health educational effect.
Drug and nondrug interventions used in treating nicotine dependence are reviewed.
Tobacco use is the leading preventable cause of death in the United States. Risks of smoking-related disease and death decline sharply when smokers quit, but 26% of Americans continue to smoke. Most smokers find it extremely difficult to quit smoking because of their nicotine addiction. Nonpharmacologic interventions used to promote smoking cessation include behavioral therapy, setting a specific date for quitting, receiving advice to quit from a health care professional, follow-up visits to review progress, self-help approaches, group counseling, filtration devices, hypnosis, and acupuncture. The efficacy of these approaches ranges from substantial to almost nil. The only pharmacologic agent with FDA-approved labeling for use in smoking-cessation therapy is nicotine. When used in conjunction with appropriate nonpharmacologic interventions, nicotine-replacement therapy roughly doubles the rate of quitting obtained with placebo. Nicotine-replacement therapies consist of nicotine transdermal (patch) systems and nicotine chewing gum. The nicotine patch is the first-line replacement therapy because it is effective when accompanied by only minimal (as opposed to more intensive) nonpharmacologic interventions and because it is easier to use and comply with than gum. Clonidine, antidepressants, and buspirone require further study to determine what role, if any, they should play in the treatment of nicotine dependence. The stages of smoking cessation are precontemplation, contemplation, action, and maintenance; interventions are selected on the basis of the stage the smoker is in.
Nicotine dependence is difficult to treat, but there are aids that boost a smoker’s chances of quitting. Nicotine patches and chewing gum offer the most effective pharmacologic options, especially when combined with behavioral interventions and counseling.
Objetivo. Evaluar la dependencia física y psicológica de los fumadores mexicanos y su asociación con factores físicos, psicológicos y sociales. Material y métodos. A partir de la Encuesta Nacional de Consumo de Drogas, Alcohol y Tabaco 2016 (n=7 331), se analizó la escala de dependencia física a la nicotina de Fagerström (FTND) y la escala corta de dependencia psicológica al tabaco (TAPDSc). Se realizaron análisis bivariados y regresiones logísticas ordinales generalizadas para evaluar los factores asociados. Resultados. 82.3% de fumadores diarios y 98.8% de ocasionales reportaron dependencia física leve, mientras que 47.9 y 37.9%, respectivamente, presentaron dependencia psicológica moderada. La edad de inicio temprana de consumo de tabaco, uso de drogas, consumo alto de alcohol y malestar emocional se asociaron con niveles altos de dependencia psicológica en todos los fumadores. Conclusión. El uso exclusivo de FNTD no permite evaluar adecuadamente a los fumadores mexicanos. La dependencia física y psicológica al tabaco debe ser diagnosticada con escalas independientes y validadas en esta población.
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