Academic literature on the topic 'Caffeine Cigarette smokers'

Cigarette smoking has been associated with delayed sleep onset and diminished sleep duration, primarily on the bases of responses to one-shot questionnaires. This study used a survey format of daily diaries to observe sleep quality. 29 smokers were matched for age, ethnicity, and gender with 29 nonsmokers. Both groups recorded information on cigarette, alcohol, caffeine consumption, daily stress, and sleep quality. While the results showed that smokers were more likely to experience poor sleep than nonsmokers, these data are difficult to interpret because smokers also used significantly greater amounts of alcohol and caffeine.

Simultaneous determination of caffeine, cotinine, and 1N-methyluric acid in urine has numerous applications in determining patterns of use by athletes, according to the World Anti-Doping Agency (WADA) which includes these substances on the Monitoring List. The method can provide information on the enzyme-inducing activity on CYP1A2 of polycyclic aromatic hydrocarbons from cigarette smoke. Urine samples from 30 people (15 smokers and 15 non-smokers) were sampled 6 hours after having consumed a beverage with a total caffeine content of 200 mg. A HPLC with UV detection method was used which allowed concomitant determination of the three analytes. The results obtained show different values of caffeine urine concentrations (6.47 � 3.63 mM / L in smokers vs 10.09 � 5.68 in non-smokers, p [0.05) and a higher elimination of N1-methyluric acid by over 50% in smokers (identifiable due to the presence of cotinine, the main metabolite of nicotine).

Non-alcoholic fatty liver disease (NAFLD) is common among 30% of American adults. Former and current smokers are at higher risk for NAFLD compared to never smokers. The ratio of urine caffeine metabolites to caffeine intake—namely, urine caffeine metabolite indices—has previously been used as a proxy for CYP1A2 activity, which is one of the main liver metabolizing enzymes. CYP1A2 activity is associated with NAFLD progression. No studies to our knowledge have examined the associations of liver enzymes, smoking intensity, and secondhand smoke (SES) with CYP1A2 activity (using caffeine metabolite indices) across smoking status. We analyzed national representative samples from the 2009–2010 National Health and Nutrition Examination Survey (NHANES). Interestingly, even within a normal range, several liver enzymes were associated with caffeine metabolite indices, and patterns of many of these associations varied by smoking status. For instance, within a normal range, aspartate aminotransferase (AST) in never smokers and bilirubin in current smokers were inversely associated with 1-methyluric acid and 5-acetylamino-6-amino-3-methyluracil (URXAMU). Furthermore, we observed a common pattern: across all smoking statuses, higher AST/alanine aminotransferase (AST/ALT) was associated with 1-methyluric acid and URXAMU. Moreover, in current smokers, increased lifelong smoking intensity was associated with reduced caffeine metabolite indices, but acute cigarette exposure as measured by SES levels was associated with increased caffeine metabolite indices among never smokers. In summary, commonly used liver enzyme tests can reflect the CYP1A2 activity even within a normal range, but the selection of these enzymes depends on the smoking status; the associations between smoking and the CYP1A2 activity not only depend on the intensity but also the duration of tobacco exposure.

Existing US epidemiological data demonstrate that consumption of smokeless tobacco, particularly moist snuff, is less harmful than cigarette smoking. However, the molecular and biochemical changes due to moist snuff consumption relative to smoking remain incompletely understood. We previously reported that smokers (SMK) exhibit elevated oxidative stress and inflammation relative to moist snuff consumers (MSC) and non-tobacco consumers (NTC), based on metabolomic profiling data of saliva, plasma, and urine from MSC, SMK, and NTC. In this study, we investigated the effects of tobacco consumption on additional metabolic pathways using pathway-based analysis tools. To this end, metabolic pathway enrichment analysis and topology analysis were performed through pair-wise comparisons of global metabolomic profiles of SMK, MSC, and NTC. The analyses identified >8 significantly perturbed metabolic pathways in SMK compared with NTC and MSC in all 3 matrices. Among these differentially enriched pathways, perturbations of caffeine metabolism, energy metabolism, and arginine metabolism were mostly observed. In comparison, fewer enriched metabolic pathways were identified in MSC compared with NTC (5 in plasma, none in urine and saliva). This is consistent with our transcriptomics profiling results that show no significant differences in peripheral blood mononuclear cell gene expression between MSC and NTC. These findings, taken together with our previous biochemical, metabolomic, and transcriptomic analysis results, provide a better understanding of the relative changes in healthy tobacco consumers, and demonstrate that chronic cigarette smoking, relative to the use of smokeless tobacco, results in more pronounced biological changes, which could culminate in smoking-related diseases.

BACKGROUND: A relationship between smoking and development of pain syndromes has been suggested in the literature. The present study examined associations between smoke exposure and other related variables, and pain response to suprathreshold electrical stimulation.METHODS: Subjects were prospectively recruited from a population referred to an electrodiagnostic clinic. Information about age, smoke exposure, caffeine and alcohol consumption was obtained, as well as documented objective signs of stress through physical assessment. One investigator applied two standardized 0.1 ms electrical stimulations (50 mA followed by 100 mA) to asymptomatic extremities at the beginning of each electrodiagnostic session, using consistent technique. Subjects used a visual analogue scale to indicate the level of pain felt after each stimulation.RESULTS: Two hundred fifteen women were included. Current smokers and those currently exposed to second-hand smoke had significantly higher pain ratings (P=0.003 for 50 mA, P=0.005 for 100 mA) than those not currently exposed to smoke. Time since exposure was negatively associated with pain ratings. Those with objective signs of stress reported higher levels of pain, which was significant for the 100 mA stimulation (P=0.046). Linear regression modelling indicated that current smoke exposure and alcohol use were associated with higher pain ratings at both 50 mA and 100 mA, while stress was associated with higher pain ratings and older age was associated with lower pain ratings at 100 mA only.INTERPRETATION: Exposure to cigarette smoke is significantly related to higher reported levels of pain experienced in response to electrical stimulation in this study population. Exposure to smoke can add 10 points to the 100-point visual analogue scale compared with subjects without exposure, with alcohol use adding another eight points. Reported pain decreases as length of time since previous exposure to smoke increases.

Little is known about environmental risk factors for hypodontia. The objective of this study was to investigate the association between hypodontia and common environmental risk factors, such as maternal smoking and alcohol and caffeine consumption during pregnancy. Eighty-nine hypodontia cases with 1 or more missing permanent lateral incisors and/or 1 or more missing premolars were enrolled in this clinic-based case-control study. Some 253 controls with no missing teeth were frequency matched to cases by age and sex. Hypodontia was diagnosed using panoramic radiographs. Sociodemographic data were collected from both the participants and their mothers, with maternal self-reported active and passive smoking, as well as alcohol and caffeine consumption during pregnancy, assessed by a questionnaire. Odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated with logistic regression to assess the strength of association between risk factors and hypodontia. OR estimates were then adjusted for possible confounders, such as maternal age at delivery, sex and gestational age of the child, and household socioeconomic background. Significant associations were found between hypodontia and maternal cigarette use during pregnancy, as well as the number of cigarettes smoked per day. The consumption of 10 or more cigarettes per day during pregnancy was associated with greater odds of having a child with hypodontia (adjusted OR, 4.18; 95% CI, 1.48–11.80; P = 0.007). Observed associations between hypodontia, second-hand smoke, and alcohol and caffeine consumption were not statistically significant. Maternal smoking during pregnancy is associated with hypodontia. Larger samples and prospective observational study designs, however, are needed to investigate this association further.

Caffeine–a methylxanthine analogue of the purine bases adenine and guanine–is by far the most consumed neuro-stimulant, being the active principle of widely consumed beverages such as coffee, tea, hot chocolate, and cola. While the best-known action of caffeine is to prevent sleepiness by blocking the adenosine receptors, caffeine exerts a pleiotropic effect on cells, which lead to the activation or inhibition of various cell integrity pathways. The aim of this review is to present the main studies set to investigate the effects of caffeine on cells using the model eukaryotic microorganism Saccharomyces cerevisiae, highlighting the caffeine synergy with external cell stressors, such as irradiation or exposure to various chemical hazards, including cigarette smoke or chemical carcinogens. The review also focuses on the importance of caffeine-related yeast phenotypes used to resolve molecular mechanisms involved in cell signaling through conserved pathways, such as target of rapamycin (TOR) signaling, Pkc1-Mpk1 mitogen activated protein kinase (MAPK) cascade, or Ras/cAMP protein kinase A (PKA) pathway.

Thesis (M.A.)--Central Connecticut State University, 1999.
Thesis advisor: Carol Shaw Austad. " ... in partial fulfillment of the requirements for the degree of Master of Arts [in Psychology]." Includes bibliographical references (leaves 17-18).

All addictive chemicals are psychoactive, but not all psychoactive compounds are addictive although they can be abused. Notable non-addictive psychoactive compounds are hallucinogens and the many mood-altering drugs marketed for depression, anxiety, epilepsy, and so forth. This chapter’s movies were chosen for the variety of psychoactive substances used by characters. They all show either drug abuse or addiction. The first few times that someone chooses to take a potentially addictive drug, they experience a rapid-onset pleasurable response followed by a slower onset, longer lasting dark side called withdrawal (Koob and Le Moal 2006; Grens 2007). Chronic use and bingeing lead to “tolerance” such that the euphoric effects are diminished even as the dose is increased. A person is said to be addicted to a drug when he or she seeks out the drug to avoid the dark side more than to induce its bright side. The bright and dark emotional and biochemical responses of euphoria, tolerance, and withdrawal are associated with a set of nerves called the “reward system” that lie at the top of the brainstem, buried deep within the human brain. We inherited these neurons from our earliest vertebrate ancestors. They are normally stimulated when we quench our thirst, stave off hunger, engage in sexual behavior, or participate in a host or other pleasurable activities. Repeated use of addictive drugs triggers the synthesis of proteins in the brain that cause anxiety or depression. Therefore, one promising line of research is to lessen the effects of withdrawal by finding other small molecules (therapeutic drugs) that bind to the receptors for the anxiety-producing or depression-inducing compounds. The “big three” legally addictive substances are nicotine, alcohol, and caffeine. About three-quarters (76%) of Americans over the age of 12 have smoked at least one cigarette in their lifetime, and 19% of Americans over the age of 12 smoke every day. From this we can calculate that 25% of users are addicted (=19%/76%), the highest addiction rate for any substance. With regard to alcohol, 51% of Americans are regular, moderate drinkers, 23% are binge drinkers, and 7% are heavy drinkers.

There is currently a great deal of interest in the diagnosis and treatment of unstable angina and silent ischemia.Many feel that these syndromes are due, in part, to periodic accumulation of platelet thrombi which subsequently embolize.In addition, anti-piatelet therapy is also considered necessary for patients after coronary artery bypass grafts (CABG'S), balloon angioplasty, and thrombolysis. Currently the two antiplatelet agents most commonly prescribed for the patient conditions mentioned above are aspirin (ASA), alone or in combination with dipyridamole (Dip). ASA reduces cardiac events in patients with unstable angina, and prolongs CABG graft patency. The addition of Dip to ASA therapy is very confusing since most studies done compared ASA + Dip to placebo. In several studies however,when an ASA group was compared to an ASA + Dip group there was no significant difference.We have developed and will describe ananimal model of coronary artery stenosis in the dog and the pig, or carotid arterystenosis in the monkey and the rabbit, with intimal damage, that simulates some ofthe conditions that exist in patients with coronary or carotid artery disease. The artery to be studied is dissected outand blood flow is continuously measured with an electromagnetic flowmeter probe. As acute platelet thrombus formation (APTF) developes in the stenosed lumen, the blood flow declines to low levels, producing ischemia until the thrombus emobolizesdistally resulting in abrupt restoration of blood flow. These cyclical flow reductions (CFR's), when they occur in the coronaries, produce ECG changes identical to those observed in patients with silent ischemia and unstable angina. They also produce significant transient regional dyskinesis of the ventricular wall, which resolves when blood flow is restored. Histologic examination of myocardial tissue in the bed distal to the stenosis shows focal areas of ischemic change presumably caused by the embolized platelet emboli.We have examined factors which exacerbate the size and frequency of these CFR"ssuch as; IV infusion of epinephrine (E) 0.4 μg/kg/min for 15 min, ventilating the animals with cigarette smoke, infusing nicotine IV, or placing chewing tobacco under the tongue.We have examined four groups of agentswhich prevent APTF in our model.1. Antiplatelet agents including ASA, indomethacin, ibuprofen and several other NSAI agentsas well as several experimental thromboxane synthetase inhibitors. These agents all block the production of TXA2and inhibit APTF in our model. Unfortunately the IV infusion of E reinstates APTtemporarily (by another biochemical pathway) until the E is metabolized. High (2-4 mg/kg) doses of Dip, alone or with sub threshold dose of ASA does nothing to I APTF.However,0.6mg/kg of chi orpromaz i ne abolishes APTF in all four species and protects agents renewal of APTF by E.2. Dietary Substances In our model, caffeine 10 mg/kg, or the extract from two garlic cloves, or enough ethanol to achieve a blood alcohol level of 0.07 mg% all significantly inhibit or abolish APTF in our model.3. Metabolic Inhibitors POCA, an oral hypoglycemic agent, which inhibits mitochondrial beta oxidation of fatty acids also inhibits APTF in our model possibly by reducing ATP production in the platelet.4. We have studied a monoclonal antibody(developed by Dr. Barry Coller) to the platelet I Ib�I I la glycoprotein receptor where fibrinogen binds platelets into aggregates and ultimately leads to APTF. This antibody 0.3 mg/kg/completely inhibits APTF, and also strongly inhibits in vitro platelet aggregation in response to either ADP or collagen given alone or each combined with E. This antibody is the most potent inhibitor of APTF that we have studied.