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Goodwin R.D.,Columbia University | Lavoie K.L.,University of Quebec at Montreal | Lavoie K.L.,Montreal Heart Institute | Lavoie K.L.,Montreal Behavioural Medicine Center | And 4 more authors.
Nicotine and Tobacco Research | Year: 2012

Introduction: Previous studies have shown links between anxiety and depression and chronic obstructive pulmonary disease (COPD), but little is known about possible mechanisms of this association. The current study examined whether the observed relationship between anxiety and depression and COPD is explained by confounding due to cigarette smoking and lifetime nicotine dependence. Methods: Data were drawn from the National Comorbidity Survey Replication, a community-based representative sample of adults in the United States. Results: Analyses suggest that the association between anxiety disorders and COPD appears to be largely explained by confounding by former cigarette smoking and lifetime nicotine dependence. The association between mood disorders and COPD appears to be largely explained by confounding by lifetime nicotine dependence. Conclusions: These findings provide initial evidence suggesting that the association between anxiety, depression, and COPD may be at least partly attributable to confounding by cigarette smoking and nicotine dependence. Efforts toward prevention of chronic lung disease may be more effective if treatment and prevention efforts aimed at smoking cessation address mental health problems. © The Author 2011. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. Source

Bourbeau J.,McGill University | Bourbeau J.,Montreal Chest Institute | Lavoie K.L.,University of Quebec at Montreal | Lavoie K.L.,Montreal Behavioural Medicine Center | Sedeno M.,McGill University
Seminars in Respiratory and Critical Care Medicine | Year: 2015

In this article, we provide a review of the literature on self-management interventions and we are giving some thought to how, when, and by whom they should be offered to patients. The present literature based on randomized clinical trials has demonstrated benefits (reduced hospital admissions and improved health status) for chronic obstructive pulmonary disease (COPD) patients undergoing self-management interventions, although there are still problems with the heterogeneity among interventions, study populations, follow-up time, and outcome measures that make generalization difficult in real life. Key to the success, self-management intervention has to target behavior change. Proper self-management support is a basic prerequisite, for example, techniques and skills used by health care providers case manager to instrument patients with the knowledge, confidence, and skills required to effectively self-manage their disease. To improve health behaviors and engagement in self-management, self-management interventions need to target enhancing intrinsic motivation to change. This will best be done using client-centered communication (motivational communication) that encourages patients to express what intrinsically motivates them (e.g., consistent with their values or life goals) to adopt certain health behavior, with the goal of helping them overcome their ambivalence about change. Finally, if we want to be able to design and implement self-management interventions that are integrated, coherent, and have a strong likelihood of success, we need to take a more careful look and give more attention at the case manager, the patient (patient evaluation), and the quality assurance. © 2015 by Thieme Medical Publishers, Inc. Source

Doonan R.J.,McGill University | Scheffler P.,McGill University | Yu A.,McGill University | Egiziano G.,McGill University | And 7 more authors.
PLoS ONE | Year: 2011

Background: Studies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals. Methods/Results: Healthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions. Conclusion: Chronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired 'vascular reserve' or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands. © 2011 Doonan et al. Source

Johnson C.,University of Sydney | Raj T.S.,The George Institute for Global Health | Trudeau L.,Jewish General Hospital | Bacon S.L.,Concordia University at Montreal | And 4 more authors.
Journal of Clinical Hypertension | Year: 2015

The authors provided a systematic review of the clinical and population health impact of increased dietary salt intake during 1 year. Randomized controlled trials or cohort studies or meta-analyses on the effect of sodium intake were examined from Medline searches between June 2013 to May 2014. Quality indicators were used to select studies that were relevant to clinical and public health. A total of 213 studies were reviewed, of which 11 (n=186,357) were eligible. These studies confirmed a causal relationship between increasing dietary salt and increased blood pressure and an association between several adverse health outcomes and increased dietary salt. A new association between salt intake and renal cell cancer was published. No study that met inclusion criteria found harm from lowering dietary salt. The findings of this systematic review are consistent with previous data relating increased dietary salt to increased blood pressure and adverse health outcomes. © 2015 Wiley Periodicals, Inc. Source

Austin A.W.,Montreal Behavioural Medicine Center | Austin A.W.,Concordia University at Montreal | Wissmann T.,University of Bern | Von Kanel R.,University of Bern
Seminars in Thrombosis and Hemostasis | Year: 2013

Numerous naturalistic, experimental, and mechanistic studies strongly support the notion that-as part of fight-or-flight response-hemostatic responses to acute psychosocial stress result in net hypercoagulability, which would protect a healthy organism from bleeding in case of injury. Sociodemographic factors, mental states, and comorbidities are important modulators of the acute prothrombotic stress response. In patients with atherosclerosis, exaggerated and prolonged stress-hypercoagulability might accelerate coronary thrombus growth following plaque rupture. Against a background risk from acquired prothrombotic conditions and inherited thrombophilia, acute stress also might trigger venous thromboembolic events. Chronic stressors such as job strain, dementia caregiving, and posttraumatic stress disorder as well as psychological distress from depressive and anxiety symptoms elicit a chronic low-grade hypercoagulable state that is no longer viewed as physiological but might impair vascular health. Through activation of the sympathetic nervous system, higher order cognitive processes and corticolimbic brain areas shape the acute prothrombotic stress response. Hypothalamic-pituitary-adrenal axis and autonomic dysfunction, including vagal withdrawal, are important regulators of hemostatic activity with longer lasting stress. Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response. Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed. Restoring normal hemostatic function with biobehavioral interventions bears the potential to ultimately decrease the risk of thrombotic diseases. © 2013 by Thieme Medical Publishers, Inc. Source

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