This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Freedland, K. E. Articles by Skala, J. A. Search for Related Content PubMed PubMed Citation Articles by Freedland, K. E. Articles by Skala, J. A. Related Collections Depression

Depression and Smoking in Coronary Heart Disease

From the Department of Psychiatry, Washington University School of Medicine, St. Louis, MO.

Address correspondence and reprint requests to Kenneth E. Freedland, PhD, Department of Psychiatry, Washington University School of Medicine, 4625 Lindell Blvd., Suite 420, St. Louis, MO 63108. E-mail: freedlak{at}wustl.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
Objective: This review examines the relationship between depression and smoking in coronary heart disease (CHD). It summarizes relevant findings from general population and smoking cessation studies and discusses the few studies that have investigated whether smoking confounds, mediates, or moderates the effect of depression on cardiac morbidity and mortality.

Methods: Qualitative review of research literature.

Results: Although many studies of the prognostic importance of depression in CHD have adjusted for smoking, there is no convincing evidence that smoking actually confounds the relationship between depression and CHD. There is also no evidence that smoking moderates this relationship. There is, however, limited evidence that smoking may partially mediate the effect of depression on morbidity and mortality in CHD.

Conclusion: We need more research on the relationship between depression and smoking in CHD to develop a more complete model of the mechanisms linking depression to cardiac morbidity and mortality.

Key Words: coronary disease • depression • depressive disorder • myocardial infarction • smoking • smoking cessation • tobacco use disorder

Abbreviations: CHD = coronary heart disease; MI = myocardial infarction.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
Depression is associated with several behavioral risk factors for the secondary progression of coronary heart disease (CHD), including smoking, unfavorable dietary patterns, physical inactivity, and nonadherence to cardiovascular medication regimens (1). Of these, smoking has received the most attention in research on the relationship between depression and heart disease, and there is extensive literature on the associations of smoking with CHD and with depression.

The purpose of this article is to consider whether smoking confounds, mediates, or moderates the relationship between depression and cardiovascular morbidity and mortality in patients with established CHD. It summarizes the cardiovascular consequences of smoking and the complex interrelationships between depression, smoking, and smoking cessation in the general population. It then reviews studies of the prognostic importance of depression in CHD that have controlled for smoking as a potential confounder, and the few studies that have specifically examined the relationship between depression and smoking in patients with CHD. The nature of this relationship has important implications for future research on the role of depression as a risk factor for morbidity and mortality in CHD.

	SMOKING AND CORONARY HEART DISEASE

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
Cigarette smoking acutely increases the rate-pressure product and myocardial blood flow at rest, decreases myocardial flow reserve, impairs endothelium-dependent vasodilation, and impedes endogenous fibrinolysis (2–4). It is associated with endothelial dysfunction in healthy young adults, suggesting that it contributes to the early development of coronary atherosclerosis (5). It is conceivable that this association might not be a result of the effects of smoking per se, but instead of behaviors that are prevalent among smokers, such as other forms of substance abuse. However, passive exposure to environmental tobacco smoke causes endothelial dysfunction in healthy young adults with no history of active smoking (6), and it increases coronary atherosclerosis in animal models (7). Thus, there is little doubt that exposure to cigarette smoke promotes the development of coronary disease.

The role of smoking in coronary atherosclerosis extends far beyond the early onset of endothelial dysfunction. Smoking increases the risk of incident CHD, especially in the context of other major risk factors such as diabetes (8). It accelerates the angiographic progression of existing coronary atherosclerosis and promotes the formation of new atherosclerotic lesions (9). It can trigger transient myocardial ischemia in patients with established coronary disease (10), and it is a potent risk factor for acute myocardial infarction (MI) and for sudden cardiac death (11–16). The risks are higher in women than men, especially in younger cohorts (14, 16).

There is some evidence that smoking may have paradoxical effects on the outcomes of acute myocardial infarction. In one study, for example, smokers had a lower case fatality rate than nonsmokers during the month following hospitalization for an acute MI. However, this appeared to be a result of a high case fatality rate among smokers who never made it to the hospital (17). Differences in background factors between smokers and nonsmokers might also help to account for some of the paradoxical findings. For example, the age at first onset of acute MI tends to occur approximately 10 years earlier in smokers than nonsmokers (18–22). Most studies have found harmful rather than beneficial effects of smoking after acute MI, including increased risks of recurrent MI and mortality (23, 24). Furthermore, smoking cessation substantially reduces these risks (24–26).

	DEPRESSION AND SMOKING

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
There is a reciprocal relationship between depression and smoking: depression is more common in smokers than nonsmokers, and smoking is more common in depressed than nondepressed individuals. A recent analysis of data from the Stirling County Study suggests that the association between smoking and depression has strengthened in recent decades. This historical trend may be a result of declining rates of smoking among psychiatrically well individuals.

Numerous epidemiological studies have found strong associations between depression and smoking (29, 31–37). One showed that the high comorbidity of smoking and depression is apparent as early as adolescence (27). Among 3213 St. Louis area adult participants in the National Institute of Mental Health Epidemiologic Catchment Area study, current smokers were significantly more likely than nonsmokers to have had an episode of major depression at some point in their lifetime (28). A history of major depression was a significant risk factor for the onset of daily smoking in a longitudinal study of more than 1000 young adults (29). A 21-year longitudinal study of a birth cohort of 1265 children in New Zealand found that major depression was a significant risk factor for daily smoking and for nicotine dependence even after controlling for confounding child and adolescent factors (30).

The Children in the Community Study is an exception. It found that juvenile smokers were more likely than nonsmokers to have developed alcohol or other substance abuse disorders by their late 20s, but they were no more likely to have new episodes of major depression (38). However, the participants were younger at enrollment and at follow-up than were most of the subjects in the other studies. It may be necessary to follow juvenile cohorts into their 30s or beyond to observe an increased incidence of major depressive disorder.

Whether there is a causal relationship between depression and smoking is unknown. However, findings from two studies suggest that the relationship may not be causal, either with respect to smoking as a cause of depression or to depression as a cause of smoking. Kendler et al. (39) found a strong association between depression and smoking in 1566 female twin pairs and used a co-twin control design to determine whether the association was causal or noncausal. The best-fitting model suggested that the association is entirely a result of genetic factors that predispose to both problems. More recently, Dierker et al. (40) conducted a case-control family study of 133 probands and 273 of their first-degree relatives. Their findings were consistent with a shared etiology between heavy smoking and dysthymia, a chronic but relatively mild form of depression. However, their results did not provide evidence of a shared etiology between heavy smoking and major depression. Further research is needed to determine whether specific genes predispose both to smoking and to depression.

It is important to recognize that these were studies of the heritability of liability to smoking and depression over the lifetime of the subjects. Even if there are genetic factors that predispose both to nicotine dependence and to depressive disorders, other kinds of relationships between smoking and depression are also possible. Mood state might affect concurrent smoking behavior and vice versa, and there may be individual differences in the strength of these effects. For example, smoking has long been thought to be a form of self-medication for depressed patients who use it to treat their dysphoric mood. In some cases, however, smoking appears to worsen rather than relieve dysphoria. Two recent studies provide some insight into these individual differences. One found that the use of smoking for self-medication is common among depressed smokers who are homozygous for the short alleles of the dopamine D4 receptor gene, but not among those who are either heterozygous or homozygous for the long alleles (41). The other found that smoking worsens rather than improves depressed mood among individuals who tend to ruminate when depressed, perhaps because smoking increases the individual’s attention to negative cognitions (42). In short, mood states can affect smoking behavior, smoking can alter mood, and genetic factors such as the dopamine D4 receptor gene polymorphism can create individual differences in whether and how these effects operate (43).

	SMOKING CESSATION

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
The adverse cardiovascular effects of smoking are reversible, at least to some extent. A recent meta-analysis (25) of 20 studies reported that among patients with CHD, those who quit smoking have a 36% reduction in the relative risk of mortality compared with patients who continue smoking. The size of this beneficial effect is similar across subgroups defined by sex, age, type of cardiac event at index, and other factors.

Unfortunately, depression may interfere with smoking cessation. Depressive symptoms at the initiation of smoking cessation predict lower success rates and higher relapse rates (44, 45). An increase in depressive symptoms after smoking cessation also raises the risk of relapse (46). There is less consistent evidence that a past history of major depression predicts poor smoking cessation outcomes. Data from the Epidemiologic Catchment Area study showed that individuals who had ever had an episode of major depression were less successful in their attempts to quit smoking than were respondents with no history of depression (47), but other studies have not replicated this finding (29, 48). In combination, these findings suggest that having a past history of major depression does not reduce the prospects for successful smoking cessation as long as depressive symptoms are absent while one is attempting to quit.

In some cases, mood improves after smoking cessation; in others, it worsens or remains unchanged (46). Depression is a common sequela of smoking cessation, primarily among individuals with a past history of major depression (28, 49, 50). The 12-month incidence of new major depressive episodes after smoking cessation is approximately 14%. Although past history of major depression is a strong predictor of incident depressive episodes during this period, smoking abstinence status is not (51). Thus, depression is probably not a consequence of nicotine withdrawal. Individuals with a past history of major depression, especially those with a history of recurrent episodes, are at risk for having additional depressive episodes regardless of their smoking status.

	DEPRESSION AND SMOKING IN CHD

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
Most studies of the prognostic importance of depression in CHD have treated smoking as a potential confounder. The earliest example was a small study of major depression in patients who had just undergone coronary angiography and who been diagnosed with coronary disease. Although smoking was more common among the depressed than the nondepressed patients, depression was retained as an independent predictor of cardiac events over the following 12 months after adjustment for smoking (52). Similar findings were subsequently reported in much larger cohorts, including studies of patients with a recent history of acute MI (e.g., 53, 54)

These studies confirm that the effect of depression on post-MI mortality and other cardiac events is not a result of the confounding effects of smoking, at least not entirely. However, they do not prove that smoking is actually a confounder. For smoking to be a true confounder, it would have to be both a cause of depression and a cause of cardiac events or mortality. However, the genetic studies discussed suggest that the association between the lifetime risks of smoking and depression is noncausal. That is, the association is a result of genetic factors that predispose to both problems. Furthermore, the studies of active smokers and of smoking cessation show that the phenotypic relationship between smoking and depression is quite complex. Smoking improves mood in some cases and worsens it in others. Smoking cessation increases depressive symptoms and raises the risk of developing a major depressive episode in some cases but not in others. Nicotine abstinence per se does not predict new depressive symptoms or episodes during attempts to quit smoking, but a past history of major depression does. In short, adjustment for smoking may be necessary to establish that depression is an independent risk factor for cardiac morbidity and mortality, just as it is necessary to adjust for indicators of disease severity and other well established predictors. However, the assumption that smoking is a true confounder is not necessarily justified.

Two recent studies have moved beyond this questionable assumption and have instead examined whether smoking mediates or moderates the effects of depression in CHD. Brummett et al. (55) studied patients with newly diagnosed coronary disease and found that depression, smoking, and sedentary behaviors were independent predictors of mortality, but they also found that smoking and sedentary behavior partially mediate the effect of depression on mortality. Smoking was modeled as a time-dependent covariate to differentiate between patients who stopped smoking after being diagnosed with coronary disease and those who continued smoking during the follow-up period. The hazard ratio for a change of 2 standard deviations on the Zung Self-Rating Depression Scale was 1.39 after adjustment for age, sex, a disease severity index, and surgical status. It dropped to 1.32 after further adjustment for current smoking. When smoking was removed from the model and replaced by sedentary behavior, the hazard ratio for depression dropped to 1.26. This suggests that current smoking may be one of the pathways linking depression to adverse cardiac outcomes, but that it is clearly not the only one. In addition to sedentary behavior, a number a physiological mechanisms that were not measured in this study (but that are reviewed elsewhere in this issue of the journal) could also partially mediate the relationship between depression and mortality in CHD.

In the same study, Brummett et al. (55) found no evidence that smoking or sedentary behavior moderates the effect of depression. In other words, the effect of depression on mortality is no better or worse in smokers than nonsmokers, or in sedentary than in physically active patients. Overall, these findings support the conclusion that one of the ways that depression increases the mortality risk in CHD is by interfering with smoking cessation.

Miller et al. (56) studied the effect of depression on the expression of inflammatory markers (C-reactive protein and interleukin-6) that have been implicated in the pathogenesis of CHD. The sample included 50 individuals with current major depression and 50 with no history of any psychiatric disorders, all of whom were in excellent health. Both inflammatory markers were significantly higher in the depressed than in the nondepressed group. Adiposity partially mediated this relationship, but neither subclinical infections with cytomegalovirus or Chlamydia pneumoniae nor smoking were mediators.

The studies by Brummett et al. (55) and Miller et al. (56) are difficult to compare because the first study was of patients with coronary disease and the other was of healthy subjects. Nevertheless, the findings from these studies suggest that if smoking partially mediates the effect of depression on mortality in CHD, it does not necessarily do so via a proinflammatory mechanism. Other cardiovascular consequences of smoking, such as its ability to trigger episodes of myocardial ischemia, are probably involved.

	CONCLUSIONS

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 
Both smoking and depression are risk factors for cardiac morbidity and mortality. There is a complex relationship between smoking and depression in the general population, one that does not necessarily support the assumption that smoking confounds the association between depression and CHD. Although adjustment for smoking as if it were a true confounder has helped to establish depression as an independent risk factor for morbidity and mortality in CHD, this practice oversimplifies the relationship between smoking and depression in CHD. Recent studies have moved beyond this approach to investigate whether smoking either mediates or moderates the relationship between depression and CHD. They have also shown that it is important to pay careful attention to how smoking is assessed and modeled in this line of research. However, this is just a beginning. We need more data on the effects of smoking, smoking cessation, depression, and depression treatment on one another in CHD patient populations. We also need to evaluate the relationships of smoking to other potential mechanisms such as cardiovascular autonomic dysregulation and procoagulant processes that might mediate the effects of depression on cardiac morbidity and mortality.

	NOTES

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 

In accordance with CME accreditation guidelines, the authors of this article disclosed no real or potential conflicts of interest.

DOI:10.1097/01.psy.0000162255.55629.9c

	REFERENCES

TOP ABSTRACT INTRODUCTION SMOKING AND CORONARY HEART... DEPRESSION AND SMOKING SMOKING CESSATION DEPRESSION AND SMOKING IN... CONCLUSIONS NOTES REFERENCES

 

1. Carney RM, Freedland KE, Miller GE, Jaffe AS. Depression as a risk factor for cardiac mortality and morbidity: a review of potential mechanisms. J Psychosom Res 2002;53:897–902.[CrossRef][Medline]
2. Czernin J, Sun K, Brunken R, Bottcher M, Phelps M, Schelbert H. Effect of acute and long-term smoking on myocardial blood flow and flow reserve. Circulation 1995;91:2891–7.[Abstract/Free Full Text]
3. Newby DE, Wright RA, Labinjoh C, Ludlam CA, Fox KA, Boon NA, Webb DJ. Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking: a mechanism for arterial thrombosis and myocardial infarction. Circulation 1999;99:1411–5.[Abstract/Free Full Text]
4. Zeiher AM, Schachinger V, Minners J. Long-term cigarette smoking impairs endothelium-dependent coronary arterial vasodilator function. Circulation 1995;92:1094–100.[Abstract/Free Full Text]
5. Celermajer DS, Sorensen KE, Georgakopoulos D, Bull C, Thomas O, Robinson J, Deanfield JE. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation 1993;88:2149–55.[Abstract/Free Full Text]
6. Celermajer DS, Adams MR, Clarkson P, Robinson J, McCredie R, Donald A, Deanfield JE. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. N Engl J Med 1996;334:150–4.[Abstract/Free Full Text]
7. Zhu BQ, Sun YP, Sievers RE, Isenberg WM, Glantz SA, Parmley WW. Passive smoking increases experimental atherosclerosis in cholesterol-fed rabbits. J Am Coll Cardiol 1993;21:225–32.[Abstract]
8. Al-Delaimy WK, Manson JE, Solomon CG, Kawachi I, Stampfer MJ, Willett WC, Hu FB. Smoking and risk of coronary heart disease among women with type 2 diabetes mellitus. Arch Intern Med 2002;162:273–9.[Abstract/Free Full Text]
9. Waters D, Lesperance J, Gladstone P, Boccuzzi SJ, Cook T, Hudgin R, Krip G, Higginson L. Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. CCAIT Study Group. Circulation 1996;94:614–21.[Abstract/Free Full Text]
10. Gabbay FH, Krantz DS, Kop WJ, Hedges SM, Klein J, Gottdiener JS, Rozanski A. Triggers of myocardial ischemia during daily life in patients with coronary artery disease: physical and mental activities, anger and smoking. J Am Coll Cardiol 1996;27:585–92.[Abstract]
11. Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997;336:1276–82.[Abstract/Free Full Text]
12. Dunn NR, Faragher B, Thorogood M, de CL, MacDonald TM, McCollum C, Thomas S, Mann R. Risk of myocardial infarction in young female smokers. Heart 1999;82:581–3.[Abstract/Free Full Text]
13. Goldenberg I, Jonas M, Tenenbaum A, Boyko V, Matetzky S, Shotan A, Behar S, Reicher-Reiss H, Bezafibrate Infarction Prevention Study Group. Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease. Arch Intern Med 2003;163:2301–5.[Abstract/Free Full Text]
14. Njolstad I, Arnesen E, Lund-Larsen PG. Smoking, serum lipids, blood pressure, and sex differences in myocardial infarction: a 12-year follow-up of the Finnmark Study. Circulation 1996;93:450–6.[Abstract/Free Full Text]
15. Parish S, Collins R, Peto R, Youngman L, Barton J, Jayne K, Clarke R, Appleby P, Lyon V, Cederholm-Williams S. Cigarette smoking, tar yields, and non-fatal myocardial infarction: 14,000 cases and 32,000 controls in the United Kingdom. The International Studies of Infarct Survival (ISIS) Collaborators. BMJ 1995;311:471–7.[Abstract/Free Full Text]
16. Prescott E, Hippe M, Schnohr P, Hein HO, Vestbo J. Smoking and risk of myocardial infarction in women and men: longitudinal population study. BMJ 1998;316:1043–7.[Abstract/Free Full Text]
17. Sonke GS, Stewart AW, Beaglehole R, Jackson R, White HD. Comparison of case fatality in smokers and non-smokers after acute cardiac event. BMJ 1997;315:992–3.[Free Full Text]
18. Ruiz-Bailen M, de Hoyos EA, Reina-Toral A, Torres-Ruiz JM, varez-Bueno M, Gomez Jimenez FJ, ARIAM Group. Paradoxical effect of smoking in the Spanish population with acute myocardial infarction or unstable angina: results of the ARIAM Register. Chest 2004;125:831–40.[Abstract/Free Full Text]
19. White HD. Lifting the smoke-screen: the enigma of better outcome in smokers after myocardial infarction. Am J Cardiol 1995;75:278–9.[CrossRef][Medline]
20. Hasdai D, Holmes DR Jr, Criger DA, Topol EJ, Califf RM, Wilcox RG, Paolasso E, Simoons M, Deckers J, Harrington RA. Cigarette smoking status and outcome among patients with acute coronary syndromes without persistent ST-segment elevation: effect of inhibition of platelet glycoprotein IIb/IIIa with eptifibatide. The PURSUIT Trial Investigators. Am Heart J 2000;139:454–60.[CrossRef][Medline]
21. Gottlieb S, Boyko V, Zahger D, Balkin J, Hod H, Pelled B, Stern S, Behar S. Smoking and prognosis after acute myocardial infarction in the thrombolytic era (Israeli Thrombolytic National Survey). J Am Coll Cardiol 1996;28:1506–13.[Abstract]
22. Grines CL, Topol EJ, O'Neill WW, George BS, Kereiakes D, Phillips HR, Leimberger JD, Woodlief LH, Califf RM. Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction. Circulation 1995;91:298–303.[Abstract/Free Full Text]
23. Njolstad I, Arnesen E. Preinfarction blood pressure and smoking are determinants for a fatal outcome of myocardial infarction: a prospective analysis from the Finnmark Study. Arch Intern Med 1998;158:1326–32.[Abstract/Free Full Text]
24. Rea TD, Heckbert SR, Kaplan RC, Smith NL, Lemaitre RN, Psaty BM. Smoking status and risk for recurrent coronary events after myocardial infarction. Ann Intern Med 2002;137:494–500.[Abstract/Free Full Text]
25. Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA 2003;290:86–97.[Abstract/Free Full Text]
26. Kawachi I, Colditz GA, Stampfer MJ, Willett WC, Manson JE, Rosner B, Speizer FE, Hennekens CH. Smoking cessation and time course of decreased risks of coronary heart disease in middle-aged women. Arch Intern Med 1994;154:169–75.[Abstract/Free Full Text]
27. Fergusson DM, Lynskey MT, Horwood LJ. Comorbidity between depressive disorders and nicotine dependence in a cohort of 16-year-olds. Arch Gen Psychiatry 1996;53:1043–7.[Abstract/Free Full Text]
28. Glassman AH, Helzer JE, Covey LS, Cottler LB, Stetner F, Tipp JE, Johnson J. Smoking, smoking cessation, and major depression. JAMA 1990;264:1546–9.[Abstract/Free Full Text]
29. Breslau N, Peterson EL, Schultz LR, Chilcoat HD, Andreski P. Major depression and stages of smoking: a longitudinal investigation. Arch Gen Psychiatry 1998;55:161–6.[Abstract/Free Full Text]
30. Fergusson DM, Goodwin RD, Horwood LJ. Major depression and cigarette smoking: results of a 21-year longitudinal study. Psychol Med 2003;33:1357–67.[CrossRef][Medline]
31. Egede LE, Zheng D. Independent factors associated with major depressive disorder in a national sample of individuals with diabetes. Diabetes Care 2003;26:104–11.[Abstract/Free Full Text]
32. Hamalainen J, Kaprio J, Isometsa E, Heikkinen M, Poikolainen K, Lindeman S, Aro H. Cigarette smoking, alcohol intoxication and major depressive episode in a representative population sample. J Epidemiol Community Health 2001;55:573–6.[Abstract/Free Full Text]
33. Hanna EZ, Grant BF. Parallels to early onset alcohol use in the relationship of early onset smoking with drug use and DSM-IV drug and depressive disorders: findings from the National Longitudinal Epidemiologic Survey. Alcohol Clin Exp Res 1999;23:513–22.[CrossRef][Medline]
34. Harlow BL, Cohen LS, Otto MW, Spiegelman D, Cramer DW. Prevalence and predictors of depressive symptoms in older premenopausal women: the Harvard Study of Moods and Cycles. Arch Gen Psychiatry 1999;56:418–24.[Abstract/Free Full Text]
35. John U, Meyer C, Rumpf HJ, Hapke U. Depressive disorders are related to nicotine dependence in the population but do not necessarily hamper smoking cessation. J Clin Psychiatry 2004;65:169–76.[Medline]
36. Murphy JM, Horton NJ, Monson RR, Laird NM, Sobol AM, Leighton AH. Cigarette smoking in relation to depression: historical trends from the Stirling County Study. Am J Psychiatry 2003;160:1663–9.[Abstract/Free Full Text]
37. Wilhelm K, Mitchell P, Slade T, Brownhill S, Andrews G. Prevalence and correlates of DSM-IV major depression in an Australian national survey. J Affect Disord 2003;75:155–62.[CrossRef][Medline]
38. Brook DW, Brook JS, Zhang C, Cohen P, Whiteman M. Drug use and the risk of major depressive disorder, alcohol dependence, and substance use disorders. Arch Gen Psychiatry 2002;59:1039–44.[Abstract/Free Full Text]
39. Kendler KS, Neale MC, MacLean CJ, Heath AC, Eaves LJ, Kessler RC. Smoking and major depression: a causal analysis. Arch Gen Psychiatry 1993;50:36–43.[Abstract/Free Full Text]
40. Dierker LC, Avenevoli S, Stolar M, Merikangas KR. Smoking and depression: an examination of mechanisms of comorbidity. Am J Psychiatry 2002;159:947–53.[Abstract/Free Full Text]
41. Lerman C, Caporaso N, Main D, Audrain J, Boyd NR, Bowman ED, Shields PG. Depression and self-medication with nicotine: the modifying influence of the dopamine D4 receptor gene. Health Psychol 1998;17:56–62.[CrossRef][Medline]
42. Richmond M, Spring B, Sommerfeld BK, MeChargue D. Rumination and cigarette smoking: a bad combination for depressive outcomes? J Consult Clin Psychol 2001;69:836–40.[CrossRef][Medline]
43. Gilbert DG, Gilbert BO. Personality, psychopathology, and nicotine response as mediators of the genetics of smoking. Behav Genet 1995;25:133–47.[CrossRef][Medline]
44. Cinciripini PM, Wetter DW, Fouladi RT, Blalock JA, Carter BL, Cinciripini LG, Baile WF. The effects of depressed mood on smoking cessation: mediation by postcessation self-efficacy. J Consult Clin Psychol 2003;71:292–301.[CrossRef][Medline]
45. Kinnunen T, Doherty K, Militello FS, Garvey AJ. Depression and smoking cessation: characteristics of depressed smokers and effects of nicotine replacement. J Consult Clin Psychol 1996;64:791–8.[CrossRef][Medline]
46. Burgess ES, Brown RA, Kahler CW, Niaura R, Abrams DB, Goldstein MG, Miller IW. Patterns of change in depressive symptoms during smoking cessation: who's at risk for relapse? J Consult Clin Psychol 2002;70:356–61.[CrossRef][Medline]
47. Glassman AH, Covey LS, Stetner F, Rivelli S. Smoking cessation and the course of major depression: a follow-up study. Lancet 2001;357:1929–32.[CrossRef][Medline]
48. Hitsman B, Borrelli B, McChargue DE, Spring B, Niaura R. History of depression and smoking cessation outcome: a meta-analysis. J Consult Clin Psychol 2003;71:657–63.[CrossRef][Medline]
49. Borrelli B, Niaura R, Keuthen NJ, Goldstein MG, DePue JD, Murphy C, Abrams DB. Development of major depressive disorder during smoking-cessation treatment. J Clin Psychiatry 1996;57:534–8.[Medline]
50. Covey LS, Glassman AH, Stetner F. Major depression following smoking cessation. Am J Psychiatry 1997;154:263–5.[Abstract]
51. Tsoh JY, Humfleet GL, Munoz RF, Reus VI, Hartz DT, Hall SM. Development of major depression after treatment for smoking cessation. Am J Psychiatry 2000;157:368–74.[Abstract/Free Full Text]
52. Carney RM, Rich MW, Freedland KE, Saini J, teVelde A, Simeone C, Clark K. Major depressive disorder predicts cardiac events in patients with coronary artery disease. Psychosom Med 1988;50:627–33.[Abstract/Free Full Text]
53. Carney RM, Blumenthal JA, Catellier D, Freedland KE, Berkman LF, Watkins LL, Czajkowski SM, Hayano J, Jaffe AS. Depression as a risk factor for mortality after acute myocardial infarction. Am J Cardiol 2003;92:1277–81.[CrossRef][Medline]
54. Frasure-Smith N, Lesperance F, Talajic M. Depression following myocardial infarction: impact on 6-month survival. JAMA 1993;270:1819–25.[Abstract/Free Full Text]
55. Brummett BH, Babyak MA, Siegler IC, Mark DB, Williams RB, Barefoot JC. Effect of smoking and sedentary behavior on the association between depressive symptoms and mortality from coronary heart disease. Am J Cardiol 2003;92:529–32.[CrossRef][Medline]
56. Miller GE, Stetler CA, Carney RM, Freedland KE, Banks WA. Clinical depression and inflammatory risk markers for coronary heart disease. Am J Cardiol 2002;90:1279–83.[CrossRef][Medline]

This article has been cited by other articles:

				M Kivimaki, J Head, J E Ferrie, A Singh-Manoux, H Westerlund, J Vahtera, A Leclerc, M Melchior, A Chevalier, K Alexanderson, et al. Sickness absence as a prognostic marker for common chronic conditions: analysis of mortality in the GAZEL study Occup. Environ. Med., December 1, 2008; 65(12): 820 - 826. [Abstract] [Full Text] [PDF]

				J. Bunde and R. Martin Depression and Prehospital Delay in the Context of Myocardial Infarction Psychosom Med, January 1, 2006; 68(1): 51 - 57. [Abstract] [Full Text] [PDF]

				D. S. Sheps and A. Rozanski From Feeling Blue to Clinical Depression: Exploring the Pathogenicity of Depressive Symptoms and Their Management in Cardiac Practice Psychosom Med, May 1, 2005; 67(Supplement_1): S2 - S5. [Full Text] [PDF]

				A. Rozanski Integrating Psychologic Approaches Into the Behavioral Management of Cardiac Patients Psychosom Med, May 1, 2005; 67(Supplement_1): S67 - S73. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Freedland, K. E. Articles by Skala, J. A. Search for Related Content PubMed PubMed Citation Articles by Freedland, K. E. Articles by Skala, J. A. Related Collections Depression