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Psychosomatics 48:54-59, February 2007
doi: 10.1176/appi.psy.48.1.54
© 2007 Academy of Psychosomatic Medicine
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Self-Reported Depression and Cardiovascular Risk Factors in a Community Sample of Women

Felice N. Jacka, B.A., Pg.Dip.Sc., Julie A. Pasco, Ph.D., Stephen McConnell, M.B.B.S., M.Psych., FRANCP, Lana J. Williams, Grad. Dip. App. Psych., B.Psych., Mark A. Kotowicz, M.B.B.S., FRACP, Geoff C. Nicholson, M.B.B.S., Ph.D., FRACP, FRCP, and Michael Berk, M.B.B.Ch., M.Med., FRANZCP, Ph.D.

Received December 5, 2005; revised January 31, 2006; accepted March 3, 2006. From The University of Melbourne, Department of Clinical and Biomedical Sciences, Barwon Health, Victoria, Australia. Send correspondence and reprint requests to Felice Jacka, The Univ. of Melbourne, Dept. of Clinical and Biomedical Sciences, Barwon Health, P.O. Box 281, Geelong 3220, Australia. e-mail: felice{at}barwonhealth.org.au


  ABSTRACT

 
TOP
 ABSTRACT
INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
The authors examined data collected from a randomly selected, representative sample of 755 women (ages 23–97 years) from southeastern Australia. Self-report questionnaires were utilized to determine lifetime rates of depression and cardiovascular risk factors within the study sample. A lifetime history of depression (LHx) was reported by 145 women (19.20%). There were no associations between indices of weight, cholesterol levels, hypertension, inactivity, diabetes, and LHx. However, a history of smoking increased the odds of reporting an LHx, whereas women with self-reported angina were more than four times more likely to report an age-adjusted LHx.


  INTRODUCTION

 
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 ABSTRACT
 INTRODUCTION
METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 
Depression and cardiovascular disease are two of the most prevalent and serious health problems in Australia. The Australian Burden of Disease (ABD) study in 1996 identified ischemic heart disease as the leading cause of both premature mortality and overall disease burden for men and women, whereas depression was the leading cause of disability in both genders, accounting for approximately 4% of total disease burden.1

There is substantial epidemiological evidence to suggest that both major depression and depressive symptoms independently increase the risk of an individual developing cardiovascular disease (CVD),2–7 and it is also the case that the presence of both depressive symptoms and major depression may predict an increased likelihood of cardiac mortality for those who have experienced myocardial infarction (MI).8–12 The association between depression and CVD is likely to be mediated by a number of behavioral and pathophysiological risk factors for CVD, including obesity and body fat distribution, physical activity levels, hypercholesterolemia, smoking, hypertension, and diabetes. In light of the evidence linking depression and heart disease, we report here on the association between self-reported depression and such CVD risk factors in a community study of women from the southeastern region of Australia.


  METHOD

 
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 ABSTRACT
 INTRODUCTION
 METHOD
RESULTS
 DISCUSSION
 REFERENCES
 
Participants
This study examined data collected from women participating in the Geelong Osteoporosis Study (GOS), which comprises an age-stratified, sample of women drawn at random from the community. Electoral enrollment in Australia is compulsory for all individuals age 18 years or older, and the participants were randomly selected from Commonwealth electoral rolls for the Barwon Statistical Division (southeastern Australia) between 1994 and 1997; there was an overall acceptance rate of 77.1%.13 The initial study group totaled 1,494 women (ages 20–94 years) who underwent a comprehensive range of medical and lifestyle assessments at baseline and have continued to return to the study center for biennial assessment. The Barwon Health Research and Ethics Advisory Committee approved the study, and written, informed consent was obtained from all participants.

Depression Assessment
Symptoms of past and present depression were ascertained by a self-report questionnaire and measured symptoms from the year between July 2000 and July 2001 (current depression), as well as a past history of depressive symptoms (lifetime). A categorical diagnosis of clinically significant self-reported depression was made on the basis of DSM-IV criteria for major depressive disorder.14 These include the presence of either dysphoria (depressed mood) or anhedonia (inability to take pleasure in daily activities) consistently over a 2-week period, with at least four accompanying symptoms, including changes in appetite, insomnia or hypersomnia, restlessness, fatigue, inappropriate feelings of guilt, loss of concentration, and suicidal ideation. Participants identified with clinically significant self-reported depression at any stage (current or lifetime) were classified as having a "lifetime history of depression" (LHx), whereas those with no clinically significant depression were classified as Nondepressed. All those participants enrolled in the GOS in 2001 (N=1,275) were sent the depression questionnaire, with a total of 758 women responding (60%). Three responses were incomplete and therefore excluded, resulting in 755 women participating in this aspect of the study.

Cardiovascular Risk Factor Assessments
All CVD and risk variables were assessed at the baseline GOS assessment, between 1994 and 1997. Height was measured in centimeters to the nearest 0.1 cm, and weight was measured to the nearest 0.1 kg while participants were barefoot and in a hospital gown. Obesity was defined as body mass index (BMI) ≥30. The presence of central body fat was calculated as waist/hip ratio (WHR). Central body fat accumulation was classified as WHR ≥0.8.

Blood pressure (mmHg) was measured (seated) with a digital meter (A&D Company, Model UA-751). Hypertension was classified as systolic blood pressure >140 mmHg and/or diastolic blood pressure >90 mmHg and/or self-reported hypertension. Smoking status was determined from the baseline questionnaire ("Have you ever smoked regularly?"). Activity levels were assessed, and participants classified as active if they undertook any regular physical exercise. Inactivity was defined by grouping together a number of items describing varying degrees of inactivity, including "no appreciable exercise, but walks reasonable distances and does normal activities of daily living," "little walking outside the home," or "sits in chair or lies in bed most of the time." Diabetes was determined if subjects had morning, fasting blood glucose levels ≥7.0 mmol/liter (as defined by WHO15) and/or self-report of having diabetes ("Have you ever had diabetes?"). Medical history of "heart attack" (MI) or anginal chest pain was determined by self-report ("Have you ever had a heart attack [myocardial infarction]?" "Have you ever had angina?"), and serum cholesterol levels (mmol/liter) were ascertained from fasting, morning blood samples. Baseline data for MI, angina, and serum cholesterol were available on only 472 women, because of the delayed inclusion of these CVD risk factor assessments in the baseline questionnaire.

Statistical Analysis
Analyses were performed with the Minitab Statistical Package (Version 13). Prevalence of self-reported depression was determined from the study population and standardized using 1996 census data from the Australian Bureau of Statistics for population figures for the Barwon Statistical Division. Differences in baseline characteristics between depressed and nondepressed groups were compared by means of a two-sample t-test for parametric data or a Mann-Whitney test for nonparametric data for all continuous variables; chi-square statistics or Fisher’s exact test were used for discrete data. Logistic regressions, yielding odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for an LHx being associated with CVD risk factors, angina, and MI, unadjusted and adjusted for age. The significance level for all tests was set at {alpha} <0.05.


  RESULTS

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
DISCUSSION
 REFERENCES
 
In this sample, 145 women (19.2%) reported an LHx. Characteristics of the whole group, women with an LHx and those with no LHx are summarized in Table 1. Women with a history of smoking and angina were more likely to report an LHx, and those women who were younger tended to report an LHx, although this finding did not reach statistical significance. Other CVD risk factors and disease measures, including levels of obesity, central body fat accumulation, cholesterol levels, hypertension, inactivity, and diabetes, were not associated with LHx. Because of the small number of participants reporting a previous MI (N=8), we were unable to test the relationship between LHx and this variable.


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TABLE 1. Characteristics for the Whole Group and Women With LHx Versus NO LHx



Table 2 summarizes the ORs for cardiovascular risk factors and CVD being associated with an LHx. A history of smoking increased the odds for reporting an LHx, and the odds of having an LHx were also increased in those with a self-reported history of angina, before and after adjustment for age. Further adjustment for smoking did not alter this relationship. Other CVD risk factors were not associated with LHx.


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TABLE 2. Unadjusted and Age-Adjusted Odds Ratio (ORs) and Confidence Intervals (CIs) for LHx Associated With Cardiac Risk Facotrs and Cardiovascular Disease




  DISCUSSION

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
REFERENCES
 
The findings of this community study offer partial support for extant literature regarding an association between depression and CVD and its risk factors. Angina, in particular, demonstrated an association with a self-reported history of depression, independently increasing the odds of an LHx after adjustment for age. A history of smoking was also associated with LHx. There were no other significant associations between CVD risk factors, including weight indices, diabetes, blood pressure, cholesterol levels, activity levels, and alcohol consumption, and an LHx.

The association between angina and depression in patients with established coronary disease is well established,16–18 whereas prospective studies have found depression to be predictive of angina pectoris in both community and clinical studies.19,20 In a recent review of the literature, Ketterer et al.21 included the following proposals regarding mechanisms for the relationship between angina and depression: that the experience of angina induces or aggravates feelings of anxiety and depression; that the distress experienced as part of a depressive state triggers ischemia/angina; that the angina in depressed individuals with coronary artery disease is due to emotional distress rather than ischemia; and finally, that depressed individuals are hypersensitive to ischemic/angina episodes because of reduced central beta-endorphin production.

It is also the case that angina/chest pain commonly occurs in the absence of demonstrable CVD22 and is associated with depression and anxiety symptoms and disorders in individuals without comorbid CVD.23–27 Of the 18 participants reporting a history of angina in this study, only five also self-reported previous MI or any other heart problems, leaving open the possibility that many of those experiencing angina did so in the absence of concomitant CVD.

The mechanisms of interaction between CVD and depression are complex, and the negative influence depression has on health behaviors, such as smoking, diet, and levels of physical activity28 is likely to be an important contributor to the relationship. Cigarette-smoking is associated with both CVD29 and depression,30–32 and a history of smoking increased the odds of an LHx. In some cross-sectional and prospective epidemiological studies,33–35 physical activity has been shown to be protective against depression in older adults; however we detected no such association in this study, nor was there an association between alcohol consumption and LHx.

There was no association between levels of obesity and LHx in this study, although there were trends, after adjustment for age, toward those with central body-fat accumulation reporting an LHx. Several cross-sectional community studies have demonstrated an association between overweight or obesity and major depression in women, but not in men.36,37 However, evidence supporting this association is equivocal, because weight loss is common in those with clinically significant major depression.38–40 The lack of association between indices of weight and an LHx in our study could be due, in part, to the methodology used to assess depression. We have previously examined those assessed as "currently depressed" by the self-report questionnaire in this same sample of women, and found them to weigh significantly more than nondepressed women.41 If a depressive episode was experienced many years before the assessment, it may be that any previous relationship between an individual’s weight and depression status would no longer be evident.

There were no associations between diabetes, serum cholesterol levels, or prevalence of hypertension and LHx. However, those participants with lower systolic blood pressure tended to report an LHx, and this is consistent with previous epidemiological studies finding hypotension to be common in older individuals with depressive symptoms.42,43 It is also the case that participants with high blood pressure were likely to be on medication for their condition, thus normalizing their blood pressure at the time of testing. As previously stated, the low number of women reporting a previous MI resulted in a lack of power to test the association between self-reported history of MI and LHx.

With regard to methodological problems affecting this study, we must acknowledge the limitations of utilizing DSM-IV criteria for major depressive disorder as a self-report diagnostic instrument, rather than using a clinical diagnostic interview. Although DSM-IV criteria are well validated, the validity of utilizing these criteria in the form of a self-report questionnaire has not yet been established. It is also possible that those identified as depressed according to their self-reported symptoms would not have been diagnosed as such by a validated clinical interview. Self-report measures are the most susceptible to the misclassification of cases.44 We are currently in the process of validating this self-report questionnaire against validated clinical interviews in this sample of women.

There was also a significant time differential between the measurement of cardiovascular variables at baseline and the depression assessment, and it may be that some participants experienced their first depressive episodes at a time-point postdating the baseline assessment. Also, new cases of angina, MI, diabetes, and other measures of cardiovascular disease may have developed in the interim period between the two assessments. Therefore, no causation can be inferred from these results.

The strength of this study lies in the randomly selected, community-based study population and the representativeness of this population in relation to the rest of Australia. Comparisons between the Barwon Statistical Division characteristics and the Australian female population indicate that the similarities between the characteristics in age, country of birth, education, marital status, employment, and income profiles afford a firm basis for extrapolating these data to national levels.13

As previously described, mounting evidence suggests that depression may be an independent risk factor for development of CVD and increased morbidity and mortality post-MI.45 However, there have been four negative or equivocal studies in recent years concerning the association between depression and cardiac mortality,46–49 and, in a recent editorial, Lesperance and Frasure-Smith50 comment that, "despite the weight of accumulated evidence, it is premature to say that depression is causally related to cardiac mortality." Nevertheless, it is important to recognize that depression is commonly underdiagnosed by cardiologists and general practitioners,51 and it has been recommended by expert working-groups in the United States and Australia that depression and other psychosocial factors should be screened for or taken into account in the assessment of cardiac patients.51,52 The rigorous identification and treatment of depression in patients with measurable cardiovascular risk factors or disease would seem to be warranted.


  ACKNOWLEDGMENTS

 
The authors gratefully acknowledge the support of the Geelong Regional Medical Research Foundation and the Victorian Health Promotion Foundation. The authors have no conflict of interest with any commercial or other associations in connection with the submitted article.


  REFERENCES

 
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 ABSTRACT
 INTRODUCTION
 METHOD
 RESULTS
 DISCUSSION
 REFERENCES
 

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