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From the Departments of Medicine (MdG., R.E.C.) and Psychiatry (MdG., R.A., K.E.F., R.E.C., P.J.L.), Washington University School of Medicine, St. Louis, Missouri.
Address reprint requests to: Mary de Groot, PhD, Washington University, Division of Health Behavior Research, Campus Box 8504, 4444 Forest Park, Ste 6700, St. Louis, MO 63108. Email: mdegroot{at}im.wustl.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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METHOD: MEDLINE and PsycINFO databases were searched for articles examining depression and diabetes complications in type 1 and type 2 diabetes samples published between 1975 and 1999. Meta-analytic procedures were used. Studies were reviewed for diabetes type, sample size, statistical tests, and measures of diabetes complications and depression. Significance values, weighted effect sizes r, 95% confidence intervals (CI), and tests of homogeneity of variance were calculated for the overall sample (k = 27) and for subsets of interest.
RESULTS: A total of 27 studies (total combined N = 5374) met the inclusion criteria. A significant association was found between depression and complications of diabetes (p < .00001, z = 5.94). A moderate and significant weighted effect size (r = 0.25; 95% CI: 0.22–0.28) was calculated for all studies reporting sufficient data (k = 22). Depression was significantly associated with a variety of diabetes complications (diabetic retinopathy, nephropathy, neuropathy, macrovascular complications, and sexual dysfunction). Effect sizes were in the small to moderate range (r = 0.17 to 0.32).
CONCLUSIONS: These findings demonstrate a significant and consistent association of diabetes complications and depressive symptoms. Prospective, longitudinal studies are needed to identify the pathways that mediate this association.
Key Words: depression • diabetes mellitus • meta-analysis
Abbreviations: CI = Confidence Interval; ES = Effect Size; BDI = Beck Depression Inventory;; SCID = Structured Clinical Interview for the DSM; SCL-90 R = Symptom Checklist 90-Item Version, Depression Subscale; DIS = Diagnostic Interview for the DSM; Zung = Zung Depression Scale; KDS-1 = Kupffer-Detre Depression Scale, Form 1; PSE = Present State Exam; CES-D = Center for Epidemiologic Studies Depression Inventory.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Chronic hyperglycemia is a well-established predictor of the onset and exacerbation of diabetes complications in both type 1 (eg (7),) and type 2 diabetes (8). If depression is associated with hyperglycemia and hyperglycemia is associated with diabetes complications, it follows that depression may also be associated with diabetes complications. Previous studies have correlated depression with a variety of diabetes complications such as diabetic neuropathy (9) and cardiovascular disease (10), yet others have failed to find an association between depression and diabetic retinopathy (11) or other complications such as nephropathy (12). Although a number of studies have examined this relationship, none have systematically reviewed the literature to assess the magnitude and consistency of the association. The demonstration of a consistent relationship is important because it lays the groundwork for exploring the pathways between depression as a psychological variable and complications as medical variables.
The purpose of the current investigation was to determine whether a consistent relationship between depression and diabetes complications among type 1 and type 2 diabetes patient samples could be established using meta-analytic techniques. We were interested in determining: 1) whether there is an association; 2) its direction, if found; and 3) whether the relationship differs among specific diabetes complications.
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METHODS |
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Statistical Analyses
Meta-analysis was developed by Glass (13), Hedges and Olkin (14), and Rosenthal (15) to estimate effect sizes across multiple studies. Effect size, the measure of the magnitude of association between two variables, may be calculated from test statistics, variance estimates, or significance values (eg, p values, odds ratios). A variety of ES indices may be used to estimate the magnitude of an effect (16). In the current study, the Pearson correlation coefficient r was used as the ES estimator. Rosenthal (15) and Cohen (16) note that r is a robust estimator that reflects the proportion of common elements between two variables. The random effects model was used to estimate effect sizes. This conservative model was chosen to reduce overestimation of effect sizes in light of the correlational nature of the studies available in the literature.
Meta-analytic techniques for data collection, aggregation, and analysis were based on the procedures recommended by Rosenthal (15). For each study meeting the inclusion criteria, the following information was gathered: sample size, diabetes type, duration of diabetes, sample source, method of depression assessment, method of diabetes complication assessment, test statistics, and statistical significance values for the association between depression and complications, and if available, effect sizes. Depression assessment methods varied from self-report symptom inventories (eg, Beck Depression Inventory (17)) to diagnostic interview protocols (eg, Diagnostic Interview Schedule (18)), as did the definition of depression (eg, depressive symptoms vs. major depression). Diabetes complication assessment methodologies varied from patient self-report symptom inventories to physiologic test protocols (eg, biothesiometers used to measure nerve conductance). Likewise, the sources of complication data varied across studies (eg, protocol evaluations vs. medical chart data).
Published test statistics, significance values and effect sizes from each contributing study were used to calculate estimates of effect sizes and combined p values. Meta-analytic software (19) was used to perform these calculations.
ES estimates were calculated using standard formulas (15) from the following source data: test statistics; means, standard deviations, and sample sizes; or p values. For studies in which ES could be derived from more than one method, test statistic values took precedence. In the case of articles that reported only nonsignificant p values and did not provide enough information to replicate test statistics, r values were set as missing and omitted from further analyses. Once calculated, effect size r values were converted to Fisher’s Zr.
To estimate the combined effect size, weighted and unweighted effect sizes r were calculated for each data aggregation. Weighted effect sizes were calculated by multiplying the Fisher’s Zr values by the respective sample size weights and dividing the sum by the sum of the sample sizes. Confidence intervals were calculated from residual variation of the effect sizes. CI represent the range of variance in the sample of effect sizes with a value of zero or less in the lower bound indicating statistical nonsignificance.
Combined p values were also calculated to estimate the probability of the null hypothesis (ie, the likelihood that the association of depression and complications is a chance occurrence) in an aggregation of studies. While combined p values provide less specific information about the magnitude of effects within a given study, they provide an estimate of the overall significance of findings. In order to evaluate all studies in the same metric, significance values for two-tailed tests were divided by two to yield one-tailed p values. Several papers referred to nonsignificant test results in the text but did not provide specific p values. In these cases, a p value of .50 was assigned. The p values were then transformed into z scores. In studies that contributed more than one significance test, the z scores were averaged and backtransformed to obtain the average p value. To calculate the combined p value, z scores from each study were multiplied by their respective sample sizes, summed, and divided by the square root of the sum of the squared sample sizes.
Homogeneity of variance concerns the degree of variability in the effect sizes in an aggregation of studies. The random effects model assumes that effect sizes are sample estimates of a true population parameter. Consequently, ES are subject to sampling error. Homogeneity of variance is estimated to measure the degree of variability associated with the effect size estimate. The homogeneity hypothesis was tested for each grouping of studies. Three tests of homogeneity of variance were calculated: residual variation, proportion of variance observed, and chi-square. The presence of heterogeneity of variance suggests that there may be other sources of systematic variance (moderator variables) in the relationship between two variables. It may also suggest the presence of "noise" or measurement error in aggregations of studies.
Finally, the Fail Safe N was calculated for each sample grouping. As noted by Rosenthal and others (15), a common criticism of meta-analysis is the "file drawer problem" or the extent to which nonsignificant results are disproportionately excluded from publication. Fail Safe N indicates the number of unpublished studies with negative findings that would be required to reduce the effect size to the r = 0.05 level (19). An effect size level of r = 0.05 was chosen as an ES approximating zero.
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RESULTS |
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c NA = Information not provided by authors.
As shown in Table 2, meta-analytic statistics for the entire sample of studies were calculated for all complications and diabetes types combined. The combined p value was significant (p < .00001, z = 5.94). The weighted effect size among studies for which sufficient information was available (k = 22) was r = 0.25 (95% CI: 0.22–0.28), indicating a moderate ES (16). The total aggregation of studies was heterogeneous according to all three tests of homogeneity of variance.
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To examine whether the association between depression and diabetes complications differs by diabetes type, studies were aggregated by type of diabetes irrespective of complications. As shown in Table 2, the aggregations yielded significant combined p values with weighted effect sizes ranging from r = 0.21 to r = 0.30 (95% CI range: 0.17–0.34). These findings indicate consistent and moderate effect sizes in the relationships between depression and complications in both type 1 and type 2 diabetes. ES and CI were similar for studies of type 1 and type 2 patient samples. Tests of homogeneity of variance indicated that the type 1 and mixed samples data aggregations were heterogeneous, suggesting the possible presence of moderator variables. Type 2 study aggregations, however, were homogeneous.
Finally, the studies were aggregated by specific diabetes complications. Studies reporting analyses for depression and several separate diabetes complications were entered into each diabetes complication aggregation for which results were available. As shown in Table 3, the specific diabetes complications represented in this literature included diabetic retinopathy (k = 10), neuropathy (k = 12), nephropathy (k = 5), sexual dysfunction (k = 4), and macrovascular complications (k = 10).
The ten studies that examined relationships between depressive symptoms and diabetic retinopathy yielded a significant combined p value (p < .0001; z = 3.84) and a small to moderate effect size (r = 0.17; 95% CI: 0.11–0.22; k = 7). Five studies examined nephropathy and yielded a significant combined p value (p = .0002; z = 3.51) and moderate effect size (r = .25; 95% CI: .19–.30; k = 5). Similar findings were obtained for the subsets of studies examining diabetic neuropathy (p = .0002; z = 3.57; r = .28; 95% CI: .22–.34; k = 10) and sexual dysfunction (p < .0001; z = 3.77; r = .32; 95% CI: .22–.42; k = 4).
Ten studies examined the association between depressive symptoms and macrovascular complications (eg, coronary artery disease, peripheral vascular disease, coronary vascular disease, ischemic heart disease, arthrosclerotic vascular disease). These studies were aggregated to form a general "macrovascular" disease category. The combined p value was significant (p < .0001; z = 5.42) and there was a moderate effect size (r = .20; 95% CI: .16–.24; k = 9).
Tests of homogeneity of variance indicated that all of the subgroups except sexual dysfunction and type 2 diabetes were heterogeneous. This suggests that additional sources of variability exist in these study aggregations.
Fail Safe N values were calculated for each data aggregation. The numbers of unpublished studies with negative findings that would be required to reduce the effect sizes to the r = .05 level are shown in Tables 2 and 3.
Effect sizes r and 95% confidence intervals are graphically represented in Figure 1 for all study aggregations. The associations between depression and diabetes complications were consistently positive. That is, increased depression was associated with increased numbers, severity, or ratings of complications. The lower 95% confidence limits did not cross zero in any of the aggregations, indicating statistically significant effect size estimates.
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DISCUSSION |
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The findings are noteworthy for their consistency. In all subgroup aggregations, the association between depressive symptoms and specific complications was statistically significant. In addition, effect sizes were similar across physiologically diverse complications such as retinopathy, nephropathy, and sexual dysfunction. It is reasonable to expect that the course and patient experience of diabetic retinopathy, for example, might differ considerably from that of macrovascular complications. Likewise, depression might be expected to have a different relationship with neuropathy, than with nephropathy. Yet, the results within these aggregations indicated that depression was consistently associated with increased severity of diabetes complications. Likewise, there was similarity in effect size in type 1 and type 2 study samples. Type 1 and type 2 diabetes are etiologically distinct diseases, with differing ages of onset, courses of illness, and treatment regimens. This consistency suggests that there may be common pathways that support the association between depression and type 1 and type 2 diabetes.
Each of these analyses indicated a positive direction of association. An increase in depressive symptoms was associated with an increase in the severity or number of diabetes complications. As shown in Table 1, 89% of all studies showed significant, positive correlations. The three exceptions to this trend reported statistically nonsignificant inverse relationships (range: -.04 to -.12) between self-report depression scores and complications (11, 22, 23). The consistency of the positive association increases confidence that these findings are replicable.
The meta-analysis has several limitations. First, a limited sample of studies were available for the analysis, which yielded small numbers of studies in each of the subgroup analyses. This may have contributed to the effect size variance found within most of the study aggregations. Second, the Fail Safe N values indicate that additional studies are needed to confidently reject the "file drawer problem" for some of the data aggregations (eg, presence/absence of complications, number of complications, type 2 samples, and retinopathy). Third, all of the studies available for analysis used cross-sectional designs, rather than prospective longitudinal approaches. Caution should be used in interpreting the strength of the association in light of the correlational nature of these studies. Finally, as noted in Tables 2 and 3, calculation of the ES in the majority of data aggregations yielded heterogeneous variance estimates indicating the possible presence of moderator variables. Heterogeneity of variance remained after studies were subdivided into logical aggregations (eg, specific complications, diabetes type). This suggests that additional variables not disclosed by the source studies may be important contributors to the association.
At this stage in the development of the literature, it is not possible to determine causal directions or mechanisms to explain the association between depression and complications due to the correlational nature of many of the contributing studies. Depression may precede and/or follow the onset of diabetes complications depending on the individual or course of disease. Depression, once established, may affect the course of complication development, promoting the onset of some, intensifying others. Depression may have an impact on some complications (eg, macrovascular disease) but little impact on the course of other complications (eg, nephropathy). It would be reasonable to speculate that underlying mechanisms linking depression and diabetes complications are a function of biological, social, and psychological variables that may interact with depression in differing ways to produce similar interactions with complications. In order to better characterize the relationship between depression and diabetes complications, three issues require further investigation: temporal relationships between depression and diabetes complications, the role of glycemic control as a potential mediating variable between depression and complications, and whether depression may accelerate the onset or progression of complications.
Temporal relationships between depressive symptoms and complications warrant clarification. The development of depression has often been considered a secondary response to the onset of complications but depression might also play a primary role in the development or exacerbation of diabetes complications. Which comes first? For whom? Are there differences in these relationships by type of diabetes? Do these relationships differ by diabetes complication? What role does duration of diabetes play in the development of depression? The majority of studies evaluated mean duration of diabetes, but no studies have used this variable as a covariate in analyses of the association between depression and complications. Precise characterization of the timing and predictors of this interrelationship is needed.
Second, the role of glycemic control as a mediating variable is suggested by the recent review by Lustman and colleagues (2). Depression has been found to be associated with worsened glycemic control. Further work is needed to identify the mechanisms underlying the association between glycemic control and depression and what predicts the onset of depression in some individuals with hyperglycemia but not in others.
Finally, further investigation is needed to establish the role depression may play in the exacerbation of diabetes complications, that is, hastening the onset or progression of complications. In a longitudinal study of 114 patients over a ten-year period, Carney and colleagues (24) found a three-fold increased likelihood of developing coronary artery disease in patients with depression. Cohen and colleagues (25) reported that patients with a lifetime history of any affective disorder had greater progression of retinopathy than patients with no psychiatric history. Findings from these two studies lend support to the hypothesis that depression may accelerate the development of diabetes complications.
Prospective longitudinal studies are needed to explore these hypotheses. Such studies would require use of control samples, stratification of samples by diabetes type and disease duration, and precision in the documentation of diabetes complication trajectories. In addition, use of standardized interview protocols and diagnostic standards would be essential to documenting the existence of depressive syndromes, episodes, and disorders.
In conclusion, this meta-analysis documents consistent and significant associations between depression and a variety diabetes complications in both type 1 and type 2 diabetes. Well-designed, longitudinal studies are needed to pinpoint depression and complication trajectories and the mechanisms that link these diseases (26–43).
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONACKNOWLEDGMENTSREFERENCES |
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Received for publication July 13, 2000.
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P. M. Trief Depression in Elderly Diabetes Patients Diabetes Spectr, April 1, 2007; 20(2): 71 - 75. [Full Text] [PDF]
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P. J. Lustman, M. M. Williams, G. S. Sayuk, B. D. Nix, and R. E. Clouse Factors Influencing Glycemic Control in Type 2 Diabetes During Acute- and Maintenance-Phase Treatment of Major Depressive Disorder With Bupropion Diabetes Care, March 1, 2007; 30(3): 459 - 466. [Abstract] [Full Text] [PDF]
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J. Wagner and G. Abbott Depression and Depression Care in Diabetes: Relationship to perceived discrimination in African Americans Diabetes Care, February 1, 2007; 30(2): 364 - 366. [Full Text] [PDF]
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D. Anderson, C. Horton, M. L. O'Toole, C. A. Brownson, P. Fazzone, and E. B. Fisher Integrating Depression Care With Diabetes Care in Real-World Settings: Lessons From the Robert Wood Johnson Foundation Diabetes Initiative Diabetes Spectr, January 1, 2007; 20(1): 10 - 16. [Abstract] [Full Text] [PDF]
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 L. C. Brown, S. R. Majumdar, S. C. Newman, and J. A. Johnson Type 2 diabetes does not increase risk of depression. Can. Med. Assoc. J., July 4, 2006; 175(1): 42 - 46. [Abstract] [Full Text] [PDF]
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A. Cherrington, G. X. Ayala, B. Sleath, and G. Corbie-Smith Examining knowledge, attitudes, and beliefs about depression among latino adults with type 2 diabetes. The Diabetes Educator, July 1, 2006; 32(4): 603 - 613. [Abstract] [Full Text] [PDF]
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J. E. Elwing, P. J. Lustman, H. L. Wang, and R. E. Clouse Depression, Anxiety, and Nonalcoholic Steatohepatitis Psychosom Med, July 1, 2006; 68(4): 563 - 569. [Abstract] [Full Text] [PDF]
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M. M. Williams, R. E. Clouse, and P. J. Lustman Treating Depression to Prevent Diabetes and Its Complications: Understanding Depression as a Medical Risk Factor Clin. Diabetes, April 1, 2006; 24(2): 79 - 86. [Abstract] [Full Text] [PDF]
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P. M. Trief, P. C. Morin, R. Izquierdo, J. A. Teresi, J. P. Eimicke, R. Goland, J. Starren, S. Shea, and R. S. Weinstock Depression and Glycemic Control in Elderly Ethnically Diverse Patients With Diabetes: The IDEATel Project Diabetes Care, April 1, 2006; 29(4): 830 - 835. [Abstract] [Full Text] [PDF]
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M. de Groot, B. Pinkerman, J. Wagner, and E. Hockman Depression treatment and satisfaction in a multicultural sample of type 1 and type 2 diabetic patients. Diabetes Care, March 1, 2006; 29(3): 549 - 553. [Abstract] [Full Text] [PDF]
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P. de Jonge, G. I.J.M. Kempen, R. Sanderman, A. V. Ranchor, C. H.M. van Jaarsveld, E. van Sonderen, W. Scaf-Klomp, A. Weening, J. P.J. Slaets, and J. Ormel Depressive Symptoms in Elderly Patients After a Somatic Illness Event: Prevalence, Persistence, and Risk Factors Psychosomatics, February 1, 2006; 47(1): 33 - 42. [Abstract] [Full Text] [PDF]
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E. H. B. Lin, W. Katon, C. Rutter, G. E. Simon, E. J. Ludman, M. Von Korff, B. Young, M. Oliver, P. C. Ciechanowski, L. Kinder, et al. Effects of Enhanced Depression Treatment on Diabetes Self-Care Ann. Fam. Med, January 1, 2006; 4(1): 46 - 53. [Abstract] [Full Text] [PDF]
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M. D. Llorente and V. Urrutia Diabetes, Psychiatric Disorders, and the Metabolic Effects of Antipsychotic Medications Clin. Diabetes, January 1, 2006; 24(1): 18 - 24. [Abstract] [Full Text] [PDF]
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S. M. Frayne, J. H. Halanych, D. R. Miller, F. Wang, H. Lin, L. Pogach, E. J. Sharkansky, T. M. Keane, K. M. Skinner, C. S. Rosen, et al. Disparities in Diabetes Care: Impact of Mental Illness Arch Intern Med, December 12, 2005; 165(22): 2631 - 2638. [Abstract] [Full Text] [PDF]
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W. J. Katon, C. Rutter, G. Simon, E. H.B. Lin, E. Ludman, P. Ciechanowski, L. Kinder, B. Young, and M. Von Korff The Association of Comorbid Depression With Mortality in Patients With Type 2 Diabetes Diabetes Care, November 1, 2005; 28(11): 2668 - 2672. [Abstract] [Full Text] [PDF]
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L. Vileikyte, H. Leventhal, J. S. Gonzalez, M. Peyrot, R. R. Rubin, J. S. Ulbrecht, A. Garrow, C. Waterman, P. R. Cavanagh, and A. J.M. Boulton Diabetic Peripheral Neuropathy and Depressive Symptoms: The association revisited Diabetes Care, October 1, 2005; 28(10): 2378 - 2383. [Abstract] [Full Text] [PDF]
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M. M. Garrison, W. J. Katon, and L. P. Richardson The Impact of Psychiatric Comorbidities on Readmissions for Diabetes in Youth Diabetes Care, September 1, 2005; 28(9): 2150 - 2154. [Abstract] [Full Text] [PDF]
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G. E. Miller, N. Rohleder, C. Stetler, and C. Kirschbaum Clinical Depression and Regulation of the Inflammatory Response During Acute Stress Psychosom Med, September 1, 2005; 67(5): 679 - 687. [Abstract] [Full Text] [PDF]
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 E. B. Fisher, C. A. Brownson, M. L. O'Toole, G. Shetty, V. V. Anwuri, and R. E. Glasgow Ecological Approaches to Self-Management: The Case of Diabetes Am J Public Health, September 1, 2005; 95(9): 1523 - 1535. [Abstract] [Full Text] [PDF]
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A. Engum, A. Mykletun, K. Midthjell, A. Holen, and A. A. Dahl Depression and Diabetes: A large population-based study of sociodemographic, lifestyle, and clinical factors associated with depression in type 1 and type 2 diabetes Diabetes Care, August 1, 2005; 28(8): 1904 - 1909. [Abstract] [Full Text] [PDF]
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L. E. Egede, P. J. Nietert, and D. Zheng Depression and All-Cause and Coronary Heart Disease Mortality Among Adults With and Without Diabetes Diabetes Care, June 1, 2005; 28(6): 1339 - 1345. [Abstract] [Full Text] [PDF]
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 A. M. Pot, D. J. H. Deeg, J. W. R. Twisk, A. T. F. Beekman, and S. H. Zarit The Longitudinal Relationship Between the Use of Long-Term Care and Depressive Symptoms in Older Adults Gerontologist, June 1, 2005; 45(3): 359 - 369. [Abstract] [Full Text] [PDF]
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 G. D. Rosson, A. L. Dellon, R. Gross, H. Sone, S. Mizuno, N. Yamada, S. Tesfaye, D. R. Witte, and J. H. Fuller Vascular Risk Factors and Diabetic Neuropathy N. Engl. J. Med., May 5, 2005; 352(18): 1925 - 1927. [Full Text] [PDF]
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The Diabetes Prevention Program Research Group Depression Symptoms and Antidepressant Medicine Use in Diabetes Prevention Program Participants Diabetes Care, April 1, 2005; 28(4): 830 - 837. [Abstract] [Full Text] [PDF]
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 A. Rozanski, J. A. Blumenthal, K. W. Davidson, P. G. Saab, and L. Kubzansky The epidemiology, pathophysiology, and management of psychosocial risk factors in cardiac practice: The emerging field of behavioral cardiology J. Am. Coll. Cardiol., March 1, 2005; 45(5): 637 - 651. [Abstract] [Full Text] [PDF]
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P. J. Lustman, R. E. Clouse, P. S. Ciechanowski, I. B. Hirsch, and K. E. Freedland Depression-Related Hyperglycemia in Type 1 Diabetes: A Mediational Approach Psychosom Med, March 1, 2005; 67(2): 195 - 199. [Abstract] [Full Text] [PDF]
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L. E. Egede Effect of Comorbid Chronic Diseases on Prevalence and Odds of Depression in Adults With Diabetes Psychosom Med, January 1, 2005; 67(1): 46 - 51. [Abstract] [Full Text] [PDF]
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 J. Haber, C. F. Toombs, E. Hamera, D. Hillyer, B. J. Limandri, S. Pagel, R. R. Staten, and M. L. Zimmerman Advanced Practice Psychiatric Nurses: 2004 Legislative Update Journal of the American Psychiatric Nurses Association, December 1, 2004; 10(6): 298 - 310. [PDF]
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L. Jack Jr. Diabetes and Men's Health Issues Diabetes Spectr, October 1, 2004; 17(4): 206 - 208. [Full Text] [PDF]
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 W. J. Katon, M. Von Korff, E. H. B. Lin, G. Simon, E. Ludman, J. Russo, P. Ciechanowski, E. Walker, and T. Bush The Pathways Study: A Randomized Trial of Collaborative Care in Patients With Diabetes and Depression Arch Gen Psychiatry, October 1, 2004; 61(10): 1042 - 1049. [Abstract] [Full Text] [PDF]
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E. H.B. Lin, W. Katon, M. Von Korff, C. Rutter, G. E. Simon, M. Oliver, P. Ciechanowski, E. J. Ludman, T. Bush, and B. Young Relationship of Depression and Diabetes Self-Care, Medication Adherence, and Preventive Care Diabetes Care, September 1, 2004; 27(9): 2154 - 2160. [Abstract] [Full Text] [PDF]
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 L. B. Dixon, J. A. Kreyenbuhl, F. B. Dickerson, T. W. Donner, C. H. Brown, K. Wolheiter, L. Postrado, R. W. Goldberg, L. Fang, C. Marano, et al. A Comparison of Type 2 Diabetes Outcomes Among Persons With and Without Severe Mental Illnesses Psychiatr Serv, August 1, 2004; 55(8): 892 - 900. [Abstract] [Full Text] [PDF]
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P. J. Lustman and R. E. Clouse Section III: Practical Considerations in the Management of Depression in Diabetes Diabetes Spectr, July 1, 2004; 17(3): 160 - 166. [Full Text] [PDF]
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J. W. Williams Jr., W. Katon, E. H.B. Lin, P. H. Noel, J. Worchel, J. Cornell, L. Harpole, B. A. Fultz, E. Hunkeler, V. S. Mika, et al. The Effectiveness of Depression Care Management on Diabetes-Related Outcomes in Older Patients Ann Intern Med, June 15, 2004; 140(12): 1015 - 1024. [Abstract] [Full Text] [PDF]
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J. L. Jackson, K. DeZee, and E. Berbano Can Treating Depression Improve Disease Outcomes? Ann Intern Med, June 15, 2004; 140(12): 1054 - 1056. [Full Text] [PDF]
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M. W. Ketterer, G. Mahr, J. J. Cao, M. Hudson, S. Smith, and W. Knysz What's "Unstable" in Unstable Angina? Psychosomatics, June 1, 2004; 45(3): 185 - 196. [Abstract] [Full Text] [PDF]
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J. D. McKellar, K. Humphreys, and J. D. Piette Depression Increases Diabetes Symptoms by Complicating Patients' Self-Care Adherence The Diabetes Educator, May 1, 2004; 30(3): 485 - 492. [PDF]
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R. D. Goldney, P. J. Phillips, L. J. Fisher, and D. H. Wilson Diabetes, Depression, and Quality of Life: A population study Diabetes Care, May 1, 2004; 27(5): 1066 - 1070. [Abstract] [Full Text] [PDF]
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W. Katon, M. Von Korff, P. Ciechanowski, J. Russo, E. Lin, G. Simon, E. Ludman, E. Walker, T. Bush, and B. Young Behavioral and Clinical Factors Associated With Depression Among Individuals With Diabetes Diabetes Care, April 1, 2004; 27(4): 914 - 920. [Abstract] [Full Text] [PDF]
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L. E. Egede Diabetes, Major Depression, and Functional Disability Among U.S. Adults Diabetes Care, February 1, 2004; 27(2): 421 - 428. [Abstract] [Full Text] [PDF]
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R. E. Clouse, P. J. Lustman, K. E. Freedland, L. S. Griffith, J. B. McGill, and R. M. Carney Depression and Coronary Heart Disease in Women With Diabetes Psychosom Med, May 1, 2003; 65(3): 376 - 383. [Abstract] [Full Text] [PDF]
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L. E. Egede and D. Zheng Independent Factors Associated With Major Depressive Disorder in a National Sample of Individuals With Diabetes Diabetes Care, January 1, 2003; 26(1): 104 - 111. [Abstract] [Full Text] [PDF]
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 M. M. Desai, R. A. Rosenheck, B. G. Druss, and J. B. Perlin Mental Disorders and Quality of Diabetes Care in the Veterans Health Administration Am J Psychiatry, September 1, 2002; 159(9): 1584 - 1590. [Abstract] [Full Text] [PDF]
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P. J. Lustman, M. L. Caudle, and R. E. Clouse Case Study: Nondysphoric Depression in a Man With Type 2 Diabetes Clin. Diabetes, July 1, 2002; 20(3): 122 - 123. [Full Text] [PDF]
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S. A. Black Diabetes, Diversity, and Disparity: What Do We Do With the Evidence? Am J Public Health, April 1, 2002; 92(4): 543 - 548. [Abstract] [Full Text]
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