Psychiatry and primary careThe relationship of depressive symptoms to symptom reporting, self-care and glucose control in diabetes
Introduction
A recent meta-analysis has shown that among patients with diabetes, the prevalence of major depression and significant depressive symptoms was 11% and 31%, respectively [1]. The presence of comorbid depressive symptoms can have a significant impact on health outcomes, health care utilization, and overall functioning in patients with diabetes [2], [3]. In a recent study of predominantly type 2 primary care diabetes patients (N=367), we found that depressive symptoms were associated with significantly poorer physical and mental functioning, decreased adherence to dietary recommendations, less adherence to oral hypoglycemic medications, higher health care costs and nonsignificant increases in HbA1c levels [4].
While a number of cross-sectional studies have shown that depression is significantly associated with hyperglycemia in type 2 diabetic patients, as many studies have found that this association is not significant [5]. When examined meta-analytically, the association between poorer glucose control and depression has been found to be more significant in type 1 as compared to type 2 diabetic patients across studies, particularly when standardized interviews were used (Effect Size 0.28 vs. 0.15) [5]. A recent cross-sectional study also found the correlation between Beck Depression Inventory scores and HbA1c levels in type 1 diabetic patients was moderately high (r=.44) as compared to that in type 2 diabetic patients (r=−.06) [6]. A number of differences in type 1 and 2 diabetes – such as different etiologies, age of onset and treatment regimens – may lead to different mechanisms operating to cause hyperglycemia in depressed type 1 and 2 diabetic patients. In type 1 diabetes, patients develop complete insulin deficiency due to an autoimmune destruction of the beta cells of the pancreas. In type 2 diabetes there is a relative lack of insulin based in part on resistance to this hormone at both the liver and the muscle. The complete insulin deficiency in type 1 diabetes may result in greater lability in glycemic control in response to behavioral or neuro-hormonal effects of depression, than may be the case in type 2 diabetes. There is also typically more treatment heterogeneity in type 2 patients who may be treated with diet and exercise only, oral hypoglycemics, insulin or a combination of these. The main – and essential – treatment in type 1 diabetes is insulin, though diet and exercise also play an important secondary role in achieving glucose control. Such differences in diabetes treatment may result in differential treatment outcomes given changes in self-care behavior resulting from depression. For example, in a type 2 diabetic patient treated with diet only, lack of treatment adherence is not likely to cause as significant an increase in glucose levels as lack of adherence to an insulin regimen in a type 1 diabetic patient.
Another important feature of the coexistence of diabetes and depression is the increased potential for symptom reporting among depressed diabetic patients. While there is overlap of symptoms associated with both disorders (e.g., fatigue, hyperphagia), depression is known to cause nonspecific symptom amplification in patients with chronic medical illnesses [7]. Thus, patients with depression may have a lower threshold in reporting all physical symptoms including common diabetes symptoms such as thirst, polyuria, and blurry vision. This tendency to amplify physical symptoms may result in higher health care use and increased laboratory testing by providers [8].
In the current study, we assessed the impact of depressive symptoms on patients with diabetes in a tertiary care university-based clinic. We sought to determine if diabetes self-care behaviors, physical functioning, diabetes symptom reporting and glucose control correlated significantly with depressive symptoms in both type 1 and 2 diabetes. We hypothesized that higher levels of depression would be significantly associated with greater diabetes symptom reporting, lower diabetes self-care, lower physical functioning in both type 1 and 2 diabetes, and we predicted that there would be effect modification so that higher levels of depression would be significantly associated with higher HbA1c levels in type 1, but not type 2 diabetes.
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Materials and methods
This cross-sectional observational study was carried out at the University of Washington Diabetes Care Center (DCC), Seattle, Washington. Eligible participants included all English-speaking DCC patients already enrolled in both 1998 and 1999, age 18 or over. Potential subjects with severe cognitive or language deficits were excluded. In July 1999, 826 potential subjects were sent an approach letter briefly describing the study. Two weeks later subjects were sent a questionnaire and consent form
Results
Of 826 patients, 475 (58%) responded to the survey, of which 276 (58%) had type 1 diabetes and 199 (42%) had type 2 diabetes. There were no significant differences between respondents and nonrespondents in age (48.8±15.9 vs. 50.0±16.4, respectively; t=1.13, df=825, P=.26) and gender (52.5% in both groups; χ2 (df=1)=0.04, P=.95). All subsequent analyses are based on those respondents who had at least one HbA1c level documented in the electronic records within a twelve-month period (N=407).
Discussion
Depressive symptoms were found to be significantly associated with lower adherence to dietary recommendations and exercise, poorer physical functioning, and higher diabetes symptom reporting among patients with type 1 and type 2 diabetes in a tertiary care diabetes specialty clinic. These associations were robust after controlling for diabetes type and complications. These results are consistent with other studies. For example, in our previous study of a primary care sample of predominantly
Acknowledgements
The authors thank Anthony D’Amico and Larry Mix for their assistance with collection of data for this study.
Supported by Group Health Cooperative/Kaiser Permanente Community Foundation Grant #66-0404 and Bayer Institute for Health Care Communication Grant #98-439 and NIDDK grant K23 DK60652-01.
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