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Psychosomatic Medicine 63:551-555 (2001)
© 2001 American Psychosomatic Society

ORIGINAL ARTICLES

Depressed Mood Is a Factor in Glycemic Control in Type 1 Diabetes

Miranda A.L. Van Tilburg, PhD, Cynthia C. McCaskill, MSN, James D. Lane, PhD, Christopher L. Edwards, PhD, Angelyn Bethel, MD, Mark N. Feinglos, MD and Richard S. Surwit, PhD

From the Duke University Medical Center, Durham, North Carolina.

Address reprint requests to: Richard S. Surwit, Box 3842, Duke University Medical Center, Durham, NC 27710. Email: Richard.Surwit{at}duke.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
OBJECTIVE: The diabetes literature contains conflicting evidence on the relationship between depression and glycemic control. This may be due, in part, to the fact that past studies failed to distinguish between patients with type 1 and type 2 diabetes. Because these are actually completely different diseases that are often treated differently and consequently make different demands on patients, the relationship between glycemic control and depressed mood in type 1 and type 2 diabetes was examined separately.

METHODS: The relationship between Beck Depression Inventory (BDI) scores and HbA1c, as an index of long-term glycemic control, was measured in samples of 30 patients with type 1 and 34 patients with type 2 diabetes.

RESULTS: Groups of patients with type 1 and type 2 diabetes did not differ in mean BDI score or HbA1c level. Correlation analysis revealed a significant positive relationship between BDI scores and HbA1c in the type 1 group (r = .44, p < .02) but not in the type 2 group (r = -0.06, p > .05). This relationship was evident throughout the entire range of BDI scores and was not restricted to scores indicative of clinical depression. Patients with type 1 diabetes who had higher HbA1c and BDI scores reported a lower frequency of home blood glucose monitoring.

CONCLUSIONS: Variations in depressive mood, below the level of clinical depression, are associated with meaningful differences in glycemic control in type 1 but not type 2 diabetes. Preliminary data analysis suggests that this effect may be mediated, at least in part, by decreased self-care behaviors in patients with more depressed mood.

Key Words: depression • type 1 diabetes • type 2 diabetes • glycemic control

Abbreviations: HbA1c = hemoglobin A1c; BDI = Beck Depression Inventory; SMBG = self-monitored blood glucose; BMI = body mass index.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Diabetes is a chronic metabolic disorder that affects almost 14 million Americans (1). Many patients with diabetes eventually develop severe complications, including amputations, blindness, kidney failure, and cardiovascular disease. The main goal of treatment is the control of blood sugar. Patients must follow rigorous daily dietary, exercise, and medication regimens for the remainder of their lives. Because successful diabetes management depends on the behavior of the patient, biopsychosocial factors are thought to contribute to clinical outcomes. One important factor is depression. Diabetes mellitus is a significant risk factor for depression. Recent prevalence studies suggest that approximately 15% of all patients with diabetes suffer from clinical depression, and even a greater percentage (about 30%) suffer from some sort of psychiatric disturbance (2–6). In addition to the negative psychological and social consequences, depression may also be a risk factor for poor metabolic control in diabetes. Some investigators have found moderate to strong associations (5, 7–12) between depression and glycemic (blood glucose) control, although others have found no relationship (13–22).

Two factors may contribute to the inconsistencies among studies. First, studies of patients with major depression do not account for the potential confounding role of psychopharmacologic treatment on metabolic control. All major classes of antidepressants have been shown to have direct pharmacologic effects on metabolic function, which could confound the relationship between measures of depression and glycemic control. Monoamine oxidase inhibitors improve glucose tolerance as a direct result of their chemical action (23–24), and selective serotonin reuptake inhibitors improve metabolic control mainly through their effect on weight loss (25–30). In contrast, tricyclic antidepressants may worsen glycemic control by causing weight gain (31–33). Many other psychoactive drugs can affect glucose as well (34). It is critical that the confounding effects be considered and controlled in studies of the relationship of measures of depression and glycemic control.

The second source of confusion in the literature is that most published studies combined patients with type 1 and type 2 diabetes or included only one group or the other. In type 1 diabetes, the insulin secreting beta cells of the pancreas are destroyed by an autoimmune reaction, leaving the patient totally dependent on exogenous insulin for survival. The onset of disease is typically abrupt and occurs before age 30 years. Multiple daily insulin injections are necessary, and equipment must be used for SMBG several times each day. In contrast, type 2 diabetes is a condition in which there is a relative insulin deficiency where, for a variety of reasons, not enough insulin is secreted to meet the needs of the body. Disease onset occurs gradually and usually after age 30 years. Although many patients with type 2 diabetes can be treated with diet and oral medications, insulin therapy is eventually required in a subset of this population as their ability to secrete insulin diminishes. Because these diseases are of different etiology and demand different degrees of lifestyle adaptation from patients, it is logical that they should be considered separately. Type of diabetes may be critical in determining the effect of mood on glycemic control. For example, a recent study found an association between a history of depression and poor glycemic control in patients with type 1 but not with type 2 diabetes (35).

The aim of the present study was to explore how depressive mood affects glycemic control and to avoid the methodological problems of earlier studies. Therefore, we tested the association between a well-standardized measure of depressive symptoms and an established index of glycemic control in separate samples of patients with type 1 and type 2 diabetes who were not taking psychoactive medication.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Participants
Patients with diabetes presenting for routine care at the Duke University Medical Center Endocrinology Clinic were asked to participate in the study. None of the patients who were approached declined participation, and all patients gave informed consent. Roughly equal numbers of patients with type 1 and type 2 diabetes were enrolled. Patients were screened before data collection, and potential participants were excluded for the following reasons: (1) type of diabetes indeterminate from the medical record and/or consultation with the attending physician; (2) current or prior psychiatric diagnosis or treatment of psychiatric illness (Detailed psychiatric charts were not available in the medical clinic. As a result, we excluded all patients with a documented history of psychiatric diagnosis because use of psychoactive medication could not be determined.); (3) history of stroke, brain surgery, or closed head injury, mild dementia, pregnancy, or recent infection or illness that could have affected glucose control; and (4) inability to independently complete the BDI questionnaire because of vision, literacy, or primary language other than English. Of all patients screened for participation, roughly 30% were excluded because of a psychiatric diagnosis or psychiatric treatment. This figure corresponds with prevalence rates of psychiatric disorders in diabetes (eg, Ref. 5–6).

The final sample contained 64 patients—34 patients who were classified as having type 2 diabetes and 30 patients classified as having type 1 diabetes. Demographic characteristics of patients in the two groups are presented in Table 1.


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  		Table 1. Characteristics of Patients with Type 1 and Type 2 Diabetes
 
Measures
Depressive symptomatology was measured by use of the Beck Depression Inventory (The Psychological Corporation, Orlando, FL). The BDI has been shown to have high reliability and validity (36). Furthermore, the BDI has been specifically validated as a tool for measuring depression in diabetes (4, 37, 38). Scores of 16 and above have been reported to indicate possible clinical depression in this population (37).

Glycemic control was assessed by HbA1c, a generally accepted index of average blood glucose level over the previous 12 to 16 weeks. All tests were conducted in a standard clinical laboratory that has met the requirements to be certified by the National Glycohemoglobin Standardization Program. HbA1c was measured by use of ion-exchange high-performance liquid chromatography, a methodology that measures only the A1c fraction of glycohemoglobin (reference range 4.3%–6.0%). HbA1c levels of the first 5 patients enrolled in the study were determined by Hitachi 911 immunoassay; these levels were converted to new method equivalents before data analysis.

Procedures
After screening and informed consent, patients were interviewed briefly to collect information on diabetes duration (in years), frequency of SMBG (by asking patients to estimate approximately how many times a week they usually monitored their blood glucose), and recent history of infections or serious illness. Patients were then asked to either complete the BDI in the clinic or to take the BDI home and return it by mail within the same week. If BDI scores exceeded the cutoff score of 16, indicating possible clinical depression, the attending physician was informed, and (s)he took appropriate action. Demographic information, height, weight, medication use, and medical history, as well as results of the routine measurement of HbA1c performed during the clinic visit, were obtained from the medical record after the visit. All procedures were approved by the Duke University Medical Center Institutional Review Board.

Analyses
Hypotheses were tested by use of correlation and linear-regression procedures provided by SAS for Windows (SAS Institute, Cary, NC). Statistical significance was declared for p < .05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
BDI scores ranged from 0 to 22 (mean 7.3; SD 5.3), and 93.8% of patients scored below the cutoff for potential clinical depression. HbA1c levels ranged from 5.7% to 11.3% (mean 8.1%; SD 1.4%). To determine the relationship of depressive symptoms to glycemic control, Pearson correlations were calculated between BDI scores and HbA1c levels. A strong positive correlation was found in patients with type 1 diabetes (r = .44, p < .02), but no association between these variables was found in patients with type 2 diabetes (r = -0.06, p > .05). The scatterplot in Figure 1 shows a linear relationship for patients with type 1 diabetes, extending across the entire range of BDI scores. The patient groups of type 1 and type 2 diabetes did not differ in mean BDI scores or HbA1c levels and had very similar variability in these measures (Table 1).



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  		Fig. 1. Relationship of BDI scores and HbA1c in patients with types 1 and 2 diabetes.

 
Although we had no prior hypothesis regarding potential mechanisms by which mood might influence diabetes control, we conducted preliminary analyses on available data in patients with type 1 diabetes. Because no association was found between HbA1c and BDI in patients with type 2 diabetes, a test of mediation was not performed in this group. Age, duration of illness, BMI, and gender were not associated with either BDI or HbA1c in patients with type 1 diabetes (as determined by Pearson correlations and t tests for gender, which were all nonsignificant) and cannot mediate the relationship between these two. Self-reported SMBG frequency, on the other hand, correlated with both BDI (r = -0.32, p < .09) and HbA1c (r = -0.47, p < .01). To test the mediating role of SMBG frequency, a stepwise linear regression was conducted to predict HbA1c. At step 1, BDI (ß = 0.10, p < .05) entered the regression equation (adjusted R2 = 0.16; F(2/28) = 6.60, p < .05). When SMBG frequency (ß = -0.04, p < .05) was added to the model, it weakened, but did not eliminate, the effect of BDI on HbA1c (ß = 0.07, p = .07; adjusted R2 = 0.26; F(2/27) = 6.21, p < .01).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results of the present study confirm and extend previous reports by showing that depressed mood as measured by the BDI is significantly related to HbA1c in type 1 but not in type 2 diabetes. In patients with type 1 diabetes, depressed mood was associated with poorer glycemic control. In the present study, we excluded any patient who might be taking psychoactive medications, which left a sample in which BDI scores were mainly within the normal range. The observed relationship between depressive symptoms and glycemic control is linear throughout the complete range of observed BDI scores and is not restricted to scores associated with clinical depression. A similar linear relationship between a measure of mood and glycemic control was observed in type 1 diabetes by Mazze et al. (9). They found that changes in Zung depression scores were associated with changes in HbA1c scores over a 36-week time period, even though the mean Zung score was clearly within the normal range. However, the Mazze study was restricted to a type 1 patient population and, the relationship of mood to glycemic control was not evaluated in patients with type 2 diabetes. Thus, our study, in combination with that of Mazze et al., indicates that mood, and not clinical depression per se, is associated with meaningful differences in glycemic control in type 1 diabetes.

Although it is well known that depression is more common in women than in men, it is unlikely that our finding was due to confounding effects of gender. In this sample of patients with type 1 diabetes, men and women did not differ in terms of either HbA1c (8.7% men vs. 8.0% women, p > .15) or BDI values (8.1 men vs. 7.1 women, p > .65).

Depressed mood could affect glycemic control through at least two plausible mechanisms, either through changes in self-care or through counterregulatory hormones. There is evidence to indicate that clinical depression may adversely affect at least some facets of diabetes self-care behavior (13, 17, 39), but it is not clear whether this phenomenon would generalize to a nonclinical population. In addition, it has been documented that counterregulatory hormones are increased in depression, (40, 41), but it is also unclear whether such changes would occur in patients with moderate changes in mood.

Although it was not the focus of the present study to test any possible mechanisms by which mood and glycemic control are related, we observed that one component of self-care, reported frequency of SMBG, contributed to the relationship of BDI to HbA1c in patients with type 1 diabetes. These analyses do not prove the existence of a cause-and-effect relationship, and one must be careful not to overgeneralize from these self-report data. If observations made in a depressed population can be generalized to a nonclinical population, depressed mood could reduce appropriate self-care behaviors, which would negatively impact glycemic control, particularly in type 1 diabetes. However, data from the current study are not sufficient to confirm or reject this hypothesis.

Although it is plausible that mood affects glycemic control through various mechanisms, the alternative hypothesis that poor glycemic control leads to more depressive symptoms deserves consideration. Patients with type 1 diabetes have no residual insulin, so maintaining good blood glucose control is much more difficult for them than it is for patients with type 2 diabetes. Patients with type 1 diabetes may therefore be prone to experience "learned helplessness" if attempts to control their disease are unsuccessful. This, in turn, could lead to depressed mood (42–44). Similar effects have been observed in patients with epilepsy, another condition in which the patient is likely to perceive a lack of control over disease-related events (45). Again, more data would be needed to determine whether "learned helplessness" can account for our observed findings. The final understanding of the relationships between depressed mood and diabetes control may require the integration of more than one mechanism.

The strength of the observed relationship between depressed mood and chronic glycemic control in patients with type 1 diabetes suggests that this phenomenon is of clinical relevance. In our type 1 sample, BDI scores account for 16% of the variance in HbA1c. The regression equation suggests that a difference in mood equal to about 10 points on the BDI is associated with a change in HbA1c of approximately 1%, which would be considered clinically meaningful (46). There are several reports that the treatment of depression improves glycemic control in diabetes (eg, 33,47,48). Our data suggest that the treatment of mild depression, or even depressed mood, may be helpful in the management of type 1 diabetes.

Received for publication February 14, 2000.


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 INTRODUCTION
 METHODS
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 DISCUSSION
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