A total of 30 studies were identified that measured the association of depression with glycemic control.
Of these studies, 28 provided information sufficient to calculate the study r; the remaining 2 did not.
These 2 studies contributed only to the calculation of the overall P. Meta-analysis revealed a significant association of depression with hyperglycemia (Z = 5.3, P 0.0001) and a small-to-moderate standardized ES (0.16; 95% CI 0.13–0.20).
However,the residual standard deviation test of interstudy variance was statistically significant,indicating heterogeneity of variance in this aggregation of studies.
This finding was not surprising given that studies with distinctly different designs and methods were included.
Consequently, the studies were divided into cross-sectional (n = 26) and RCT (n = 5) subsets. The RCT subset was heterogeneous by all 3 tests of interstudy ES variance, and these studies were therefore not subjected to meta-analysis.
The tests uniformly indicated that the cross-sectional subset was homogeneous.
The characteristics of these 26 studies are described in Table 1. Weighted and unweighted ESs,BESDs, fail-safe N’s, and tests of ES variance are reported in Table 2 for all and for subsets of the cross-sectional studies.
Meta-analysis of the cross-sectional studies Of the 26 cross-sectional studies, 10 (38.5%) examined the association of depression with GHb in patients with type 1 diabetes, 6 (23.1%) involved only patients with type 2 diabetes, and 10 (38.5%) included a mixed sample of patients with type 1 or type 2 diabetes.
Of the 26 studies,20 (76.9%) used self-report questionnaires to assess depression, 5 (19.2%) used a structured diagnostic interview, and 1 (3.8%) used both methods.
The mean sample size in the studies of type 1 patients was smaller but not statistically different from that in the studies of type 2 patients (93 vs.144, P0.2), and neither of these were statistically different from the mean sample size (119) of the studies of subjects with either type 1 or type 2 diabetes.
In these mixed-sample studies, roughly equal proportions of the subjects had type 1 versus type 2 diabetes (50.4 vs. 49.6%).
Twenty-four (92.3%) of the 26 crosssectional studies provided enough information to calculate the individual ES.
These 24 studies had a total of 2,817 subjects.
The combined effect showed that depression was significantly associated with hyperglycemia (Z = 5.4, P 0.0001).
The standardized ES was small to moderate (0.17) and statistically significant (95% CI 0.13–0.21). ESs for the overall group and for homogeneous subsets are displayed in Fig. 1. The ES was similar in studies of type 1 compared with type 2 diabetes (ES: 0.19 vs. 0.16) and greater in studies that used interview-based diagnoses rather than selfreport measures of symptom severity to assess depression (ES 0.28 vs. 0.15).
RCTs
Five studies were identified that measured the covariation over time of depression and glycemic control (33–37) with experimental perturbation of 1 of the variables.
Although these studies did not meet the meta-analytic requirement of homogeneity,they provided additional data reflecting on the character of the depression–hyperglycemia association.
The findings of the 5 studies are summarized in Table 3. Three of the RCTs were studies of psychological (cognitive behavior therapy) or psychopharmacological (nortriptyline, fluoxetine) treatments for depression in adults with diabetes (33–35). In all 3 of these trials, the active treatment was significantly more effective than the control treatment in relieving depression.
Treatment-related improvements in glycemic control were noted in 2 of the studies (33,35), and 2 of 3 studies reported that reduction in depression severity was directly associated with significant reductions in GHb (33,34).
The other 2 RCTs assessed the comparative efficacy of 2 diabetes interventions.
In both trials, glycemic control was the primary dependent variable, and depression was a secondary (28) or ancillary (38) outcome measure.
The first trial found no differences in GHb level between treatments (28).
However, pre- to posttreatment changes in GHb and depression severity were correlated (r = 0.46, P = 0.001), showing that as metabolic control improved, so did depression, or vice versa.
In the second study (38), participants were randomized to diet titration with either glipizide or placebo for 12 weeks.
Glipizide-treated patients had significantly better glycemic control and less depression compared with placebo-treated patients (P 0.05).
จำนวน 30 การศึกษาได้ระบุที่วัดความสัมพันธ์ของภาวะซึมเศร้ามี glycemic ควบคุม ของการศึกษาเหล่านี้ 28 ให้ข้อมูลเพียงพอที่จะคำนวณการศึกษา r 2 ที่เหลือไม่ เหล่านี้ส่วนเฉพาะการคำนวณของการรวม P. Meta-analysis การศึกษา 2 เปิดเผยความสัมพันธ์ที่สำคัญของภาวะซึมเศร้ากับ hyperglycemia (Z = 5.3, P มาก 0.0001) และเล็กให้ปานกลางมาตรฐาน ES (0.16; 95% CI 0.13-0.20) อย่างไรก็ตาม การทดสอบเหลือส่วนเบี่ยงเบนมาตรฐานของผลต่าง interstudy ถูกทางสถิติอย่างมีนัยสำคัญ ระบุ heterogeneity ของความผันแปรนี้รวมการศึกษา ค้นหานี้ไม่น่าแปลกใจที่ศึกษากับการออกแบบที่แตกต่างกันอย่างเห็นได้ชัดและวิธีได้รวม ดังนั้น การศึกษาได้แบ่งออกเป็นเหลว (n = 26) และ RCT (n = 5) ชุดย่อย ชุดย่อย RCT แตกต่างกัน โดยการทดสอบ 3 ทั้งหมดของ interstudy ES ต่าง และการศึกษาเหล่านี้ได้ดังนั้นไม่ต้อง meta-analysis การทดสอบสม่ำเสมอเมื่อเทียบเคียงระบุว่า ย่อยเหลวเป็นเนื้อเดียวกัน ลักษณะของการศึกษาเหล่านี้ 26 ไว้ในตารางที่ 1 ถ่วงน้ำหนัก และ unweighted ESs, BESDs, fail-safe N และการทดสอบผลต่างของ ES มีรายงานในตารางที่ 2 ทั้งหมด และ สำหรับชุดย่อยของศึกษาเหลวMeta-analysis of the cross-sectional studies Of the 26 cross-sectional studies, 10 (38.5%) examined the association of depression with GHb in patients with type 1 diabetes, 6 (23.1%) involved only patients with type 2 diabetes, and 10 (38.5%) included a mixed sample of patients with type 1 or type 2 diabetes. Of the 26 studies,20 (76.9%) used self-report questionnaires to assess depression, 5 (19.2%) used a structured diagnostic interview, and 1 (3.8%) used both methods. The mean sample size in the studies of type 1 patients was smaller but not statistically different from that in the studies of type 2 patients (93 vs.144, P0.2), and neither of these were statistically different from the mean sample size (119) of the studies of subjects with either type 1 or type 2 diabetes. In these mixed-sample studies, roughly equal proportions of the subjects had type 1 versus type 2 diabetes (50.4 vs. 49.6%).Twenty-four (92.3%) of the 26 crosssectional studies provided enough information to calculate the individual ES.These 24 studies had a total of 2,817 subjects.The combined effect showed that depression was significantly associated with hyperglycemia (Z = 5.4, P 0.0001). The standardized ES was small to moderate (0.17) and statistically significant (95% CI 0.13–0.21). ESs for the overall group and for homogeneous subsets are displayed in Fig. 1. The ES was similar in studies of type 1 compared with type 2 diabetes (ES: 0.19 vs. 0.16) and greater in studies that used interview-based diagnoses rather than selfreport measures of symptom severity to assess depression (ES 0.28 vs. 0.15).RCTsFive studies were identified that measured the covariation over time of depression and glycemic control (33–37) with experimental perturbation of 1 of the variables.Although these studies did not meet the meta-analytic requirement of homogeneity,they provided additional data reflecting on the character of the depression–hyperglycemia association. The findings of the 5 studies are summarized in Table 3. Three of the RCTs were studies of psychological (cognitive behavior therapy) or psychopharmacological (nortriptyline, fluoxetine) treatments for depression in adults with diabetes (33–35). In all 3 of these trials, the active treatment was significantly more effective than the control treatment in relieving depression. Treatment-related improvements in glycemic control were noted in 2 of the studies (33,35), and 2 of 3 studies reported that reduction in depression severity was directly associated with significant reductions in GHb (33,34).The other 2 RCTs assessed the comparative efficacy of 2 diabetes interventions. In both trials, glycemic control was the primary dependent variable, and depression was a secondary (28) or ancillary (38) outcome measure. The first trial found no differences in GHb level between treatments (28). However, pre- to posttreatment changes in GHb and depression severity were correlated (r = 0.46, P = 0.001), showing that as metabolic control improved, so did depression, or vice versa. In the second study (38), participants were randomized to diet titration with either glipizide or placebo for 12 weeks. Glipizide-treated patients had significantly better glycemic control and less depression compared with placebo-treated patients (P 0.05).
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