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Longitudinal study of depressive symptoms and progression of insulin resistance in youth at risk for adult obesity.

Shomaker LB, Tanofsky-Kraff M, Stern EA, Miller R, Zocca JM, Field SE, Yanovski SZ, Hubbard VS, Yanovski JA - Diabetes Care (2011)

Bottom Line: RESEARCH DESIGN AND METHODS A non-treatment-seeking sample of 115 children (aged 5-13 years), oversampled for being at risk for adult obesity, was assessed at baseline and again ~6 years later.CONCLUSIONS In this study, depressive symptomatology at baseline predicted the progression of insulin resistance during child and adolescent development independent of changes in BMI.Research is needed to determine whether early intervention to decrease elevated depressive symptoms in youth ameliorates later development of insulin resistance and lessens the risk of type 2 diabetes.

View Article: PubMed Central - PubMed

Affiliation: Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.

ABSTRACT
OBJECTIVE The purpose of this study was to determine whether having childhood depressive symptoms is a risk factor that prospectively predicts impairment in glucose homeostasis. RESEARCH DESIGN AND METHODS A non-treatment-seeking sample of 115 children (aged 5-13 years), oversampled for being at risk for adult obesity, was assessed at baseline and again ~6 years later. Children self-reported depressive symptoms using the Children's Depression Inventory at baseline. Insulin resistance was assessed at baseline and follow-up with the homeostasis model assessment of insulin resistance index (HOMA-IR). RESULTS Children's depressive symptoms were a significant predictor of follow-up HOMA-IR, fasting insulin, and fasting glucose in models accounting for baseline HOMA-IR, insulin, or glucose values; sex; race; baseline age; baseline BMI; change in BMI at follow-up; family history of type 2 diabetes; and time in the study (P < 0.01). CONCLUSIONS In this study, depressive symptomatology at baseline predicted the progression of insulin resistance during child and adolescent development independent of changes in BMI. Research is needed to determine whether early intervention to decrease elevated depressive symptoms in youth ameliorates later development of insulin resistance and lessens the risk of type 2 diabetes.

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Compared with children with lower depressive symptoms at baseline (n = 97; CDI total score <13), youth with elevated depressive symptoms at baseline (n = 18; CDI total score ≥13) had greater follow-up: insulin resistance (HOMA-IR: [means ± SE] 2.8 ± 0.2 vs. 4.3 ± 0.4, P < 0.001) (A), fasting insulin (13.2 ± 0.8 µU/L vs. 19.4 ± 1.7 µU/L, P = 0.001) (B), and fasting glucose (85.3 ± 0.8 mg/dL vs. 92.9 ± 1.7 mg/dL, P < 0.001) (C), adjusting for the respective baseline values, sex, race, family history of type 2 diabetes, baseline age, baseline BMI, BMI change, and time in study.
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Figure 1: Compared with children with lower depressive symptoms at baseline (n = 97; CDI total score <13), youth with elevated depressive symptoms at baseline (n = 18; CDI total score ≥13) had greater follow-up: insulin resistance (HOMA-IR: [means ± SE] 2.8 ± 0.2 vs. 4.3 ± 0.4, P < 0.001) (A), fasting insulin (13.2 ± 0.8 µU/L vs. 19.4 ± 1.7 µU/L, P = 0.001) (B), and fasting glucose (85.3 ± 0.8 mg/dL vs. 92.9 ± 1.7 mg/dL, P < 0.001) (C), adjusting for the respective baseline values, sex, race, family history of type 2 diabetes, baseline age, baseline BMI, BMI change, and time in study.

Mentions: Table 2 summarizes the analyses examining baseline depressive symptoms as a predictor of follow-up insulin resistance, fasting insulin, and fasting glucose. Controlling for all other variables in the models, children’s baseline depressive symptoms predicted greater insulin resistance and higher fasting insulin and glucose at follow-up (P < 0.01). Baseline depressive symptoms explained 8% of the variance in follow-up insulin resistance (P < 0.001), 7% of the variance in follow-up fasting insulin (P < 0.001), and 4% of the variance in follow-up fasting glucose (P = 0.019), after accounting for the other variables in the model. An identical pattern of results was observed when depressive symptoms were considered categorically. Youth with elevated depressive symptoms at baseline (n = 17) had higher insulin resistance, fasting insulin, and fasting glucose at follow-up than youth with lower depressive symptoms at baseline (P ≤ 0.001) (Fig. 1). As an exploratory analysis, we also tested whether baseline insulin resistance predicted follow-up depressive symptoms, accounting for baseline depressive symptoms and a parallel set of covariates. Insulin resistance was not a significant predictor of follow-up depressive symptoms (P = 0.99).


Longitudinal study of depressive symptoms and progression of insulin resistance in youth at risk for adult obesity.

Shomaker LB, Tanofsky-Kraff M, Stern EA, Miller R, Zocca JM, Field SE, Yanovski SZ, Hubbard VS, Yanovski JA - Diabetes Care (2011)

Compared with children with lower depressive symptoms at baseline (n = 97; CDI total score <13), youth with elevated depressive symptoms at baseline (n = 18; CDI total score ≥13) had greater follow-up: insulin resistance (HOMA-IR: [means ± SE] 2.8 ± 0.2 vs. 4.3 ± 0.4, P < 0.001) (A), fasting insulin (13.2 ± 0.8 µU/L vs. 19.4 ± 1.7 µU/L, P = 0.001) (B), and fasting glucose (85.3 ± 0.8 mg/dL vs. 92.9 ± 1.7 mg/dL, P < 0.001) (C), adjusting for the respective baseline values, sex, race, family history of type 2 diabetes, baseline age, baseline BMI, BMI change, and time in study.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3198302&req=5

Figure 1: Compared with children with lower depressive symptoms at baseline (n = 97; CDI total score <13), youth with elevated depressive symptoms at baseline (n = 18; CDI total score ≥13) had greater follow-up: insulin resistance (HOMA-IR: [means ± SE] 2.8 ± 0.2 vs. 4.3 ± 0.4, P < 0.001) (A), fasting insulin (13.2 ± 0.8 µU/L vs. 19.4 ± 1.7 µU/L, P = 0.001) (B), and fasting glucose (85.3 ± 0.8 mg/dL vs. 92.9 ± 1.7 mg/dL, P < 0.001) (C), adjusting for the respective baseline values, sex, race, family history of type 2 diabetes, baseline age, baseline BMI, BMI change, and time in study.
Mentions: Table 2 summarizes the analyses examining baseline depressive symptoms as a predictor of follow-up insulin resistance, fasting insulin, and fasting glucose. Controlling for all other variables in the models, children’s baseline depressive symptoms predicted greater insulin resistance and higher fasting insulin and glucose at follow-up (P < 0.01). Baseline depressive symptoms explained 8% of the variance in follow-up insulin resistance (P < 0.001), 7% of the variance in follow-up fasting insulin (P < 0.001), and 4% of the variance in follow-up fasting glucose (P = 0.019), after accounting for the other variables in the model. An identical pattern of results was observed when depressive symptoms were considered categorically. Youth with elevated depressive symptoms at baseline (n = 17) had higher insulin resistance, fasting insulin, and fasting glucose at follow-up than youth with lower depressive symptoms at baseline (P ≤ 0.001) (Fig. 1). As an exploratory analysis, we also tested whether baseline insulin resistance predicted follow-up depressive symptoms, accounting for baseline depressive symptoms and a parallel set of covariates. Insulin resistance was not a significant predictor of follow-up depressive symptoms (P = 0.99).

Bottom Line: RESEARCH DESIGN AND METHODS A non-treatment-seeking sample of 115 children (aged 5-13 years), oversampled for being at risk for adult obesity, was assessed at baseline and again ~6 years later.CONCLUSIONS In this study, depressive symptomatology at baseline predicted the progression of insulin resistance during child and adolescent development independent of changes in BMI.Research is needed to determine whether early intervention to decrease elevated depressive symptoms in youth ameliorates later development of insulin resistance and lessens the risk of type 2 diabetes.

View Article: PubMed Central - PubMed

Affiliation: Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.

ABSTRACT
OBJECTIVE The purpose of this study was to determine whether having childhood depressive symptoms is a risk factor that prospectively predicts impairment in glucose homeostasis. RESEARCH DESIGN AND METHODS A non-treatment-seeking sample of 115 children (aged 5-13 years), oversampled for being at risk for adult obesity, was assessed at baseline and again ~6 years later. Children self-reported depressive symptoms using the Children's Depression Inventory at baseline. Insulin resistance was assessed at baseline and follow-up with the homeostasis model assessment of insulin resistance index (HOMA-IR). RESULTS Children's depressive symptoms were a significant predictor of follow-up HOMA-IR, fasting insulin, and fasting glucose in models accounting for baseline HOMA-IR, insulin, or glucose values; sex; race; baseline age; baseline BMI; change in BMI at follow-up; family history of type 2 diabetes; and time in the study (P < 0.01). CONCLUSIONS In this study, depressive symptomatology at baseline predicted the progression of insulin resistance during child and adolescent development independent of changes in BMI. Research is needed to determine whether early intervention to decrease elevated depressive symptoms in youth ameliorates later development of insulin resistance and lessens the risk of type 2 diabetes.

Show MeSH
Related in: MedlinePlus