TY - JOUR
T1 - Seasonal affective disorder and seasonal changes in weight and sleep duration are inversely associated with plasma adiponectin levels
AU - Akram, Faisal
AU - Gragnoli, Claudia
AU - Raheja, Uttam K.
AU - Snitker, Soren
AU - Lowry, Christopher A.
AU - Stearns-Yoder, Kelly A.
AU - Hoisington, Andrew J.
AU - Brenner, Lisa A.
AU - Saunders, Erika
AU - Stiller, John W.
AU - Ryan, Kathleen A.
AU - Rohan, Kelly J.
AU - Mitchell, Braxton D.
AU - Postolache, Teodor T.
N1 - Funding Information:
The authors would like to thank the participants and the Amish community for supporting the study, and the staff and Amish liaisons at the Amish Research Clinic in Lancaster, PA, USA for their exceptional contribution to this project. We acknowledge Sonia Y. Postolache for contributions in data collection and management, and proofreading the manuscript. The study was funded by the National Institute of Mental Health of the National Institutes of Health via the K18MH093940 (PI Postolache), and in part by The Mid-Atlantic Nutrition Obesity Research Center (NORC) developmental sub-project (PI Postolache, co-PI Snitker), supported by grant P30 DK072488 from the NIH National Institute of Diabetes and Digestive and Kidney Diseases (PI Mitchell). Claudia Gragnoli and Teodor Postolache are supported by NICHD 5R01HD086911-02 (PI Gragnoli). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, US Air Force, Department of Defense, or the US Department of Veterans Affairs.
Funding Information:
The authors would like to thank the participants and the Amish community for supporting the study, and the staff and Amish liaisons at the Amish Research Clinic in Lancaster, PA, USA for their exceptional contribution to this project. We acknowledge Sonia Y. Postolache for contributions in data collection and management, and proofreading the manuscript. The study was funded by the National Institute of Mental Health of the National Institutes of Health via the K18MH093940 (PI Postolache), and in part by The Mid-Atlantic Nutrition Obesity Research Center (NORC) developmental sub-project (PI Postolache, co-PI Snitker), supported by grant P30 DK072488 from the NIH National Institute of Diabetes and Digestive and Kidney Diseases (PI Mitchell). Claudia Gragnoli and Teodor Postolache are supported by NICHD 5R01HD086911-02 (PI Gragnoli). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, US Air Force, Department of Defense, or the US Department of Veterans Affairs.
Publisher Copyright:
© 2020
PY - 2020/3
Y1 - 2020/3
N2 - Overlapping pathways between mood and metabolic regulation have increasingly been reported. Although impaired regulation of adiponectin, a major metabolism-regulating hormone, has been implicated in major depressive disorder, its role in seasonal changes in mood and seasonal affective disorder-winter type (SAD), a disorder characterized by onset of mood impairment and metabolic dysregulation (e.g., carbohydrate craving and weight gain) in fall/winter and spontaneous alleviation in spring/summer, has not been previously studied. We studied a convenience sample of 636 Old Order Amish (mean (± SD), 53.6 (±14.8) years; 50.1% males), a population with self-imposed restriction on network electric light at home, and low prevalence of total SAD (t-SAD = syndromal + subsyndromal). We calculated the global seasonality score (GSS), estimated SAD and subsyndromal-SAD after obtaining Seasonal Pattern Assessment Questionnaires (SPAQs), and measured overnight fasting plasma adiponectin levels. We then tested associations between plasma adiponectin levels and GSS, t-SAD, winter-summer difference in self-reported sleep duration, and self-reported seasonal weight change, by using analysis of co-variance (ANCOVA) and linear regression analysis after adjusting for age, gender, and BMI. Participants with t-SAD (N = 14; 2.2%) had significantly lower plasma adiponectin levels (mean ± SEM, 8.76 ± 1.56 μg/mL) than those without t-SAD (mean ± SEM, 11.93 ± 0.22 μg/mL) (p = 0.035). In addition, there was significant negative association between adiponectin levels and winter-summer difference in self-reported sleep duration (p = 0.025) and between adiponectin levels and self-reported seasonal change in weight (p = 0.006). There was no significant association between GSS and adiponectin levels (p = 0.88). To our knowledge, this is the first study testing the association of SAD with adiponectin levels. Replication and extension of our findings longitudinally and, then, interventionally, may implicate low adiponectin as a novel target for therapeutic intervention in SAD.
AB - Overlapping pathways between mood and metabolic regulation have increasingly been reported. Although impaired regulation of adiponectin, a major metabolism-regulating hormone, has been implicated in major depressive disorder, its role in seasonal changes in mood and seasonal affective disorder-winter type (SAD), a disorder characterized by onset of mood impairment and metabolic dysregulation (e.g., carbohydrate craving and weight gain) in fall/winter and spontaneous alleviation in spring/summer, has not been previously studied. We studied a convenience sample of 636 Old Order Amish (mean (± SD), 53.6 (±14.8) years; 50.1% males), a population with self-imposed restriction on network electric light at home, and low prevalence of total SAD (t-SAD = syndromal + subsyndromal). We calculated the global seasonality score (GSS), estimated SAD and subsyndromal-SAD after obtaining Seasonal Pattern Assessment Questionnaires (SPAQs), and measured overnight fasting plasma adiponectin levels. We then tested associations between plasma adiponectin levels and GSS, t-SAD, winter-summer difference in self-reported sleep duration, and self-reported seasonal weight change, by using analysis of co-variance (ANCOVA) and linear regression analysis after adjusting for age, gender, and BMI. Participants with t-SAD (N = 14; 2.2%) had significantly lower plasma adiponectin levels (mean ± SEM, 8.76 ± 1.56 μg/mL) than those without t-SAD (mean ± SEM, 11.93 ± 0.22 μg/mL) (p = 0.035). In addition, there was significant negative association between adiponectin levels and winter-summer difference in self-reported sleep duration (p = 0.025) and between adiponectin levels and self-reported seasonal change in weight (p = 0.006). There was no significant association between GSS and adiponectin levels (p = 0.88). To our knowledge, this is the first study testing the association of SAD with adiponectin levels. Replication and extension of our findings longitudinally and, then, interventionally, may implicate low adiponectin as a novel target for therapeutic intervention in SAD.
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UR - http://www.scopus.com/inward/citedby.url?scp=85078505641&partnerID=8YFLogxK
U2 - 10.1016/j.jpsychires.2019.12.016
DO - 10.1016/j.jpsychires.2019.12.016
M3 - Article
C2 - 31981963
AN - SCOPUS:85078505641
SN - 0022-3956
VL - 122
SP - 97
EP - 104
JO - Journal of Psychiatric Research
JF - Journal of Psychiatric Research
ER -
