Diagnosis and body mass index effects on hippocampal volumes and neurochemistry in bipolar disorder

D. J. Bond, L. E. Silveira, E. L. MacMillan, I. J. Torres, D. J. Lang, W. Su, W. G. Honer, R. W. Lam, L. N. Yatham

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

We previously reported that higher body mass index (BMI) was associated with greater hippocampal glutamate+glutamine in people with bipolar disorder (BD), but not in non-BD healthy comparator subjects (HSs). In the current report, we extend these findings by examining the impact of BD diagnosis and BMI on hippocampal volumes and the concentrations of several additional neurochemicals in 57 early-stage BD patients and 31 HSs. Using 3-T magnetic resonance imaging and magnetic resonance spectroscopy, we measured bilateral hippocampal volumes and the hippocampal concentrations of four neurochemicals relevant to BD: N-acetylaspartate+N-acteylaspartylglutamate (tNAA), creatine+phosphocreatine (Cre), myoinositol (Ins) and glycerophosphocholine+phosphatidylcholine (Cho). We used multivariate factorial analysis of covariance to investigate the impact of diagnosis (patient vs HS) and BMI category (normal weight vs overweight/obese) on these variables. We found a main effect of diagnosis on hippocampal volumes, with patients having smaller hippocampi than HSs. There was no association between BMI and hippocampal volumes. We found diagnosis and BMI effects on hippocampal neurochemistry, with patients having lower Cre, Ins and Cho, and overweight/obese subjects having higher levels of these chemicals. In patient-only models that controlled for clinical and treatment variables, we detected an additional association between higher BMI and lower tNAA that was absent in HSs. To our knowledge, this was the first study to investigate the relative contributions of BD diagnosis and BMI to hippocampal volumes, and only the second to investigate their contributions to hippocampal chemistry. It provides further evidence that diagnosis and elevated BMI both impact limbic brain areas relevant to BD.

Original languageEnglish (US)
Article numbere1071
JournalTranslational psychiatry
Volume7
Issue number3
DOIs
StatePublished - 2017

Bibliographical note

Funding Information:
Dr Bond has received speaking/consulting fees or research grants from AstraZeneca, Bristol Myers Squibb, the Canadian Institutes of Health Research (CIHR), the Canadian Network for Mood and Anxiety Treatments (CANMAT), the Canadian Psychiatric Association (CPA), Janssen-Ortho, Myriad Genetics, Otsuka, Pfizer, Sunovion and the University of British Columbia (UBC) Institute of Mental Health/Coast Capital Depression Research Fund. Dr Torres has received speaking/consulting fees or research grants from CIHR, Lundbeck Canada and Sumitomo Dainippon. Dr Honer has been on advisory boards for In Silico, Otsuka/Lundbeck, Roche and Eli Lily. He was additionally supported by the UBC Jack Bell Chair in Schizophrenia. Dr Lam has been on speaker/advisory boards for, or has received research support from AstraZeneca, Bristol Myers Squibb, CANMAT, CPA, CPA Foundation, CIHR, Eli Lilly, Litebook Company, Lundbeck, Lundbeck Institute, Merck, Mochida, Pfizer, Servier, St Jude Medical, UBC Institute of Mental Health/Coast Capital Depression Research Fund, Takeda and Wyeth. Dr Yatham has been on speaker/advisory boards for, or has received research support from AstraZeneca, Bristol Myers Squibb, CANMAT, CIHR, Eli Lilly, GlaxoSmithKline, Janssen, the Michael Smith Foundation for Health Research, Pfizer, Servier and the Stanley Foundation. The remaining authors declare no conflict of interest.

Funding Information:
The data for this manuscript were generated from the Systematic Treatment Optimization Program for Early Mania, which was supported by an unrestricted to LNY from AstraZeneca Canada.

Publisher Copyright:
© 2017 The Author(s).

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