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Bidirectional causal associations between plasma metabolites and bipolar disorder

Abstract

Altered levels of human plasma metabolites have been implicated in the etiology of bipolar disorder (BD). However, the causality between metabolites and the disease was not well described. We performed a bidirectional metabolome-wide Mendelian randomization (MR) analysis to evaluate the potential causal relationships between 871 plasma metabolites and BD. We used DrugBank and ChEMBL to evaluate whether related metabolites are potential therapeutic targets. Finally, Bayesian colocalization analysis was performed to identify shared genomic loci BD and identified metabolites. Our MR results showed that six metabolites were significantly associated with a reduced risk of BD, including arachidonate (20:4n6) (OR: 0.90, 95% CI: 0.84–0.95) and sphingomyelin (d18:2/24:1, d18:1/24:2) (OR: 0.92, 95% CI: 0.87–0.96), while five metabolites were significantly associated with an increased risk of BD, including 1-palmitoyl-2-linoleoyl-GPE (16:0/18:2) (OR: 1.09, 95% CI: 1.05–1.13). However, our reverse MR analysis showed that BD was not associated with the levels of any metabolite. Additionally, the leave-one-out analysis revealed SNPs within chromosome 11 loci harboring MYRF, FADS1, and FADS2 as ones with the potential to influence partial causal effects. Druggability evaluation showed that 10 of the BD-related metabolites, such as sphingomyelin and cytidine, have been targeted by pharmacologic intervention. Colocalization analysis highlighted one colocalized region (chromosome 11q12) shared by 11 metabolites and BD and pointed to some genes as possible players, including FADS1, FADS2, FADS3, and SYT7. Our study supported a causal role of plasma metabolites in the susceptibility to BD, and the identified metabolites may provide a new avenue for the prevention and treatment of BD.

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Fig. 1: Flowchart of the study.

Fig. 2: Forest plot of causal effects of plasma metabolites on BD (FDR < 0.05).

Fig. 3: Forest plot of causal effects of BD on plasma metabolites (P < 0.05).

Fig. 4: Druggability of plasma metabolites with a causal effect on BD.

Fig. 5: One colocalized region between metabolites and BD.

Data availability

All data generated or analyzed during this study are included in this published article and its supplementary information files.

References

Vieta E, Berk M, Schulze TG, Carvalho AF, Suppes T, Calabrese JR, et al. Bipolar disorders. Nat Rev Dis Primers. 2018;4:18008.

PubMedGoogle Scholar

Merikangas KR, Jin R, He JP, Kessler RC, Lee S, Sampson NA, et al. Prevalence and correlates of bipolar spectrum disorder in the world mental health survey initiative. Arch Gen Psychiatry. 2011;68:241–51.

PubMedPubMed CentralGoogle Scholar

Plans L, Barrot C, Nieto E, Rios J, Schulze TG, Papiol S, et al. Association between completed suicide and bipolar disorder: A systematic review of the literature. J Affect Disord. 2019;242:111–22.

CASPubMedGoogle Scholar

Vigo D, Thornicroft G, Atun R. Estimating the true global burden of mental illness. Lancet Psychiatry. 2016;3:171–8.

PubMedGoogle Scholar

Smoller JW, Finn CT. Family, twin, and adoption studies of bipolar disorder. Am J Med Genet Part C, Semin Med Genet. 2003;123c:48–58.

PubMedGoogle Scholar

Baker SA, Rutter J. Metabolites as signalling molecules. Nat Rev Mol Cell Biol. 2023;24:355–74.

CASPubMedGoogle Scholar

Shin SY, Fauman EB, Petersen AK, Krumsiek J, Santos R, Huang J, et al. An atlas of genetic influences on human blood metabolites. Nat Genet. 2014;46:543–50.

CASPubMedPubMed CentralGoogle Scholar

Chen Y, Lu T, Pettersson-Kymmer U, Stewart ID, Butler-Laporte G, Nakanishi T, et al. Genomic atlas of the plasma metabolome prioritizes metabolites implicated in human diseases. Nat Genet. 2023;55:44–53.

PubMedPubMed CentralGoogle Scholar

Wishart DS. Metabolomics for investigating physiological and pathophysiological processes. Physiol Rev. 2019;99:1819–75.

CASPubMedGoogle Scholar

Bartel J, Krumsiek J, Schramm K, Adamski J, Gieger C, Herder C, et al. The human blood metabolome-transcriptome interface. PLoS Genet. 2015;11:e1005274.

PubMedPubMed CentralGoogle Scholar

Bartoli F, Cioni RM, Cavaleri D, Callovini T, Crocamo C, Misiak B, et al. The association of kynurenine pathway metabolites with symptom severity and clinical features of bipolar disorder: an overview. Eur Psychiatry. 2022;65:e82.

PubMedPubMed CentralGoogle Scholar

Ribeiro HC, Sen P, Dickens A, Santa Cruz EC, Orešič M, Sussulini A. Metabolomic and proteomic profiling in bipolar disorder patients revealed potential molecular signatures related to hemostasis. Metabolomics. 2022;18:65.

CASPubMedGoogle Scholar

Lan MJ, McLoughlin GA, Griffin JL, Tsang TM, Huang JT, Yuan P, et al. Metabonomic analysis identifies molecular changes associated with the pathophysiology and drug treatment of bipolar disorder. Mol Psychiatry. 2009;14:269–79.

CASPubMedGoogle Scholar

Kageyama Y, Kasahara T, Morishita H, Mataga N, Deguchi Y, Tani M, et al. Search for plasma biomarkers in drug-free patients with bipolar disorder and schizophrenia using metabolome analysis. Psychiatry Clin Neurosci. 2017;71:115–23.

CASPubMedGoogle Scholar

Lawlor DA, Harbord RM, Sterne JA, Timpson N, Davey Smith G. Mendelian randomization: using genes as instruments for making causal inferences in epidemiology. Stat Med. 2008;27:1133–63.

PubMedGoogle Scholar

Chen F, Cao H, Baranova A, Zhao Q, Zhang F. Causal associations between COVID-19 and childhood mental disorders. BMC Psychiatry. 2023;23:922.

CASPubMedPubMed CentralGoogle Scholar

Baranova A, Chandhoke V, Cao H, Zhang F. Shared genetics and bidirectional causal relationships between type 2 diabetes and attention-deficit/hyperactivity disorder. Gen Psychiatry. 2023;36:e100996.

CASGoogle Scholar

Baranova A, Zhao Q, Cao H, Chandhoke V, Zhang F. Causal influences of neuropsychiatric disorders on Alzheimer’s disease. Transl Psychiatry. 2024;14:114.

PubMedPubMed CentralGoogle Scholar

Zhang L, Yang F, Ma J, Hu Y, Li M, Wang C, et al. The impact of testosterone on Alzheimer’s disease are mediated by lipid metabolism and obesity: a mendelian randomization study. J Prev Alzheimer’s Dis. 2024;11:507–13.

CASGoogle Scholar

Hemani G, Zheng J, Elsworth B, Wade KH, Haberland V, Baird D, et al. The MR-Base platform supports systematic causal inference across the human phenome. Elife. 2018;7:e34408.

PubMedPubMed CentralGoogle Scholar

Giambartolomei C, Vukcevic D, Schadt EE, Franke L, Hingorani AD, Wallace C, et al. Bayesian test for colocalisation between pairs of genetic association studies using summary statistics. PLoS Genet. 2014;10:e1004383.

PubMedPubMed CentralGoogle Scholar

Mullins N, Forstner AJ, O’Connell KS, Coombes B, Coleman JRI, Qiao Z, et al. Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology. Nat Genet. 2021;53:817–29.

CASPubMedPubMed CentralGoogle Scholar

Emdin CA, Khera AV, Kathiresan S. Mendelian Randomization. JAMA. 2017;318:1925–6.

PubMedGoogle Scholar

Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol. 2015;44:512–25.

PubMedPubMed CentralGoogle Scholar

Bowden J, Del Greco MF, Minelli C, Zhao Q, Lawlor DA, Sheehan NA, et al. Improving the accuracy of two-sample summary-data Mendelian randomization: moving beyond the NOME assumption. Int J Epidemiol. 2019;48:728–42.

PubMedGoogle Scholar

Burgess S, Thompson SG. Avoiding bias from weak instruments in Mendelian randomization studies. Int J Epidemiol. 2011;40:755–64.

PubMedGoogle Scholar

Wishart DS, Feunang YD, Guo AC, Lo EJ, Marcu A, Grant JR, et al. DrugBank 5.0: a major update to the DrugBank database for 2018. Nucleic Acids Res. 2018;46:D1074–d82.

CASPubMedGoogle Scholar

Mendez D, Gaulton A, Bento AP, Chambers J, De Veij M, Félix E, et al. ChEMBL: towards direct deposition of bioassay data. Nucleic Acids Res. 2019;47:D930–d40.

CASPubMedGoogle Scholar

Wallace C. Eliciting priors and relaxing the single causal variant assumption in colocalisation analyses. PLoS Genet. 2020;16:e1008720.

CASPubMedPubMed CentralGoogle Scholar

Wei J, Zhao L, Du Y, Tian Y, Ni P, Ni R, et al. A plasma metabolomics study suggests alteration of multiple metabolic pathways in patients with bipolar disorder. Psychiatry Res. 2021;299:113880.

CASPubMedGoogle Scholar

Kasahara T, Takata A, Kato TM, Kubota-Sakashita M, Sawada T, Kakita A, et al. Depression-like episodes in mice harboring mtDNA deletions in paraventricular thalamus. Mol Psychiatry. 2016;21:39–48.

CASPubMedGoogle Scholar

Gaebel W, Zielasek J. Schizophrenia in 2020: Trends in diagnosis and therapy. Psychiatry Clin Neurosci. 2015;69:661–73.

PubMedGoogle Scholar

Cho DH, Park JH, Joo Lee E, Jong Won K, Lee SH, Kim YH, et al. Valproic acid increases NO production via the SH-PTP1-CDK5-eNOS-Ser(116) signaling cascade in endothelial cells and mice. Free Radic Biol Med. 2014;76:96–106.

CASPubMedGoogle Scholar

Feinstein DL. Potentiation of astroglial nitric oxide synthase type-2 expression by lithium chloride. J Neurochem. 1998;71:883–6.

CASPubMedGoogle Scholar

Yokoyama S, Yasui-Furukori N, Nakagami T, Miyazaki K, Ishioka M, Tarakita N, et al. Association between the serum carnitine level and ammonia and valproic acid levels in patients with bipolar disorder. Therapeutic Drug Monit. 2020;42:766–70.

CASGoogle Scholar

Kadriu B, Farmer CA, Yuan P, Park LT, Deng ZD, Moaddel R, et al. The kynurenine pathway and bipolar disorder: intersection of the monoaminergic and glutamatergic systems and immune response. Mol Psychiatry. 2021;26:4085–95.

PubMedGoogle Scholar

Claes S, Myint AM, Domschke K, Del-Favero J, Entrich K, Engelborghs S, et al. The kynurenine pathway in major depression: haplotype analysis of three related functional candidate genes. Psychiatry Res. 2011;188:355–60.

CASPubMedGoogle Scholar

Lavebratt C, Olsson S, Backlund L, Frisén L, Sellgren C, Priebe L, et al. The KMO allele encoding Arg452 is associated with psychotic features in bipolar disorder type 1, and with increased CSF KYNA level and reduced KMO expression. Mol Psychiatry. 2014;19:334–41.

CASPubMedGoogle Scholar

Pramod AB, Foster J, Carvelli L, Henry LK. SLC6 transporters: structure, function, regulation, disease association and therapeutics. Mol Asp Med. 2013;34:197–219.

CASGoogle Scholar

Mazei-Robison MS, Couch RS, Shelton RC, Stein MA, Blakely RD. Sequence variation in the human dopamine transporter gene in children with attention deficit hyperactivity disorder. Neuropharmacology. 2005;49:724–36.

CASPubMedGoogle Scholar

Rapoport SI, Basselin M, Kim HW, Rao JS. Bipolar disorder and mechanisms of action of mood stabilizers. Brain Res Rev. 2009;61:185–209.

CASPubMedPubMed CentralGoogle Scholar

Rapoport SI. Lithium and the other mood stabilizers effective in bipolar disorder target the rat brain arachidonic acid cascade. ACS Chem Neurosci. 2014;5:459–67.

CASPubMedPubMed CentralGoogle Scholar

Cheon Y, Park JY, Modi HR, Kim HW, Lee HJ, Chang L, et al. Chronic olanzapine treatment decreases arachidonic acid turnover and prostaglandin E2 concentration in rat brain. J Neurochem. 2011;119:364–76.

CASPubMedPubMed CentralGoogle Scholar

Lee HJ, Ghelardoni S, Chang L, Bosetti F, Rapoport SI, Bazinet RP. Topiramate does not alter the kinetics of arachidonic or docosahexaenoic acid in brain phospholipids of the unanesthetized rat. Neurochem Res. 2005;30:677–83.

CASPubMedGoogle Scholar

Gracia-Garcia P, Rao V, Haughey NJ, Bandaru VV, Smith G, Rosenberg PB, et al. Elevated plasma ceramides in depression. J Neuropsychiatry Clin Neurosci. 2011;23:215–8.

CASPubMedPubMed CentralGoogle Scholar

Gulbins E, Palmada M, Reichel M, Lüth A, Böhmer C, Amato D, et al. Acid sphingomyelinase-ceramide system mediates effects of antidepressant drugs. Nat Med. 2013;19:934–8.

CASPubMedGoogle Scholar

Kornhuber J, Müller CP, Becker KA, Reichel M, Gulbins E. The ceramide system as a novel antidepressant target. Trends Pharmacol Sci. 2014;35:293–304.

CASPubMedGoogle Scholar

Gabandé-Rodríguez E, Boya P, Labrador V, Dotti CG, Ledesma MD. High sphingomyelin levels induce lysosomal damage and autophagy dysfunction in Niemann Pick disease type A. Cell Death Differ. 2014;21:864–75.

PubMedPubMed CentralGoogle Scholar

Keam SJ. Olipudase alfa: first approval. Drugs. 2022;82:941–7.

CASPubMedGoogle Scholar

McCormack PL, Goa KL. Miglustat. Drugs. 2003;63:2427–34.

CASPubMedGoogle Scholar

Vykoukal J, Fahrmann JF, Gregg JR, Tang Z, Basourakos S, Irajizad E, et al. Caveolin-1-mediated sphingolipid oncometabolism underlies a metabolic vulnerability of prostate cancer. Nat Commun. 2020;11:4279.

CASPubMedPubMed CentralGoogle Scholar

Ikeda M, Takahashi A, Kamatani Y, Okahisa Y, Kunugi H, Mori N, et al. A genome-wide association study identifies two novel susceptibility loci and trans population polygenicity associated with bipolar disorder. Mol Psychiatry. 2018;23:639–47.

CASPubMedGoogle Scholar

Stahl EA, Breen G, Forstner AJ, McQuillin A, Ripke S, Trubetskoy V, et al. Genome-wide association study identifies 30 loci associated with bipolar disorder. Nat Genet. 2019;51:793–803.

CASPubMedPubMed CentralGoogle Scholar

Yamamoto H, Lee-Okada HC, Ikeda M, Nakamura T, Saito T, Takata A, et al. GWAS-identified bipolar disorder risk allele in the FADS1/2 gene region links mood episodes and unsaturated fatty acid metabolism in mutant mice. Mol Psychiatry. 2023;28:2848–56.

CASPubMedPubMed CentralGoogle Scholar

Stacey D, Benyamin B, Lee SH, Hyppönen E. A metabolome-wide mendelian randomization study identifies dysregulated arachidonic acid synthesis as a potential causal risk factor for bipolar disorder. Biol Psychiatry. 2024;96:455–62.

CASPubMedGoogle Scholar

Kaeser PS, Regehr WG. Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release. Annu Rev Physiol. 2014;76:333–63.

CASPubMedGoogle Scholar

Bhalla A, Tucker WC, Chapman ER. Synaptotagmin isoforms couple distinct ranges of Ca2+, Ba2+, and Sr2+ concentration to SNARE-mediated membrane fusion. Mol Biol Cell. 2005;16:4755–64.

CASPubMedPubMed CentralGoogle Scholar

Shen W, Wang QW, Liu YN, Marchetto MC, Linker S, Lu SY, et al. Synaptotagmin-7 is a key factor for bipolar-like behavioral abnormalities in mice. Proc Natl Acad Sci USA. 2020;117:4392–9.

CASPubMedPubMed CentralGoogle Scholar

Bertolino A, Frye M, Callicott JH, Mattay VS, Rakow R, Shelton-Repella J, et al. Neuronal pathology in the hippocampal area of patients with bipolar disorder: a study with proton magnetic resonance spectroscopic imaging. Biol Psychiatry. 2003;53:906–13.

PubMedGoogle Scholar

Wang QW, Wang YH, Wang B, Chen Y, Lu SY, Yao J. Synaptotagmin-7-mediated activation of spontaneous NMDAR currents is disrupted in bipolar disorder susceptibility variants. PLoS Biol. 2021;19:e3001323.

CASPubMedPubMed CentralGoogle Scholar

Keogh CE, Kim DHJ, Pusceddu MM, Knotts TA, Rabasa G, Sladek JA, et al. Myelin as a regulator of development of the microbiota-gut-brain axis. Brain, Behavior, Immun. 2021;91:437–50.

CASGoogle Scholar

Wang LN, Zhang Z. [Mendelian randomization approach, used for causal inferences]. Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi. 2017;38:547–52.

CASPubMedGoogle Scholar

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Acknowledgements

The authors thank all investigators and participants from the groups for sharing these data.

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Authors and Affiliations

Department of Psychiatry, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, China

Qian Zhao & Fuquan Zhang

School of Systems Biology, George Mason University, Fairfax, 22030, USA

Ancha Baranova & Hongbao Cao

Research Centre for Medical Genetics, Moscow, 115478, Russia

Ancha Baranova

Department of Radiology, Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, 210008, China

Dongming Liu

Institute of Neuropsychiatry, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, 210029, China

Fuquan Zhang

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Qian Zhao

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Contributions

QZ: Writing – Original Draft; Writing – Review & Editing; Visualization. AB, DL, and HC: Writing – Review & Editing. FZ: Conceptualization; Formal Analysis; Supervision. All authors contributed to the revision of the manuscript. All authors approved the final version. FZ is the guarantor of this work and, as such, has full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

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Correspondence to Fuquan Zhang.

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This study adheres to the STROBE-MR guidelines. The genome-wide association study cohorts used in this research received ethical approval, and informed consents were obtained as documented in the original studies from which these datasets were derived.

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Zhao, Q., Baranova, A., Liu, D. et al. Bidirectional causal associations between plasma metabolites and bipolar disorder. Mol Psychiatry (2025). https://doi.org/10.1038/s41380-025-02977-3

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Received:24 September 2024

Revised:03 March 2025

Accepted:21 March 2025

Published:02 April 2025

DOI:https://doi.org/10.1038/s41380-025-02977-3

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