Dataset Information

[Bipolar disorder vulnerability: The vitamin D path].

ABSTRACT:

Objectives

Bipolar disorder (BD) etiopathogenesis is still not well elucidated. It has recently been proven that 25-hydroxy vitamin D (25OHD) has an anti-inflammatory and neuroprotective role. Our objectives were to measure 25OHD plasma levels in patients with BD in acute decompensation and compare them with patients with schizophrenia (SCZ) or schizoaffective disorder (SAD) and with healthy controls.

Methods

This is a cross-sectional case-control study including male inpatients with a decompensation of their disease who were diagnosed with BD, SCZ or SAD according to DSM-5 criterias. The control group was constituted by unrelated healthy subjects, age-and-sex matched.

Results

The 25OHD level was significantly higher only in patients with BD compared to controls. 25OHD was also positively correlated to the PANSS scale (r = 0.282, p < 0.001) and to different MOCA scores (r = 0.326, p = 0.006) as well as aspects related to abstraction, attention and memory capacity. Multivariate analysis found that BD acute decompensation was independently related to the rise in plasma 25OHD (p = 0.012; OR =1.157, [1.032 -1.297]).

Conclusion

Our study shows that BD acute decompensation is associated with the rise in plasma 25OHD synthesis. However, the vitamin D dosage relevance as a biomarker of this disease warrants a verification in other studies.

SUBMITTER: Naifar M

PROVIDER: S-EPMC7019462 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Publications

[Bipolar disorder vulnerability: The vitamin D path].

Naifar Manel M Maalej Bouali Manel M Guidara Wassim W Ellouze Ahmed Slim AS Jmal Khalil K Omri Sana S Messedi Meriam M Zouari Lobna L Elleuch Aida A Maalej Mohamed M Chaabouni Khansa K Charfi Nada N Turki Mouna M Jihène Ben Thabet BT Ayadi Fatma F

Canadian journal of psychiatry. Revue canadienne de psychiatrie 20190821 3

<h4>Objectives</h4>Bipolar disorder (BD) etiopathogenesis is still not well elucidated. It has recently been proven that 25-hydroxy vitamin D (25OHD) has an anti-inflammatory and neuroprotective role. Our objectives were to measure 25OHD plasma levels in patients with BD in acute decompensation and compare them with patients with schizophrenia (SCZ) or schizoaffective disorder (SAD) and with healthy controls.<h4>Methods</h4>This is a cross-sectional case-control study including male inpatients w ...[more]

PMID: 31434497

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Project description:ObjectiveBipolar disorder (BD) is highly heritable. Neuroimaging studies comparing unaffected youth at high familial risk for BD (i.e., those with a first-degree relative with the disorder; termed "high-risk" [HR]) to "low-risk" (LR) youth (i.e., those without a first-degree relative with BD) and to patients with BD may help identify potential brain-based markers associated with risk (i.e., regions where HR+BD≠LR), resilience (HR≠BD+LR), or illness (BD≠HR+LR).MethodDuring functional magnetic resonance imaging (fMRI), 99 youths (i.e., adolescents and young adults) aged 9.8 to 24.8 years (36 BD, 22 HR, 41 LR) performed a task probing face emotion labeling, previously shown to be impaired behaviorally in youth with BD and HR youth.ResultsWe found three patterns of results. Candidate risk endophenotypes (i.e., where BD and HR shared deficits) included dysfunction in higher-order face processing regions (e.g., middle temporal gyrus, dorsolateral prefrontal cortex). Candidate resilience markers and disorder sequelae (where HR and BD, respectively, show unique alterations relative to the other two groups) included different patterns of neural responses across other regions mediating face processing (e.g., fusiform), executive function (e.g., inferior frontal gyrus), and social cognition (e.g., default network, superior temporal sulcus, temporo-parietal junction).ConclusionIf replicated in longitudinal studies and with additional populations, neural patterns suggesting risk endophenotypes could be used to identify individuals at risk for BD who may benefit from prevention measures. Moreover, information about risk and resilience markers could be used to develop novel treatments that recruit neural markers of resilience and attenuate neural patterns associated with risk. Clinical trial registration information-Studies of Brain Function and Course of Illness in Pediatric Bipolar Disorder and Child and Adolescent Bipolar Disorder Brain Imaging and Treatment Study; http://clinicaltrials.gov/; NCT00025935 and NCT00006177.

Project description:ImportanceUnderstanding the origins of clinical heterogeneity in bipolar disorder (BD) will inform new approaches to stratification and studies of underlying mechanisms.ObjectiveTo identify components of genetic liability that are shared between BD, schizophrenia, and major depressive disorder (MDD) and those that differentiate each disorder from the others and to examine associations between heterogeneity for key BD symptoms and each component.Design, setting, and participantsUsing data from the Bipolar Disorder Research Network in the United Kingdom, components of liability were identified by applying genomic structural equation modeling to genome-wide association studies of schizophrenia, BD, and MDD. Polygenic risk scores (PRS) representing each component were tested for association with symptoms in an independent BD data set. Adults with DSM-IV BD or schizoaffective disorder, bipolar type, were included. Data were collected from January 2000 to December 2013, and data were analyzed from June 2020 to February 2022.Main outcomes and measuresPRS representing the components of liability were tested for association with mania and depression, psychosis, and mood incongruence of psychosis in participants with BD, measured using the Bipolar Affective Disorder Dimensional Scale.ResultsOf 4429 included participants, 3012 (68.0%) were female, and the mean (SD) age was 46.2 (12.3) years. Mania and psychosis were associated with the shared liability component (mania β = 0.29; 95% CI, 0.23-0.34; P = 3.04 × 10-25; psychosis β = 0.05; 95% CI, 0.04-0.07; P = 2.33 × 10-13) and the components that differentiate each of schizophrenia (mania β = 0.08; 95% CI, 0.03-0.14; P = .002; psychosis β = 0.03; 95% CI, 0.01-0.04; P = 1.0 × 10-4) and BD (mania β = 0.14; 95% CI, 0.09-0.20; P = 1.99 × 10-7; psychosis β = 0.02; 95% CI, 0.01-0.03; P = .006) from the other disorders. The BD differentiating component was associated with mania independently of effects on psychosis (β = 0.14; 95% CI, 0.08-0.20; P = 4.32 × 10-6) but not with psychosis independently of mania. Conversely, the schizophrenia differentiating component was associated with psychosis independently of effects on mania (β = 0.01; 95% CI, 0.003-0.03; P = .02), but not with mania independently of psychosis. Mood incongruence of psychosis was associated only with the schizophrenia differentiating component (β = 0.03; 95% CI, 0.01-0.05; P = .005). Depression was associated with higher MDD differentiating component (β = 0.07; 95% CI, 0.01-0.12; P = .01) but lower BD differentiating component (β = -0.11; 95% CI, -0.17 to -0.06; P = 7.06 × 10-5).Conclusions and relevanceIn this study of BD, clinical heterogeneity reflected the burden of liability to BD and the contribution of alleles that have differentiating effects on risk for other disorders; mania, psychosis, and depression were associated with the components of genetic liability differentiating BD, MDD, and schizophrenia, respectively. Understanding the basis of this etiological heterogeneity will be critical for identifying the different pathophysiological processes underlying BD, stratifying patients, and developing precision therapeutics.

Dataset Information

[Bipolar disorder vulnerability: The vitamin D path].

Objectives

Methods

Results

Conclusion

Publications

[Bipolar disorder vulnerability: The vitamin D path].

Similar Datasets

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