The association between BDNF levels and risperidone-induced weight gain is dependent on the <i>BDNF</i> Val66Met polymorphism in antipsychotic-naive first episode schizophrenia patients: a 12-week prospective study

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Abstract

A growing number of studies have shown that brain-derived neurotrophic factor (BDNF) is associated with weight gain during antipsychotic treatment in schizophrenia patients. However, there is still a lack of research results in the initial stage of antipsychotic treatment. This study aimed to evaluate the relationship between weight gain caused by risperidone monotherapy for 12 weeks and BDNF level in antipsychotic-naive and first-episode (ANFE) patients with schizophrenia, and we hypothesize that this may depend on BDNF Val66Met gene polymorphism. In a 12-week longitudinal trial, 225 ANFE patients were enrolled and treated with risperidone. Body weight was measured at baseline and during the 12-week follow-up. After treatment, the average weight of ANFE patients increased by 2.6 kg. Furthermore, we found that in patients with Val/Val genotype, the increase in serum BDNF levels was negatively correlated with risperidone-induced weight gain ( r = −0.44, p = 0.008). Regression analysis showed that the baseline BDNF level was a predictor of weight gain after treatment ( β = −0.45, t = −3.0, p = 0.005). Our results suggest that the BDNF signaling may be involved in weight gain caused by risperidone treatment. Furthermore, the negative association between weight gain and increased BDNF levels during risperidone treatment in ANFE schizophrenia depends on the BDNF Val66Met polymorphism.

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The relative effectiveness of second-generation (atypical) antipsychotic drugs as compared with that of older agents has been incompletely addressed, though newer agents are currently used far more commonly. We compared a first-generation antipsychotic, perphenazine, with several newer drugs in a double-blind study. A total of 1493 patients with schizophrenia were recruited at 57 U.S. sites and randomly assigned to receive olanzapine (7.5 to 30 mg per day), perphenazine (8 to 32 mg per day), quetiapine (200 to 800 mg per day), or risperidone (1.5 to 6.0 mg per day) for up to 18 months. Ziprasidone (40 to 160 mg per day) was included after its approval by the Food and Drug Administration. The primary aim was to delineate differences in the overall effectiveness of these five treatments. Overall, 74 percent of patients discontinued the study medication before 18 months (1061 of the 1432 patients who received at least one dose): 64 percent of those assigned to olanzapine, 75 percent of those assigned to perphenazine, 82 percent of those assigned to quetiapine, 74 percent of those assigned to risperidone, and 79 percent of those assigned to ziprasidone. The time to the discontinuation of treatment for any cause was significantly longer in the olanzapine group than in the quetiapine (P<0.001) or risperidone (P=0.002) group, but not in the perphenazine (P=0.021) or ziprasidone (P=0.028) group. The times to discontinuation because of intolerable side effects were similar among the groups, but the rates differed (P=0.04); olanzapine was associated with more discontinuation for weight gain or metabolic effects, and perphenazine was associated with more discontinuation for extrapyramidal effects. The majority of patients in each group discontinued their assigned treatment owing to inefficacy or intolerable side effects or for other reasons. Olanzapine was the most effective in terms of the rates of discontinuation, and the efficacy of the conventional antipsychotic agent perphenazine appeared similar to that of quetiapine, risperidone, and ziprasidone. Olanzapine was associated with greater weight gain and increases in measures of glucose and lipid metabolism. Copyright 2005 Massachusetts Medical Society.

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Author and article information

Contributors

Meihong Xiu: xiumeihong9797@gmail.com

Xiangyang Zhang:

ORCID: http://orcid.org/0000-0003-3326-382X

zhangxy@psych.ac.cn

Journal

Journal ID (nlm-ta): Transl Psychiatry

Journal ID (iso-abbrev): Transl Psychiatry

Title: Translational Psychiatry

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2158-3188

Publication date (Electronic): 4 September 2021

Publication date PMC-release: 4 September 2021

Publication date Collection: 2021

Volume: 11

Electronic Location Identifier: 458

Affiliations

[1 ]GRID grid.268099.c, ISNI 0000 0001 0348 3990, The Affiliated Kangning Hospital of Wenzhou Medical University, ; Wenzhou, China

[2 ]GRID grid.413259.8, ISNI 0000 0004 0632 3337, Neurology Department, , Xuan Wu Hospital of Capital Medical University, ; Beijing, China

[3 ]GRID grid.410645.2, ISNI 0000 0001 0455 0905, Qingdao Mental Health Center, , Qingdao University, ; Qingdao, China

[4 ]GRID grid.414351.6, ISNI 0000 0004 0530 7044, Peking University HuiLongGuan Clinical Medical School, Beijing HuiLongGuan Hospital, ; Beijing, China

[5 ]GRID grid.454868.3, ISNI 0000 0004 1797 8574, CAS Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Science, ; Beijing, China

Author information

Xiangyang Zhang http://orcid.org/0000-0003-3326-382X

Article

Publisher ID: 1585

DOI: 10.1038/s41398-021-01585-3

PMC ID: 8418607

PubMed ID: 34482368

SO-VID: e4246f0c-4c73-486d-aeb4-19281c321416

License:

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