Clinical features of methamphetamine-induced paranoia and preliminary genetic association withDBH-1021C→T in a Thai treatment cohort

Abstract

Aims To explore clinical features of methamphetamine-induced paranoia (MIP) and associations between MIP and a genetic polymorphism in dopamine β-hydroxylase (DBH −1021C→T). Design Retrospective analysis of clinical presentation and genetic association by chi-square test and logistic regression analysis. Setting A Thai substance abuse treatment center Participants 727 Methamphetamine-dependent (MD) individuals Measures Clinical: Semi-Structured Assessment for Drug Dependence and Alcoholism (SSADDA) and the Methamphetamine Experience Questionnaire (MEQ). Genetic: DBH −1021C→T. Findings Forty percent of individuals (289 of 727) with MD had MIP. Within-binge latency to MIP onset occurred more rapidly in the most recent compared with initial MIP episode (p=0.02), despite unchanging intake (p=0.89). Individuals with MIP were significantly less likely to carry lower (TT/CT) compared with higher (CC) activity genotypes (34% vs 43%; χ21=5, p=0.03). DBH effects were confirmed (OR=0.7, p=0.04) after controlling for associated clinical variables (MD severity, OR=3.4, p<0.001; antisocial personality disorder, OR=2.2, p<0.001; alcohol dependence, OR=1.4, p=0.05; and nicotine dependence, OR=1.4, p=0.06). TT/CT carriers were more likely to initiate cigarette smoking (OR=3.9, p=0.003) and probably less likely to be dependent on alcohol (OR=0.6, p=0.05). Conclusions Among methamphetamine-dependent individuals, paranoia appears to occur increasingly rapidly in the course of a session of methamphetamine use. Severity of methamphetamine dependence and antisocial personality disorder predicts methamphetamine-induced paranoia. The genetic polymorphism in dopamine β-hydroxylase is associated with methamphetamine-induced paranoia and influences smoking initiation.

Sex Differences in Methamphetamine Use and Dependence in a Thai Treatment Center

“…Subjects agreed to be hospitalized for four months of residential (i.e., inpatient) drug treatment at the Princess Mother National Institute on Drug Abuse and Treatment (Thanyarak Institute) located in central Thailand (near Bangkok) during 2007-2011 (Kalayasiri et al, 2010, Intharachuti, 2012, Kalayasiri et al, 2014), a period immediately following implementation of the Thai government's new drug policies. The treatment program mainly used a modified therapeutic community program.…”

“…The treatment program mainly used a modified therapeutic community program. Subjects and measures have been described elsewhere (Kalayasiri et al, 2014), but in brief, individuals aged 18 years or older with more than 10 episodes of lifetime MA (often called “yaba”) use were included without sampling; all available patients were invited for screening and informed consent, excluding those with primary psychotic (schizophrenia or bipolar affective disorder) or neurological (e.g., cerebrovascular disease, epilepsy) disorders. We also excluded participants with mood disorders due to small samples (five males and one female) or other primary illicit substance (opioid, cannabis, inhalants, kratom or Mitragyna speciosa) dependences (n = 208), resulting in a final study sample of 782 MA-using individuals.…”

“…The SSADDA was previously translated into Thai for the study of the genetics of opioid (Malison et al, 2011) and MA dependence (Kalayasiri et al, 2014) and been previously shown to have a high inter-rater/inter-instrument reliability (Malison et al, 2011, Kalayasiri et al, 2014). Rigorous quality control (including ten practice-interviews required for each beginning interviewer prior to data collection and regular cross-editing) for the SSADDA interview was applied based on established practice with the English version in the US (Kalayasiri et al, 2014). The instruments were administered as computerized versions and performed onsite at the treatment center by a team of six interviewers, each with a bachelor's degree in psychology or higher and specifically certified in the SSADDA protocol.…”

Paranoid schizophrenia and methamphetamine-induced paranoia are both characterized by a similar LINE-1 partial methylation profile, which is more pronounced in paranoid schizophrenia

“…We recruited subject with MIP who were admitted to the Princess Mother National Institute Methamphetamine Experience Questionnaire (MEQ) -Thai version (Kalayasiri et al, 2014) by exploring paranoid experiences during MA use. We have excluded paranoid schizophrenia patients who were diagnosed with substance use disorder, while we excluded MIP subjects who were diagnosed with primary psychotic disorders or schizophrenia.…”

Animal models of gene–environment interaction in schizophrenia: A dimensional perspective

“…Briefly, those genetic association studies found positive association between METH induced psychoses and certain haplotypes of neurotransmission associated genes. These genes included dopamine β-hydroxylase (Kalayasiri et al, 2014), dopamine transporter (Ujike et al, 2003), dopamine receptor 2 ( DRD2 ) (Harano et al, 2004), DRD4 (Chen et al, 2004), COMT (Jugurnauth et al, 2011; Suzuki et al, 2006), glycine transporter-1 (Morita et al, 2008), PICK1 (Matsuzawa et al, 2007), G72 (Kotaka et al, 2009), GRM2 (Tsunoka et al, 2010), GRIN1 (Chanasong et al, 2013), Serotonin transporter ( 5- HTTLPR ) (Ezaki et al, 2008), serotonin 1A receptor (Kishi et al, 2010), serotonin 6 receptor (Kishi et al, 2011) and monoamine oxidase-A (Nakamura et al, 2009). Additional associations have been seen with various other genes such as alpha-synuclein (in females only) (Kobayashi et al, 2004), glutathione-S-transferase (Hashimoto et al, 2005; Hashimoto et al, 2008), quinone oxireductase (Ohgake et al, 2005), dysbindin (Kishimoto et al, 2008a), frizzled-3 (Kishimoto et al, 2008b), estrogen receptor alpha gene (Kishi et al, 2009), and neuropeptide Y1 receptor (Okahisa et al, 2009).…”