The illegal use of methamphetamine (MA) is a growing public health concern globally and results in a series of negative effects. The prominent detrimental effect of MA use is MA-related psychiatric symptoms (MAP) and is observed at a much higher incidence compared to the general population. MAP often includes multiple dimensions of cognitive impairment and induces adverse consequences such as, violence and suicide. However, the assessment methods for MAP are not standardized. Hence, it is necessary to investigate factors that affect the progression of psychiatric symptoms in individuals who use MA. A review of published studies was performed by searching the following databases: PubMed, EMBASE, and PsycINFO from inception to 31 May, 2018. The search strategy included methamphetamine, dependence, psychiatric symptoms, and risk factor terms. We reviewed the different features of MAP and the various types of assessment instruments and summarized MAP risk factors from MA use-related factors, socio-demographic characteristics, life events, and genetic factors. We found that MAP was consistently and causally associated with MA use, particularly as it relates to the frequency and amount of MA use. Other MAP-related risk factors like life events and genetics were relatively inconsistent in their association with MAP. Hence, causal and longitudinal studies that focus on multilateral comparisons are required. This review provides high quality evidence for MAP risk factors and would be helpful for developing early prevention and treatment strategies for MAP.

Background and aims Genomic and transcriptomic findings greatly broaden the biological knowledge regarding substance use. However, systematic convergence and comparison evidence of genome‐wide findings is lacking for substance use. Here, we combined all the genome‐wide findings from both substance use behavior and disorder (SUBD) and identified common and distinguishing genetic factors for different SUBDs. Methods Systemic literature search for genome‐wide association (GWAS) and RNA‐seq studies of alcohol/nicotine/drug use behavior (partially meets or not reported diagnostic criteria) and alcohol use behavior and disorder (AUBD), nicotine use behavior and disorder (NUBD) and drug use behavior and disorder (DUBD) was performed using PubMed and the GWAS catalog. Drug use was focused upon cannabis, opioid, cocaine and methamphetamine use. GWAS studies required case–control or case/cohort samples. RNA‐seq studies were based on brain tissues. The genes which contained significant single nucleotide polymorphism (P ≤ 1 × 10−6) in GWAS and reported as significant in RNA‐seq studies were extracted. Pathway enrichment was performed by using Metascape. Gene interaction networks were identified by using the Protein Interaction Network Analysis database. Results Total SUBD‐related 2910 genes were extracted from 75 GWAS studies (2 773 889 participants) and 17 RNA‐seq studies. By overlapping the genes and pathways of AUBD, NUBD and DUBD, four shared genes (CACNB2, GRIN2B, PLXDC2 and PKNOX2), four shared pathways [two Gene Ontology (GO) terms of ‘modulation of chemical synaptic transmission’, ‘regulation of trans‐synaptic signaling’, two Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of ‘dopaminergic synapse’, ‘cocaine addiction’] were identified (significantly higher than random, P < 1 × 10−5). The top shared KEGG pathways (Benjamini–Hochberg‐corrected P‐value < 0.05) in the pairwise comparison of AUBD versus DUBD, NUBD versus DUBD, AUBD versus NUBD were ‘Epstein–Barr virus infection’, ‘protein processing in endoplasmic reticulum’ and ‘neuroactive ligand‐receptor interaction’, respectively. We also identified substance‐specific genetic factors: i.e. ADH1B and ALDH2 were unique for AUBD, while CHRNA3 and CHRNA4 were unique for NUBD. Conclusions This systematic review identifies the shared and unique genes and pathways for alcohol, nicotine and drug use behaviors and disorders at the genome‐wide level and highlights critical biological processes for the common and distinguishing vulnerability of substance use behaviors and disorders.