With the revised DSM-5 SUD criteria, the substance abuse ‘legal problems’ criterion was removed and a psilocybe semilanceata habitat craving criterion was added. Compton, Dawson, Goldstein, and Grant (2013) found that a threshold of ⩾4 DSM-5 criteria (i.e. moderate severity) demonstrated optimal correspondence with DSM-IV dependence for alcohol, cocaine, and opioid use disorders. Updates about mental health topics, including NIMH news, upcoming events, mental disorders, funding opportunities, and research.
Definition of SUD
Thinking of addiction as genetic begins with understanding that addiction is a chronic relapsing brain disorder. “In many ways, it’s no different than having a family history with heart disease or diabetes,” says Dr. Anand. There has been limited knowledge of the molecular genetic underpinnings of addiction until now.
Rare and Common Variants
The coding variants in these genes provide a protective effect for AUD by producing aversive effects when drinking alcohol, often resulting in lower levels of consumption and AUD risk (Edenberg & Mcclintick, 2018). However, it is likely that thousands of additional genetic loci play a role beyond the genes encoding alcohol metabolizing enzymes. Additional studies have examined subdomains of alcohol consumption, suggesting potential etiological differences between alcohol consumption frequency and alcohol consumption quantity (Mallard et al., 2020; Marees et al., 2020b). Specifically, alcohol consumption quantity was found to be more genetically similar to AUD and psychopathology, while frequency demonstrated negative relationships with AUD and other psychiatric outcomes, and was found to be influenced by measures of SES (Mallard et al., 2020; Marees et al., 2020b). Thus, evidence of genetic dissimilarity between consumption and AUD may be being driven by frequency of drinking, which in turn, is being influenced by indices of SES. Further studies probing this relationship will be needed to fully disentangle the nuance of the shared and unique genetic etiology across the maverick house sober living spectrum of alcohol consumption levels (e.g. normative consumption, binge drinking) and AUD.
NIH study reveals shared genetic markers underlying substance use disorders
Another issue is that there is no certain way to cross-map animal and human phenotypes, limiting the opportunities for translation. The majority of GWAS of SUDs to date are composed primarily of individuals of European-ancestry, and thus, the generalizability of these findings to other ancestry groups is uncertain. This gap has the potential to further exacerbate health disparities for individuals of diverse ancestry. This raises the need for efforts to study SUDs in transancestral populations, such as the All of Us Research Program.
Mark S. Gold, M.D., is a pioneering researcher, professor, and chairman of psychiatry at Yale, the University of Florida, and Washington University in St Louis. His theories have changed the field, stimulated additional research, and led to new understanding sober house boston and treatments for opioid use disorders, cocaine use disorders, overeating, smoking, and depression. The world around you also can play a significant role in opening a door that leads to problematic substance use, notes Dr. Anand. About half of your susceptibility to developing a substance use disorder (SUD) can be hereditary. Genetics can mark you as more prone to use alcohol, tobacco products or drugs such as cocaine, heroin and opioids. Personalized medicine in addiction treatment considers individual differences in behavioral and psychological factors.
- The latest information and resources on mental disorders shared on X, Facebook, YouTube, LinkedIn, and Instagram.
- Given the public health burden of SUDs, a better understanding of SUD etiology is of wide-reaching importance.
- Further, most clinical trials and behavioral studies have focused on individual substances, rather than addiction more broadly.
- Thus, evidence of genetic dissimilarity between consumption and AUD may be being driven by frequency of drinking, which in turn, is being influenced by indices of SES.
- This special issue also includes the results from a GWAS of nicotine addiction in individuals of Asian descent (Yoon et al. 2012).
Integration of functional genomic data and cross-species translational models
Moreover, the persistent nature of the changes induced by drugs in the brain reward pathway (and other circuits), along with the chronicity of the addictive process, are known to be closely linked to pathological neuroplasticity (Van den Oever et al. 2012; Kalivas and Volkow 2011). “Using genomics, we can create a data-driven pipeline to prioritize existing medications for further study and improve chances of discovering new treatments. In 2021, more than 46 million people in the United States aged 12 or older had at least one substance use disorder, and only 6.3% had received treatment.
Such studies, however, cannot yet address the critical mechanistic question about how genetic diversity influences the sensitivity to either adverse or protective environments vis á vis abuse and addiction trajectories. One overarching question that has emerged from the first-generation of well-powered SUD GWAS is whether measures of non-problematic substance use have divergent genetic underpinnings from SUDs, and if so, to what extent. Another area of interest has been dissecting the genetic relationships between SUDs, other psychiatric disorders, and relevant complex traits; by leveraging large GWAS and advanced statistical genetics methods e.g. Cross-trait genetic correlations, genomicSEM (Grotzinger et al., 2019), interesting patterns of pleiotropy have emerged (Abdellaoui, Smit, Van Den Brink, Denys, & Verweij, 2021; Hatoum et al., 2021; Jang et al., 2020).
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