Background: Over 100 people die daily from opioid overdose and $78.5B per year is spent toward treatment efforts, however the real societal cost is multifold greater. Alternative strategies to eradicate/manage drug misuse and addiction need consideration. The perception of opioid addiction as a social/criminal problem has evolved to evidence-based considerations of them as clinical disorders with a genetic basis. We present evaluations of the genetics of addiction with ancestry-specific risk profiles for consideration. Objective: Studies of gene variants associated with predisposition to substance use disorders (SUDs) are monolithic, and exclude many ethnic groups, especially Hispanics and African Americans. We evaluate gene polymorphisms that impact brain reward and predispose individuals to opioid addictions, with a focus on the disparity of research which includes individuals of African and Hispanic descent. Methodology: PubMed and Google Scholar were searched for: Opioid Use Disorder (OUD), Genome-wide association studies (GWAS); genetic variants; polymorphisms, restriction fragment length polymorphisms (RFLP); genomics, epigenetics, race, ethnic group, ethnicity, ancestry, Caucasian/White, African American/Black, Hispanic, Asian, addictive behaviors, reward deficiency syndrome (RDS), mutation, insertion/deletion, and promotor region. Results: Many studies exclude non-White individuals. Studies that include diverse populations report ethnicity-specific frequencies of risk genes, with certain polymorphisms specifically associated with Caucasian and not African-American or Hispanic susceptibility to OUD or SUDs, and vice versa. Conclusion: To adapt precision medicine-based addiction management in a blended society, we propose that ethnicity/ancestry-informed genetic variations must be analyzed to provide real precision-guided therapeutics with the intent to attenuate this uncontrollable fatal epidemic.

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The heroin epidemic has existed for decades, but a sharp rise in opioid overdose deaths (OODs) jolted the nation in the mid-twenty-teens and continues as a major health crisis to this day. Although the new wave of OODs was initially approached as a rural problem impacting a White/Caucasian demographic, surveillance records suggest severe impacts on African Americans and urban-dwelling individuals, which have been largely underreported. The focus of this report is on specific trends in OOD rates in Black and White residents in states with a significant Black urban population and declared as hotspots for OOD: (Maryland (MD), Illinois (IL), Michigan (MI), and Pennsylvania (PA)), and Washington District of Columbia (DC). We compare OODs by type of opioid, across ethnicities, across city/rural demographics, and to homicide rates using 2013–2020 data acquired from official Chief Medical Examiners’ or Departments of Health (DOH) reports. With 2013 or 2014 as baseline, the OOD rate in major cities (Baltimore, Chicago, Detroit, Philadelphia) were elevated two-fold over all other regions of their respective state. In DC, Wards 7 and 8 OODs were consistently greater than other jurisdictions, until 2020 when the rate of change of OODs increased for the entire city. Ethnicity-wise, Black OOD rates exceeded White rates by four- to six-fold, with fentanyl and heroin having a disproportionate impact on Black opioid deaths. This disparity was aggravated by its intersection with the COVID-19 pandemic in 2020. African Americans and America’s urban dwellers are vulnerable populations in need of social and political resources to address the ongoing opioid epidemic in under-resourced communities. Supplementary Information The online version contains supplementary material available at 10.1007/s40615-022-01384-6.

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Selenium (Se) is a trace element required for normal body function. Its supplementation of human diet at standard optimum amount prevents oxidative damages in cells and could be a viable method in the prevention of diseases related to DNA damage, including cancer, neurodegenerative diseases and aging. While Se anticancer properties have been linked to its ability to remove excess Reactive Oxygen Species (ROS) in cells, the underlying molecular mechanism remains unknown. Recent studies have shown that the removal of ROS alone cannot account for Se anticancer properties. To really comprehend the molecular basis of Se anticancer properties, current researches now focus on the metabolism of Se in the cell, especially Se-containing amino acids. Selenocysteine (Sec) is a novel amino acid and one of the seleniumcontaining compounds in the cell. It is essential in the maintenance of the integrity of its parent proteins, some of which include enzymes such as Glutathione Peroxidases (GPXs) and Thioredoxin Reductases (TrXs). We propose in this study that the overproduction of Sec via the overexpression of Selenocysteine synthase (SecS) gene and Se supplementation induced cell death in Prostate Carcinoma (PC-3) cells. Although the mechanism underlying the cell death induction is unknown, we propose it could be due to the random incorporation of Sec into proteins at high concentration, causing premature protein degradation and cell death. The outcome of this study showed that increasing the concentration of intracellular Se-containing amino acids may provide important clinical implications for the treatment of cancer.