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    • d-biotin Substance use disorder is characterized by drug

    2018-11-07

    Substance use disorder is characterized by drug craving and loss of control over drug consumption, including inordinate amounts of time spent pursuing or using the drug and continued use despite negative consequences. Consequences of SUD involve a failure to fulfill work, school, and home obligations, and the development of social and interpersonal problems, physical or psychological harm, and tolerance and withdrawal symptoms (APA, 2013; NIDA, 2014). While many adolescents experiment with drugs, the transition to dependence is marked by compulsive and habitual substance use (Everitt et al., 2008; Volkow and Fowler, 2000). In the present review we use the term addiction or substance dependence in reference to more severe forms of SUD, which are characterized by chronic drug seeking and drug use (APA, 2013; NIDA, 2014).
    An evolutionary understanding of adolescent risk behaviors To understand how the developing d-biotin can become vulnerable to drugs of abuse during adolescence, we first turn to evolution and the adaptive role of reward and risk-related behaviors. Our tenet is that the adaptive adolescent strategies, which evolved for survival, manifest today as risk behaviors that can be commuted to substance use disorder (SUD) in vulnerable individuals. Adolescence is maturational period unique to mammals, during which time puberty occurs before peripheral and neurological growth is complete (Bogin and Smith, 1996). Gonadal hormones released during puberty stimulate the development of adult social behaviors (Bogin and Smith, 1996). The adolescent stage allows individuals to practice more complex physical and social skills before adulthood is reached, to increase survival and reproductive fitness (Bogin and Smith, 1996; Darwin, 1871). Behaviors that emerged during adolescence to promote survival and reproduction may no longer be adaptive, but instead can increase an individual’s likelihood to experiment with, use, and become dependent on drugs (Bardo et al., 1996; de Wit, 2009; Hester and Garavan, 2004; Kreek et al., 2005; Naneix et al., 2012; Potvin et al., 2014; Vonmoos et al., 2013). For example, aggression and risk-taking in males can be a competitive strategy that increases reproductive fitness by increasing mating opportunities and genetic diversity (Gluckman and Hanson, 2006). Yet, data from the National Epidemiological Study of Alcohol and Related Conditions (a survey of n=43,084 individuals 18 years and older) shows that violent behavior increases risk of SUD 2.42-fold (Schwartz et al., 2015). Other traits, including hyperactivity, novelty seeking, and impulsivity were advantageous to early humans by promoting exploration of the environment and acquisition of resources (Bjorklund and Pellegrini, 2000), but are also associated with substance abuse (Belin et al., 2008; Gruber et al., 2014; Khurana et al., 2013; Mitchell et al., 2014; Sonntag et al., 2014; Volkow et al., 1999). The early-onset of puberty may represent a unique risk factor for substance abuse due to early initiation of adolescent risk behaviors. As a risk factor early puberty is of particular concern for females, who on average mature up to two years earlier than males (Tanner, 1962). Early puberty onset is associated with earlier initiation and increased frequency of nicotine and alcohol use in adolescent males and females (Harrell et al., 1998; Patton et al., 2004; Wilson et al., 1994). Today puberty occurs at increasingly earlier ages, up to 3 years earlier than 100 years ago (Gluckman and Hanson, 2006). Earlier onset has been attributed to a number of factors, including improved nutrition, lower rates of disease in childhood, reduced early mortality, exposure to growth hormones through cow’s milk, other endocrine-disrupting toxins (i.e., bisphenol A), genetic polymorphisms, and childhood obesity (Gluckman and Hanson, 2006; Parent et al., 2011; Surbey, 1998). Regardless of the cause, earlier-onset puberty has resulted in increasingly wider gaps between an individuals’ cognitive and reproductive maturity (Hawley, 2011). In some cases, interventions aimed at limiting factors that accelerate puberty may therefore be protective against SUD risk (Houben et al., 2011).