Introduction
Drugs such as cocaine, amphetamine, nicotine, alcohol, and marijuana are commonly used for their mood- and mind-altering properties. These substances also have the potential to be addictive. In some people, regular use leads to “addiction” or “dependence,” i.e., compulsive and repetitive drug-seeking behavior despite negative health and social consequences. However, this type of behavior does not occur in all users (see Fig. 1). Many people who experiment with drugs do not find the effects rewarding and avoid them in the future. Some people enjoy the effects of the drugs and use them recreationally without ever becoming dependent. For others, however, the drugs gain powerful control over their lives and may replace all other healthy pursuits (see Fig. 1). The majority of people who self-administer drugs of abuse begin during adolescence. Epidemiological studies have shown that earlier onset of drug intake is associated with greater likelihood of development of substance use problems. However, there is debate about whether early onset uniquely affects brain development in such a way as to promote pathological behavior or whether the same genetic and environmental factors that make an individual likely to develop drug problems also make them likely to initiate early. This review summarizes results from animal models in which the effect of age of onset has been examined.
The terms “addiction,” “drug abuse,” and “drug dependence” are used interchangeably in the vernacular and have varying definitions in psychological, sociological, and neuroscience literature. For the sake of clarity, we will refer to the two substance use disorders (SUDs), drug dependence and drug abuse, as they are defined by the Diagnostic and Statistical Manual of Mental Disorders version IV (DSM-IV 1994).
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For a diagnosis of drug abuse, a patient must present at least one of the following four characteristics:
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For a diagnosis of drug dependence, a patient must present three of the following seven characteristics:
Two of the criteria for drug dependence, withdrawal and tolerance, relate to physiological phenomena that ensue from repeated drug taking and are relatively easy to measure in animal models. New behavioral methods are approaching success at modeling increased intake, intake despite negative consequences, and the choice between drug intake and other activities, as described below.
The DSM-IV criteria provide a “snapshot” that clinicians can use when a patient requires diagnosis or treatment. However, drug dependence is actually a progressive disease, with several defined stages that often overlap with adolescence (Kreek et al. 2005; see Figs. 1 and and2).2). Drug dependence necessarily begins as experimental drug use; no person can become dependent without first taking a drug. Most people try drugs (at least alcohol or tobacco) at some point in their lives, typically experimenting during the late teenage years and early 20s (Chen and Kandel 1995). Some users repeat drug use under recreational circumstances. Recreational drug use can vary widely but is defined by the fact that the user has control over it. Recreational users seek drugs for their rewarding properties and not out of compulsion (Kalivas and Volkow 2005). Drug abuse and dependence begin to emerge when use becomes compulsive. The likelihood of progression from experimentation to recreational use to dependence varies by drug. Figure 1 provides a visual interpretation of this point by depicting the percentage of the population of the USA over age 12 that has ever taken a particular drug, uses regularly, or is dependent. Although the percentage that develops dependence varies by drug and is likely influenced by cultural and legal factors, the dependent population represents a small subset of those who have experimented with a drug. A key research question, therefore, is why do some drug users develop SUDs, while others can remain purely recreational?
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Epidemiological studies have provided insight into some factors that explain the difference between recreational users and those with SUD. One frequently observed correlation is that people who begin use at a young age are more likely to develop SUDs (Robins and Przybeck 1985; Meyer and Neale 1992; Lewinsohn et al. 1999; Prescott and Kendler 1999; DeWit et al. 2000; Lynskey et al. 2003; Brown et al. 2004; Patton et al. 2004) and tend to progress faster from experimentation to problem use (Chen and Kandel 1995; Chen et al. 1997). This correlation is the focus of the present review. Other contributing factors include family history of SUDs (Hoffmann and Su 1998; Hill et al. 2000) and psychopathology such as depression, anxiety, attention deficit disorder, schizophrenia, and conduct disorder (Deykin et al. 1987; Russell et al. 1994; Burke et al. 1994; Abraham and Fava 1999; Compton et al. 2000; Shaffer and Eber 2002; Costello et al. 2003). All of these factors are associated with increased risk of development of SUDs, but causality is difficult to address in human populations. In this review, we will examine attempts in animal models to address the question of whether drug taking at a young age is causal or merely coincidental in SUD development.
It is crucial at this point to define what we mean by “young.” Experimentation with alcohol, tobacco, and marijuana typically begins during the teenage years (SAMHSA 2008). Use of alcohol peaks around age 18-20 and declines into adulthood (Chen and Kandel 1995). Marijuana and tobacco use peaks slightly later, between ages 19 and 22 (Chen and Kandel 1995). Cocaine use peaks in the early to mid-20s and also declines into adulthood (Chen and Kandel 1995). The typical age-related pattern of drug use involves experimentation in the late teens and early 20s, so those who experiment before these typical times (alcohol and cigarettes in late childhood or the early teens or illegal drugs in the teens) are the most at risk. While many studies use an age of onset before 15 years as the cutoff for “early onset,” there is, in general, an inverse correlation: younger users are more likely to develop SUDs.
While the inverse correlation between age of onset and SUD liability is well established in humans, it does not tell us whether early use is causal. Epidemiological studies to test causality require twin or longitudinal studies which are difficult and rare. Two twin studies have resulted in conflicting results, albeit with different substances. One large study examining the risk for alcohol abuse and dependence reported that age of onset was correlated with but not causal in development of alcohol use disorders (Prescott and Kendler 1999). In contrast, a smaller study of twins who were discordant for early-onset marijuana use reported that age of onset was causal in development of later drug use and abuse problems (Lynskey et al. 2003). Thus, there is sparse evidence and lingering debate within the epidemiological literature regarding the causality of early-onset drug use as it relates to later drug problems. Human studies show that family history and psychopathology both increase the likelihood of early initiation (Tarter et al. 1999; Franken and Hendriks 2000; McGue et al. 2001a, b). Do these biological and environmental effects, therefore, operate through early initiation to increase vulnerability to SUDs? Or would users with a family history and/or psychopathology develop SUDs no matter when they initiate? These questions are difficult to address in human studies. To fully address the causality of early drug exposure on later SUD, animal models are necessary.
Animal models have the distinct advantage of experimental control. Experimenters can randomly assign the age of initial exposure, as well as the drug, dose, duration, and timing of exposure, whereas, in human studies, these conditions are determined by the user. For this reason, animal models have provided much valuable information. However, one drawback to animal use is that no model completely recapitulates the stages in development of SUD. For this reason, we must integrate results from multiple behavioral and neurobiological models to achieve a full understanding.
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