Biological Contributions to Addictions in Adolescents and Adults: Prevention, Treatment, and Policy Implications

People differ in the degree to which they like or dislike a particular addictive substance or activity. Some people may enjoy a substance or activity so much that it becomes very tempting and difficult to resist. Another person would not experience this difficulty because they do not experience a similar enjoyment. Likewise, the ability to temper impulsive desires with rational thought is a brain function that varies among different people. Some people may have a deficiency in their capacity to resist certain types of impulses.

Why is the biopsychosocial model of addiction important?

A BPS model provides a foundation for understanding both the causes of addictive disorders and the best treatments for them. The BPS model also fits well with the definition of addiction developed by the American Society of Addiction Medicine (ASAM), which incorporates physiology, psychology, and environment.

The factors that increase an individual’s risk for addiction are numerous, yet they all find their place in the biopsychosocial model of addiction (Marlatt & Baer, 1988). Taken together, this model provides a holistic conceptualization of addiction that acknowledges the complexity of the disorder and provides guidance toward a solution, which must necessarily be multifaceted and holistic as well. The more we know about the biopsychosocial model, the more we can foster accurate empathy for those with addiction and work toward effective treatment and prevention efforts. In this article, sober house we provide a narrative review of current biological models for addictions with a goal of placing existing data and theories within a translational and developmental framework targeting the advancement of prevention, treatment, and policy strategies. One important approach that has been employed for the past decade involves the study of intermediary phenotypes or endophenotypes [146]. This approach considers that multiple factors, including multiple gene variations, likely contribute to psychiatric disorders like addictions, and that these disorders represent heterogeneous groupings.

Persistent impacts of smoking on resting-state EEG in male chronic smokers and past-smokers with 20 years of abstinence

It is important to note that one person’s reaction to the reward experience may be quite different from another’s. This realization should help us cultivate empathy for those with addiction—it is very likely that others truly do not know how drugs make them feel. Although there is no “addiction gene” to definitively identify a person as being at risk for addiction, it is evident through twin studies, adoption studies, family studies, and more recently, epigenetic studies that addiction has a genetic component. Individuals who are genetically predisposed for addiction enter the world with a greater risk of becoming addicted at some point in their lives. The growing body of data on the neurobiology of addiction has the potential to address more effectively one of the major public health problems facing societies today.

Despite significant efforts, excessive patterns of alcohol, tobacco and other drugs have been estimated to cost the United States alone over $400 billion annually [4]. Worldwide, addictions are prevalent and low- and middle-income countries may not have the resources to adequately address these disorders [5, 6]. The impact of addictions typically is widespread, with some estimates indicating seven people being affected for each identified addicted individual, and there often exist substantial social consequences [7]. Addictions may influence employers as well as families, and the impact may be felt trans-generationally as parents with addictions may neglect children or model unhealthy behaviors [8]. Consistent with this notion, adolescents and young adults as compared to children and older adults have high rates of addictions [11]. As biological studies identify specific brain pathways and chemicals that may underlie specific aspects of addictions and addiction vulnerability [12], the knowledge gained holds significant potential to advance prevention, treatment and policy interventions.

Chronic and relapsing, developmentally-limited, or spontaneously remitting?

Hence, small environmental or chemical stimuli can reactivate addictive behaviours even after long periods of abstinence. Stress and major depression produce similar changes in the reward circuits, compounding the effect. Some of the substance-induced changes occur at the epigenetic level and may be transmitted to descendants.

biological model of addiction

Furthermore, efficacy of treatment approaches such as contingency management, which provides systematic incentives for abstinence [107], supports the notion that behavioral choices in patients with addictions remain sensitive to reward contingencies. In recent years, the conceptualization of addiction as a brain disease has come under increasing criticism. When first put forward, the brain disease view was mainly an attempt to articulate an effective response to prevailing nonscientific, moralizing, and stigmatizing attitudes to addiction. According to these attitudes, addiction was simply the result of a person’s moral failing or weakness of character, rather than a “real” disease [3]. To promote patient access to treatments, scientists needed to argue that there is a biological basis beneath the challenging behaviors of individuals suffering from addiction.

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