Other studies also show that when an addicted person is given a stimulant, it causes a smaller release of dopamine than when the same dose is given to a person who is not addicted. Until recently, much of our knowledge about the neurobiology of substance use, misuse, and addiction came from the study of laboratory animals. Although no animal model fully reflects the human experience, animal studies let researchers investigate addiction under highly controlled conditions that may not be possible or ethical to replicate in humans. These types of studies have greatly helped to answer questions about how particular genes, developmental processes, and environmental factors, such as stressors, affect substance-taking behavior. Review of the current state of knowledge of individual differences with regard to physiological effects of illicit drugs is beyond the scope of this chapter.
However, such differences (see Chapter 3) are expected to be key factors in the formulation of theories regarding the etiology of drug abuse. Physiological influences that may exacerbate an individual’s vulnerability to drug abuse could include neurochemical system impairment and heightened susceptibility to a drug because of biologically determined responsiveness. Although there has been substantial research on individual differences in response to ethanol and nicotine, less is known regarding the effects of the major classes of illicit drugs of abuse, such as opioids, stimulants, and cannabis.
Biopsychosocial Model
These environmental factors critically include availability of drugs, but also of healthy alternative rewards and opportunities. As we will show, stating that brain mechanisms are critical for understanding and treating addiction in no way negates the role of psychological, social and socioeconomic processes as both causes and consequences of substance use. To reflect this complex nature of addiction, we have assembled a team with expertise that spans from molecular neuroscience, through animal models of addiction, human brain imaging, clinical addiction medicine, to epidemiology.
- Therefore, repeated injection into nucleus accumbens evoked a behavioural response, but not sensitisation, whereas repeated injection into VTA produced no behavioural response, but did cause sensitisation, providing evidence for the critical role of VTA in sensitisation.
- This nucleus accumbens has at times been termed the brain’s “reward center” given that all known drugs with abuse potential, as well as natural rewards, lead to dopamine release in this structure [37, 38].
- It has been argued that a genetic contribution cannot support a disease view of a behavior, because most behavioral traits, including religious and political inclinations, have a genetic contribution [4].
- However, adverse caregiving experiences in early life may in particular foster the aforementioned deficits, as they lead to conflicting mental representations of self and others (Fonagy & Target, 2008).
- Such interactions appear to have important clinical implications with respect to addictive behaviors in adolescents; for example, greater stress-induced risk-taking has been linked to poorer treatment outcome in adolescent smokers [168].
The authors outlined an agenda closely related to that put forward by Leshner, but with a more clinical focus. This paper, too, has been exceptionally influential by academic standards, as witnessed by its ~3000 citations to date. What may be less appreciated among scientists is that its impact in the real world of addiction treatment has remained more Alcoholic ketoacidosis Information New York limited, with large numbers of patients still not receiving evidence-based treatments. This review has considered the value of synthesizing neurobiological and psychodynamic perspectives to better understand addictions, identifying potential pathways to the initiation of substance use, as well as mechanisms that may maintain substance use and abuse.
Addictive Substances “Hijack” Brain Reward Systems
For example, effective tax strategies that have helped curtail tobacco use particularly amongst adolescents and young adults may be used to model similar efforts with respect to food taxation [31, 206]. It may also be that certain foods (e.g., highly caloric, “hyper-palatable” processed foods) may possess greater addictive potential than do other foods and thus may warrant increased attention from public health and policy perspectives [31]. With respect to adolescents, limiting fast food and sugared sodas https://trading-market.org/alcohol-intolerance-diagnosis-treatment/ (e.g., in school cafeterias and vending machines) warrant consideration. Similarly, policy efforts could restrict the availability of substances with addictive potential that might lead to greater adolescent initiation or use (“bidis” or flavored cigarettes and alcohol-containing caffeinated beverages). Using information related to individual differences in biologies may help to optimize such policies, and the resulting policies may have substantial impact on reducing the societal burdens of addictions.
Environmental risk factors tend to operate most strongly in children with genetic vulnerability (Rutter et al., 1990). It is therefore critical to identify the joint role of environmental and genetic factors in the etiology of drug abuse. In recent years, the conceptualization of addiction as a brain disease has come under increasing criticism.
Book Title: Theories and Biological Basis of Addiction
Several studies comparing alcoholics with nonalcoholics have found decreased platelet MAO activity levels among alcohol abusers (von Knorring et al., 1985; Pandey et al., 1988; Tabakoff et al., 1988). MAO is an enzyme that is important in the metabolism of a variety of brain neurotransmitters that affect behavior, including dopamine, norepinephrine, and serotonin. Etiological research focuses primarily on the likely causes and correlates of drug use; it has identified many factors that affect drug use, although no single variable or set of variables explains drug use by an individual.
Estimates of the heritability of CocUD range from ~0.40 to 0.80, with evidence of a common genetic vulnerability with other SUDs, especially cannabis, and little evidence of cocaine-specific genetic influences (Kendler et al., 2007). Measurement of neurotransmitter release in localised brain areas during behaviour and/or in response to drugs is really important in understanding underlying neurotransmitter actions. Over the last few decades, two main methods have been employed, both of which can be used in awake, freely moving experimental animals. These are forms of neuroadaptation which are important in many aspects of neuronal function, and are particularly important in understanding processes of drug addiction.
A developmental model of addiction
Incentive salience, or ‘wanting’ on the other hand, represents the motivational importance of stimuli, making otherwise unimportant stimuli able to attract attention, making them attractive and ‘wanted’. This dissociation of the two components accounts for the observation that addicts continue to seek and take drugs, even when they derive little or no pleasure from it, and when they are fully aware of the physical, emotional and social damage it is causing. Importantly, the dissociation between ‘wanting’ and ‘liking’ has also been demonstrated experimentally, indicating that it is not simply a theoretical concept, but does actually occur. We therefore argue that a contemporary view of addiction as a brain disease does not deny the influence of social, environmental, developmental, or socioeconomic processes, but rather proposes that the brain is the underlying material substrate upon which those factors impinge and from which the responses originate.
Therefore some of these so called ‘addictive behaviours’ share many of characteristics of drug addiction, and evidence suggests that they may share similar neural mechanisms. A major research focus is aimed at identifying whether they are indeed different manifestations of the same process or different processes. Considering the site of action of the different drugs accounts for why animals will self-administer morphine into the VTA and amphetamine and cocaine into the nucleus accumbens, as these are the regions where the respective drugs activate mesolimbic function.