“Whether or not we look at addiction as a “disease,” we can clearly see that changes in the brain do occur that promote continued use.”
In the past, addiction was viewed as stemming from an individual’s moral failing and weakness of will (NIH, 2010). With the advances in scientific research, biological theories of addiction as a “brain disease” are now widely accepted; however, this point of view is still controversial. Many prefer to characterize it as a condition that requires continued management, rather than a disease, as it promotes the idea that addiction can be managed through behavioral changes and that the individual is ultimately in control of the condition.
The disease model is supported by the changes that occur in the brain as a result of continued substance use. Through a process of adaptation, the brain attempts to adapt to the presence of a substance in effort to function normally. The disease model asserts that while initial choice to use the substance may have been voluntary, over time behavioral choice is lessened as these neurobiological changes occur.
Not only do these changes modify one’s initial response to a substance, they regulate:
- The development of craving.
- The distress associated with periods of abstinence (which is a key factor in relapse).
Whether or not we look at addiction as a “disease,” we can clearly see that changes in the brain do occur that promote continued use — both due to the rewarding feelings that the substance can initiate in the brain and also due to avoidance of withdrawal symptoms that present when dependence develops.
The Brain and Addiction
The most complex body organ, the brain, is impacted by substance use in 3 central areas:
- The brain stem. This controls basic bodily functions, including breathing, sleeping, and heart rate.
- The cerebral cortex. This controls executive functions, such as decision-making, planning, and sensory information processing.
- The limbic system. This is the body’s emotional reward circuitry and controls our ability to experience pleasure and motivation for survival sustaining activities, which is activated by drugs of abuse (NIDA, 2014).
The Role of Neurotransmitters in Addiction
Neurons communicate via dendrites and axons, sending electrical impulses down the axon, converting them to chemical signals at the axon terminal, releasing neurotransmitters (chemical messengers) across synaptic gaps (narrow space between the axon terminal and the dendrite of another neuron), and attaching to the receiving neuron’s receptor site.
The dendrite receives the neurotransmitter and converts it back to electrical signals. This process happens between billions of neurons in the brain. Communication between neurons functions to control behavior, cognition, mood, and movement (NIDA, 2013).
Drugs of abuse, whose chemical structures mimic natural neurotransmitters, interfere with normal neuronal processing, releasing neurotransmitters in excessive amounts, providing greater pleasure than naturally pleasing survival activities (e.g., eating or sex) and preventing normal chemical reuptake, meaning that an excessive amount of neurotransmitters are left in the synapse, ultimately affecting the behavior of other communicating neurons, which subjectively alters our mood. (NIDA, 2013).
The brain’s reward system is activated when an individual engages in survival activities, providing euphoric feelings and reinforcing behavior. When activated, information travels from the ventral tegmental area (VTA) to the nucleus accumbens and then to the prefrontal cortex (Van Wormer & Davis, 2013).
The neurotransmitter dopamine is responsible for incentive, reward and motivation, and is a key neurotransmitter involved in addiction.
Drugs of abuse activate reward pathways, releasing excessive dopamine. Dopamine surges produce:
- Strong behavioral reinforcement.
- Cravings or compulsions to perform certain behaviors.
The brain adjusts to such surges by reducing dopamine production and the number of receptors that can receive signals.
Dopamine depletion, along with disruption in other neurotransmitters, reduces one’s ability to experience pleasure (NIDA, 2013). Dopamine depletion following cocaine use may account for binges, tolerance, and craving (Van Wormer & Davis, 2013).
Serotonin, the neurotransmitter involved in sleep, sensory experiences, and sense of well-being, may also play a key role in addiction. Decreased serotonin levels have been linked to behaviors associated with:
- Poor impulse control.
- Suicidal behavior.
Another neurotransmitter, glutamate, the primary excitatory brain neurotransmitter stimulating brain cells to fire, is associated with learning and memory, and has been implicated in the perpetuation of addiction.
Research has demonstrated that glutamate, operating independently and interacting with the dopaminergic system, fosters the development and maintenance of addiction through:
- Conditioning (cues in one’s daily routine become associated with use).
- Relapse (Tzschentke & Schmidt, 2003).
The Disease Theory
The disease concept of addiction is helpful in that it fosters our understanding that addiction is not simply a lack of willpower. The model, however, is not without limitations.
What presents a challenge is how to answer this question: With exposure to a substance, why will some individuals become addicted and others will not? (West, 2013).
Canadian psychologist, Bruce K. Alexander, argues the disease model makes one of two claims:
- Claim A: All or most people who use heroin or cocaine beyond a certain minimum amount become addicted.
- Claim B: No matter what proportion of the users of heroin and cocaine become addicted, their addiction is caused by exposure to the drug.
Alexander (2001) argues that historical and clinical evidence fails to support this view. He states that during the 19th century, opiate consumption in America and England was more prevalent than it is now, but less than 1% of the population became dependent or addicted and the numbers were declining at the end of the century even before certain laws were passed restricting use.
In the United Kingdom, Alexander notes, heroin was widely used as a medication for chronic pain, cough, and diarrhea. In 1972, British physicians prescribed large doses of heroin, yet British statistics showed a surprisingly low number of people who’d become addicted to heroin as a result (Trebach,1982: p. 83).
This challenges the disease theory, in addition to the assertion that exposure to certain substances will result in addiction in most people.
Do Substances Cause Addiction?
Reference to research on self-administration of drugs by laboratory animals is often used as an argument to support the construct of substance-induced addiction. In the 1960s, researchers at the University of Michigan created devices that allowed rats to self-administer drugs by pressing a lever. These types of experiments were conducted throughout the 1970s and demonstrated that rats, mice, monkeys, and other mammals will self-inject large doses of heroin, cocaine, amphetamines, and other drugs (Woods, 1978), seemingly proving that these substances are irresistibly addicting.
In the 1970s, Alexander and associates conducted the Rat Park study. Alexander posited that addiction was substance-dependent, and that the evidence for opiate addiction seen in laboratory rats was attributable to living conditions rather than to the drugs’ addictive properties (Alexander, 2001). To prove his premise, Alexander built Rat Park, a housing colony approximately 200 times more spacious than a regular laboratory cage, with half dozen rats of both sexes living with ample provision of food, toys, and space for socializing, mating and raising litters.
Experiments conducted in Rat Park indicated that rats who were living in a better environment had little appetite for morphine (Alexander, 2001).
By report, rats that had been forced to consume morphine hydrochloride daily for nearly two months were brought to Rat Park and given the opportunity to choose between tap or morphine-laced water. Alexander (2001) reports that the rats for the most part chose plain water. Control groups of rats isolated in small cages consumed more morphine in this and subsequent experiments.
Alexander believes that the Rat Park experiments demonstrate that animal self-administration studies provide no empirical evidence for the theory of substance-induced addiction. The closing of Rat Park left unresolved questions as to the cause of addiction and the reason for the current high prevalence of addiction to drugs and other habits.
The Role of Personal History
Further evidence to refute the theory of drug-induced addiction is depicted in heroin use during the Vietnam War, when many American soldiers were routinely using heroin. Ten months after returning home, only 5% of those solders considered addicted were still using. This is an excellent recovery rate, not accounted for by treatment.
It begged the question: Is a substance intrinsically addicting, or do other life experiences determine compulsive use? (Felitti, 2004).
Findings of the Adverse Childhood Experiences (ACE) study demonstrate that unrecognized adverse childhood experiences are a major factor underlying addiction. These adverse childhood experiences result in neurodevelopmental changes and emotional damage (Felitti, 2004). These experiences can predispose one to negative emotional states and create a strong motivation for seeking relief through psychoactive substance use which provides short-term benefit in the face of long-term risks.
Is Addiction Hereditary?
There are multiple ways in which genetic and environmental factors may result in variation in vulnerability to addiction (West, 2013). According to NIH (2010), genes account for approximately 50% of an individual’s risk of becoming addicted.
Three attributes influence an individual’s disposition to engage in a specific behavior:
- Capability – the physical or psychological capacity to engage in behavior.
- Motivation – the mental process that guide behavior, both automatic (e.g. euphoria after ingesting cocaine) and reflective (e.g. attitude that marijuana is harmless).
Opportunity – environmental factors that either promote or constrain behavior. Includes:
- The physical environment (e.g. ease of access to a substance).
- Social factors, such as peer attitudes (West, 2013).
- Although substance use at any age can progress to addiction, onset of use is highly predictive.
- Adolescents are quite vulnerable as their brains are still developing.]
Environment plays a major role in it, as well. The interplay between an individual and his environment gives rise to behavior. There are many influences in one’s environment, including:
- Social network.
- Socioeconomic status.
- Parental involvement.
- Personal history, such as physical or sexual abuse, or neglect.
To combat addiction, exposure to environmental and internal factors that foster strong motivations to use must be reduced and countered with other motivators (West, 2013). From a harm reduction standpoint, delaying onset of use may be highly beneficial.
For example, targeted prevention and outreach efforts toward adolescents and their networks, including family and teachers, have successfully demonstrated changes in attitudes and behaviors with respect to youth tobacco use (NIH, 2010).
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- West, R. (2013). Models of Addiction. European Monitoring Centre for Drugs and Drug Addiction Insights Series 14. Lisbon: Publication Office of the European Union.
- Woods, J. H. (1978). Behavioral pharmacology of drug self-administration. In M.A. Lipton, A. DiMascio, and K.F. Killam (Eds.), Psychopharmacology: A generation of progress. New York: Raven.