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Analysis of behavioural response to substance is a critical point of discussion when formulating a assertion around addiction/substance use disorders. The diagnosis manual, referred to in psychiatry is used to define the different psychiatric diagnoses that are presented within societal groups which is commonly known as the DSM. Advances in neuroscience identified addiction as a chronic brain disease alluding to strong genetic, neurodevelopmental and social components that offer a debate towards classification of a personal lifestyle choice or a biological vulnerability. This discussion will explore the history of drug abuse and addiction, societal’s response, epidemiology, neuroplasticity of dopamine circuits, brain-behaviour relationships and new approached to treatment and prevention.
Substance abuse or substance dependance are terms previously used in the DSM-4 to define a diagnosis of substance use disorder, however numerous iteration have been made to redefine and clarify a diagnosis between the DSM-4 and DSM-5. The key differential feature between these two diagnoses are physiological symptoms of tolerance and withdrawals. The change from DSM-4 to DSM-5 was significant as the DSM-5 deemphasised the physiologic pieces attached to this disorder allowing the DSM-5 to define and incorporate behavioural components as its core attribute. Through reconceptualising addiction as a chronically relapsing mental illness, it allows for a deeper analysis of potential heritability rates, compliance of treatments and treatment response for patients suffering with a substance abuse diagnosis. This triggers a response to the relegated stigmas attached to this disorder.
Neuroplasticity is heavily classified in relation to defining addiction as a disease. Results of extensive research into addiction it has draw conclusions towards substances that the brain hold traumatic memories that manifest itself by reflex activation brain circuits primarily involving the reward system. This manifestation results in motivation to return to a substance consumption behaviours when triggers or cues are encountered. Using a substance that activates the reward system produces the potential for the development of addiction while vulnerability to a substance use disorder is influenced by complex genetic and environmental factors.
Neuroplasticity can be seen in tolerance to the substance, manifesting through reduced effects from exposed dosage and the physical dependance presented through withdrawal symptoms. Another significant form for neuroplasticity can be seen in compulsive substance seeking behaviour. Brain imaging studies has provided clear evidence of the rapid activation through the increase of blood flow to the reward pathways when patients who are involved in remission are exposed to substance related stimuli. This is a result of the brain interpreting a craving and the reward system is activated. The level of craving of the substance is directly related to the level of endogenous dopamine released in the reward structures.
Individuals who are vulnerable to addiction and experience repetitive exposure to substance agents, can induce long-lasting neuroadaptive changes to the nervous system that promote drug seeking behaviours and can lead to persistent and uncontrollable patters of use that constitute addiction. The neuroadaptive changes form the foundation to tolerance, craving, withdrawal and can lead to a motivational shift which is driven by impulsivity and positive reward signals. Extensive research has been undertaken to assess the functionality of the orbitofrontal cortex within the brain in people with substance use disorder to understand the involvement in the inhibitory decision making process related to reward value and environmental stimuli. Dopamine plays a key role in the processing of reward-related stimuli with a strong association to drug use which allows for a further understanding of addiction and certain vulnerabilities to addiction. Traditionally, dopamine increases in response to natural rewards to food, water and sex in comparison to an artificial serve of dopamine which triggers an exaggerated reward.
Addicts and patients that surfer from substance use disorder have clinically shown to have reduced ability to inhibit impulses. This directly correlates with decreased activity in the frontal lobe of the brain. Patient who don’t suffer from this disorder can activate normal frontal lobe control mechanisms when triggered by a stimuli like sexual arousal however patients that struggle with SUD are unable to inhibit cravings when exposed to substance related stimuli. Frontal lobe activation is a intervention is used to condition patients to learn to activate inhibitory structures and inhibit specific substance cravings. This therapeutic cognitively introduces new learning to addictive behaviour. The continual study of neuroplasticity markers and mechanisms active in patients will correspond directly with new pharmacological and behaviour treatments towards prevention and subduing the growth of substance use disorders.
In the persecute to developing a comprehensive understand of addiction, debates have been conducted that conceptualise drug addiction as a chronic disease while others provide evidence of the role that choice has in addiction. A strong advocate of choice operating as the foundational block to the substance use disorder is Gene Heyman. Heyman’s “A disorder of choice (2009)” focuses on a range of relationships and descriptions that provide a central point for depicting normality and rational choice processes that lead to long-term outcomes like addiction. While Heyman acknowledges the genetic contributions he argues that genetic influence lacks a sound basis for concluding that drug abuse is a disease process which can be further challenged through related twin studies. A defining perspective discussed is the evidence showing that brain activity and neuronal functions appear differently in drug abusers and non-abusers which draws the conclusion that addiction is tied to changes in brains structure and function which defines it as a disease. This statement is challenged by Heyman as any persistent change in behaviour is directly associated with change in the central nervous system.
A complex theory was developed by Gary Becker and Kevin Murphy to categorise choice theory and define addiction as a rational economic choice. Becker and Murphy’s applied economic theory to the psychology of addiction and developed a model that hinged on the rationality of addictive behaviour and its similarity to consumers and the commodity of the consumption. This commodity is a representative of a substance for addicts and implies a cost/benefit analysis when consuming the substance. The rational theory invokes the significants of distress acting as a superficial trigger and pathway to using a substance as a benefit to reducing the emotional stress being felt by the user. Therefore, the user is balancing the complexities of the cost/benefit analysis and the considerations towards seeking treatment. As a result of the distress it can become a triggering event of the addiction but also the key component in maintaining the addiction. Becker and Murphy conceptualised the theory of addicts self medicating conditions like depression or anxiety and shaping a conscious choice to use a substance as a benefit of medicating to cope with feelings indicative of depression or other disorders. Both theories operate under the principle that addicts and people suffering with addictive disorders are making rational and logical choices towards their own addiction and using a cost/benefit analysis to determine an imbalance that may lead to prevention and treatment.
Treatments that attempt to reverse learnt behaviours exhibited in addiction can involve a variety of different interventions including Cognitive-Behavioural therapy (CBT). CBT in relation to substance use disorder has become progressively more relevant as a effective tool to combat and improve the mental health for the patient though behavioural and cognitive behavioural intervention. Strategies developed in CBT address both the association and operant consequence conditioning methods.
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