This post will provide a discussion of the physiological effects of short and long term opioid use with special attention of brain-behavior correlations. While the research on the physiological aspects of opioid use is ongoing, the influence and value of the research on the field of psychology is already significant as opioid usage in the United States has reached a degree of a nationwide epidemic.We will begin by providing a brief history of opioid use before moving into a discussion of the prevalence. The etiological factors for opioid use is multifaceted and considerations will be briefly discussed while concluding with a discussion on the treatments for opioid use.
According to Merrer, Becker, Befort,and Kieffer (2009), the human opioid system has been engaged since ancient history. Opium, which is extracted from the seeds of a naturally growing flower, has natural and extremely effective pain relieving properties. In addition to the pain relieving benefits of opium, a feeling of euphoria is produced once the opium is introduced to the body. The first commercialized synthetic form of opium was produced in the 19th century and was called morphine. Morphine found its way into the United States in the 19th century during the US Civil War, through the channels of modern medicine as a pain killer for wounded soldiers. It was soon discovered that morphine had some highly addictive qualities, so heroin was introduced as the first non-addictive opium pain killer. In time, heroin proved to be just as, if not more, addictive than morphine and was soon outlawed; however, although the legality of heroin was changed the prevalence of heroin as an illicit drug has only increased overtime (Merrer et al., 2009).
In today’s market, there are many different forms of opioid based medications, which are designed to decrease pain. According to Schuckit (2016), contemporary commercial opioid medications such as oxycodone and hydrocodone are two of the most popular pain medications used today. Opioid based pain medications continue to undergo modifications as even though the risk factors for opioid use are well documented, opioids effectiveness as a pain killer is undeniable. Many complications arise when trying to effectively treat pain levels for individuals suffering from chronic pain. There is a current emphasis on the use of methadone, an opioid based pain killer, for chronic pain relief due to modifications made to the drug that manipulates the euphoric effect of the opioid, with the hope that it will reduce abuse reinforcement (Schuckit, 2016).
According to the American Psychiatric Association (2013), there is a 12 month prevalence rate of aproximentally 0.37% of individuals diagnosed with opioid use disorder. It is important to note that the 0.37% may not be an accurate representation of the generalizability of the disorder as many individuals are undiagnosed. According to Schuckit (2016), there is an estimated 400,000 individuals which have used heroin (i.e., synthetic opioid) in the past month alone and over four million individuals have used nonmedical (i.e., not prescribed to them by a medical professional) opioid based prescription pain relievers.
According to the American Psychiatric Association (2013), rates of opioid use are higher in males than they are in females. The male-to-female ratio generally falls around 1.5:1 for general opioid use; however, when heroin is isolated as the drug of choice than the ratio changes radically to 3:1. Prevalence significantly decreases with age with a peak prevalence rate at 28 years old. African Americans represent the lowest prevalence of opioid disorder (0.18%), while Native Americans account for the highest (1.25%). White Americans fall almost directly on the national average (0.38%) (American Psychiatric Association, 2013).
Research on biological etiology is ongoing, however to date there has been very few discoveries in regards to identifying one biological disposition that serves as the indicator for opioid use. According to Adisetiyo and Gray (2017), there is a significant correlation between attention-deficit/hyperactivity disorder (ADHD) and substance abuse. ADHD is a neurodevelopmental disorder that is commonly found in children in the United States, with over an 11% prevalence rate. One of the more significant risk factors for individuals diagnosed with ADHD is the engagement of some sort of substance abuse, which includes opioid use. Children that have been diagnosed with ADHD are three times more likely to end up developing a substance abuse problem, than an individual who has not been diagnosed with ADHD (Adisetiyo & Gray, 2017).
According to Groenman et al. (2013), due to the conclusive scientific research establishing ADHD as a high risk factor for the development of a substance abuse problem, major resources need to be infused into the study towards, and the development of, early intervention methods. Stimulant treatment for individuals diagnosed with ADHD is one of the leading treatment methods. Stimulant treatment can lower the risk for the development of a comorbid substance abuse problem (Groenman et al., 2013).
According to Hicks, Iacono, and McGue (2014), one option for determining etiology for opioid use is to identify the most prominent psychological characteristics that promote underlying risk. A few characteristics that serve as identifiers are as follows: impulsivity, rebelliousness, defiance, and aggressiveness. Research is ongoing, however the opportunity to substantiate psychological characteristics as etiological factors for opioid use is promising. In contrast, socialism (i.e., conformity to rules and conventional values) and boldness (i.e., social assurance and stress resilience) are psychological characteristics that are found to be resilience factors for the development of opioid use problem (Hicks et al., 2014).
According to Evren and Bozkurt (2017), impulsivity is a complex characteristic that can be defined as a predisposition towards not planned and rapid reactions to circumstances or stimuli. There is an increasing amount of scientific support for the strong association between impulsivity and substance abuse. Impulsivity can increase the risk for substance experimentation; furthermore, unique to opioid use disorder, continuous abuse of the opioid substance actually modifies the neurological makeup of the brain. This particular modification actually increases the levels of impulsivity in the individual, increasing the severity of the problem (Evren & Bozkurt, 2017).
According to Goodman (2017), adverse childhood experiences (ACEs) help measure levels of toxic stress that an individual has endured. High levels of toxic stress serves as one of the etiological factors considered for opioid use. Children’s exposure to traumatic experiences, also known as toxic stress, is widespread with 4 out of 10 children under the age of 10 being exposed to at least one component of toxic stress in the United States alone. Research has continued to conclude that there is an undeniable interconnectedness between the experiencing of adverse childhood experiences and the ensuing underlying drivers that contribute to the development of a substance abuse problem, and even more specifically, an opioid use dependency (Goodman, 2017).
According to Merrer et al. (2009), opioid receptors are broadly distributed throughout the brain and more specifically, throughout the peripheral and central nervous system. There are three primary opioid receptors, the mu, the kappa, and the delta. More recently, a fourth opioid receptor has been located and is identified as the nonopioid orphaninFQ. Opioid receptors play a major role in the regulation and manipulation of both the central nervous system (i.e., pain stimuli regulation) and the reinforcement system of the brain. The primary role of the opioid system is to regulate pain; however, the opioid system also regulates multiple other physiological functions such as respiration, gastrointestinal transit, stress response, and immune functions (Merrer et al., (2009).
According to Merrer et al. (2009), once the opioids are introduced into the system they rush to any available opioid receptor in order to form a bond. As previously mentioned, opioid receptors are found throughout brain and central nervous system. Once the opioid bonds with the opioid receptor on the nerve, the pain signal which was radiating from the nerve actually decreases in its intensity and in some cases, the signal stops altogether. The effect is the mitigation of the feeling of pain (i.e., pain killer). It is important to note that the opioid has no actual physiological healing or corrective component, it simply removes the signal to the brain that pain in the body exists (Merrer et al., 2009).
According to Kosten and George (2002), the mu opioid receptor is the primary receptor associated with reinforcement. Once the opioids are introduced into the blood system, they doc with the mu opioid receptor found in the mesolimbic (i.e.,midbrain) reward system. The results of the mu receptor activation is the activation of the ventral tegmental area producing and then releasing dopamine into the brain. This dopamine rush serves as a primary reinforcement factor of the opioid, as feelings of eurphoria and pleasure flood the brain. Dopamine also circulates through the amygdala, commonly known as the brains fear center,which results in an immediate decrease in stress and anxiety (Kosten &George, 2002).
Long Term Effect
Continued use of opioids over a sustained period of time can lead to an individual enduring some of the long term physiological effects of opioid use. Long term effects can vary in scope and in severity. Three of the long term effects of opioid use are discussed below: tolerance, dependence, and addiction. Brain abnormalities are a direct result of habitual use of opioids, these abnormalities produce changes in tolerance, dependence, and addictive behavior.Tolerance and dependence are two significant bi-factors of prolonged opioid use and are serious risk factors necessary to be considered for individuals using or prescribing opioids; however, these two bi-factors fail in comparison to the complex, broad, and severe, long-lasting effects of an opioid addiction (Merreret al., 2009).
According to Merrer et al. (2009), the continued use of opioids can have significant physiological effects. The immediate effects (i.e., pain relief and euphoria)gradually start to change as the pain relief received from the opioid begins to decrease, while in addition, the feeling of pleasure or euphoria also begin to decrease. This physiological phenomenon is referred to as tolerance. According to Keane and Hamill (2010), as tolerance increases the dosage required to maintain the same levels of pain relief and pleasure received from the opioid also increases. According to Kosten and George (2002), the continued exposure to increased dosage of opioids actually causes the brain to alter functions.This “altered function” presents itself by almost reversing behavior and cognition so that “normal” displays of cognition and behavior manifests when the opioid is in the system and “abnormal” displays are present when opioids are not in the system. Increases in tolerance can quickly result in a physiological dependence for opioids (Kosten & George, 2002.
According to Kosten and George (2002), opioid dependence can be described by the increased vulnerability to withdrawal symptoms. Withdrawal symptoms of opioid dependence can be severe, dangerous, and even life threatening. Some common withdrawal symptoms are nausea, headache, and severe diarrhea. In cases of sever withdrawal, an individual with an opioid dependence may experience depression,severe muscle cramping, and even seizures. Even if the opioid user desires tostop opioid use, whether it is due to the fact that tolerance has increased and as a result the effectiveness has decreased or due to the fact that actual pain has decreased to the point where the pain killer is no longer necessary, if a physiological dependence has been established than the individual may continue use for the primary reason of withdrawal symptom avoidance. Once a full opioid dependence has been established, than unfortunately the next phase is often addiction (Kosten & George, 2002).
According to Keane and Hamill (2010), there are two popular versions of addiction. The first being the neuroscientific model of addiction which can be categorized as a brain disease and the second is the behavioral model of addiction which is developed through the repeated exposure to an addictive stimulate (e.g., opioids). The neuroscientific model suggests that addiction is a biological brain disease and can be traced back to the molecular level. This model exposes itself to some obvious critique, the largest being that it limits the social influencers of addiction. According to Kosten and George (2002), there is a general understanding and consensus amongst professionals that repeated exposure to opioids does in fact modify the neurological pathways in the pre fontal cortex.The prefrontal cortex is the located in the front portion of the brain and is primarily involved in higher cognitive functions including planning and foresight. Some individuals may be predisposed with a higher susceptibility to the modification of those neurological pathways; however, there is limited research available that would actually prove the molecular determinant of addiction (Kosten & George, 2002).
According to Krebs, Kerr, Wood, and Nosyk (2016), course of treatment for individuals with an opioid use problem can differ depending upon the modality for treatment. Due to the high prevalence of opioid use, there is a continuing development of treatment methods; however, the three most prominent treatment modalities are pharmacology, out-patient treatment coupled with psychotherapy,and in-patient treatment coupled with psychotherapy. Depending upon severity of withdraw symptoms, often the initial course of treatment is pharmacology, which is performed through the administration of an opioid agonist treatment (e.g.,methadone, suboxone). Typical length of the opioid agonist treatment in order to treat withdraw symptoms is less than six days; however, it is important to note that methadone can be used as a long term pain suppressant for those suffering with chronic pain (Krebs et al., 2016).
According to Bilici et al. 2014, in-patient treatment and out-patient treatment can vary in course length (e.g., one to six months or more). In-patient treatment differs from out-patient treatment in the fact that in-patient is 24 hours per day (i.e., eat, sleep, therapy), compared to out-patient therapy which can vary from two to five intensive psychotherapy hours every day to two to five psychotherapy hours every week. The one consistent variable between all three treatment modalities discussed, is the fact that abstinence from opioid use is absolutely required. One of the main prognostic barriers to treatment is finances. In-patient and out-patient treatment can be considerably expensive,which makes some treatments inaccessible. Some health insurance companies do cover opioid treatments, however not every person has access to health insurance. An additional prognostic barrier is motivation for treatment. Many opioid users, even individuals that have been diagnosed with opioid use disorder, either are in denial that they have a problem or they simply lack the motivation to change their opioid use behavior (Bilici et al., 2014).
While research on identifying and evaluating etiological factors for opioid use disorder is ongoing, limited progress has been made in identifying symptoms which is critical for the development of accurate and early preventive measures.Early assessment and proper treatment of opioid use problem in individuals is highly important, as childhood and adolescent development stages are critical stages of development and serve as indicators for individual’s overall quality for mental health. Further research in early detection and evaluation of etiological factors for opioid use disorder for children and adolescents is advised.
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