The Biopsychosocial Model of Chronic Cocaine Addiction

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The Biopsychosocial Model of Chronic Cocaine Addiction

Post by cutthecashflow » Fri Jun 18, 2010 9:16 am

Christopher A. XXXXXX
Psychology 481
Dr. XXXXXXX XXXXXXX




Abstract
This paper explores the biopsychosocial (BPS) model of chronic cocaine addiction (CCA). A brief introduction is given stating the purpose of the paper. Then the biological, psychological, and social aspects of CCA are explored, followed by the interaction of these variables. Within each category of the BPS model individual studies are looked into to determine the significance of CCA. Potential therapeutic treatment approaches and future prevention approaches are discussed from a biological, social, and psychological perspective. A brief review of the paper is given, followed by potential implications of this paper and a personal experience with CCA.

The Biopsychosocial Model of Chronic Cocaine Addiction
This paper explores the biopsychosocial (BPS) aspects behind chronic cocaine addiction (CCA). More specifically, each individual area (biology, psychology, sociology) of cocaine addiction will be broken down to assess the individual affects that each area contributes to CCA. Likewise, special attention will be paid to the interaction of these three areas with respect to CCA.
Importance will be given to the factors that cause and contribute to the behavior of individuals suffering from CCA, as well as, factors that contribute to this debilitating disease. In addition, research based on current treatments and prevention approaches will be explored along with reflections on health issues associated with CCA from the perspective of the BPS model. Lastly, personal experience with a friend who has suffered from amphetamine abuse for the past eight years will be reflected upon to bring personal light onto the subject.

Factors That Contribute to Chronic Cocaine Addiction
It has been noted that CCA is a chronic brain disorder with psychosocial and neurobiological determinants (Fumagalli, Caffino, Racagni, & Riva, 2009; Schifano & Corkery, 2008; Vorel et al., 2001). Likewise, stress is often times a strong trigger for cocaine abuse that can cause cravings for cocaine while sensitizing behavioral and neurochemical responses to cocaine; leading to the facilitation and reinstatement of drug-seeking behavior after extinction periods of cocaine administration (Fumagalli et. al, 2009). The major potential for cocaine addiction has to do with increased dopamine levels; where natural rewards such as sex and food can double dopamine levels; self administration of cocaine can raise dopamine levels up to five times their normal levels (You, Wang, Zitman, Azari, & Wise, 2007).To better understand the BPS model of CCA each of the stages of the BPS model of CCA will be broken down into subsequent sections followed by an interaction section that will better guide the reader to a complete understanding of the BPS model with respect to CCA.

Biology
The most recent models to date have characterized CCA as a disruption of neural systems and synaptic plasticity involved in reward, motivation, learning, and memory (Fox, Jackson, & Sinha, 2009; Jones, 2008; Ungless, Whistler, Malenka, & Bonci, 2001). Cocaine acts as a dopamine agonist by blocking the reuptake of cocaine into the presynaptic neuron, this allows for increased levels of dopamine to be released in the Central nervous system (CNS), and hence the euphoric feeling that cocaine provides (Beveridge, Smith, Nader, & Porrino, 2005; You et. al, 2007).

More specifically, according to Ungless et. al (2001) the number and function of α-amino-3-hydroxl-5-methyl-isoxazole-propionate (AMPA) receptors at the postsynaptic membrane are increased following cocaine exposure. This implies that cocaine is causing learning to occur with respect to its reward. Likewise, cocaine withdrawal results in increased surface expression of AMPA receptors within the nucleus accumbens (Jones, 2008), ventral tegmental area (VTA), and hippocampus (Vorel et al., 2001). This is an important concept, because the aforementioned brain structures are highly implemented in the reward and learning process in both humans and rats. More specifically, Vorel et al. (2001) have shown that reinstatement of cocaine-seeking behavior in the rat has high validity for relapse in the human addict; and the rat and human share common triggers of relapse: cocaine, stress, and stimuli conditioned to cocaine.

In a carefully controlled study that was published in Nature Grimm, Hope, Wise, & Shaham (2001) trained seven groups of rats to press a lever for intravenous cocaine injection (.5 mg per kg body weight per lever press). The lever press was cued by a 5-second tone-light signal that accompanied each earned injection. The rats were put through this same experimental procedure for a period of 10 days of 3-hour training sessions twice daily. After the ten days the animals went through a withdrawal period of 1, 2, 4, 7, 15, 29, or 60 days. After the withdrawal period the rats were again exposed to the cuing paradigm (tone-light signal) and remarkably all groups of rats showed elevated neural responses (increased dopamine) to the tone-light signal alone; in absence of an intravenous injection of cocaine. This study illustrates that dopamine can be released in anticipation of reward without actually receiving the reward itself.

Psychology
Not only does cocaine act on a biological level, but it also is prevalent in many psychological behaviors. For instance, preclinical models of addiction have shown that stress and corticosterone-related mechanisms contribute both to learning deficits and drug-seeking in rats (Fox et. al, 2009). Likewise, cocaine dependent individuals show difficulties in executive control, attentional tasks of cognitive flexibility, motor skills, verbal learning, and memory (DeLeon, Grimes, Connor, & Melloni, 2002; Do Couto, Aguilar, Lluch, Rodriguez-Arias, & Minaro, 2009; Fox et. al, 2009), and often times show an increased level of anxiety and emotional negativity (Fox et. al, 2009; Fumagalli et al., 2009).

Relapse to cocaine addiction is frequently associated with subjective reports of craving, a state that accompanies and precedes cocaine seeking behavior (Grimm et. al, 2001). DeLeon et. al (2002) have shown that repeated cocaine use in humans and hamsters has directly led to elevated states of aggression. Evidence for CCA on psychological variables is therefore prevalent in a wide variety of cases. Fox et. al (2009) undertook a study with thirty-six treatment seeking cocaine dependent individuals (18 M/18 F). All participants underwent the following dependent measures: Salivary cortisol, perceived stress scale (PSS), and the Rey Auditory Verbal Learning Test (RAVLT). In this study, high cortisol, as measured by the salivary cortisol measure, in cocaine dependent patients and increased scores on the PSS in all participants was associated with worse learning on the RAVLT. This study and the aforementioned literature show that CCA individuals are at risk for a multitude of psychological disorders.

Sociology
Social environment can alter the responsiveness to addictive drugs, and adverse life experiences may make an individual more vulnerable to developing an addiction to drugs and relapse into drug seeking (Atkinson, Williams, Timpson, & Schonnesson, 2010;Do Couto et. al, 2009; Heinz, Witkiewitz, Epstein, & Preston, 2009; Schifano & Corkery, 2008). For instance, Atkinson et. al (2010) has shown that multiple partnering and non-condom use have been associated with the use of crack cocaine; with more frequent and intense use of crack being associated with greater numbers of sex partners, larger numbers of drug-injecting sex partners, greater frequency of sex while high on alcohol or other drugs, trading sex for money or drugs, and unprotected sex.

Married individuals are less likely to participate in drug seeking behavior than their single counterparts. Heinz et. al (2009) elaborate in great detail about The Monitoring the Future study, which found that 3.8% of married men and 2.0% of married women reported cocaine use, while 11.4% of unmarried men and 5.1% of unmarried women reported using cocaine. Similarly, it has been shown that negative environmental conditions such as crowding of adult mice, isolation, and social defeat, increase vulnerability of cocaine reinstatement; whereas positive environmental conditions, such as crowding during adolescence, cohabitation with a female, or an agnostic encounter with a nonaggressive male, produce protective effects against the reinstatement induced by cocaine (Anker & Carroll, 2010; Do Couto et. al, 2009).

Schifano & Corkery (2008) undertook data analysis in the United Kingdom (1990-2004) in relation to cocaine consumption, treatment demand, seizures, related offenses, prices, average purity levels, and deaths. Their research shows that most cocaine consumption takes place at clubs, raves, and similar venues. It was also shown that cocaine seems to have played a determinant role in between 1% and 15% of drug related deaths in the United Kingdom during this time period. They state that the recent rise in the popularity of cocaine is because of the increasing prices of commonly available psychoactive compounds, such as alcohol and tobacco. This increase in price decreases the demand for these drugs and at the same time cocaine has shown a drop in price in recent years, contributing to its increasing popularity. Cocaine therefore presents itself through many social venues and is an increasing problem throughout society.

Interaction through the BPS Model
It is important to note that the aforementioned variables do not work independently of one another; rather they are interchangeably influencing one another on a continuous basis. Once cocaine is administered it immediately begins to mediate its effects on the biological level, causing an increase in dopamine throughout the reward pathways of the brain. The CC addicted individual eventually requires more and more of the drug to gain prior effects and the absence of the drug leads to a negative change in psychological variables (aggression, anxiety, depression, learning and memory deficits). Further use of the drug begins to deteriorate prior healthy social networks and in turn unhealthy social situations are presented to the CC addicted individual (unhealthy sexual encounters, loss of social support, jail, and death). This entire cycle can begin with perceived stress to a situation where the individual finds immediate relief through cocaine administration (Fumagalli et. al, 2009). Eventually however, the euphoric feeling fades, stress increases, and unhealthy social behaviors ensue (Schifano & Corkery, 2008); perpetuating the individual into unhealthy habits and unwanted social situations (Anker & Carroll, 2010).

Current Treatment and Prevention Approaches
Cocaine treatment has been studied extensively in medical fields as well as in clinical psychology. Often times however, treatment efforts are hampered by high relapse rates (Grimm et. al, 2001; Schifano & Corkery, 2008; Vorel et. al, 2001). In light of this however there have been some promising treatment effects in the field of CCA.
It has been shown that glutamanergic agents such as Modafinil, have been shown to prolong cocaine abstinence; while at the same time improve both executive control and episodic memory in CC addicted patients (Fox et. al, 2009). This implies that improvement in learning and memory function in cocaine dependence could serve as an added marker of drug efficacy in future treatment development research. Likewise, potential improvements in mnemonic function could be acquired through psychotherapy or neuro-biofeedback. Another biological method of treatment has been suggested by Fumagalli et. al (2009), they have shown that brain derived neurotrophic factor (BDNF) injected into the prefrontal cortex attenuates cocaine seeking. This has only been shown in rats and ethical limitations limit the ability to test BDNF on humans, however, if a safe standard could be established BDNF could potentially curb CCA.

When considering treatment from a social perspective Heinz et. al (2009) state that treatment options should focus on protective factors, particularly marital satisfaction and closeness, during the course of interventions for those with substance abuse disorders. Anker & Carroll (2010) state that the earlier drug use is initiated, the more likely that an individual will have life-long problems with drug addiction. Due to this, it is vital that drug prevention programs be set up in schools at an early age to deter kids from experimenting with mind altering substances. Likewise community awareness to the dangers of cocaine use needs to be implemented in run-down urban areas, where the potential for cocaine/crack use is more prevalent (Atkinson et. al, 2010). Through a wide array of biological, psychological, and social treatment methods cocaine use can be attenuated and the prevalence of use in future generations can be significantly reduced.

Reflections from the Perspective of the BPS Model and Personal Experience with CCA
It appears from the preliminary research stuck into this paper that biological factors are the strongest link between health behaviors and chronic cocaine addiction. Once an individual makes the decision to self administer cocaine a series of biological events takes place rewarding the individual for their choice to ingest the drug. The stage is now set for repeated use and it is after these biological events take place that the individuals psychosocial behavior begins to change for the worse, leading them down a path of poor decision making and undesirable social situations. More research needs to be examined with respect to the social aspect of CCA, perhaps an individual’s environment that they grow up in predisposes them to risky decision making; this is one area that this paper did not pursue and future research should be guided in this direction.

I have a friend who has been using amphetamines (cocaine, methamphetamine, Ritalin, Adderal, etc.) for a period of approximately eight years. It started when his doctor initially prescribed him Concerta, everything was fine until he started snorting his pills, because of this he eventually graduated to harder amphetamines (cocaine, meth). I hardly see him anymore, but his behavior has changed drastically; he is impulsive, makes risky decisions, does not think about the future, lacks executive control, and he is often broke or without money due to his addiction. He has been fired from multiple jobs because he stays up for days at a time and he becomes a hazard at the work place. He has been in treatment several times and every time has failed, this implies that future treatment methods need to be explored. His parents, friends, and family have given up on him and his addiction I fear will lead him to an early grave. It is unfortunate, because this kid was full of potential growing up, he was smart, funny, and good with the ladies. Now his life is a living hell from which he cannot escape. I wish him the best of luck.



References
Anker, J.J., & Carroll, M.E. (2010). Reinstatement of cocaine seeking induced by drugs, cues, and stress in adolescent and adult rats. (2010). Psychopharmacology, 208, 211-222.
Atkinson, J.S., Williams, M.L., Timpson, S.C., & Schonnesson, L.N. (2010). Multiple sexual partnerships in a sample of African-American crack smokers. AIDS Behavior, 14, 48-58.
Beveridge, T.J.R., Smith, H.R., Nader, M.A., & Porrino, L.J. (2005). Effects of chronic cocaine self-administration on norepinephrine transporters in the non human primate brain. Psychopharmacology, 180, 781-788.
DeLeon, K.R., Grimes, J.M., Connor, D.F., & Melloni, R.H. (2002). Adolescent cocaine exposure and offensive aggression: Involvement of serotonin neural signaling and innervation in male Syrian hamsters. Behavioural Brain Research, 133, 211-220.
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Ungless, M.A., Whistler, J.L., Malenka, R.C., & Bonci, A. (2001). Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons. Nature, 411, 583-587.
Vorel, S.R., Yeshiva, U., Liu, X., Hayes, R.J., Spector, J.A., & Gardner, E.L. (2001). Relapse to cocaine-seeking after hippocampal theta burst stimulation. Science, 292, 1175-1178.
You, Z.B., Wang, B., Zitman, D., Azari, S., & Wise, R.A. (2007). A role for ventral tegmental glutamate release in cocaine seeking. The Journal of Neuroscience, 27, 10546-10555.
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