Development of Addiction and the Vulnerability of Addiction Relapse - Essay Example

Development of Addiction and the Vulnerability of Addiction Relapse; In relation to Acute and Chronic Stress. Adam ______ of Word Count: 4005 words (Excluding References). Abstract The paper seeks to explore the relation between Stress (Acute and Chronic) and the development of Addiction, along with the vulnerability to Addiction Relapse in a manner detailed enough to discuss the topic in the light of Neurobiological and Psychological Processes that connect the chemical and physiological systems that are responsible for or a consequence of the attained stress of whatever type it may be. This link will then be applied to the theories formulated with respect to behavioural addictions such as ‘Gambling’ and similarities and dissimilarities discussed in comparison with ‘substance addiction’. Development of Addiction and the Vulnerability of Addiction Relapse; In relation to Acute and Chronic Stress In order to elucidate the link mentioned in the title of the paper and to delve deep into the connections to be discussed, one must first explore the ‘meaning’ and to what the title represents as Stuart Hall states: It is by our use of things, and what we say, think and feel about them – how we represent them – that we give them a meaning (Hall, 1968). Meaning is important and extremely necessary to communicate the understanding of general terms, and is, in this case, important to represent a connection which will be theorised further into the paper. Basically (and by ‘basically’ the general idea is implied), stress is a state of mind which depicts the fact that something would have caused strain and strain being responsible for the production of stress that we feel mentally and physically another way to define it would be: The term stress is frequently defined as a process involving perception, interpretation, response and adaptation to harmful, threatening, or challenging events (Lazarus & Folkman, 1984). An example of stress and its interrelation to the mind and the body, would be to consider stress as a psychological value and then evaluate what could the outcomes be in physical form, for instance chronic stress could cause physical effects to the body in the form of fatigue or could cause the changes in physiological processes which could in turn cause the change in the blood chemistry and lead to a weaker immune system hence the physical or the biological (to be more precise) effect of a psychological function: stress. Likewise, stress can be caused by biological variables as in toxins, loud noise or drugs. Hence the relation; been established between stress and the way it interacts with the brain in a ‘superficial form’, one can proceed to discuss the link between Stress and Addiction and later on; stress and addictive behaviour. What we observe from our society and even the media is the fact that various ‘addictions’ have surfaced in this modern era. Be it drugs or other substance, be it behavioural or be it anything we feel we must keep on doing in a repetitive manner and involves the feeling of euphoria, for a part. What remains important is not the information ‘about’ stress but how the very ‘feeling’ is created and the basic neurological processes that support and present that feeling. The role that stress, be it acute or be it chronic, does play in the development of addictions is based on certain Neural Systems and their interrelated functions that in turn produce the feeling and response to stress. Events and occurrences that lead to stress always generate responses generalised as fear, anxiety, anger, excitement, pleasure and sadness (Sinha, 2001). Evaluation of an event or an occurrence conduct through the sensory nervous system’s circuits which also include the Thalamus, Insula and other sensory associative areas. Meaning and the importance of occurrences are a consequent of the Limbic-affective processing circuits which also include the Amygdala Interactions with sub-cortical and pre-frontal cortical areas; specifically orbito-frontal and medial pre-frontal cortices (Sinha, 2001). Another mechanism which is responsible for our defensive reactions is the input; direct to the Amygdala and the limbic-affective processing circuits from the thalamus and the frontal regions. The mentioned circuitry interacts with the biological adaptive systems and result in the production of stress-induced neuro-endocrine responses. The interconnectedness with Nucleus accumbens structures and the prefrontal cortex play an important role in approach and avoidance response selection and the mediation of goal directed behaviours, processes important in behavioural coping (Lovallo, 1997). The biological adaptive mechanisms with relation to stress majorly consist of two very important components of the brain stress circuitry. These two components involved in adaptation are ‘Corticotrophin Releasing Factor (CRF)’ and the brain stem (Locus Coeruleus); (Sinha, 2001). The CRF is released from Para-Ventricular Nucleus (PVN) of the Hypothalamus whereas noradrenergic activation is initiated in the Locus Coeruleus. Both of these components are activated through affective processing circuits which play a role in perceiving the occurrences which produce stress. This perception of a stressful occurrence sets in motion certain “central and Peripheral events” (Sinha, 2001) which involve the activation of the Hypothalamic – Pituitary – Adrenal Axis (HPA), along with the limbs of the activation of the autonomic nervous system. Mesolimbic Dopamine and brain Catecholamines in other limbic forebrain regions along with Endogenous Opiates are released and consequently contribute to augment adaptation to stressful occurrences. The Serotonin, Acetylcholine and GABA also contribute to the modulation of brain CRF and noradregenric circuits (Arborelius, Owens, Plotsky, & Nemeroff, 1999). Exposure to Chronic or Acute stress may encourage an individual to either adapt to and get used to or reduce or completely overcome stress through various Coping Strategies. These strategies are generalized as those that involve behavioural coping through which the individual directly deals with the stress accepting its source and then either altering it or one’s own exposure to that source. Another strategy to cope with stress includes the self regulation of one’s own emotional distress while another strategy includes the total avoidance of the stressful occurrence, denial in its existence and the lack of recognition of the event (Lazarus & Folkman, 1984). Numerous theories of addiction hypothesize that acute and chronic stress play an important role in the motivation to abuse addictive substances (Marlatt & Gordon, 1985). The stress coping model of addiction proposes that the use of addictive substances not only reduces negative affect but also increases the positive affect hence creating this ‘charm’ of the addictive substance in the perception of the abuser who then considers the abuse of addictive substances as, not only an effective but; the best coping strategy (Shiffman, 1982). A relapse prevention model, specifically referred to as ‘Marlatt’s relapse prevention model’ states that the individuals with poor coping resources are at an increased risk of addictive behaviour and substance abuse as opposed to other bio-psychosocial risk factors such as parental substance abuse, peer pressure and positive expectancies with respect to substance abuse (Marlatt & Gordon, 1985). The two models ‘Tension Reduction’ and ‘Self-Medication Hypothesis’ both reflect that if an individual is going through Acute or Chronic Stress; then the individual is compelled to cope with that stress he/she is experiencing through substance addiction which may enhance or alleviate emotional distress. Initially a drug may be used to modulate stress or to cope with distress but then...with repeated success it may lead to a sensation of an ever present response to stress or an excuse for mood enhancement (Sinha, 2001). Both these postulates suggest that however the situation may present itself: be the drug only be used for stress relief or be it for mood enhancement purposes, the vulnerability of the abuser to addiction is greatly increased. Based on Pre-Clinical findings it was observed “that stress leads to state related changes in the Brain Reward Circuits” (Sinha, 2001) and hence increasing the sensitivity to the reinforcing properties of drugs and thus consequent in the increased motivational characteristic to apply drugs instinctively. Accordingly, stress may act in a manner that changes the Brain reward systems which results in an enhanced efficacy of drugs, particularly those vulnerable to drug abuse (Piazza & Le Moal, 1998). Hence in simple words, stress may be considered to bring about changes in the brain systems that promote the effects of drugs and hence the matter may evolve into addiction and drug abuse. Research conducted on chronically stressed infant monkeys depict; increased levels of CRF in Cerebrospinal Fluid (CSF). Hypersensitivity of this kind pertaining to the CRF-HPA system has been linked to chronic distress states including anxiety (Arborelius et al, 1999). Studies on human subjects have shown that adverse life events, chronic distress and substance addiction are inter-related positively and affect each other (Sinha, 2001). Hence individuals that have experienced stress in a chronic form are at a risk to substance abuse so are adolescents with high levels of stress. These substances may include Alchohol, marijuana and nicotine (Sinha, 2001). The prevalance of high levels of chronic stress in adolescents is reported to cause high levels of addiction to substances such as alchohol, nicotine and marijuana (Riggs, Mikulich, Whitmore, & Crowley, 1999). In relation to the addictions acquired through exposure to Acute Stress; studies display that exposure to brief foot shock stress ‘reinstated’ drug seeking behaviour after extinction trials in animals dependent on heroin, cocaine, alchohol and nicotine (Buczek, Le, Stewart, & Shaham, 1999). Acute stress has similar affects on humans and increases the input of drugs and other substances as opposed to other non stressed subjects, thus resulting in addiction to those substances. Studies also represent that stress ‘co-activates’ the brain stress circuits and the putative reward circuitry in a manner simultaneous to each other and thus may enhance the drug taking experience and thus consequent in self administration and addiction (Sinha, 2001). Most of the common substances abused include Alcohol, Nicotine, Cocaine, Amphetamines, Opiates and Marijuana that stimulate Brain Reward Pathways also consequent in the activation of the brain stress systems (Kreek & Koob, 1998). And the activation of the Brain Stress Systems consequent in the increase of dopaminergic neurotransmission in brain reward pathways. These both systems; the neural circuitry in Brain Stress and the Reward Pathways, are known to overlap and the neuroadaptations in these circuits increase the vulnerability to stress and relapse in addiction (Sinha, 2001). Uncomplicated deductions from the discussions presented include that chronic stress, whatever the type of occurrence be, is reasoned to cause substance addiction so as to ‘cope’ with the stress experienced. These substances abused are then enhanced by the overlapping of the Brain Reward system and the Brain stress circuitry; this enhancement of the drug affects, leads to the dependence upon their euphoria effects as a coping strategy against chronic stress and hence result in Chronic Addiction, or simply long term addiction. These chronic addictions cause long term changes in the Brain and are responsible for addiction relapse. These long term changes in the brain caused by chronic addiction include the alterations in the brain stress circuits, namely the CRF – HPA and Noradrenergic Systems. For instance; chronic smokers, Alcoholics and Cocaine addicts depict ‘hypercortisolism’ (Wand & Dobs, 1991). Opiate addicts, on the other hand, depict low levels of ACTH and Cortisol (Facchinetti, et al., 1985). The acute withdrawal states are characterised by the increase in the CRF levels in the CSF, plasma ACTH, cortisol, Nor-epinephrine (NE) and epinephrine (EPI) levels (Kreek & Koob, 1998). Neurochemical tolerance in the HPA response to cocaine, alcohol, nicotine and opiates with chronic abuse has been reported (Mendelson, Mello, Teoh, & Sholar, 1998). These studies depict that the chronic addictions have a long term effect on the brain and are hence, in a way, responsible for addiction relapse pertaining to any substance abused. Alterations in the brain stress circuits during long term addictions are generally held responsible for relapse (Sinha, 2001). Chronic addiction or chronic drug abuse has known to cause long term alterations in the Brain Reward Pathways about which it is hypothesised that these alterations may be responsible for craving, drug seeking behaviour and addiction relapse (Robinson & Berridge, 2000). Data pertaining to alterations in the frontal and striatal regions of the dopaminergic pathways may be associated with affective, behavioural symptoms during addiction relapse (Porrino & Lyons, 2000). Robinson and Berridge postulated that neuroadaptations in the brain reward pathways due to chronic addiction underlie the ‘wanting’ and the ‘need’ an individual feels; the craving and the drug seeking behaviour may however, consequent in addiction relapse (Robinson & Berridge, 2000). Following discussion tends to conclude as to what relation there might be of stress to addiction relapse. Several studies were carried out to explore the relation of stress to addiction relapse, of which one was conducted using a unique animal model of relapse and results deduced by brief foot shock stress in drug free, yet dependent rats; depicted the reinstatement of drug seeking behaviour in rats (Buczek, et al, 1999) and hence the deduction that the rats experienced addiction relapse due to acute stress. Studies point out to the fact that brain CRF and NE circuits are directly involved in stress induced drug seeking, in ‘dependent’ animals (Sinha, 2001). In the case of Human Studies; clinical samples of drug abusers or addicts or alcoholics often cite ‘stress’ and negative affect as reason for relapse to drug use (Marlatt & Gordon, 1985), people who are in the phase of quitting smoking are susceptible to relapse if stressful occurrences are experienced (Shiffman, 1982), similar would be the case in recovering alcoholics, heroin addicts and cocaine addicts thus invoking addiction relapse in all of these cases if exposed to stress (Marlatt & Gordon, 1985). Behavioural addiction is not necessarily always a bad habit or process that should be avoided, ‘provided’ the behavioural addiction is kept in control; it might even help cope with day to day stress. It is in fact an affiliation that offers support to the addict. Seeing that almost everyone has a means to make themselves feel better or certain habits that make them feel better and optimistic in nature. But it is these very habits that if unchecked may lead to behavioural addiction. Let us consider the instance of ‘Gambling’ as an addictive behaviour. When a gambler behaves mindlessly and irrationally; the common reaction was, in the past, to treat him as a criminal or was rejected by friends and family. With the advent of the 1970s, studied and research material about this very situation was acquired and people began to see a compulsive gambler as an addict, or a behavioural addict to be more exact, but what happens with time is that the compulsive gambler loses control over the behaviour, denies that he/she has a problem, is easily depressed, and has a low self image (Engs, 1987). If a subject gambles under control or self restraint and keeps gambling in check; the behaviour has a positive value and helps cope with daily stress. Hence the gambling makes the person feel better and creates a sense of euphoria within the subject. An individual can become addicted, dependent, or compulsively obsessed with any activity, substance, object, or behaviour that gives him/her pleasure (Engs, 1987). But it is this sense of euphoria that creates a substantial divergence of a simple habit to a behavioural addiction. ‘Compulsive’; the term refers to doing something repeatedly or an irresistible impulse to act according to a certain behaviour. This (compulsive behaviour) in turn creates a good feeling and hence lays the grounds for behavioural addiction. We can say that behaviours are compulsive. The fact that Gambling is a compulsive behaviour puts almost everyone at risk for gambling addiction, but what matters most is the state of mind, the environment and the family history of the subject under consideration with respect to Gambling as a Behavioural Addiction. In most of the societies Gambling is a common habit (whatever the type of gambling be) and it is the promotion of this habit that most people in a society have, that may attract people to the development of Gambling addiction. Another influence could be the habits or in some cases addictions to gambling in a family, be it through the parents or blood relatives, do enforce the influence required to develop a gambling addiction. Another driving factor could be the role of genetics in gambling addiction; most cases include not only the influence of a strong genetic component or even a sociological or psychological component. This genetic transmission of the vulnerability to become a behavioural addict is strongest from father to son. Hence if a father has a gambling addiction, the chances of the son being another gambling addict would be high, though the uncertainty pertaining to Behavioural Addiction being driven by genetic, social or psychological factors exists in a manner not to be neglected and demands further research. The initial aspect of a behavioural addiction is of vital importance to the subject for if a good feeling is attained in this phase the chances of developing the addiction are immensely increased. For instance if a gambler wins big during the initial phase of the gamble or the acquisition of the gambling habit, it is more likely that gambling addiction will be developed. Gamblers who started gambling as a habit at a younger age are more susceptible to the development of Gambling Addiction at an older age as a compulsive form of behavioural addiction. This development of gambling addiction slowly pushes away the ‘good feeling’ from other activities and the person is left with solely one method of feeling good and hence will not leave gambling and be dependent on it even if faced with dire consequences. But as long as other aspects of acquiring the ‘good feeling’ is maintained, a gambler who plays frequently cannot be referred to as an addict or be accused of developing a behavioural addiction. Theoretically there are three stages that the Compulsive gambler experiences: the first phase is known as the ‘winning phase’ and it is in this initial phase that the gambler starts to develop the habit of gambling. Winning are high and morale is elevated due to the constant wins and the behaviour (gambling) is under control (Engs, 1987). The second phase is of ‘loosing’ that the gambler experiences. What happens is that the gambler starts losing money and out of frustration and in order to recover the lost amount, tries to borrow from friend and family. He/ she then tries to hide this loosing habit and hence is isolated from the worthy connections of the society (Engs, 1987). The last phase is of ‘depression’ in which the gambler looses all of his savings and investments and then starts to steal from his/ her family or friends or anybody, the main focus being; to win back what he / she had lost. This phase usually ends with the gambling addict losing his/ her job family friends and is isolated. Depression is common and in some cases suicides have also been reported (Engs, 1987).Behavioural addictions are often accompanied by Cross – Behavioural Addictions which include the abuse of Alcohol and Smoking. Hence the development of Behavioural Addictions such as gambling addiction is accompanied by the development of Smoking and Alcoholism as a Cross – Behavioural Addiction. With the passage of time Gambling Addicts may realise the absence of other activities in their life that produce the same level of ‘the-good feeling’ and hence find that the only interesting activity they’re left with is Gambling and this theory weighs more stress on them and may result in consequences of which the results vary greatly. Some addicts of gambling may recover out of it while others might even find themselves in serious life threatening consequences. In reality all addictions are the same be it substance - related addictions or be it behavioural addictions such as Gambling. As long as the same level of euphoria is communicated to the addict, it does not matter as to what the addiction might be. For any substance, procedure or behaviour to be addictive, it must convey a feeling of euphoria to the addict. Pharmacologically and biologically both; the substance addiction and the behavioural addictions, are almost at the same level and the brain is found to release the same chemicals, in both cases, so as to create an experience pleasant to the addict. It is speculated that, as in other addictive behaviours, perhaps beta-endorphines are produced in the brain, which causes the individual to repeat the behaviour to obtain the pleasant feeling. It is interesting to note that during treatment, compulsive gamblers undergo withdrawal symptoms similar to symptoms of persons addicted to depressant drugs: headaches, abdominal pain, diarrhoea, cold sweats, tremor, and nightmares (Engs, 1987). With respect to behavioural addiction, ‘gambling’ being the specific behavioural addiction under consideration for this paper; studies reveal that behavioural addiction or gambling addiction to be more precise, is a lot similar to substance addiction and abuse, in nature of the neurological functions within and the aspect of psychological dependence. Studies show that some Gambling Addicts have a lower level of ‘norepinephrine’ which is also evidently present in substance abusers’ NE circuitry and contribute in a way to self – administration (Sinha, 2001). Norepinephrine is also connected to states of stress and thrill. Studies also indicate the role of serotonin levels in both, the behavioural and substance addictions (Arborelius, et al, 1999). Some studies that have studied the connection report: A classic disorder of compulsive behaviour, patients are markedly impaired on this task and also show impaired olfactory identification (a further probe of OFC integrity) (Stekelenburg, Maruff, Olver, Purcell, & Pantelis, 2004). Interestingly, patients with OFC lesions show dissociation between knowledge and behaviour on the gambling task and other paradigms that test reward based decision-making (Bechara, Damasio, Tranel, & Damasio). Compulsive behaviour, as seen in both intractable addiction and OCD, requires dysfunction within two highly interconnected cortical systems (ACC and OFC) critically involved in self-regulation (i.e. the inhibitory system) (Goldstein & Volkow, 2002). Behavioural Addictions require a fundamentally potent and working routine that depict a repetitive manner in order to satisfy the requirements of the addict. The study of Parkinsons disease patients provides fascinating new insight into the brain mechanisms that underlie a predisposition to behavioural addictions, such as pathological gambling and shopping (Valerie Voon, 2010). The decision faced by a gambling addict is to make a choice between alternatives which could result in substantial negative outcomes. Hence, the possibility of the disturbed decision making ability: for those who demonstrate these compulsive behaviours (Valerie Voon, 2010). ‘Prediction Error’ which serves to help us determine and influence future choices has been hypothesised to play a role in Substance abuse cases but not yet associated with behavioural addictions. Dr. Valerie Voon in her study explains: A constellation of pathological behaviours, including gambling, shopping, binge eating, and hyper sexuality, is seen in13% of Parkinsons disease patients taking dopamine agonists. These behaviours are associated with factors predisposing to general substance abuse disorders, thus emphasizing a common underlying susceptibility (Valerie Voon, 2010). The results as documented by Dr. Voon and her Colleagues report: The results highlight a key decision-making process dysregulated by dopamine agonists in a population susceptible to compulsive behaviours and provide clues to mechanisms that underlie behavioural escalation in a disorder of behavioural addiction. The mechanism may also explain why anecdotally some patients describe the onset of their gambling symptoms after experiencing a win (Valerie Voon, 2010). The connection of Acute and Chronic Stress to the development of addiction and vulnerability to addiction relapse been explained in a detailed manner with respect to neurobilological and psychological mechanisms and the common grounds between Substance Addiction and Behavioural Addiction, regarding which ‘Gambling’ was taken into consideration; the concludory lines can be stated in lieu of the above discussion. The emerging Field of Biopsychology was one of the enabling factors which facilitated the thought process and provided the grounds for research with respect to the theme of the paper, in almost all the studies mentioned and referenced. Studies point towards more of the similarities in the mechanisms behind substance abuse/addiction and behavioural addiction than the potential differences between the mechanisms occurring in the neural pathways. References Arborelius, L., Owens, M. J., Plotsky, P. M., & Nemeroff, C. B. (1999). 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