Theoretical Study of Substance Use Disorder and Emotional Dysregulation
John W. Airsman, PsyD
Distributed with Permission
Scope of Study: The scope of this theoretical review was in response to the problematic issue of high relapse rates in recovering from substance use disorders. Significant associated areas linked with the problem were thoroughly accounted for in the literature review. Key areas included theories of addiction, emotional dysregulation, interpersonal trauma, intergenerational trauma, and alexithymia. These areas were filtered through three research questions, asking questions about potential relationships between these topics, gaps in literature, and potential new theoretical approaches in considering a much more comprehensive picture of etiologies of substance use disorder. An interpersonal neurobiology was utilized as a theoretical lens to suggest an expanded theoretical interpretation for results. Significant themes emerged suggesting potential relationships between early childhood trauma and dopamine dysregulation, while suggesting a more comprehensive treatment modality in treating emotional dysregulation. Finally, a more complete definition, to supplement the ASAM definition, to encompass deeper and unrecognized underpinnings potentially linked to addictive disorders and relapse back into symptoms. Clinical implications of the study suggest a more comprehensive approach to treating emotional dysregulation, as well as underpinnings of addiction highlighted in the study. Creative ways of breaching the alexithymic barrier, that may be shielding unresolved interpersonal trauma may have benefits to improving motivation and reducing relapse.
OVERVIEW OF STUDY
Substance use disorder is problematic worldwide, as it destroys lives, disrupts and divides families, and influences criminal activity. Approximately 4.9% of adults in the world are plagued with alcohol use disorder (Gowing et al. 2015). What is more problematic is, that individuals who seek out treatment and attempt to put the diagnosis of substance use disorder in remission, have a high occurrence of reoccurring symptoms (Kassani, Niazi, Hassanzadeh & Menati, 2015). A theoretical systematic draw from previous literature will be utilized to establish a foundation for understanding substrates of addictive disorders and to comprehending the complexities of substance use disorder. Potential etiologies of substance use disorder such as emotional dysregulation through developmental trauma, will be researched utilizing an interpersonal neurobiological lens. The aim of the study will be to outline the problem underlying addictive tendencies and relapse potential. To mitigate the addictive epidemic, a theoretical review will be utilizing to establish a better working conceptual presentation of the problem.
Background of the Problem
Approximately 240 million adults wordwide, suffer from alcohol use disorder. Another 15 million individuals inject psychoactive drugs (Gowing, et al., 2015). Individuals diagnosed with substance use disorder, who attempt to put the diagnosis in remission, through engagement in treatment, report an 80% relapse rate during the first six months of treatment (Kassani, Niazi, Hassanzadeh, & Menati, 2015). Robinson, Robinson, and Menati, (2014) reported a 64% lapse in recovery after the first six months suggesting that the primary problem with substance use disorder is repetitive relapse. Relapse is not limited to individuals in early recovery from SUD symptoms. People with significant periods of abstinence, still may have a high affinity towards their drugs of choice (Robinson, Robinson, & Menati, 2014). Sixty percent of individuals relapse within the first three months of treatment. Another 75% return to their addictive behaviors within one year (Robinson, Robinson, & Menati, 2014). Mohammadpoorasl, Fakhari, and Akbari (2012) state that 75% of reoccurring symptoms can be traced to negative affective conditions, interpersonal undercurrents, ineffective social support, and socio-economical dynamics. This data reflects data that is indicative of a significant undeniable social problem.
According to Reavis (2013) assert that utilizing a treatment modality focused primarily on reductions of target behaviors (crime), avail poor results. It is imperative to focus therapeutically on neurobiological insults to the brain, in a determination to establish/reestablish healthy neurological connections that are integrated and supported socially. The data regarding criminality etiologies parallels other problematic behaviors stemming from interpersonal neurobiological origins. Among these other damaging behaviors is substance abuse (Reavis, 2013).
Emotional well-being is a result of connecting to healthy relationships. The essentials for a healthy psyche, psychological resilience, and regulatory functions for emotions are contingent upon building healthy social connections. Mindful focus improves linkages between the prefrontal cortex, limbic system and brainstem. These integrative systems in connection with healthy relationships produce healthy regulatory capabilities, in terms of improving overall executive control. Childhood relationships and attachment styles are critical times in developing significant capacities to self-regulation. Conversely, they are necessities for maintaining and improving nurturing relationships (Siegel, 2001, 2014).
Dysfunction in emotional regulatory functions can increase risk factors for developing substance use disorders (Stasiewicz, et al., 2012). O’Daly, et al. (2012) posit that research involving patients with numerous relapses/detoxifications, reflected changes in functions to emotionally regulate. These lacks of emotional necessities may impede the ability to socially interact, thus increasing capacities to isolate and exacerbating addictive tendencies.
Pre-existing or coexisting emotional states may be present with substance use disorders. Alexithymia can be a resulting internal condition stemming from lack of emotional regulation (Stasiewicz, et al., 2012). Alexithymia is characteristic of the inability to identify various emotions and express the emotion. Dysfunction of these components can manifest as dysregulation, lack of comprehension and identification of emotion, adverse temperament (mood) regulation, and self-sabotaging behaviors (Spence & Courbasson, 2012). According to Stasiewicz (2012), in alcohol-dependent adults, associations were reflected in the data indicating a relationship between alcohol dependence and emotional dysregulation. Alexithymia is a presenting condition that is associated with deficiencies in regulatory skills, thus increasing alcohol dependence. Spence and Courbasson (2012) assert that alexithymia has a direct relationship with inabilities to verbalize feelings. The capacity to describe and communicate emotions seems to be a vital part of emotional regulation. What becomes even more challenging are deficiencies not only with identification and verbalization of problematic emotion, but the emotions that are generated from the dysregulation dynamic that can create more difficult emotions, such as despair and confusion (Spence & Courbasson, 2012). Reward Deficiency Syndrome is a condition asserted by Blum (2014) that explains possible compulsive and impulsive seeking for psychoactive substances and behaviors that alter dopaminergic levels. This condition is characterized by irritability, dysthymia, and stress. People with this genetic polymorphism will seek to regulate their emotional condition. Alcoholic patients subjected to numerous withdrawals/relapses showed reductions in capacities to emotionally regulate from the prefrontal cortex areas of the brain (O’Daly, et al., 2012). Yan, et al (2012) found similarities in difficulties to emotionally regulate in samples of heroin-dependent users and pathological gamblers. This broadens the problem of emotional regulation to behavioral addictive patterns. Dvir, Ford, Hill, and Frazier (2014) suggested that childhood insults have a significant impact on later adulthood cognitions and behaviors, placing individuals at risk for developing substance use disorder (SUD). In agreement with this assertion is the fact that, childhood trauma can alter biological stress systems that can potentially increase vulnerability for the onset of SUD (Bettis, 2002). Both alterations in cognitions, behaviors, and changes in how one deals with stress can affect regulatory skills (Bettis, 2002; Dvir, Ford, Hill, & Frazier, 2014).
According to Enman and Unterwald (2014), nearly 52% of men and 28% of women have a comorbidity of alcohol use disorder and posttraumatic stress disorder. Individuals with PTSD have a high risk of developing SUD, which likely suggests that there is a coinciding neurological basis for both diagnoses, although more research needs to be conducted in this area (Enman & Unterwald, 2014). Tang, Posner, Rothbart, and Volkow (2015) assert that by improving self-regulatory circuits, there is improved executive functioning, and a reduction in negative emotion. Improvement in regulatory functions could mitigate cravings and relapse. This work suggest a significant association between self-regulation and self-control, as a means to regulate impulsivity.
Statement of the Problem
Relapse is a common theme among individuals attempting to recover from substance use disorder (Robinson, Robinson, & Berridge, 2014; Kassani, Niazi, Hassanzadeh, & Menati, 2015). Relapse can be preceded by inabilities to regulate negative affect, which can have their underpinnings in interpersonal trauma (Yan, et al., 2014; Bettis, 2002; Dvir, Ford, Hill, & Frazier, 2014). Blum (2014) posits that a deficiency of dopamine receptors influences negative affect, thus creating a neurological necessity for substance driven dopamine increase. Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013 assert that significantly high relapse rates suggest the possibility that underlying issues are going undiagnosed and untreated. More research and focus relative to these undiagnosed and untreated conditions is necessary to mitigate the social consequences of this complex issue.
Purpose of the study
A more complete understanding of emotional dysregulation is necessary to comprehend the underlying problem with addiction and relapse. A more extensive comprehension of dysfunctional regulation could facilitate mitigation of symptoms associated with interpersonal trauma, reward deficiency, substance use disorder and pre-existing conditions. This will require an extensive look at why relapse rates are high among recovery populations. A growing body of research illuminates trauma, inadequate stress systems, and reward deficiency syndrome as potential pre-existing conditions that precede substance use disorder, and therefore relapse back into substance use disorder (Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). It is hoped, that by helping individuals improve stress coping, enhance skills to engage in positive social connections, that this will increasing overall contentment with sobriety.
It will be the purpose of the study, based on the information noted previously, to answer specific research questions. What causes the underlying substrate of substance use disorder relative to emotional dysregulation? What are the underpinnings of emotional dysregulation that contribute to relapse? What is the relationship between interpersonal trauma and substance use disorders?
A theoretical framework of interpersonal neurobiology, and its assertions regarding healthy development of the psyche is supportive and essentially necessary in investigating what research results reflect concerning emotional dysregulation. A solid theoretical understanding of relationships and their effect on neurobiology will set the tone for comprehending problematic issues with emotional regulation that may lead to the necessity to use psychoactive substances. Viewing the problems of relapse and substance use disorder through an interpersonal neurobiological lens, may give insight to untreated conditions associated with affronts to childhood development issues, explaining the footholds of relapse.
Interpersonal neurobiology was introduced by Daniel Siegel, M.D. in 1999, and attempts to explain neurobiological development within the context of healthy social connection (Siegel, 2014). It asserts that the mind, brain, and relationships work together as an integrated system. Vigorous development is contingent upon relationships that foster the development and connectivity of all these vital three components. Early childhood relationships, through the process of attunement and mindfulness via caretakers, is the essential element in the development of systems that promote well-being, regulatory functions, functional stress systems, and the capacity to bond socially in a way that promotes mental health (Siegel, 2001, 2014).
Occurrences during childhood that are traumatic in nature can cause alterations neurologically to the systems that regulate stress (Wiet, 2017). This is the commencement of inabilities to cope and regulate stressors, which place these individuals at risk later in life for developing substance use disorder (Dvir, Ford, Hill, & Frazier, 2014; Wiet, 2017; Bettis, 2002). Caregivers transmit to their youth their capacities to regulate and self soothe, if this dynamic is not present within the caregiver’s psyche, the child will essentially take on the neurological features of the adult’s neurobiology (Siegel, 2001). Lack of significant attachments, are causation for potential insecure attachments. This interpersonal crisis can be traumatic in nature. Due to this, it provides explanations for how trauma can be transmitted generationally (Siegel, 2001). Comprehension of interpersonal neurobiological dynamics sheds light on explanations for emotional dysregulation, and the need to alleviate negative affect. It also explains could explain persisting conditions of alexithymia leading to sabotaging behaviors and relapse (Spence & Courbasson, 2012).
The study methodology was conducted utilizing a systematic review. This entailed collection and organization of data, analysis, and presentations of limitations. Keyword searches in numerous databases were utilized to accumulate an extensive collection of 107 journal articles, which were organized into a filing system using the Mendeley application. Publications were analyzed while identifying themes, gaps in literature, and potential associations between themes (Creswell & Poth, 2018). These pre-filter articles were used to formulate conclusions about relapse, substance use disorder, and emotional dysregulation.
Significance of the study
The outcomes of the study will be beneficial to clinicians that treat substance use disorder, as well as those individuals that suffer from substance use disorder. High relapse rates, deaths, and disrupted lives necessitate the need for a comprehensive approach to substance use disorder, which penetrates deeper than the behaviors of compulsive consumption. Underlying substrates, such as emotional dysregulation, influenced by reward deficiency, interpersonal trauma, and impaired stress coping systems, are the undiagnosed etiologies that drive substance use disorder and relapse cravings (Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). The results of this study will provide scientific literature with a more comprehensive cause of relapse, thus educating clinicians and researchers with a more complete approach to substance use disorder. This will substantiate the necessity for more development and research, which considers the components of interpersonal neurobiology and applies them to substance use disorder treatment.
Definition of Terms
Alexithymia is problematic awareness of identification and expression of emotional states (Stasiewicz et al., 2012).
Emotional dysregulation is the impairment of the necessary systems to control and modify affect(Parolin et al., 2016)
Emotional regulation is a multifaceted function that allows individuals to sustain and/or adjust affective conditions, which includes the capacity to modulate interval and strength of emotions (Parolin et al., 2016)
Relapse is a reappearance of symptoms related to substance use disorder after a period of absence. Primary symptoms being using the chemical in excess, coupled with the loss of control (Vengeliene, Bilbao, & Spanagel, 2014).
Organization of the study
The primary aim of the study will be to investigate substance use disorder dynamics and their relationship/interaction with emotional dysregulation A detailed look at the underpinnings of emotional dysregulation will be presented in a manner that gives a solid comprehension of the complexities of substance use disorder, which will require necessary focus on reward deficiency syndrome, interpersonal trauma, and dis-regulated stress systems. It is hoped that through the study, a clear revelation will reveal the necessity for additional research in the area of emotional dysregulation to mitigate high relapse rates.
An explanation and presentation of a systematic review utilizing Creswell’s spiral analysis was applied to article selection; followed by and an exhaustive presentation of results and definitive findings. This will necessitate an extensive literature review of the many facets that underlie the complexities of substance use disorder (Creswell, 2013).
The nature of relapse/ substance use disorder and possible associations and underpinnings with emotional dysregulation, necessitates an exhaustive exploration of literature. The literature review is organized into two sections. These sections are indicative of substance use disorder and emotional dysregulation. Section one gives a comprehensive review related to the vital theories of addiction. Although these theories overlap, each subsection integrates research and assertions on the components, concepts, and terminology of each modality of addiction and relapse. Subsections include, the role of genetics in addiction, incentive sensitization theory, reward deficiency syndrome, addiction is a stress disorder, and neurotransmitter dysfunction.
Section two gives an exhaustive review of the multiple aspects of emotional regulation. The necessity of healthy regulation is presented, followed by subsections related to multiple complications of dysregulation. Important subsections of consideration are, alexithymia, interpersonal trauma, intergenerational transmission, adolescent development, self-medication model, and attachment.
Theoretical Etiologies of Addiction/Relapse
The complex nature of addiction requires a comprehensive review of literature pertaining to the subject matter. Relapse and emotional dysregulation are an integrated dynamic of substance use disorder. Due to the density and interconnectivity of the features of substance use disorder, it is imperative to take a broad view of substance use disorder (SUD) in order to fully cognize and comprehend the immensity of the diagnosis. A command of relapse will also require a complete methodical perspective on several key theoretical etiological assertions regarding the nature of addiction. It is therefore significant to understand the many substrates contributing to SUD, to appreciate why so many individuals return to their self-sabotaging patterns of substance intake for the purpose of self-regulation (Parolin et. al, 2016).
Agrawal et al. (2013) strongly suggest that craving is an essential feature of SUD, which has an association with genetic predispositions. Agrawal (2013) discovered a significant higher number of a-synuclein in the alcoholics. This specific protein had positively correlated data linking it with craving for alcohol Schuckit et al., (2012) asserts the fact that certain individuals are labeled as low responders, when they require larger amounts of alcohol than higher responders. This genetic attribute requires low responders to increase alcohol intake to gain an effect equivalent to higher responders. This genetic phenotype is therefore a predictor of development of alcohol use disorder. Results suggest that there is underlying neurological substrate underpinning alcoholic low responding consumption of alcohol.
Identifying and isolating certain genetic factors that contribute to substance use disorder has been a perplexed process. This is due in part to the fact that, addiction genetics is far more complex than a solitary polymorphism. It is more likely that genetics of substance use disorder is a combination of a variety of genotypes. However, neurological imagery suggests that genetic variations along the dopaminergic pathway, which directly affect reward salience and sensitivity, are strong genetic contributory factors to substance use disorder (Sweitzer, 2012). Juli and Juli (2015) postulate that genetic tendencies tend to overlap relative to specific substance of addiction. There seems to be a common genetic pathway with smoking, alcohol, and opioid use disorders. Sun et al. (2013) postulate that the following phenotypes were observed with the three disorders, DRD2 and corticotrophin releasing hormone receptor. The DRD2 genotype was not a significant variant in alcoholism. Taiwanese studies agree with opioid Mu receptor genotypes in heroin users. The Opioid Mu and brain derived neurotrophic factor were present in opioid and alcohol systems. The DRD2 Taql RFLP allele exhibited the possibility of genetic predisposition to drug cues and craving (Sun et al., 2013). Most current research focuses specifically on specific typologies of drug of choice related to a relevant gene. More research is needed on commonalities of genetic pathways (Juli & Juli, 2015).
Dopamine is a significant neurotransmitter in reward learning behavior. However, connecting the chronic nature and relapsing potential of substance use disorder with genetic factors that influence dopamine receptor types, continues to be problematic to define(Gorwood, et al., 2012) There is enough evidence to suggest that there is a genetic relationship to dopamine receptors, however some data suggest that there may be connectivity to genetic factors surrounding impulsivity, that influence substance use disorder (Gorwood, et al., 2012). Ducci and Goldman (2012) expand on this assertion by including anxiety and reward genes alongside impulsivity. Monoamine oxidase A, SLC6A4, associated with serotonin, and catechol-O-methyl transferase (COMT) have commonalities associated with substance use disorder and other psychological diagnosis (Ducci & Goldman, 2012).
Incentive Sensitization Theory
Berridge and Robinson (2016) assert the Incentive Sensitization Theory of addiction. This lays forth the fact that the dopaminergic system is believed to be no longer the pleasure center of the brain. Instead, the mesolimbic dopamine pathway facilitates motivation, desire, and wanting. Learning and pleasure are facilitated by a separate system which involves the psychological process of liking. The neurological system responsible for liking is predicated upon the utilization and flow of endogenous opioids. (Berridge & Robinson, 2016; Blum, Gardner, Oscar-Berman, & Gold, 2012). Craving or wanting the substance of choice becomes the neurological response related to mesolimbic dopamine and glutamate alterations, due to introducing these neural pathways to high levels of the substance (Sinha, 2013).
Experimentation lesions were targeted at eliminating dopamine activity on rats. Results of this procedure showed that rats continued to respond to pleasurable stimuli, however motivation was eradicated (Robinson & Berridge, 1989). This brought into focus the idea of the mesolimbic system facilitating the psychological dynamic of wanting, rather than liking. The incentive sensitization concept was launched from this study. Incentive salience is a critical term in understanding this explanation for drug addiction underpinnings. Sienkiewicz-Jarosz et al. (2013) bridged incentive sensitization over to human neurology by asserting that patients with Parkinson’s disease do not suffer reductions in enjoyment in consumption of pleasant foods.
Incentive sensitization occurs after repetitive exposure to addictive substance to the mesolimbic system. This results in neural plasticity, resulting in hypersensitive development of the dopaminergic system. Due to hypersensitivity, the individual experiences an incentive salience. This incentive salience is a significantly high spike in the flow of dopamine. This results in powerful associations to the drug and environmental cues. These changes in cells and circuits have a high longevity, which persist long after acute withdrawal has ceased (Noël, Brevers, & Bechara, 2013; Berridge & Robinson, 2016; Volkow, Koob, & McLellan, 2016). It is possible that some of these neurological modifications are permanent (Berridge Robinson, 2016). It is this very dynamic that places individuals at risk for relapse, even after years of absence, which can manifest as unconscious wanting the drug and conscience craving (Noël, Brevers, & Bechara, 2013). This psychopathological (craving or wanting) response can be initiated by exposure to the drug itself, stress, or environmental cues (Berridge & Robinson, 2016; Sinha, 2013). Blum, Gardner, Oscar-Berman, and Gold (2012) assert that two separate systems modulating wanting and liking (Berridge & Robinson, 2016), is to unsophisticated, due to the fact that the complexity of the dopaminergic system is a dynamic involving multiple transmitters facilitating cascading flow. It is therefore not possible to explain this intricacy in terms of a single neurotransmitter (Blum, Gardner, Oscar-Berman, & Gold, 2012).
Sinha (2013) asserts that high levels of negative emotion or anxiety are not predictors of relapse, however intensification of the craving dynamic is a conjecturer of relapse. Although negative affect may increase during a craving episode, speculation by Sinha (2013) says that it is not the primary driving force behind relapse. A contextual perspective of a dysregulated (high arousal) state, is that craving predicts relapse. The stronger the craving, the higher the possibility of engagement in drug consumption (Sinha, 2013).
There are contrary assertions about the role dopamine in addiction. Volkow (2016) indicates that dopamine responses are displaced and inhibited during substance consumption. This is in no way correlated with environmental triggers and cues, rather this dopaminergic reaction is linked directly to the chemical ingested. This is in direct opposition to incentive sensitization reward salience. Berridge and Robinson (2016) challenge these postulations with the argument that diminishment of dopamine elicited by drug intake is not a consistent finding in research. Yoder (2016) suggest that dopamine is enhanced in the striatum in response to alcohol consumption by individuals diagnosed with alcohol use disorder. Berridge and Robinson (2016) assert there is an emerging body of research backing their earlier assertions that dopamine is not connected with hedonic facilitation. If substance usage is a means to negate dopamine deficiencies, in an effort to experience pleasure rather than anhedonia, this is in direct conflict with functionality of dopamine, according to the emerging evidence from studies.
The incentive sensitization theory gives evidence for relapse potential, even after months of absence. This is due in part to the fact that these neurological changes, due to incentive salience remain intact, meaning the sensitization dynamic remains embedded in the neurology of the mesolimbic system for considerable time. A stronger assertion indicates that during abstinence that sensitization may increase (Berridge & Robinson, 2016). Pickens et al. (2011) labels this dormant relapse potential as incubation of drug craving. This negates the claim that relapse later in abstinence is related to withdraw or neural suppression, because acute withdrawal symptoms have resolved within several weeks after ceasing substance consumption (Berridge & Robinson, 2016).
Reward Deficiency Syndrome
Blum, Gardner, Oscar-Berman, and Gold (2012) assertions regarding dopamine suggests that individuals susceptible to substance use disorder have a genetic predisposition to low levels of the neurotransmitter. This neurological condition can also be brought about by exposure to intense durations of stress, as well as exposure to addictive substance. The term reward deficiency syndrome (RDS) is the term that labels a dysregulation or dysfunction in the brain reward cascade pathway.
The deficiency of dopamine (RDS) has been traced to a deficiency in the DRD2 receptor gene. This genetic disruption influences reward cascade system which in turn leads to reward deficiency syndrome. Symptomology of RDS includes cravings and abnormal behaviors. It is this underlying dysphoric condition that compels individuals to seek out chemical substance that relieve the dopamine deficiency condition (Blum, Gardner, Oscar-Berman, & Gold, 2012). This asserts that relapse back into symptoms are result of individuals attempting to regain the dopaminergic affect after the system has become tolerant of exposure to the reward. Long-term use will diminish the dopamine response leaving the individual in a state of dysphoric disappointment. It this condition that drives the individual to utilize a substance to alleviate the dysphoria, or lack of a functional amount of dopamine (Blum, Gardner, Oscar-Berman, & Gold, 2012). This dynamic does not agree with Berridge & Robinson, (2016), in that the postulations suggest that relapse is brought about by an incentive salience dynamic that remains incubated well into abstinence, and can quickly be activated by cues and triggers. However, Blum, Gardner, Oscar-Berman, and Gold (2012) have similarities in agreement with Volkow (2016) in their assertions of low amounts of dopamine being an underlying condition in addiction/relapse. They differ slightly in the fact that (Blum, Gardner, Oscar-Berman, & Gold, 2012) suggest that this could be a condition that preexists before addictive patterns develop. Blum, et al. (2015) postulate that relapse is directly connected to insufficient dopaminergic functioning.
Stress and Motivation
Volkow, Koob, and McLellan (2016) propose that substance use disorder involves impulsivity and compulsivity encapsulated in a three-stage process. The initial stage is termed binge and intoxication, and is characterized classical conditioning occurring by repeated pattern of the reward of the chemical and contextual stimuli. Over a period of time this results in a decrease in dopaminergic response to the chemical ingested (Koob, 2015). This is very similar to the reward salience theory (Berridge & Robinson, 2016). It is suggested that compulsivity in drug intake can be explained by the fact that for natural rewards once satiety is achieved, dopamine response as the diminished. This is unlikely the case with addictive substance, due to the environmental cues and triggers (Koob, 2015;Volkow, Koob, & McLellan, 2016).
Volkow, Koob, and McLellan (2016) suggest a second stage of progression for substance use disorder termed withdrawal and negative affect. This phase is characterized by mitigating reward responses to healthy and ordinary stimuli. This is due to a reorientation of the reward system by means of conditioning. The psyche becomes quite inflexible, as the addicted individual comes hyper focused on drug and its associated cues. From a neurological perspective, lower amounts of dopamine are being released as subsequent attempts to use the chemical result in exacerbating disappointment. In regards to relapse, this restructuring of the motivational/reward system is believed to have durability well beyond termination of abuse (Koob, 2015).
Continued exposure to dopaminergic enhancement chemicals causes neurological alterations in the extended amygdala. This fosters a hyperactivity to stress, resulting in negative affective conditions. Pursuit of the effects of the chemical become simply a means to mitigate or eradicate feelings of dysphoria. This results in an intense push-pull dynamic, for the individual feels pulled towards the reward, and pushed out of avoidance of negative mental conditions (Koob, 2015; Volkow, Koob, & McLellan, 2016).
Volkow, Koob, and McLellan (2016) suggest that the final stage of addiction results in neurological dysfunction in the prefrontal cortex. This is caused by diminishing effectiveness of the role of the prefrontal cortex to facilitate decision-making, cognitive flexibility, self-regulation, and executive functioning (Lu & Richardson, 2014; Volkow, Koob, & McLellan, 2016). This is caused by an impairment to dopaminergic and glutamatergic structures. With the limitations of these necessary functions to regulate self, attempts at changing lifestyles are difficult to achieve (Koob, 2015).
Koob (2015) asserts that substance use disorder can be described as an allostatic brain dysregulation involving the dopaminergic reward and stress system. It is suggested that maybe incentive salience occurs during the first usage of the substance (Berridge & Robinson, 2016; Koob, 2015). Subsequently, the brains stress axis is activated during the binge/intoxication phase (Koob, 2015; Volkow, Koob, & McLellan, 2016). This is followed by a cascading flow of occurrences beginning with activation of the hypothalamic–pituitary–adrenal (HPA) axis, while corticotropin releasing factor activates in the prefrontal cortex and amygdala (Lu and Richardson, 2014). This effects the release of dynorphin in the ventral striatum. Lu and Richardson (2014) suggest a neurological conduit alterations, due to exposure to alcohol and stress hormones, which essentially causes adaptive changes in the prefrontal cortex. This dynamic impact on prefrontal cortex PFC functions could have a direct sway on inhibiting the neuroendocrine system, thus increasing dependency and exacerbating relapse potential. Longevity of large consumptions of alcohol impact glucocorticoid alterations to the HPA axis and prefrontal cortex, which in turn cause dysfunctional conditions in the neuroendocrine system (Lu & Richardson, 2014).
Resting State Dysfunction (GABA and Glutamate)
Moeller, London, and Northoff (2016) suggest that substance use disorders are a dysregulation of the brains neurological resting state. Glutamate (excitatory) and gamma-aminobutyric acid (GABA)(inhibitory) are regulatory neurotransmitters, that cooperatively collaborate to balance the system, in critical areas of the brain anterior cingulate cortex , prefrontal cortex, insula, and striatum). Neuroimaging indicated decreased GABA dispersal and accessibility in subjects that were diagnosed with SUD. This data was limited to nicotine, cocaine and alcohol addiction. PET scans for GABA in nicotine and polysubstance abuse showed an increase of GABA activity. Additional research is needed for marijuana, methamphetamine, and opioids. Magnetic resonance spectroscopy revealed depleted activity of glutamate for alcohol, nicotine, opioids, and methyl amphetamine, and cannabis users. Cocaine indicated no noticeable differences between the test groups. PET scan data was positive for reduced glutamate functioning in individuals utilizing nicotine, cocaine, and polysubstance abusers (Moeller, London, & Northoff, 2016). More research needs to be conducted to sort out inconsistencies and validate existing research.
Glutamate plays a significant role in the acquisition of addictive patterns in the brain (Burnett, Chandler, & Trantham-Davidson, 2016; D’Souza, 2015). Unlike natural rewards, chemicals of addiction produce a high level of dopamine release in the mesolimbic system (Berridge and Robinson, 2016; D’Souza, 2015). Due to the intensity of drug effects, in some cases occasional recreational uses translates into compulsive seeking and usage of the chemical. Glutamatean excitatory transmitter is abundantly present within the synapses of the nervous system (D’Souza, 2015; Moeller, London, & Northoff, 2016). Chemicals of addiction increase synaptic transmissions of glutamate in the ventral tegmental area, which is instrumental in initiating the firing of the dopaminergic system (Berridge and Robinson, 2016; Blum, Gardner, Oscar-Berman, and Gold, 2012; D’Souza, 2015). Compulsive chemical consumption fosters neuroadaptations via neuroplasticity. This is believed to cause an imbalance in the resting system, thus creating an abundance of glutamate (Moeller, London, & Northoff, 2016). This in turn becomes problematic when chemical use terminates, copiousness amounts of glutamate activity are believed to be the underlying substrate for craving and relapse. Detoxification from alcohol presents with a high level of anxiety, negative affect, dysregulation of stress systems, and significant dysphoria. Excessive glutamate is the underpinning neurotransmitter imbalance that drives these symptoms in humans and rodents (Burnett, Chandler, & Trantham-Davidson, 2016).
D’Souza (2015) asserts that blocking glutamate activity reduces drug rewards. Targeting glutamate transmissions with medication can also have unanticipated effects on memory, learning, and rewards from natural stimuli. The necessity of medication assisted treatment that targets glutamate as it relates to dopaminergic facilitation of drugs of high salience. Scofield, et al. (2016) assert that drugs of addiction produce long-standing alterations in glutamate transmissions. Relapse potential has a strong neurobiological component.
Genetic predisposed progressive deterioration, due to substance use disorder, adversely affects major brain systems (Agrawal et al., 2013; Schuckit et al., 2012; Gorwood, 2012). The dopaminergic, neuroendocrine, and prefrontal cortex regulatory functions are susceptible to dysfunctional states (Noel, Brevers, & Bechara, 2013; Berridge & Robinson, 2016; Volkow, Koob, & McLellan, 2016). As addiction progresses, dopamine responses are diminished, while corticotropin release factor (CFR) and dynorphin exert stress in an opponent process dynamic to establish allostatis (Koob, 2015). What is problematic, is that once chemical intake has ceased, the stress systems remain active for a considerable period during abstinence. This creates a mental environment of anxiety, irritability, and hyperkatifeia. The combination of drug cues/triggers, exacerbated stress systems, and limited function PFC creates a high relapse potential (Koob, 2015; Noel, Brevers, & Bechara, 2013; Berridge & Robinson, 2016; Volkow, Koob, & McLellan, 2016).
Emotional regulation (ER) is a mental strategy/process that facilitates control over affective mental conditions (Dvir, Ford, Hill, & Frazier, 2014; Tang, Tang, & Posner, 2016; Parolin et. al, 2016). Self-regulation (SR) is an integrative function of attention, incentive, and behavioral response. From a definitional perspective, very similar to emotional regulation, as it involves inhibitory functions behaviorally, and mental regulatory abilities to mitigate emotional content (Busch & Hofer, 2012). Bridgett, Burt, Edwards, and Deater-Deckard (2015), indicates that self-regulation is psychological flexibility in the domains of cognition, behavior, and emotion. Deater-Deckard (2015), acknowledge the variety of terminology utilized to describe regulation, but generally agree in its multifaceted component of disposition that includes a biological and genetic basis. They add that it is also a process and is created over a period of time, and is influenced biologically, genetically, and environmentally. Emotional dysregulation is contrary to healthy regulation and can manifest in a multitude of ways resulting in psychopathology, negative affect, externalizing behaviors, and substance use disorders (Banducci, Hoffman, Lejuez, & Koenen, 2014; Guina, Nahhas, Goldberg, & Farnsworth, 2016). Research suggests that emotional dysregulation can stem from lack of interpersonal development, which can be transmitted generationally (Bridgett, Burt, Edwards, & Deater-Deckard, 2015).
Processes/Concepts of Emotional Regulation
Research data suggests that there is a substantial link between self-regulatory functions and well-being; as well the possibility of this neurological mechanism being instrumental in the development of personality. Attainment of self-regulation may be a catalyst to successful development in other critical areas (Busch & Hofer, 2012). This ability extends to regulating duration and intensity of emotional experience, as well as expression (Dvir, Ford, Hill, & Frazier, 2014; Tang, Tang, & Posner, 2016; Parolin et. al, 2016). Eisenberg and Sulik (2012) indicate that ER is a mental function that coordinates emotional intensity and intrinsic emotional motivation. It also includes regulation of physiological responses to emotions, as well as behavioral response.
Dvir, Ford, Hill, and Frazier (2014) suggest that emotional regulation(ER) is an intricate function of numerous complex progressions/processes involving psychological, biological, and interpersonal domains. Cognitive and emotional functions link in an interchange to select, adapt conditions, position attention, assimilate information, make decisions, and select the appropriate reaction. Researchers generally agree regarding ER definitionally, however there some disagreement about whether extrinsic influences should be included in the description e.g., parental attunement (Eisenberg & Sulik, 2012). Parolin et. al, (2016) advocates that ER is a function of both intrinsic and extrinsic influences, although agrees with the previous accepted definitions among most researchers. Explicit and implicit processes have been implicated in the functioning of this mental system. Eisenberg and Sulik (2012), assert that although numerous researchers agree that ER is initiated at both the conscious (effortful control) and unconscious (reactive control) level, automated unconscious regulatory functions are possibly more consistent and effective.
Busch and Hofer (2012) in presenting the necessities for self-control as an intricate necessity across a lifespan, hone into three specific components that encompass effort control. Attentional control, giving psychological flexibility to move attention off a distressing stimulus parallels attentional deployment, the concept of attentional deployment related to emotional regulation (Eisenberg & Sulik, 2012). Activation control, is essentially a degree of control over the ability to recruit motivation for action with the desire to engage a behavior when lacking impetus (Busch & Hofer, 2012). The third component of self-regulation, is termed inhibitory control, which is the mental capability to not engage in impulsive behavior. Having a high degree of functionality with effort control, enables an individual to experience a high degree of emotional satisfaction. The capacity for psychological flexibility, via attentional control, seems to be a stable construct at the age of seven throughout the remainder of a lifetime (Busch & Hofer, 2012).
Attentional deployment, cognitive reappraisal, and emotional awareness are vital to the process of emotional regulation. Attention deployment governs the focus on the situational aspects of the stimulus. This component can influence emotion to become increasingly negative (ruminating) or alleviated intensity through altering focus. Eisenberg & Sulik (2012) label this process effort control meaning having possession of psychological flexibility, to shift attention as situations necessitate appropriate responses. Cognitive reappraisal is the changing or altering the thought interpretation/meaning of the stimulating circumstances. Emotional awareness is the ability to identify and differentiate emotions. This feature is utilizing to appraise and assess emotions in self and other human beings. This is an essential component for social cognition, which is the capacity to relate to connect others, through empathy, logic and emotions (Dvir, Ford, Hill, & Frazier, 2014). Gross (2015) assert a similar model for emotional regulation, involving situation selection, situation modification, attentional employment, cognitive change, and response modulation. Situation selection involves making a choice that would increase or mitigate the potential for emotional reactivity. Situation modification, simply is defined as actions or choices within the selected situation to modify emotion. Attention deployment, is in agreement with (Eisenberg & Sulik, 2012), asserts the necessity for focusing with the intention of regulating or influencing a response. Cognitive change is essentially modification of the situation through utilization of appraisal. Finally, response modulation has a direct impact on behavioral and physiological responses to the previous stages (Gross, 2015).
Eisenberg & Sulik (2012) assert that emotional regulation begins in childhood and continues through adolescence. This process begins early in life during infancy, through the caregiver’s gentleness and responsiveness to the infant’s needs. Critical years for acquiring regulatory necessities begins during toddler years. This is done through parental or caregiving adults engaging young children during emotional intensity in a manner that self-soothes the child. Siegel (2001) suggests that consistent and nurturing connectivity between a child and a safe parent generates a secure attachment. This produces a neurological interpersonal necessity for the development of effective self-regulation.
Bridgett, Burt, Edwards, & Deater-Deckard (2015) indicate that inadequate self-regulatory abilities have been consistently associated with negative behaviors. Healthcare costs, criminality, problematic student behavioral issues within the education system, and a significantly greater potential for development of substance use disorders. Self-regulation has also been cited as a substrate feature of low self-esteem (Busch & Hofer, 2012).
Deficiencies in mental abilities to mitigate bodily responses to intense feelings, utilizing flexibility in choice during cognitive appraisal, choice during selection of focus, and selection of a behavioral response constitute emotional dysregulation (Nobile, et al., 2016). Spence and Courbasson (2012) suggests that emotional dysregulation is a failure of functionality of three processes. These are recognition and description of emotions (alexithymia), inabilities to regulate negative affect, and poor choices in behavioral responses.
Problematic dysfunction with the regulatory system may result in deficiencies to regulate emotion and may be a precursor to common mental diagnosis, such as depression, borderline personality disorder, bipolar disorder, and substance use disorders (Dvir, Ford, Hill, & Frazier, 2014). Tice, Bratslavsky, and Baumeister (2001) suggest that individuals with significant internal distress will make choices to regulate themselves. Essentially, the need to emotionally regulate supersedes the control of impulsivity. Thus, compelling behavior that quickly mitigates and medicates uncomfortable feelings. Banducci, Hoffman, Lejuez, and Koenen (2014) assert that emotional dysregulation is a multifaceted dynamic, involving low levels of awareness, complications in comprehension of feelings, difficulties validating emotions, and problematic expression. A unique contributing factor to emotional dysregulation asserted, is the low motivation and/or unwillingness to endure uncomfortable emotions to achieve or attain a purposeful goal. Any discomfort while striving for self-actualization or improvement in quality of life, is quickly subverted due to inabilities to cope with stress and feelings associated with behaviors outside of familiarity (Banducci, Hoffman, Lejuez, & Koenen, 2014).
Tang, Tang, and Posner (2015) propose that substance use disorders consistently coexist with symptoms such as, deficiencies of self-control, difficulties regulating stress, and problematic regulation emotion. In general, literature agrees that negative affect contributes to problematic drinking, as this in turn contributes to inabilities to make mental adjustments to mitigate emotional intensity. Research is lacking on exploring which facet of emotional dysregulation contributes or predicts alcohol use disorder (Veilleux, Skinner, Reese, & Shaver, 2014). Parolin et. al (2016) suggests that addictive disorders consistently present with inadequate regulation abilities.
Wilens et. al (2013) asserts a different terminology in describing emotional dysregulation. Deficits in emotional self-regulation (DESR) is essentially similar to other research definitions of emotional dysregulation, but specifically include irritability and inappropriate displays of emotion such as laughter or crying. Current research is attempting to focus on DESR and its association with addiction, specifically nicotine and substance use disorders. There is also data that suggests a relationship between marijuana and opioid use, and deficiencies of self-regulation (Wilens et. al, 2013). There is consideration of the fact that DESR may be a stable construct, as it persists after substance consumption have terminated. Wilens et. al (2013) highlight a significant result in research which targeted 325 infants at risk for substance use disorder over a 19-year time span. This longitudinal study suggested that DESR did not predict any mental health diagnosis, but indicated correlations with suicidal ideation, inadequate self-regulation, and substance use disorders. Unlike definitions for emotional dysregulation, DESR includes that both positive and negative affect. Positive affect pertaining to symptoms such as mania. Effortful control is also considered part of the affect regulatory problem (Busch & Hofer, 2012; Wilens et. al 2013; Eisenberg & Sulik, 2012). DESR may be an underlying substrate in the development and maintenance of substance use disorders. A vital concluding fact, regarding SUD and DESR, is that there is a significant overlay in neurological mechanisms (Cheetham, Allen, Yücel, & Lubman, 2010; Wilens et. al, 2013). There is developing research that reflects an association between dysfunctions in emotional learning and children showing biological and genetic markers to future alcoholism (Cheetham, Allen, Yücel, & Lubman, 2010). Cheetham et. al. (2014) conducted research that suggests that structural abnormalities to the anterior cingulate cortex (ACC), specifically the left portion of the ACC, predicted alcohol consumption that was problematic. The ACC is instrumental in emotional/self-regulation. Although this portion of the brain is involved in affective functions, the research suggested that problems related to alcohol consumption and abuse were linked with increased levels of negative affect. The research data was unable to correlate the ACC with negative affect. Recent research targeting the orbital frontal cortex (OFC), which is a brain structure handling effort control, indicated that adolescence with an atypical smaller volume of this region of the brain, has the potential increase in developing substance use disorders (Cheetham et. al., 2017). The studies by Cheetham at. al (2014, 2017) assert a biological and potentially genetic basis for deficiencies in emotional self-regulation.
Alexithymia and Substance Use Disorder
Alexithymia is a condition with difficulties in identifying and describing emotions. This malady can be coexisting with substance use disorders (Krentzman, Higgins, Staller, & Klatt, 2015; Parolin et. al, 2016). Krentzman, Higgins, Staller, and Klatt (2015) suggest data that reflects 45% to 67% of alcohol use disorder subjects with presenting symptoms of alexithymia. Parolin et. al, 2016 asserts that alexithymia is a component of emotional dysregulation, which is a trademark feature of substance use disorders. Krentzman, Higgins, Staller, and Klatt, (2015) expands the defining of alexithymia by including problematic symptoms with somatic issues, as well as underdeveloped ego defense mechanisms. Craparo, Ardino, Gori, and Caretti (2014) agree with the latter definitions, but have unique perspective, by indicating that the psychological numbing present with alexithymia reflects a parallel to what is observed in dissociative disorders. The emotional avoidance dynamic present in alexithymia and disassociation are viewed as a survival strategy to help trauma survivors manage the flooding of intense negative emotion. More research is needed understanding and explaining the associations of interpersonal trauma, alexithymia, and disassociation. The data suggest that dependency on alcohol could be considered a dissociative condition.
Stasiewicz et al. (2012) suggest data that alexithymia is related to emotional dysregulation, and presents symptoms of ineffective abilities to achieve mindfulness, and reduced effectiveness in utilizing coping skills in both genders. Craparo, Ardino, Gori, and Caretti (2014) suggests that early insults in the development of a child disrupt cognitive and affective processes. These neural adaptions later in life make identification and expression of emotion a daunting and difficult task. These individuals may present symptoms such as, feeling overwhelmed, due to the buildup and intensity of unexpressed emotion. This may foster a necessity to manage emotional numbing and intense negative affect by consuming alcohol.
Spence and Courbasson (2012) define alexithymia as difficulties in identifying emotion, describing emotion, emotional differentiation, and emotional expression. Individuals suffering with alexithymia tend to focus on extrinsic stimulating factors, rather than their own unique emotional experience. Alexithymia is a common feature with substance use issues (Spence & Courbasson, 2012). Although multiple studies suggest a relationship between alexithymia and alcohol use disorder, research is limited in viewing this relationship from the perspective that encompasses genetic and environmental factors (Stasiewicz, et al. 2012). Parolin et. al, 2016 differentiates primary from organic alexithymia, and asserts that the conditions onset is due to genetic predisposition to a personality trait. The organic type (secondary) is derived from mental disease or brain trauma. Stasiewicz et al. (2012) agrees with the latter definitions from other researchers, but asserts a unique perspective indicating that alexithymic individuals are prone to utilizing suppressive coping skills, rather than cognitive reappraisal. These individuals will have intrinsic tendencies to suppress negative feelings, while inhibiting expression outwardly of these internal conditions.
Petit et al. (2015) concurred with numerous other clinical definitions explaining the alexithymia, as well as agree that it may be a central symptom associated with alcohol use disorder(AUD). Further assertions, integrate the importance of social connectivity being contingent upon healthy regulatory functioning. Krentzman, Higgins, Staller, & Klatt, (2015) agree by positing that adaptability to emotional cues are essential to social functioning, and that alexithymic symptoms may interfere with this critical component to interacting with the environment. In referencing response modulation (Gross, 2015), Petit et al. (2015) indicates that response modulation is associated with negative responses. Individuals with AUD will be prone to responding with negative responses during the final response stage which provokes some type of action. Conversely, an emotionally regulated human would demonstrate efficacy during the cognitive change stage. This condition that impairs cognitive change in alcohol use disorder may stem from cognitive deficiencies directly related to intense exposures and long durations of alcohol consumption (Petit et el., 2015). Long-term exposure to intoxicating substance have an insulting impact on vital functions of the prefrontal cortex. This may give explanations for decrease abilities to utilizes earlier stages in the emotional regulation process (Gross, 2015).
It is possible that treatment modalities that focus on facilitating addicted individuals with attentional employment may have good outcomes in attenuating relapse; since data suggests that craving/relapse is seemingly associated with utilization of response modulation (Petit et al. ,2015). It is suggested that craving is a response to the negative affect, due to lack of efficient regulatory interventions during the latter stages of the process. This gives validity to the self-medication hypothesis, which serves as a negative means by which to regulate painful and intense negative affect (Khantzian, 2012; Petit et al. ,2015). Another possibility of impaired healthy functioning during the early stages of the regulatory functions, may be the significant strength of substance wanting (Berridge & Robinson, 2016; Petit at al., 2015). Krentzman, Higgins, Staller, and Klatt (2015) reported data that suggested that individuals with diminished emotional regulatory capabilities were more prone to relapse after discharge from treatment. Stasiewicz et al. (2012) suggest data that there is a limited relationship between alexithymia and successful treatment goals in elimination of the drinking problem. Parolin et. al, (2016) conclude several relevant facts about alexithymia and addiction. Emotional dysregulation indicates a lower emotional intelligence. Specifically, difficulties in stress regulation and managing intense emotions. Individuals reported significant difficulties in achieving and maintaining positive emotions and well-being. With problematic issues surrounding interpersonal and intrapersonal domains, this condition can complicate the necessity for social connections during treatment, and relapse prevention.
Krentzman, Higgins, Staller, and Klatt (2015) inadvertently during research became aware of data that suggested that individuals with alcohol use disorder reported improved affect after being subjected to a psychometric instrument, measuring change and affect. Individuals with alexithymia tend to have a low motivation or inability to internalize their emotionality and expressions (Parolin et. al, 2016). By actively inquiring, this facilitated motivation to activate some emotional regulation skills. This suggests that inquiry into the affective conditions of individuals with emotional dysregulation and alexithymic problems, may improve affect.
Emotional dysregulation and Trauma
Research suggest a high occurrence of childhood abuse in adults diagnosed with substance use disorder (Banducci, Hoffman, Lejuez, & Koenen, 2014; Guina, Nahhas, Goldberg, & Farnsworth, 2016). Craparo, Ardino, Gori, and Caretti (2014) agree that childhood traumatic experiences are a predictor of the cooccurrence of alcohol use disorder and a trauma diagnosis. Barahmand, Khazaee, and Hashjin (2016) confirm a well-documented association between utilization of substance and childhood insults in young adults. Childhood sexual abuse has been realted to several problematic psychological issues such as, depression, suicide, sexual dysfunction, posttraumatic stress disorder, and substance use. Research has suggested an association between childhood physical abuse and criminal behavior, suicidal ideation, aggression, complications with emotions, and substance use. Childhood emotional abuse, although lacking in reviews, data does suggest a linkage to depressive states, learned helplessness, poor view of self, negative affect, and emotional dysregulation (Banducci, Hoffman, Lejuez, & Koenen, 2014a). Banducci, Hoffman, Lejuez, and Koenen (2014b) propose data that reflects an increase in mental health issues, substance use issues, and physiological health concerns linked to trauma and abuse inflicted during childhood development. The cumulative consensus of these studies suggests that childhood maltreatment increases susceptibility to developing addictive tendencies later in life, furthermore the likelihood of co-occurring diagnosis is significantly probable (Banducci, Hoffman, Lejuez, & Koenen, 2014b).
To better understand the relationship between trauma and psychological complications later in life, two models have been proposed. The general effects modality of explanation asserts that all modes of trauma, childhood sexual abuse (CSA, childhood physical abuse (CPA), and childhood emotional abuse (CEA) may have a general impact on affect and behavioral functionality later in life. The differential effects model assumes that manifestation of psychological dysfunction is contingent upon specificity of trauma experienced (Barahmand, Khazaee, & Hashjin, 2016; Banducci, Hoffman, Lejuez, & Koenen, 2014a). The data generated from subjects diagnosed with substance use disorder, suggested that CSA can lead to sexual behaviors motivated by the necessity for intimacy and approval. CPA may have an impact on social functioning and increased aggressive behavior. CEA can result in impairments on affect regulation (Banducci, Hoffman, Lejuez, & Koenen, 2014a). Barahmand, Khazaee, and Hashjin (2016) give additional assertions highlighting that many times multiple types of abuse happened simultaneously or concurrently, and that individuals subjected to multiple angles of abuse and neglect are at risk for developing substance use disorders. Although comprehension of underlying etiologies underpinning the association between childhood insults and substance use disorder are not fully grasped, recent research has exposed emotional dysregulation as a go-between dynamic between these two co-occurring topics (Barahmand, Khazaee, & Hashjin 2016; Weiss, Tull, Lavender, & Gratz, 2013).
Emotional regulation is the necessity for mental health and well-being. It is also essential to social functioning, thus extending and exchanging neurological energy, via relationships, within a social context (Siegel, 2015). Deviations from healthy development of emotional regulation can be problematic, as it places individuals at risk for various psychopathologies and substance abuse disorders (Dvir, Ford, Hill, & Frazier, 2014; Tang, Tang, & Posner, 2015). As previously presented, alexithymia is a condition that is associated with difficulties regulating emotion. This causes difficulties in identifying, coping, and communicating problematic emotions (Krentzman, Higgins, Staller, & Klatt, 2015; Parolin et. al, 2016). These underlying conditions cause complications in attempts to put substance use disorder symptoms in remission. Emotional dysregulation could have a strong link to relapse potential (Parolin et. al, 2016; Stasiewicz et al., 2012).
Regulation and the Self-Medication Theory
Fletcher, Nutton, and Brend (2014) propose that substance use disorder susceptibility results from a combination of chemical intake and the desire to negate internal emotional distress, dissatisfaction, and lack of comprehension of emotions. This was the assertion of the Self-Medication Hypothesis that was proposed in the 1970s by Khantzian and Duncan. Drugs become a means by which to comfort and soothe, rather than indulgence in hedonic desires. Wilens et. al (2013) suggest research data that agrees with the later by giving evidence of the self-medication model of addiction. Deficiency in regulatory functions may be symptomatic causing irritability and reactivity, which may be an intrinsic drive to obtain neurological homeostasis.
Kober (2014) asserts that drugs become significantly purposeful to individuals that are prone to dysregulation, as the drug provides numerous psychological benefits. This includes gaining positive reinforcement, as well as alleviating negative affect. There is evidence that suggests that drug choices are specific to the type of dysregulation. This gives validity to the self-medication theory of drug use. This gives evidence as to why alcohol and benzodiazepines are used to mitigate anxiety (Guina, Nahhas, Goldberg, & Farnsworth, 2016). Depressive states can be alleviated through use of stimulants, such as cocaine and methamphetamine. Individuals with intense emotional pain may gravitate towards opioids to reduce symptoms (Kober, 2013; Padykula & Conklin, 2010). Padykula and Conklin (2010) suggest that anhedonia symptoms maybe negated by use of stimulants. Research is yielding data that suggests that problematic emotional regulation is a vital substrate of addiction. It is therefore hoped that pending longitudinal studies related to emotional regulation will open the door to a deeper understanding of its role in addiction/relapse (Kober, 2013).
Khantzian (2012) claimed that addiction is a dysregulation of self-regulation in accordance with the psychodynamic approach. This modality of explaining addiction suggests that individual with addictive tendencies and difficulties, self-worth, social connections, and behavioral responses. These necessary domains in human functioning, are modeled and transferred through environmental and childhood interactions. Garland, Pettus-Davis, and Howard (2012) posit that adverse environmental conditions have impact on development, and may lead to posttraumatic disorder symptoms. The casual systematic linkages between trauma, addiction, and psychological distress is still considered indeterminate. Research does suggest that trauma exposure leads to a dysregulated hypothalamic pituitary adrenal (HPA) axis and sympathetic nervous system. This results in an enduring state of disrupted stress adaptation, resulting in negative affect and dysphoria. Substance intake becomes the means to mitigate irritation, unease, and general dissatisfaction with life, resulting in high risk for developing addictive tendencies and craving/relapse (Garland, Pettus-Davis, & Howard, 2012). Although, genetics and biological functions are substrates of substance use disorder, parental nurturing is essential in the epigenetic flow of childhood development. The lack of optimum developmental environments occurs, usage of substances becomes an intrinsic necessity to fix or find balance, which in the long run, the chemical becomes the end, rather than the means to the end (Khantzian, 2012).
Dysregulation and Attachment
Parental-childhood relationships and interactions have a significant impact on emotional functioning later in life (Fletcher, Nutton, & Brend, 2014; Kreis, Gillings, Svanberg, & Schwannauer, 2016). Consistent parental/caregiver availability will serve to reduce stress, as the adult figure becomes an object associated with security. This results in development that which precipitates secure attachments into adulthood (Wedekind, et al, 2013).
Kreis, Gillings, Svanberg, and Schwannauer (2016) argue that human connectivity(attachment) is an essential ingredient in well-being and overall good mental health. The crux of attachment theory in the efficacy to pursue and obtain assistance socially to increase survivability and down regulate responses from the amygdala (Ein-Dor & Hirschberger, 2016). De Bellis and Zisk (2014) posit the necessity for nurturing maternal relations during breast-feeding, thus the release of oxytocin. This hormone is responsible for healthy attachment, empathetic feelings, emotional regulation, and development of the social brain. Wedekind, et al. (2013) postulate that research consistently suggests that mental health is contingent upon early childhood experiences within the context of a nurturing and supportive environment. Conversely, genetic predispositions may also affect attachment styles (Wedekind, et al, 2013).
Bowlby’s explanation for the necessity of attachment included genetic, neuroscience, and developmental necessities to establish neural connectivity that could support and regulate stress, mitigate anxiety, establish resilience, and launch development of personality. Compromiseddevelopment results in psychopathological deviations from normal development (Ein-Dor & Hirschberger, 2016; Wedekind, et al ,2013). Ein-Dor and Hirschberger (2016)indicates that this primitive system is essential to survival by alleviating stress, and assessing unsafe conditions to preserve survival.
Complications and lack of healthy development along this developmental continuum can cause problematic issues with attachment and relationships. This may result in attachment anxiety. Individuals with inabilities to mitigate anxiety, are described as self-sufficient and have avoidance attitudes towards social connections. Responses are primarily directed by the amygdala in reaction to stress and survival issues. This translates into these individuals initiating behavioral, in response to perceived stress and danger that expedites a quick accessible solution (Ein-Dor & Hirschberger, 2016).
Wedekind, et al (2013) assert three types of attachment dysfunctions. These are secure, insecure avoidant, insecure anxious, insecure ambivalent, and disorganized. Research suggests an association between alcohol use disorder and insecure attachment styles
Siegel (2015) asserts a neurobiological perspective on the major categories of attachment. Avoidance attachment occurs in approximately 20% of the US population. This results from lack of attunement, intentional parental focus, by the parent during early childhood. Consequently, the individual may have difficulty monitoring or linking to their inner self. This may include a disconnect from a somatic perspective. Ambivalent attachment affects 50% of the population, and results from inconsistent attunement or parental invasions. During later years, the individual will lack confidence about their internal workings. Lastly, disorganized attachment accounts for only five percent. This is a significant disorganized attachment system, resulting from abuse and neglect. This results in massive neural adaptions within the brainstem, due to feeling threatened/unsafe, while the upper cortical regions compensate by attempting to form an attachment to the unsafe parent (Siegel, 2015). The child’s brain to find homeostasis and safety, will attempt to lead to the parental figure, this results in a secure attachment which is vital for emotional self-regulation (Wedekind, et al, 2013). This causes problematic interpersonal issues and can lead to disassociation and self- dysregulation (Dvir, Ford, Hill, & Frazier, 2014; Siegel, 2015).
Problematic dysfunction of attachment in early childhood results in a higher prevalence in acquiring substance use disorders and emotional dysregulation. Some experts referred to addiction as an attachment disorder. Due to an inability to regulate emotion and mitigate anxiety from attachment dysfunction, individuals may resort to chemical substances to induce a GABAergic stability (Wedekind, et al, 2013).
Research suggests that fearful-avoidant attachment is associated with substance use disorders. Fletcher, Nutton, and Brend (2014) argue that due to attachment dysfunction, individuals will gravitate towards substance use as a substitute to forming healthy supportive social contacts. Kreis, Gillings, Svanberg, and Schwannauer (2016) assert complications in interpersonal relationships, with families and other intimate relations, leading to substance abuse and criminality in woman. Consequences of damaging interpersonal relationships are traumatic in nature, and caused significant pain and problematic issues attachment. Insecure attachment may result in emotional dysregulation, which can lead to substance abuse. This creates a vicious cycle, where the use of the chemical consumption can exacerbate an pre-existing dis-regulated system.
Therapeutic modalities that facilitate repair/healing to attachment dysfunction may have considerable success in relapse prevention. This gives validity to the necessity for twelve-step programs, which serve as an alternative to using the substance. Essentially, the individual learns new attachment patterns within the context of 12 step communities (Fletcher, Nutton, & Brend, 2014).
Intergenerational Transmission of Regulation
Bridgett, Burt, Edwards, and Deater-Deckard (2015) postulate that in the face of the evidence that self-regulation is transmitted intergenerational, research in this area has been limited and to some degree ignored. Of more interest, is the mechanisms responsible for self-regulation and how they are transmitted generationally. Self-regulatory mechanisms are transmitted to children during critical years of development in childhood and adolescence. Parental capabilities of self-regulatory functions are thus passed on to the following generation. Childhood regulation development is contingent upon parental efficacy in modulating/regulating their own emotions and behavior (Bridgett, Burt, Edwards, & Deater-Deckard, 2015; Siegel, 2001, 2012).
Bridgett, Burt, Edwards, and Deater-Deckard (2015) assert data that suggests an association between maternal effort control and a newborns ability to regulate orientation. Additional data in longitudinal study suggested that the same newborns, that transitioned into toddlerhood, showed similar abilities in effort control, as the mother. Bridgett, Burt, Edwards, and Deater-Deckard (2015) suggested data confirmed a negative correlation between maternal effort control and childhood dishonesty. Lack of maternal regulation resulted in an increase in cheating during a laboratory study. Cuevas, et al. (2014) assert that an essential bio-social process is at the core of maternal-child relationships that facilitate the transmission of adult effort control from infancy into preschool years of development. This is backed by data that suggests a positive correlation of executive functioning processes, in a longitudinal study on mother and child. This plethora of data gives a strong case for intergenerational transmission of effort control. Burt, Edwards, and Deater-Deckard (2015) assert that a positive correlation between mother-child vagal tone at ages two and five months. Additional studies on vagal tone conducted at later dates, yielded data that conflicted with Borstein and Suess. Buckholdt, Parra, and Jobe-Shields (2014) postulate that parental emotional dysregulation is significantly associated with adolescent complications in regulatory functions. Additional data suggest that parents with these regulatory emotions have patterns of invalidating their child’s emotionality. The psychological complications associated with invalidation, then led to emotional dysregulation and externalizing behaviors. Thus, the ability to regulate affect and reactions are seemingly predicated upon the parental figures capabilities and neurology of self-regulation. This places the role of parent/caregiver in a powerful position to convey, transmit, and model neurological functions that regulate bottom-up processes, through a developed top-down regulatory override of the sub cortical regions of the brain (Bridgett, Burt, Edwards, & Deater-Deckard, 2015; Cuevas, et al., 2014).
Dysregulation and Dysthymia
Diaz, Horton, and Weiner (2012) defined dysthymia as a subtype of a mood disorder. Compared with individuals diagnosed with major depressive disorder, dysthymic symptoms have been associated with greater frequencies of social problems, hospitalizations, and suicidal ideation. Primary symptoms are depressive affect, which present in lower intensity levels than major depressive disorder. Research data suggest that individuals with co-occurring dysthymia and substance use disorder are significantly higher than individuals that cooccur with major depressive disorder and substance use disorder. Gubin and Sultanov (2012) indicate that individuals with dysthymia report less than adequate quality of life, problematic alcohol intake, and numerous admits to addiction treatment centers. There is a limited amount of research studying the relationship between substance use disorders and dysthymia
Adolescence, Addiction, and Emotional Regulation
Shadur and Lejuez (2015) assert that emotional regulation is a dynamic enduring developmental process. During early childhood, this development proceeds rapidly. Dvir, Ford, Hill, and Frazier (2014) proclaim that improvements in self-control and reductions of emotional lability occur, due to the maturing of the neuroendocrine system. This maturation process continues into adolescence (Dvir, Ford, Hill, &Frazier, 2014). Nobile, et al. (2016) contends that family structure has a direct impact on the development and maturation of emotional regulation. Although genetic and behavioral components are a substantial underpinning, the role of the environment, mediated by family structure weights in considerably as to whether an adolescence will develop successful regulation skills or dysregulation.
Busch and Hofer (2012) assert that adolescents with well-developed self-regulatory functions showed a significant probability of successfully navigating through adolescent identity issues, which was associated with welfare. Quinn and Harden (2012) suggests that, regarding adolescent the maturation process, and adolescent that becomes less impulsive over a longer period, is a greater risk for developing substance use disorder. All adolescence struggle with impulsivity, but those that improve in self-regulation more rapidly, will be less prone to development of addictive disorders.
It is believed to be a moderately constant conglomeration of neurobiological factors. The developing adolescent brain is vulnerable to problematic growth of emotional regulation. It is during this significant vulnerable period of development that mental health conditions become observable (Shadur, & Lejuez, 2015). Exacerbating factors include, increased stress related to identity necessities, increases in peer group connectivity and acceptance, and development of secondary sex characteristics. The cumulative impact of these significant life changes leave teenagers vulnerable to negative affect and intensity of emotional experienced. This explains the irrationality and impulsivity of adolescent thinking and behavior. Hence, an increase of potential for the development of substance use disorders (Shadur & Lejuez, 2015). Quinn and Harden, (2012) suggest a similar assertion, but indicate that a slower decline in impulsivity during adolescence, is linked with sensation seeking, and therefore a greater risk of recreational chemical usage. A mitigation of thrillseeking and impulsivity as it relates to development, may be explained by variations and personality development.
Bridgett and Deater-Deckard (2015) conceptualize self-regulation by dividing it into two separate categories; one being a top-down process, and the other is a bottom-up progression. The dorsolateral prefrontal cortex and dorsal anterior cingulate cortex are instrumental in initiating executive control functions, as well as the necessity of effort control for healthy regulation. Psychological flexibility, per neurological imagery, has been linked to the dlPFC as well.
The PFC facilitates control over thoughts/emotions and impulsivity, executive functioning, preparation and decision-making (De Bellis & Zisk, 2014; (Shadur, & Lejuez, 2015). The orbital frontal cortex (OFC) and ventrolateral prefrontal cortex (vlPFC) have been associated with working memory (Bridgett & Deater-Deckard, 2015). Yan, et al. (2014) presented data that suggested that opioid dependent individuals may have problematic deficiencies in cognitive impairments and working memory, which may contribute to addiction and relapse. These assertions were strongly challenged by researchers who indicate that it is difficult to differentiate as to whether the impairments are associated with chemical usage or other non-substance related underpinnings. These objections were quickly supplanted by research on compulsive gamblers, that suggest poor cognitive abilities associated with low working memory. Brooks (2016) postulates and agrees that low working memory may be a substrate linking cognitive impairment with substance use disorder, but adds that compulsivity associated with anorexia nervosa may parallel addiction dynamics. There is a significant amount of research and data indicating that top-down neurological processes responsible for self/emotional regulation is significantly focused in the frontal cortex and anterior cingulate cortex (Bridgett & Deater-Deckard, 2015; Yan, et al., 2014).
Bottom-up mechanisms involved the limbic system, and includes the amygdala, central nucleus, and the hippocampus. The structures facilitate fear and stress reactivity. Individuals who have a systematic imbalance of a dominant bottom-up process will be susceptible to anxiety, stress, and social anxiety. Unregulated impulsivity tends to be a hallmark feature of a hyperactive unregulated subcortical region of the brain (Bridgett & Deater-Deckard, 2015; Shadur & Lejuez, 2015).
Neurobiological adaptations associated with dysregulation are focused in the prefrontal cortex(PFC) and limbic-striatal systems. The limbic-striatal system necessitates survival , such as drive, response, reward salience, arousal, and sensation seeking. Problematic cognitions and behaviors occur, due to a functional limbic system without the aid of a regulating prefrontal cortex (Shadur & Lejuez, 2015). Neural imagery indicates increases in emotional cue salience with the adolescent brain. This may explain impulsivity and irrationality in choices and behaviors. The amygdala is the core brain component regulating the danger response system. Trauma is channeled through the amygdala to activate the body’s physiological response system to stress and danger (De Bellis & Zisk, 2014). Activation of the amygdala to environmental cues was significantly higher for individuals that were exposed environmentally to stimulus with a parent with substance use disorder. This explains emotional dysregulation patterns within family systems. Research indicates clear differences in how and adolescent brain operates neurological (bottom/up) (Shadur & Lejuez, 2015). Dvir, Ford, Hill, and Frazier (2014) agree with these dual systems working in conjunction to produce and regulate emotion, however this mode of conceptualizing this complex process, does not account for the numerous regions of the brain that are needed for both emotional content and regulatory processes. It is not as simplistic as a mere dual system.
Neurological images indicate that the anterior cingulate cortex, and medial prefrontal cortex are involved in initiating and carrying out regulatory functions. The ACC is responsible for emotional and cognitive features, while the MPFC facilitates primarily the emotional aspects (Tang, Tang, & Posner, 2016). Dvir, Ford, Hill, and Frazier (2014) asserts that neural imagery is located specific regions relating to emotion. Frontal cortical areas such as the medial, orbital and lateral portions of the cortex indicated activation while facilitating emotional processes. Other significant areas of activation include the boundless, hypothalamus, striatum, amygdala, and periaqueductal gray.
The hypothalamus pituitary-adrenocortical axis plays a key role in activation/regulation of the bodily response system (De Bellis & Zisk, 2014). Development of the hypothalamus-pituitary-adrenocortical axis and parasympathetic nervous system are critical benchmarks for emotional development. These neural adaptions occur early in childhood and is contingent upon parental/caregiving exchanges (Siegel, 2015). The parent essentially transmits or models emotional regulatory capacities through their interactions with young developing brains (Dvir, Ford, Hill, & Frazier, 2014). Childhood insults on the young brain can disturb and disrupt the HPA axis, as indicated from data for both animal and human subjects (De Bellis & Zisk, 2014).
Dvir, Ford, Hill, and Frazier (2014) further assert that since these neurological transitions happen in early childhood, it may be possible that experiential endangerment in childhood results in an alteration in the threshold of limbic reactions. This in turn causes dysfunction in perceptions of stimulus and breakdowns in the ability to effectively appraise unsafe situations. Two possible discriminatory patterns can result from these neurological adaptions. A hyperarousal can manifest as anxiety and dysphoria. Hypo-arousal may lead to psychic numbing and disassociation.
De Bellis and Zisk (2014) assert that increased intensity of trauma from a biological perspective has yielded data to suggest that frequency of disassociation is a possible occurrence. This leaves the individual with an inability to consolidate a sense of self with memories and emotions. This is a defensive posture to mitigate and protect against anxiety, which may lead to problematic issues with connecting to others. This is a significantly different state than depression and anxiety. Neurologically, increased levels of norepinephrine in the locus coeruleus, a primitive neurological component of the brain that facilitates the activation of the sympathetic nervous system, have been associated with trauma, and cause complications in emotional regulation, thus promoting isolation and dissociation (De Bellis & Zisk, 2014).
Bale (2015) postulates the significant influence environment can have over the animal brain. Variables such as stress, nutritional deficiencies, and other medical complications can alter the developmental path, thus resulting in neurological alterations. The Barker hypothesis declares that neurological adaptability occurs during the postnatal phase of development, due to an evolutionary anticipation of analogous postnatal conditions. According to this hypothesis, complications arise when there is an imbalance between these two environments, thus Barker proposes that this is the etiology of potential stress and disease prevalence.
Interpersonal neurobiology (IPNB) is lens through which to research, examine, and more fully comprehend substrates of substance use disorder and emotional dysregulation. Emotional dysregulation seems to be a driving neurological force and underpinning of SUD and relapse (Dvir, Ford, Hill, & Frazier, 2014). Emotional dysregulation is linked to inadequate stress coping, lack of supporting relationships, and in some cases, unresolved interpersonal issues. Interpersonal integrity, as an emotional stability construct, is a necessity for regulating affect and having essential social support necessary for mental health. Breakdowns in interpersonal domains may have consequences throughout a lifetime, and can be passed on generationally (Bridgett, Burt, Edwards, & Deater-Deckard, 2015; Siegel, 2001, 2012).
IPNB gives a theoretical account and explanation for why these dysfunctions happen and how they are passed on from caregiver to child. Emotional dysregulation, due to lack of a healthy integration of mind, body, and social connections, is a multifaceted complex dynamic that is present with many mental health diagnoses (Dvir, Ford, Hill, & Frazier, 2014; Siegel, 2001, 2012, 2014).). IPNB probes beneath emotional dysregulation and theorizes about causes and conditions that underpin emotional dysregulation (Siegel, 2001, 2012, 2014).
Interpersonal neurobiology was pioneered in 1999 Daniel Siegel, M.D. This theoretical approach explains development neurologically and his relationship to social connections (Siegel, 2014). The brain, mind, and relationships are viewed as a functioning whole that is integrated. Well-being and healthy psychology are all contingent upon the unification and integration of these three key areas. Insults in early childhood can compromise interpersonal neurobiological development. Attunement is the parental feature that allows a parent to self -soothes a young child when dysregulation. Mindsight is being cognitive of another’s emotionality. A breakdown or not consistent presence of these two key factors can cause emotional dysregulation to development, causing problems later in childhood and adulthood(Siegel, 2001, 2012, 2014).
A complete comprehension of the necessity for healthy relationships for development of healthy neurology through an interpersonal neurobiological perspective, sheds light on problematic issues with emotional dysregulation and substance use disorder. Interpersonal neurobiological lens through which to consider underpinnings of substance use disorder and emotional dysregulation provide insights and considerations for potential treatment options.
Insults childhood development in early years can significantly reroute neurological and healthy development and disrupt the formation of the well-formed stress regulation system Wiet, 2017). Lack of development of coping and regulatory functions in the brain during early childhood years may place individuals later in life that is developing substance use disorders to regulate inadequate development (Dvir, Ford, Hill, & Frazier, 2014; Wiet, 2017; Bettis, 2002).
An interpersonal neurobiological lens explains how influence in child rearing, can directly influence the neurological development of the child’s brain. Essentially, a well-regulated adult brain will be able to transmit regulatory functions to the child through specific means, specifically mindsight, mindfulness, and attunement. Disruptions in this vital transmission of neurological functions, can cause problematic issues emotional dysregulation and dysfunction of attachment styles later in life(Siegel, 2001). A breakdown of intergenerational transmission of healthy coping neurological functions, can cause interpersonal trauma issues. Exhaustive comprehension of interpersonal neurobiological dynamics illuminates why problems with emotional dysregulation may exist, and the necessity for utilize substances to mitigate or eliminate negative affect(Spence & Courbasson, 2012).
Alterations in healthy development of emotional regulation can lead to problematic inabilities to regulate emotion, identify emotion, express emotions, appraise feelings, connect socially, and respond to stressful situations in a manner that promotes well-being and health (Dvir, Ford, Hill, & Frazier, 2014; Tang, Tang, & Posner, 2016; Parolin et. al, 2016). Traumatic experiences early childhood can severely dysregulated stress systems, and increase development of substance use disorders. Chemical usage can become the means to mitigate negative affect and irritability produced the substrates of genes, biology’s, stress, and childhood experiences (Banducci, Hoffman, Lejuez, & Koenen, 2014; Guina, Nahhas, Goldberg, & Farnsworth, 2016). Attachment styles from childhood insults can set individuals up for development of addictive patterns solution (Ein-Dor & Hirschberger, 2016). Self-regulatory patterns associated with attachment styles, can be transmitted across generations (Bridgett, Burt, Edwards, & Deater-Deckard, 2015).
Relapse is a common theme among individuals attempting to recover from substance use disorder (Robinson, Robinson, & Berridge, 2014; Kassani, Niazi, Hassanzadeh, & Menati, 2015). Studies reflect significantly high relapse rates, associated with reoccurring symptoms related to substance use disorder, which suggest the possibility that underlying issues are going undiagnosed and untreated (Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). Spence and Courbasson (2012) suggests that emotional dysregulation is a failure of functionality of the self-regulatory system. This results in problems with recognition and description of emotions (alexithymia), inabilities to regulate negative affect, and poor choices in behavioral responses. Problematic dysfunction within the regulatory system may result in deficiencies to regulate emotion and may be a precursor to substance use disorders (Dvir, Ford, Hill, and Frazier, 2014; Stasiewicz, et al., 2012). Tice, Bratslavsky, and Baumeister (2001) suggest that individuals with significant internal distress will make choices to regulate themselves. Tang, Posner, Rothbart, and Volkow (2015) assert that by improving self-regulatory circuits, there is improved executive functioning, and a reduction in negative emotion. Improvement in regulatory functions could therefore mitigate cravings and relapse and improve remission of symptoms associated with substance use disorder.
Underlying substrates, such as emotional dysregulation, influenced by reward deficiency, interpersonal trauma, and impaired stress coping systems, are the undiagnosed etiologies that drive substance use disorder and relapse cravings (Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). Researchers assert the necessity for additional research in key areas associated with emotional dysregulation and SUD. Enman & Uterwald (2014) in connection with, their assertion regarding traumatic victims being at high risk for developing SUD, they conclude that more research needs to be conducted to explore the commonalities from a neurological perspective on both PTSD and SUD. Juli and Juli (2015) postulate the necessity for more research regarding typologies of choice of drug and possible associations with genetic underpinnings of this selection of chemical intake. Craparo, Ardino, Gori, and Caretti (2014) strengthen the necessity for more research by indicating the necessity of understanding and explaining the associations of interpersonal trauma, alexithymia, and disassociation.
A systematic review of literature will be employed for the analysis of literature. Key assumptions related to systematic reviews to categorize, evaluate, investigate, and infer themes and gaps in existing published literature. A hallmark feature of the systematic or systematic review is the exhaustive and comprehensive planning design. Equally important is the necessity of a purposeful and planned search for literature. The objective is the mitigation of identification, assessment, and synthesis of information from an unbiased methodology (Uman, 2011).
There are limitations to a systematic review. This includes the commonality of a poor quality of articles that may misrepresent or mislead on a topic or thematic presentation. Lacking in data and journals may also create confounding issues to substantiate and answer research questions. Generalizing answers to research questions through systematic review, may be problematic when applying these answers to a specific treatment need (Biondi-Zoccai, Lotrionte, & Modena, 2011). Nevertheless, systematic reviews provide quality insights into lacking data and research, that may have been overlooked, or outside the scope of the specific study. Due to the comprehensive analysis through systematic reviews, articles can be significantly exploited, while applying this aggressive analysis and synthesis to the entire journal, rather than generalizing about findings in an abstract or conclusion (Biondi-Zoccai, Lotrionte, & Modena, 2011). Systematic studies enhance, broaden and highlight existing literature, while offering potential new interpretations (Creswell, 2013).
The plethora of studies provide two significant reasons for the importance and necessity of a systematic study. Due to the numerous amounts of journals and research, it is challenging for clinicians and researchers to stay abreast and informed of current research. A systematic review is effective at giving a synopsis for what research has uncovered. The essence of the bottom line, becomes an effective way to stay informed, rather than wading through cumbersome methodologies and data discussions (Uman, 2011).
A secondary reason for the choice of a systematic review is relevant to the previously presented issue of a plethora of research journals pertinent to substance use disorder and emotional dysregulation. A quantitative or qualitative research design would merely replicate and coincide with existing research that attempts to answer the research questions. It was deemed necessary to glean from already conducted research to interpret, analyze, and organize existing information for the purpose of consideration of novel ideas and the comprehension of etiologies of substance use disorder, thus suggesting future research for interventions and treatment.
A primary example the limited usage and conduction with qualitative or quantitative research designs, considers the research question inquiring about underlying conditions relative to substance use disorder and emotional dysregulation. Yan, et al., (2014); Bettis, (2002); Dvir, Ford, Hill, and Frazier, (2014) assert the notion that reoccurring symptoms of substance use disorder tend to be preceded by difficulties in regulating negative emotion. Rather than employing a research design that mimics or closely parallels prior existing research by these researchers, it is best suited to utilize a systematic design to thoroughly examine these assertions and data findings.
Numerous databases were utilized to obtain appropriate literature for the study. The following are the databases that were searched: Google Scholar, National Center for Biotechnology Information (NCBI), Research Gate, Springer Link, Akadémiai Kiadó, PubMed Central Canada, PubMed, Academia, MDPI, Yale University Clinical and Affective Neuroscience Laboratory, Frontiers, Cambridge University Press, Science Central, Biological Psychiatry, and ProQuest Psychology Journals. References from numerous journals were utilize for the acquisition of other relevant literature. All searches were limited to publishing dates between 2012 and 2017. The California Southern University library was instrumental in obtaining seven key articles on the inner library loan system. Several key journal articles that were published beyond the five-year period were chosen due to the relevance of the study. These seminal articles included were: Cheetham et al., 2010), (De Bellis, 2002), (Myers, Swett, & Miller, 1973), (Schuckit et al., 2011), (Siegel, 2001), (Robinson & Berridge, 1993), (Pickens et al., 2011), (Tice, Bratslavsky & Baumeister, 2001), Robinson & Berridge, 2008), (Berridge, Venier, & Robinson, 1989). Keyword searches were conducted in the listed databases. The following were entered: addiction and dysregulation, substance use disorder and emotional regulation, interpersonal neurobiology, stress and addiction, dopamine and dysregulation, attachment and SUD, intergenerational trauma, interpersonal trauma and addiction, reward deficiency syndrome, incentive salience theory, and addiction and PTSD.
Over 107 journal articles and one book were methodically viewed, evaluated, and organized. The organizational flow of these articles was governed by the research questions. The research questions were then answered, while being supported by each section of articles allocated to support and coincide with each individual research question. Additional research was added, as the need frequently fostered the necessity for additional searches for more enquiry.
Scholarly publications were chosen predicated upon significance to the study, which encapsulated articles focused on substance use disorder and emotional dysregulation. Creswell’s (2013) Analysis Spiral, which utilizes a cyclic progression of systematic analysis, will be utilized to reduce selection bias. This is a five stage process, starting with organization, perusal, clarification, and synthesis of data and literature (Creswell, 2013).
Once an article was chosen, it was organized into a preset system utilizing the electronic application, Mendeley. This digitalized organizational program had enabling features which allow for subcategories to be established. The first level of organization coincided with the topic of the study, which was substance use disorder and emotional dysregulation. Second-level subcategories were then developed to further organize literature. Journal articles placed by second-level folder under substance use disorder, were theories of addiction, genetic predisposition, reward deficiency syndrome, motivation and choice, memory and learning, stress and allostasis, and neuroscience of addiction. Within the emotional dysregulation level 1 folder, there were sub second-level folders. Among these were theories of dysregulation, development of healthy regulation, dysregulation and trauma, dysthymia/anhedonia, epigenetics, disrupted mood dysregulation, and disassociation/substance use disorder, social problems, memory systems, and neurotransmitters. Under emotional dysregulation, there is a third level of sub-files. The second level trauma folder was divided down into attachment, interpersonal trauma, neurobiology of trauma, and intergenerational trauma folders.
The data management system permitted effective and accurate organization of subject matters. Articles will be then be more thoroughly scrutinized. This process will involve objective reflections, noting specific relevance to research questions. This also will require making notations and highlighting on the articles themselves. The Mendeley application had numerous tools that improve the effectiveness of this stage of analysis. There was also minor reorganization of the database in considering thematic integration, as well as differentiating subject matter that was contrary to agreements in assertions regarding concepts and themes. This investigative stage will be useful in preparing for the following more precise stage of investigation and inquiry. Thematic categories will be developed based on interpretive findings. Creswell’s (2013) analytical spiral will be utilized to synthesize qualitative data, while organizing information into the category themes.
A systematic review of literature identifying common themes, exposing gaps in previous research, while suggesting potential new necessities for research. Synthesizing information through this review will be the essential role of the study, for additional insights and information to the treatment of substance use disorder. High relapse rates associated with emotional dysregulation, will be the premise of the following chapter. This will lead to a methodical approach to answering the proposed research questions (Robinson, Robinson, & Berridge, 2014; Kassani, Niazi, Hassanzadeh, & Menati, 2015).
Reoccurring symptoms of substance use disorders is problematic, significantly high relapse rates may give concern for potential undiagnosed and untreated substrates underline the addictive epidemic (Robinson, Robinson, & Berridge, 2014; Kassani, Niazi, Hassanzadeh, & Menati, 2015; Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). Emotional dysregulation is a common symptom associated with numerous mental diagnoses. Inabilities to regulate emotion may possibly be related to susceptibility to the development of substance use disorders (Dvir, Ford, Hill, and Frazier, 2014; Stasiewicz, et al., 2012). Tice, Bratslavsky, and Baumeister (2001) suggests that underpinnings associated with substance use disorder and relapse, may include problems with emotional regulation, which have been influenced by insults deviating development of interpersonal integrity, leading to complications and dysregulation in stress coping. There is evidence supporting the fact that enhancement of regulatory functions have demonstrated in improvements in reducing reoccurring symptoms of substance use disorder (Tang, Posner, Rothbart, and Volkow, 2015).
Enman & Uterwald (2014) indicate that more research is needed to substantiate linkages neurologically between posttraumatic stress disorder and substance use disorder. Comprehending overlapping and shared neurological pathways may shed light on undiagnosed trauma related to substance use disorder. Craparo, Ardino, Gori, and Caretti (2014) conclude that lack of comprehension relating interpersonal issues, disassociation, and alexithymia necessitate additional research.
Interpersonal neurobiology presents the theoretical basis for explaining regulated and dysregulated psychological states predicated up on healthy attachment during early childhood (Siegel, 2001, 2014). Utilizing IPNB as a theoretical lens, the following research questions will be filtered, organize, analyze and synthesized. This in turn will suggest a more accurate comprehension and assessment of substance use disorders. Giving insight and explanations for significant high relapse back into substance use disorder symptoms (Mohammadpoorasl, Fakhari, & Akbari, 2012).
Question 1: What causes the underlying substrate of substance use disorder relative to emotional dysregulation?
Question 2: What are the underpinnings of emotional dysregulation that contribute to relapse?
Question 3: What is the relationship between interpersonal trauma and substance use disorders?
The results of this section of the study, will be a result of being thoroughly sifted through each specific research question. Due to the overlapping nature of the research questions, it is hoped that substantial and qualitative findings will formulate novel themes. New evolving themes will be used to determine potential new relationships, and validate innovative findings.
Research Question One What causes the underlying substrate of substance use disorder relative to emotional dysregulation?
Research question one inquiries about etiologies or underpinnings of substance use disorder that are associated with problematic regulation of emotion. Multiple themes emerged as a result of utilizing a systematic review. An analysis of 74 articles produced justifiable results in accordance with the first research question.
Dopamine Dysregulation in the Midbrain/Mesolimbic System
The first emerging thematic construct from research question one centered on problematic issues with the mesolimbic system. There is evidence suggesting genetic tendencies for the development of dysregulation developments of the mesolimbic system and midbrain, and having emotional dysfunction as a subsidiary condition (Blum, Gardner, Oscar-Berman, & Gold, 2012; Duci &Goldman, 2012). The concept is also related to an inadequate neurological condition that explains negative affect, which may give rise to a neurochemical drive to alleviate an adverse inner condition. Deficiencies of dopaminergic flow operate at less than optimum levels, due to genetic possession of the DRD2 A1 allele (Blum, et. al., 2015). Chemical seeking and consumption becomes a default mode whereby the individual attempts to use the chemical effects to override a significant depletion of dopamine (Blum, Gardner, Oscar-Berman, and Gold, 2012; Blum, et. al., 2015). Negative affect caused by genetic determinations of low amounts of dopamine in the synapse, becomes the problem that is responsible for relapse and development of addictive disorders (Blum, et. al., 2015).
Increased flow of oxygenated blood flow in the right orbital frontal cortex, bilateral anterior cingulate, right nucleus accumbens, right dorsolateral prefrontal cortex, right caudate nucleus, and bilateral medial frontal cortex was observed in response to trigger condition cues (Blum, Gardner, Oscar-Berman, and Gold, 2012). Increased flow of dopamine decreases anhedonia and poor affective conditions, in response to potential incentives. Drug-seeking therefore becomes a means to alleviate negative affect produced by reward deficiency syndrome (Blum, Gardner, Oscar-Berman, and Gold, 2012; Blum, et. al., 2015). There are arguments against the dopamine hypothesis, indicating that dopamine depletions drive substance intake. Berridge and Robinson (2016) indicate that reward deficiency syndrome suggests dopamine being associated with hedonic factors, and that this is in conflict with the emerging studies suggesting that dopamine facilitates motivation towards survival goals, rather than hedonic features.
The incentive sensitization theory asserts explanations for the craving dynamic, that underpins and exacerbates substance use disorder. However, this theory gives no evidence linking emotional dysregulation with the craving for substances. It does give essential explanations for how the same brain system associated with reward salience, is also utilized when a fear salience is experienced. The role of dopamine can elicit dopamine salience in response to a fearful stimulus, as well as a pleasurable salience (Berridge and Robinson, 2016). Sinha (2013) gives reasonable assertions that negative affect does not forecast reoccurring symptoms of substance use disorder. Craving is the necessary dynamic that precedes and predicts relapse into symptoms. Negative affect may parallel the craving energy, but it is the craving that necessitates return to chemical consumption. Assertions by Sinha (2013) argue against negative affects association with reoccurring symptoms of substance use disorder.
Deficits in Emotional Self-Regulation Leading to Distress to Regulate through Substances
Emotional regulation development is contingent upon many factors. Genetical influences through epigenetic dynamics can determine development of healthy or dysfunctional (Deater-Deckard, 2015). Deficits in emotional self-regulation (DESR), according to Cheetham, Allen, Yucel, & Lubman, (2010); Wilken et. al, (2012), give plausible evidence for the fact that DESR as being a genetically influenced substrate of substance use disorder. Neuroimaging related to deficits in emotional self-regulation have yielded data suggesting structural dysfunction with the anterior cingulate cortex (ACC), which predicts the capacity to develop alcohol use disorder. This specific region of the brain is also known to facilitate emotional regulation (Cheetham, Allen, Yucel, & Lubman, 2010). Alexithymia commonly presents itself with alcohol use disorder. However, research is limited in associating genetic factors linking these conditions (Pombo, 2014; Stasiewicz et al. 2012). Parolin et. al, (2016) conclude that alexithymia presents symptoms, due to a genetic predisposition associated with a personality trait. Inabilities to identify and describe emotion from alexithymia conditions during abstinence, can certainly complicate recovery goals (Krentzman, et al., 2015)
Alterations in Brains Stress System/Inadequate Coping
Over time there is a reduction in reward induced by chemical substances. A neurological state develops, that may be long-term or even chronic. This results in a hyper active extended amygdala, resulting in stress and negative affect. Chemical consumption becomes the driving force to reduce negative affect (Volkow, Koob, & McLellan). This dynamic dysregulation over time diminishes connectivity to the prefrontal cortex. Complications and alterations from glutamate and dopamine pathways caused significant diminishment in self-regulatory functions (Lu & Richardson, 2014; Volkow, Koob, & McLellan).
The concept of a severe dysregulation of the brains stress system gives plausible answers to potential underpinnings of substance use disorder related to regulatory issues. Large consumptions of chemicals in response to tolerance related to decreasing levels of reward responses, cause dysfunctional rerouting and reorganizing, which included perversions to the hypothalamic pituitary system. This results in abundance of unnecessary stress hormones, creating negative affect in a powerful craving dynamic. The critical prefrontal cortex area of the brain is essentially off-line to promote regulation (Koob, 2015; Lu & Richardson, 2014; Volkow, Koob, & McLellan).
GABA/Glutamate Dysfunction Link to Relapse/Emotional Dysregulation
Dysfunctional gamma-aminobutyric acid and glutamatergic systems are resulting factor underpinning and exacerbating substance use disorder. This results in increased levels of anxiety and dysphoric affect (Moeller, London, and Northoff, 2016; Burnett, Chandler, & Trantham-Davidson, 2016). This is termed, a resting State dysfunction. Essential systems associated with the anterior cingulate cortex, prefrontal cortex, insula, and striatum function systematically to create GABAergic stability. Although studies of this nature are limited to subjects with known alcohol, nicotine, opioids, methamphetamine, and marijuana abuse, neuroimaging presents data of lower levels of GABAergic flow, compared to the control group (Moeller, London, and Northoff, 2016). Conversely, resting State dysfunction is associated with high levels of glutamate. High levels of dopamine exposure, associated with chemical intake, causes glutamate levels to rise. Excessive glutamate therefore creates conditions associated with negative affect (Burnett, Chandler, & Trantham-Davidson, 2016). The emerging theme filtering through research question one, gives credible evidence for neurobiological undesirable affective conditions, underpinning substance use disorder (Moeller, London, and Northoff, 2016; Burnett, Chandler, & Trantham-Davidson, 2016).
Predisposition Due to Genetic Vulnerability
There is evidence suggesting, not only are there genetic components extenuating impulsivity that impacting substance use disorder; that there are plausible assertions for anxiety/reward genetic basis for SUD coexisting with impulsivity (Ducci & Goldman, 2012; Gorwood, et al., 2012). This is referencing monoamine oxidase and catechol-O-methyltransferase (COMT). These genetic directives coordinate formation of enzymes essential for mental health. The presence of anxiety and substance use disorder, according to this study, presents the possible assertion of a genetic basis for addiction and emotional dysregulation (Ducci & Goldman, 2012). Agrawal et al. (2013) suggest a potential genetic component to craving for alcohol relative to the dopaminergic system, in subjects with alcohol use disorder. More research focusing on other neurotransmitters and their effect on craving needs to be conducted. Gorwood, et al. (2012) conclude that it is still premature research perspective to identify specific genes associated with the dopaminergic system in the development of addictive disorders. Additional research focusing on phenotypes linked to other related issues such as impulsivity, stress systems, novelty seeking, and allocation of attention.
Deficits in Emotional Self-Regulation Leading to Distress in Addiction
Problematic issues with emotional regulation a substrate of substance use disorders. Dysfunction of regulatory abilities or common issues and other mental diagnosis. Disorder such as depression and bipolar disorder are known to have underline regulatory dysfunction. Borderline personality disorder is also symptomatic of emotional dysregulation (Dvir, Ford, Hill, & Frazier, 2014). In some cases, individuals with specific disorders may attempt to regulate their negative internal environment by gravitating towards substance use. This is more than just impulsive behavior, as this is a means to improved affect (Tice, Bratslavsky, and Baumeister, 2001). It is not uncommon for substance use disorders to coincide poor coping skills, deficiencies in regulating behavior, and difficulties mitigating a coping with negative affect (Tang, Tang, and Posner, 2015). Deficits in emotional self-regulation (DESR) could be a potential underlying substrate of substance use disorder that is relatively stable mental construct. This means that this condition can extend and remain present even after symptoms of substance use disorder have been placed in remission (Wilens et. al, 2013).
Gross (2015) asserts five components that comprise and make up emotional regulatory functions. These include, situation selection, situation modification, attentional deployment, cognitive change, and response modulation. Although most literature agrees that negative affect exacerbates consumption of alcohol, there is a necessity for research exploring which of these facets is most commonly linked to alcohol use disorder ((Tang, Tang, and Posner, 2015; Veilleux, skinner, Reese, & Shaver, 2014). According to Cheetham, Allen, Yucel, &Lubman, (2011); Wilens et. al, (2013) there is a similar neurology with substance use disorder and DESR.
Research Question Two What are the underpinnings of emotional dysregulation that contribute to relapse?
Research question two explores the underpinnings of dysfunctional emotional regulatory functions that lead to reoccurring symptoms of substance use disorder. Although there were frequent overlapping emerging themes from question one, additional themes emerged as etiological conditions related to abnormal emotional regulation. A total of 33 articles were assessed and analyzed for this specific question.
Emotional Dysregulation/Trauma Underlying Substance Use Disorders
De Bellis and Zisk (2014) suggests that trauma intensity may lead to disassociation. This can cause complications with ability to acquire a sense of self and the presenting emotions associated with that state. Essentially this is a defense mechanism to guard against future harm, however this process creates a dissociative state. This can cause difficulties connecting oneself and other humans. As norepinephrine increases in the locus coeruleus, which is essential to stimulation of the sympathetic nervous system. This may foster the need to isolate protection, generating significant interpersonal internal issues. Dvir, Ford, Hill, and Frazier (2014) postulate that these neurological adaptions for safety they promote changes in limbic system functions. To potential deviating patterns are hypo-arousal and hyperarousal. It is concluded that disassociation and psychic numbing may be an underlying cause stemming from hypo-arousal states.
Dysregulated stress systems are known to cause negative affect. These systems can be damaged and rerouted from heavy doses of addictive substance. There is the possibility of an existing disruption and dysfunction caused by breaches to interpersonal integrity. Multiple studies reflect well-predictable and high incidences of childhood insults predicting development of substance use disorders (Banducci, Hoffman, Lejuez, & Koenen, 2014a; Guina, Nahlas, Goldberg, & Farnsworth, 2016; Craparo, Ardino, Gori, and Caretti, 2014; Barahmand, Khazaee, and Hashjin, 2016). Research results suggest specific symptoms associated with typologies of childhood abuse (Table 4.1)
|Symptom||Sexual abuse||Physical abuse||Emotional abuse|
|Post-traumatic stress disorder||x|
|Substance use disorder||x||x|
Psychiatric Symptoms Associated with Types of Abuse
(Banducci, Hoffman, Lejuez, & Koenen, 2014a)
Certain symptoms do cluster around specific types of abuse experience during childhood (see Table 4.1). Barahmand, Khazaee, and Hashjin (2016) conclude that combinations of types of abuse and neglect to make individuals significantly inclined to developing substance use disorder. Emotional dysregulation tends to be a bridging construct between interpersonal trauma and addictive disorders.
Underpinnings of Dysregulation
Functional and healthy regulatory capabilities are precursor for good mental health. Emotional regulation is the critical underlying feature of healthy social support. It’s emotional regulatory skills, that assist a human in exchanging emotional energy within a social framework, that nurture and support (Siegel, 2015). Maladaptive development in emotional regulatory circuitry will increase vulnerability to development of mental diagnosis, including substance use disorders (Dvir, Ford, Hill, & Frazier, 2014; Tang, Tang, & Posner, 2015). Specific features contributing to relapse related to emotional regulation, specifically alexithymia, is that due to symptoms stemming from alexithymic conditions, can set the stage for difficulties with insightfulness and self-honesty, and can be linked to poor therapeutic progress that is essential for recovery and relapse prevention (Parolin et. al, 2016).
Neuroimaging Specific to Emotional Dysregulation/Substance Use Disorder
Wilcox, Pommy, and Adinoff (2016) research regarding specific neural circuit impairment relative to substance use disorders and regulatory dysfunction gives significant information related to conditions contributing to relapse into substance use disorder. Neuroimaging indicated that individuals with mental diagnosis without substance use disorder displayed increased activity in the amygdala and insula. Hyperactivation of oxidized blood flow was limited to the rostral anterior cingulate cortex, ventromedial prefrontal cortex, dorsal medial prefrontal cortex, and lateral prefrontal cortex. Known that substance use disorder indicated reduced activity in the rACC/vmPFC, although there was an exception related to cocaine use disorder that did not reflect mitigated activity in this region of the brain. Findings for substance use disorder parallel neurological regulatory functions with disorders such as borderline personality disorder, depression, and anxiety. A significant finding was the fact that with substance use disorder, regulatory functions did not increase blood flow in the amygdala/insula. Psychiatric diagnosis not occurring with substance use disorder did display imaging that substantiated increase activity in these essential emotional generating and processing areas of the brain. A vital caveat is that a single study with women subjects, discovered hyperactivation in the amygdala/insula region. Resting state linkages between regulatory areas and emotional generating regions showed weak linkages between these two regions in both SUD and non-SUD related diagnosis. This is believed to be related to lack of veracity with white matter areas.
Wilcox, Pommy, and Adinoff (2016) conducted neuroimaging specific to emotional dysregulation and substance use disorder. Currently there is no other research as precise as these areas of focus, relative to this theoretical review. Although this study gives credible neurological insights into emotional dysregulation and substance use disorder, several key limitations need to be noted (Wilcox, Pommy, & Adinoff , 2016). Data was obtained from individuals who had approximately 14 days of abstinence from any substance usage. Therefore, the study is unable to delineate between pre-existing conditions and conditions developing from chemical usage. It needs to be noted that research does suggest that alterations from chemical usage can present symptoms even after usage has ceased. Other potential emotional regulating brain functions such as the hippocampus and striatum were not studied. Finally, studying the complex nature of co-occurring disorders were beyond the scope of this study (Wilcox, Pommy, & Adinoff, 2016).
Working Memory Undergirding Dysregulation and Addiction
Limited capacity in working memory, associated with the orbital frontal cortex and ventrolateral prefrontal cortex, maybe be linked with deficiencies in cognitive process (Bridgett & Deater-Deckard, 2014; Yan, et al. 2014). Yan, et al. 2014 specifies that opioid dependency may be linked to impairments with working memory and cognitive functions. Brooks (2016) agrees that deficiencies in working memory may be an etiology bridging substance use disorder and lack of cognitive functioning for regulatory purposes. There is disagreement about whether substance use causes this cognitive impairment or whether it is a pre-existing condition. Yan, et al. (2014) supersedes this argument asserting that these maladaptive cognitive impairments and deficiencies in working memory are present and pathological gamblers. This indicates that this may be a predisposed condition, and the launching pad for addictive patterns.
Research Question Three What is the relationship between interpersonal trauma and substance use disorder?
Research question three focuses on the specific question inquiring about the relationship between interpersonal trauma and emotional dysregulation. Although, again there are significant overlaps between previous questions, this specific inquiry explores the dynamics of primarily pre-existing conditions that may precede the development of substance use disorder. Sixteen articles were organized, assessed, and synthesized to answer research question three.
Intergenerational Transmission of Dysfunctional Interpersonal Development
Transmission of emotional regulatory functions emerged as a theme related to how mental constructs are transmitted generationally. Bridgett, Burt, Edwards, and Deater-Deckard (2015) indicate that research studies focusing on intergenerational dynamics is limited and to a small degree has been overlooked. Parental regulatory mechanisms are transmitted during critical years of childhood and adolescence. The emerging theme of normal development or abnormal growth hinging upon adult caregiver’s capacity to regulate emotion, gives plausible explanations for how regulatory functions become and intergenerational dynamic (Siegel, 2012).
Interpersonal traumatic insults target the amygdala in order to activate the body’s response system to danger (De Bellis & Zisk, 2014). Shadur and Lejuez (2015) assert data that suggests that stimulation of the amygdala to environmental stimuli was of greater intensity with subjects that had a caregiver with substance use problems. This gives credibility to emotional regulation being transmitted generationally.
Research data focused on intergenerational transmission of emotional regulation indicates that the cognitive construct of effort control from a maternal influence has a significant impact on development of childhood regulatory functions (Bridgett, Burt, Edwards, and Deater-Deckard, 2015). Negatively correlated data suggested that a decrease in the ability to regulate emotion by a mother was associated with increases in children’s lack of integrity and dishonesty. There is also data suggesting a positive correlation between effort control capabilities and infantile orientation. Mother and childhood vagal tone were also positively correlated between 2 months to 5 years of age (Bridgett, Burt, Edwards, and Deater-Deckard, 2015). Cuevas, et al. (2014) conclude from research that executive functioning (EF) development in early childhood is contingent on parental modeling. A possible neurological substrate according to Cuevas, et al. (2014) of executive functioning related to maternal to childhood transmission, is the manufacturing and operation of dopamine. Genetic variants of the catechol-O-methyltransferase (COMT) and DRD4 may have a heritability influence on mother and child linkages associated with executive functioning.
Addiction as an Attachment Disorder
Development of healthy interpersonal integrity related to capabilities to regulate emotion are strongly predicated upon attachment theory. The role of oxytocin release during breast-feeding is a necessity neurologically from which healthy attachment develops. This is a significant dynamic that is conducive for neurology of emotional regulation and capacities to engage socially throughout a lifetime (De Bellis & Zisk, (2014). Consistent with other emerging themes related to research question three, is the necessity for environmental conditions prompted by parental support and connectivity to the child, to facilitate how children are affected by attachment style (Wedekind, et. al, 2013).
Disruptions in the development of this primal brain system results in a chronic dysregulation state in which the individual feels habitually threatened and/or problematic functions with monitoring of internal states (Siegel, 2015). Wedekind, et al (2013) assert that, individuals will be susceptible to development of substance use disorders, due to this severely regulatory deficit to cope with stress and form healthy attachments. Therefore, addiction has been referred to as an attachment disorder.
Thematic conflicts did emerge contrary to attachment disorders pre-existing substance use disorders. Attachments dysregulation implies disruption and a hyper-active amygdala and insula (Siegel, 2015). Emotional dysregulation neurology related to substance use disorder neuroimaging, reflected data that did not implicate the emotional generating components (limbic system) of the brain. Although these systems are considerably illuminated from oxidative blood flow related to other diagnosis, which incur problematic issues with emotional regulation (Wilcox, Pommy, & Adinoff, 2016).
Research has established linkages between childhood development and development of capabilities to handle stress and process negative emotion throughout a lifetime (Fletcher, Nutton, & Brend, 2014; Kreis, Gillings, Svanberg, & Schwannauer, 2016). Deviations in healthy development of interpersonal integrity, due to defective parenting and attachment, sets the stage for future problems with emotional dysregulation (Div, Ford, Hill, & Frazier, 2014; Siegel, 2015). Fletcher, Nutton, and Brend (2015) postulate that fearful avoidant attachment styles found to be associated with substance use disorder. Khantzian (2012) expands upon this theme by asserting that lack of interpersonal integrity complicates necessity for interpersonal relationships. This happens because of inabilities to recognize emotions and a sense of self. This produces separation from the concept of self and the need for relationships. It is this state of isolation that is the underpinning of dysphoric feelings, which in turn may increase vulnerability to utilize substances. Substitutionary use of substance then becomes the new object for attachment needs Khantzian (2012). Fletcher, Nutton, and Brend (2015) assert that twelve-step programs provide attachment needs while recovering individuals learn to function abstinent while utilizing the group and twelve-step relationships as a new object of attachment.
Chapter four illuminated significant themes relative to three specific research questions. Dopaminergic dysfunction was a consistent theme through numerous articles. Underlying this regulated stress systems contributing to problems with emotional dysregulation and substance use disorder was another consistent theme. Neurotransmitter and underlying issues with emotional dysregulation relative to genetic components emerged as a consistent problem with substance use disorder. Regarding the second research question, describe regulation function due to trauma and working memory emerged as thematic constructs. Research question three yielded two major themes. Intergenerational transmission of dysregulation and attachment dysfunction due to early childhood experiences were considerable themes.
Substance use disorder is a significant social problem, characterized by failed attempts to put the diagnosis into remission. This is a disconcerting problem, as it confounds the problem of SUD, fostering concerns about possible underlying untreated conditions and what is the nature of this nebulous diagnosis (Robinson, Robinson, & Berridge, 2014; Kassani, Niazi, Hassanzadeh, & Menati, 2015; Mohammadpoorasl, Fakhari, & Akbari, 2012; Reavis, 2013). A commonality with mental diagnosis is a symptom of emotional dysregulation. Dysregulation of affect has been linked to addictive disorders (Dvir, Ford, Hill, and Frazier, 2014; Stasiewicz, et al., 2012).
Based upon these facts, a more precise comprehension of the dynamics of substance use disorder and emotional dysregulation is required. Inquiries about underpinnings of these two problems is not sufficient. A detailed inspection of the relationships between maladaptive emotional coping and addictive patterns is necessary to fully comprehend the complexity of the diagnosis. The purpose of this theoretical systematic review was to potentially demystify and clarify the nature of substance use disorder which could provide clinicians with additional insights and clinical tools. It is hope that this also serve to mitigate the shame stigma associated with addictive disorders and the numerous failed attempts to put the diagnosis in remission. Finally, by illuminating gaps in numerous previously conducted research; more studies will be pursued to close the space in research.
Discussion of Findings
Thirteen themes emerged from three specific questions about the nature of emotional dysregulation and substance use disorder, and the potential shared relationships. In general, themes were related to problematic neurobiology, dopamine dysregulation, insufficient stress coping, interpersonal issues, generational transmission, attachment, and trauma. These essential findings of the themes will be discussed, while applying an interpersonal neurobiological framework.
Dopamine Dysregulation/Interpersonal Development
Cuevas et al. (2014) postulated based on research, a link between human development in early years predicated upon parental interactions, to dopaminergic manufacturing and processes. This may suggest a connection/intersection between two research questions. Research question one was primarily concerned with underpinnings of substance use disorder and associations with inabilities to emotionally regulate. Research question three was based on specific relationships between substance use disorder in interpersonal development related to traumatic occurrences during development. According to Siegel (2012) trauma related to lack of healthy development of interpersonal constructs from an interpersonal neurobiological perspective, be a considerable lack of vital parental attunement and mindsight. Mindsight is an open focus on one’s internal awareness and subjective conditions of others. Attunement is the manner in which focus occurs in obtaining information about self and others subjective perceptions and interpretations (Siegel, 2012).
Cuevas et al. (2014) related to child and maternal relationships in the early development, asserted the development of effort control having a genetic basis. This genetic polymorphism could therefore be responsible for dopaminergic functionality and the acquisition/development of effort control. Metabolism for dopamine are linked to genetic variants of the COMT and DRD2 genes. This is a genetic contributory to effort control.
De Bellis & Zisk (2014) assert that inner disassociation and social isolation is a result of interpersonal insults. Diaz, Horton, and Weiner (2012); Mohammadpoorasl, Fakhari, and Akbari (2012) highlight the fact that substance use disorder is linked with social problems. It becomes clearer that trauma/interpersonal injuries distance the individual with substance use disorder from self and others, exacerbating an already dysregulation system. It is possible that, early childhood abnormal development sets the stage for dysregulation in the dopaminergic system. Siegel (2012) concludes that activation of the dopaminergic circuity occurs when there is a reaching out to others for relationship and/or aiding others.
A genetic predisposition to develop abnormal executive functioning, once an individual is subjected to parenting that is void of attunement and mindsight. Lack of these essential mental constructs, could therefore causes conditions to isolate socially, thus further reinforcing faulty neurology, to remain isolated and dysregulated. The very means to activate the dopaminergic reward circuitry through social engagement, becomes not a viable option due to trauma already sustained to that brain system (Siegel, 2012). A lack of social connectivity to stimulate dopamine, coupled with deficiencies in executive functioning could set the stage for development of substance use disorder.
The incentive sensitization theory contributes a number of clarifications of the nature of addiction. This theory assert that the inflow of addictive substances into the mesolimbic system cause a significantly high spike in in dopamine. This surge is no longer believed to be a hedonic spike, but an evolutionary response to promote the chances of the behavior being repeated in the future form a potential survival perspective. It is termed the wanting system, which is different from the endogenous opioids liking system (Berridge & Robinson, 2016; Blum, Gardner, Oscar-Berman, & Gold, 2012). The massive surge of dopamine ensures that any environmental or internal contextual information present at the time of the rapid increase in dopamine will be encoded causing a powerful and long lasting effects through conditioning (Berridge &Robinson, 1993).
Blum, Gardner, Oscar-Berman, and Gold (2012) assert the reward deficiency syndrome, which states that addictive patterns are caused by genetically predisposed low levels of dopamine. Thus, chemical seeking in consumption becomes a way to self-medicate and imbalance of the dopamine neurotransmitter (Fletcher, Nutton, and Brend, 2014). Although Berridge & Robinson (2016) argue against Blum’s position on the role of dopamine, there assertions on abnormal/dysfunctional levels dopamine are in agreement.
Berridge and Kringelbach (2016) conclude that the system although active during a reward salience experience, can be triggered by fear. Thus, a fear salience in induced, following the same principles as reward salience. This means that environmental cues associated with the salience of fear will stored in memory. This reversal of the salience dynamic that can be attributed to the plasticity of mesolimbic motivation. For example, a cocaine user initially experiencing euphoria followed by drug-induced cocaine psychosis. The experience of the cocaine becomes a source of paranoid fear.
This brings the experience of trauma and negative interpersonal development into focus. Dvir, Ford, Hill, Frazier (2014) conclude that early experiences during childhood development are critical periods of time for the development of regulatory functions of the parasympathetic nervous system. Additionally, development of the hypothalamic-pituitary-adrenocortical axis is equally critical at this juncture in human development. Complications and abnormalities to the development of these essential regulatory systems in potential cause to inabilities to regulate emotion, and produce individuals with significant maladaptive emotional responses to stress. Early insults in childhood development could therefore set the stage for maladaptive development of the dopaminergic system, based on exposures to experiences that produce a fear salience.
Domain Specific Targeting for Treatment of Substance Use Disorders
Themes related to all three research questions give focus to consideration to numerous concepts and insights into addiction comprehension and treatment, which focus on the domains of emotional regulation and complications that may arise at each regulation stage. Emotional dysregulation has been linked to development of substance use disorders (Dvir, Ford, Hill, Frazier, 2014). Brain regulatory functions for modulating emotions are divided into specific functions. There are slight variations in what researchers deem as necessary components to regulate. Gross (2015) asserts five domains of emotional regulation that is widely accepted. These domains are situation selection, situation modification, attentional employment, cognitive change, and response modulation. Each of these components facilitate specific functions in the goal to regulate. Emotional dysregulation becomes problematic when there is abnormal functioning within these domains. Therefore, it becomes of particular interest as to which domain or domains are linked to the development of substance use disorders. It is therefore pertinent to look at each of these domains in detail, and draw from existing research to link potential risk factors in the development of substance use disorder/relapse with possible maladaptive functions at specific components of emotional regulation.
Situation selection involves making a choice anticipating the probability of or absence of an emotional response. The nature of the response can be positive or negative. This is a critical domain relative to recovery from substance use disorder. The idea of placing one in favorable environments to avoid trigger cues related to the incentive salience (Berridge & Robinson, 2016). The premise of this domain is the aspect of choice or selection. Situational modification is also based off the choice. The choice is a matter of altering the situation to affect the emotional consequences. Attention deployment(reappraisal) is the directing or redirecting of attention anticipating a shift in affect for more desirable conditions. The are reappraisal phase can be dis-regulated leading to unhealthy risk behaviors, and decreased awareness of potential consequences (Panno, Lauriola, & Figner, 2013). In addition to situation selection, this is an essential focal point for addiction treatment. Cognitive change involves modulation or governing the evaluation of the situation. The therapeutic reframe is an accurate description of this domain. Response modulation is essentially the reaction or response. This includes extrinsic coping mechanisms. Substance use patterns would be an action to regulate or modulate affect responses (Gross, 2015). From these descriptions, it is obviously apparent that the focus relating to emotional regulation and substance use disorders centers on to specific stages. Meaning the environmental trigger stage (situational selection) and the response phase (response modulation). Skinner, Reese, and Shaver (2014) postulate that emotional dysregulation is a multi-domain process, however research is limited at which specific component is potentially predictive of problematic consumption of alcohol.
Due to the strong possibilities of emotional dysregulation being a considerable substrate of substance use disorders, it possible that treatment modalities aimed at focusing on each specific domain may foster increases in regulatory functions, and therefore improve recovery rates from SUD. Therefore, experimentation with clinical interventions that help with situational modification, attentional employment, and cognitive change, within the context of interpersonal neurobiology, is a significant point of interest. Triggering situations (situational selection) and action-based reactivity (response modulation) only account for the beginning and ending of the emotional regulation process, while neglecting stages in the process that identify emotion and motivate positive changes extrinsically and intrinsically to mitigate negative affect or reduce intensity (Gross, 2015). Spence and Courbasson (2012) although referencing a more simplistic explanation of emotional regulation, mentioning reappraisal, selection of focus, and behavioral response, suggest that dysregulation is a breakdown of all processes. This could mean that addressing all aspects of emotional dysregulation, may improve inabilities to emotionally regulate.
An interpersonal neurobiological focus would foster improved relations with others and self, while mitigating the necessity to emotionally regulate through substances. Therapeutic interventions that facilitate mindsight, attunement, and integration of mind, brain and connections socially will promote enhanced abilities for prefrontal cortex operations to override and regulate the limbic generated emotions (Siegel, 2012).
Underpinnings, Associations, and Overlaps to Substance Use Disorder
Numerous underline conditions have surfaced as potential underlying issues of substance use disorder. Possible patterns and associations have also emerged in themes and the relationships to the literature review. Siegel (2015) asserts that positive mental health is hinged upon abilities to regulate emotional energy while maintaining a social network can use it to the exchange of neurological energies to foster necessary support for integration and regulation. Dvir, Ford, Hill, and Frazier (2014); Tang, Tang, and Posner (2015) agree that dysfunction of emotional regulation systems exacerbate vulnerabilities to development of substance use disorder. Dvir, Ford, Hill, and Frazier (2014) postulates a relationship between social functioning and emotional regulation. The interplay between these two functions is critical to emotional health. Capabilities to experience empathy, mindsight, and emotional understanding are pertinent features in emotional intelligence. Research has established a positive correlation between healthy emotional regulation and social efficacy. Therefore, emotional regulation is essential to social connections, and social connections support and contribute to emotional regulation. Conversely, poor aptitudes in these areas produce susceptibility to externalizing behaviors such as substance abuse.
Interpersonal trauma has been recognized as a condition causing complications in the ability to emotionally regulate and regulate stress (Tice, Bratslavsky, & Baumeister, 2001). Khantzian (2012) postulates that deficiencies in dysfunctions in integrity related to interpersonal issues leads to difficulties with relationships that foster interpersonal integrity. Craparo, Ardino, Gori, and Caretti (2014) postulate the necessity for more research relative to alexithymia, disassociative states, and interpersonal integrity. This could mean that there is a connection between maladaptive interpersonal integrity, underpinning emotional dysregulation and social dysfunction. This in turn can lead to increased vulnerability to the development of substance use disorder to medicate underlying conditions.
Fletcher, Nutton, and Brend (2015) conclude that attachment problems can undergird substance use disorder. A fearful avoidant attachment style has been associated with SUD. Addiction has been referred to as a deregulatory attachment disorder (Wedekind, et al, (2013). According to Siegel (2015) problematic dysregulation related to attachment problems induces a hyperactive state of the amygdala and insula. Although research by Wilcox, Pommy, and Adinoff (2016) reported neuroimaging that did not implicate activation of the symptom relative to emotional regulation. More studies are needed to address this discrepancy in research.
Parental influence at critical stages during childhood development set the stage for development of attachment emotional dysregulation. Alternatively, child-parental relations that are void of interpersonal neurobiological attunement and mindsight because dysfunction in these areas (Dvir, Ford, Hill, & Frazier, 2014; Siegel, 2015). This is possibly interpreted as difficulties with both emotional regulation and social needs being difficult functions stemming from interpersonal matters.
Bridgett, Burt, Edwards, and Deater-Deckard (2015) indicate that self-regulation mechanisms can be transmitted intergenerational. Although, research has been minimized in this area, seems to be a vital importance in understanding and indirect relationship with substance use disorder. Yehuda et al. (2016) studied the epigenetic dynamics between stress affects intergenerational transmission. Neurological adaptions associated with stress disorders can emerge in individuals who sustain no significant trauma. However, the neurological dysfunctions of parents exposed to traumatic stimulus, seems to be transmitted to the offspring. It is also a possibility that trauma to parents early in childhood, may have lasting effects to abilities to emotionally regulate, coping stress, and sustain and nurture healthy interpersonal relationships.
Addiction has been cited as a genetic disease. There is significant research to support the fact that polymorphisms from an epigenetic perspective, become active in the mesolimbic system once exposed to stress and intoxicating substances (Sweitzer, 2012). It may be more accurate to refer to substance use disorder/addiction as an inter-generationally transmitted dysregulation of interpersonal dysfunction, stress dysregulation, social ineptness, and maladaptive attachments disorder. This does not undermine or disregard the American Society of Addiction Medicine definition, which suggests that addiction is a problematic issue with diseased reward, motivation, and memory systems (Smith, 2012). The model (figure 5.1) suggest a more comprehensive comprehension of underlying etiologies and why these systems maybe diseased/dysregulated.
Alexithymia seems to be a hidden and overlooked underlying problem with substance use disorders. It manifests as inadequacies in identifying and describing problematic emotions (Parolin et.al, 2016). Research suggests that it clicks nearly 45% to 67% with individuals diagnosed with alcohol use disorder (Krentz, Higgons, Staller, and Klatt, 2015). Craparo, Ardino, Gori, and Caretti (2014) assert that alexithymia presents itself with a psychic numbing similar to dissociative disorders. Stasiewicz et al. (2012) conclude that alexithymia impedes abilities to become mindful, while reducing effectiveness with coping skills in both men and women. An inability to identify and express emotions, may therefore result in unmanageable negative affect resulting in the necessity to self-medicate. Although, this could be a defense mechanism stemming from trauma, more studies director that the dynamic associations between alexithymia and interpersonal struggles needs further refinement.
This could mean that alexithymia is a condition that camouflages underlying interpersonal trauma. This also can be interpreted as why interpersonal issues are minimized and /or denying the impact of early childhood insults. Alexithymia can possibly be a blockade to underpinnings of emotional dysregulation leading to substance abuse (figure 5.1). Minimizing emotions and denying the impact of early childhood experiences can complicate treatment modalities aimed at substance use disorder. Potentially two conclusions, requiring more research, may be reasons for development of addiction and high relapse rates. The first is the role of alexithymia in minimizing damaging experiences to the psyche, while minimizing and ignoring past and current affective of conditions. Secondly, through intergenerational transmission of interpersonal trauma, perhaps many individuals are unaware that they have been affected by trauma in previous generations. These require further research and inquiry into their obstructions and interfering role with therapeutic gain in substance use treatment.
Recommendations for Practice
Etiologies of substance use disorder and emotional regulation complex, and remain somewhat nebulous, as the mysteries of the brain still have not yielded all secrets. There is definitive evidence that the mesolimbic system is a specific area of interest to addiction science. Epigenetics attempts to fill in the gap for why certain individuals go on to develop substance use disorder, while others may regulate their substance intake or cease consumption for logical life-changing reasons. Emotional dysregulation is a powerful force underlying many mental diagnoses. Khantzian (2012) assertions about self-medication to alleviate undesirable conditions, is not an oversimplification of the addiction dynamic. A dysregulated individual will gravitate towards a substance or some type of behavioral intervention to find relief. Blum (2015) adds plausible evidence to the fact that individuals prone and susceptible to addictive disorders, may have an underlying condition that predates their first initial use of substance. It is suggested that possibly under dynamics of interpersonal trauma, sustained either earlier in life, or as a result of being parented by a dysregulation parent, give some explanation for why emotional regulation becomes the default affective condition. Alexithymia, and complicates the issue, due to the fact that is difficult to discern or detect underlying complications with affect. It is not uncommon to see a client for substance use disorder, who denies any childhood insults, and indicate that they had a great childhood upbringing. Months later, it is revealed that many of their negative coping skills and lack of stress management, dates back to what they have learned from their parents. In some cases, they may have been shamed for attempting to operate healthy, by asking for help for complicated emotions. Therefore, interpersonal trauma may not come in the form of moderate to severe neglect and abuse. But can possibly occur from caregivers who lack empathy, attunement, and the ability to have mindsight. In homes where these are viewed as weak or cowardly, the shame incurred by rejecting these healthy psychological attributes and actions, can leave children disillusioned, confused, and emotional dysregulation. A comprehensive model for understanding the complexities that underlie emotional dysregulation and substance use disorder is necessary to improve treatment modalities, increase client awareness, and prepare clinicians for the deeper work underpinning substance use disorders.
Recommendations for Practice
Etiologies of substance use disorder and emotional regulation complex, and remain somewhat nebulous, as the mysteries of the brain still have not yielded all secrets. There is definitive evidence that the mesolimbic system is a specific area of interest to addiction science. Epigenetics attempts to fill in the gap for why certain individuals go on to develop substance use disorder, while others may regulate their substance intake or cease consumption for logical life-changing reasons. Emotional dysregulation is a powerful force underlying many mental diagnoses. Khantzian (2012) assertions about self-medication to alleviate undesirable conditions, is not an oversimplification of the addiction dynamic. A dysregulated individual will gravitate towards a substance or some type of behavioral intervention to find relief. Blum (2015) adds plausible evidence to the fact that individuals prone and susceptible to addictive disorders, may have an underlying condition that predates their first initial use of substance. It is suggested that possibly under dynamics of interpersonal trauma, sustained either earlier in life, or as a result of being parented by a dysregulation parent, give some explanation for why emotional regulation becomes the default affective condition. Alexithymia, and complicates the issue, due to the fact that is difficult to discern or detect underlying complications with affect. It is not uncommon to see a client for substance use disorder, who denies any childhood insults, and indicate that they had a great childhood upbringing. Months later, it is revealed that many of their negative coping skills and lack of stress management, dates back to what they have learned from their parents. In some cases, they may have been shamed for attempting to operate healthy, by asking for help for complicated emotions. Therefore, interpersonal trauma may not come in the form of moderate to severe neglect and abuse. But can possibly occur from caregivers who lack empathy, attunement, and the ability to have mindsight. In homes where these are viewed as weak or cowardly, the shame incurred by rejecting these healthy psychological attributes and actions, can leave children disillusioned, confused, and emotional dysregulation. A comprehensive model for understanding the complexities that underlie emotional dysregulation and substance use disorder is necessary to improve treatment modalities, increase client awareness, and prepare clinicians for the deeper work underpinning substance use disorders (figure 5:1).
From a clinical perspective, it is significantly disappointing when a client has done good work on numerous issues for months, then for unknown reasons engagement in treatment decreases, followed by the news that the client has relapsed back into substance use disorder symptoms. This study has yielded numerous possible underlying etiologies that seem to be interrelated. Although not everyone with substance use disorder symptoms will have underlying interpersonal trauma. But they will possess some form of dysfunction in regulatory functions. This raises questions as to why they are dysregulation.
The disease concept of addiction has served to bridge the neurological conditions for substance use disorder with improve treatment modalities, while mitigating the shame associated with such a diagnosis. Therefore, those that disagree with the addiction concept as being a diseased brain, will have a difficult time arguing against referring to addiction as a dysregulation of mesolimbic system functions. More importantly, this state of dysregulation remains intact while in a state of abstinence. This poses important questions about the nature of dysregulation, anhedonia states that camouflage underlying conditions, and intergenerational transmission of interpersonal struggles. Thus, this was the intent of the study.
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Dr. John Airsman is a Clinical Director and valued team member at Midwest Institute for Addiction.