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Table of contents
- Biological and Psychological Mechanism
- Chronic Stress, Drug Use, and Vulnerability to Addiction
- Stress and Addiction
- Chronic Stress, Drug Use, and Vulnerability to Addiction
The effects of distal events occurring more than 1 year prior and proximal stress experiences events during the most recent 1-year period , and their effects on meeting criteria for substance use disorders were also assessed. The findings indicate that the cumulative number of stressful events was significantly predictive of alcohol and drug dependence in a dose-dependent manner, even after accounting for control factors. Both distal and proximal events significantly and independently affected addiction vulnerability. The types of adverse events significantly associated with addiction vulnerability were parental divorce or conflict, abandonment, forced to live apart from parents, loss of child by death or removal, unfaithfulness of significant other, loss of home to natural disaster, death of a close one, emotional abuse or neglect, sexual abuse, rape, physical abuse by parent, caretaker, family member, spouse, or significant other, victim of gun shooting or other violent acts, and observing violent victimization.
These represent highly stressful and emotionally distressing events, which are typically uncontrollable and unpredictable in nature.
Table 1 summarizes the types of life events, chronic stressors, maltreatment, and individual level variables associated with addiction risk. There is some evidence from animal studies to support the notion that acute exposure to stress increases initiation and escalation of drug use and abuse see 30 , 83 for reviews.
For example, in animal models, social defeat stress, social isolation, tailpinch and foot-shock, restraint stress, and novelty stress are known to enhance acquisition of opiates, alcohol, and psychostimulant self-administration, with caveats relating to stressor type, genetic background of animals, and variations by drug type see 84 — 87 for reviews. Nonetheless, there is evidence that stress increases drinking and nicotine smoking see 83 for review , but the effects of drinking history, history of adversity, social stress, and expectancies are known to play a role in these experimental studies.
As evidence using diverse approaches has accumulated in support of a significant effect of stress on risk of addiction, this section examines research on neurobiological links between stress and reward pathways activated by abusive drugs. It is well known that the reinforcing properties of drugs of abuse involve their activation of the mesolimbic dopaminergic DA pathways, which include dopamine neurons originating in the ventral tegmental area and extending to the ventral striatum and the prefrontal cortex PFC.
However, stress exposure and increased levels of glucocorticoids GC also enhance dopamine release in the NAc. There is also evidence that, like drugs of abuse, stress and concomitant increases in CRF and glucocorticoids enhance glutamate activity in the VTA, which in turn enhances activity of dopaminergic neurons. In addition to a role in reward, a growing body of human imaging studies and preclinical data indicate that the ventral striatum is also involved in aversive conditioning, in experience of aversive, pain stimuli, and in anticipation of aversive stimuli.
Research has also examined whether stress-related increases in acquisition of drug self-administration are mediated by corticosterone cortisol in humans. Findings indicate that HPA-activated corticosterone release is important for acquisition of drug self-administration. Mice with deletion of the GR gene show a dose-dependent decrease in motivation to self-administer cocaine. Although in nonhuman primates the link between cortisol, dopamine, and drug self-administration has not been reported, there is evidence that stress related to social subordination is associated with lower levels of D2 receptors and higher cocaine self-administration.
For example, in a small-sample study, Pruessner and colleagues found that healthy individuals with low early-life maternal care showed greater dopamine release in the ventral striatum during an acute psychological stress task as compared to those with a history of high early-life maternal care. More recently, the same group has also shown a similar significant relationship between cortisol levels and dopamine release in the VS using a psychological stress task.
There is growing evidence from basic science studies that early-life stress and chronic stress significantly affect the mesolimbic dopamine pathways and play a role in drug self-administration. Repeated and prolonged exposure to maternal separation MS in neonatal rats significantly alters the development of central CRF pathways. Early-life stress and prolonged and repeated stress also adversely affect development of the prefrontal cortex, a region that is highly dependent on environmental experiences for maturation.
High levels of glucocorticoid receptors are also found in the PFC, and chronic GC treatment results in a dramatic dendritic reorganization of PFC neurons similar to that seen in the hippocampus. High emotional stress is associated with loss of control over impulses and an inability to inhibit inappropriate behaviors and to delay gratification.
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In a recent PET imaging study, Oswald examined the effects of chronic stress and impulsivity on amphetamine-induced striatal dopamine release. These findings indicated that high trait impulsivity was associated with blunted right VS dopamine release. However, these effects were modified by a significant interaction with chronic life events stress. With low to moderate stress, dopamine release was greater in low than in high impulsive subjects, but with high stress, both groups showed low DA release.
These findings demonstrate the important effects of stress and impulsivity on mesolimbic dopamine transmission and highlight the fact that both factors need to be carefully considered to fully understand the role of stress and impulsivity on addiction risk. Figure 1 presents a schematic model of stress effects on addiction. It highlights cross-sensitization of stress and drug abuse on specific behavioral and neurochemical responses and indicates the common neurobiological pathways upon which both stress and drugs of abuse act. Column A lists three types of vulnerability factors: Specific synaptic changes in these pathways at molecular and cellular levels , provide the basis for the mechanism by which stress and individual and genetic factors in column A interact to increase risk of maladaptive behaviors represented in column C.
The model suggests that stress experiences in the presence of these vulnerability factors result in maladaptive stress and self-control responses that increase addiction risk. The specific mechanism by which the maladaptive stress responding increases this risk involves dysregulation in brain stress circuits, particularly the CRF and NE systems, and their interactions with the mesocorticolimbicstriatal dopamine pathways and its modulation by glutamate and GABA.
A schematic model of stress effects on addiction, representing the cross-sensitization of stress and drugs on behavioral and neurochemical responses, that are mediated by the stress and reward pathways. Each of these factors influences each other to significantly affect alterations in neurobiological pathways involved in stress regulation and cognitive and behavioral control Column B. Such changes at least partially mediate the mechanisms by which stress and individual and genetic factors in column A interact to increase risk of maladaptive behaviors represented in column C when an individual is faced with stress or challenge situations.
Acute administration of the most commonly abused drugs such as alcohol, nicotine, cocaine, amphetamines, and marijuana that activate brain reward pathways mesocorticolimbic dopaminergic systems also activate brain stress pathways CRF-HPA axis and the autonomic nervous system pathways with increases in plasma adrenocorticotropic hormone ACTH and corticosterone, changes in heart rate and blood pressure, and skin conductance responses. For example, changes in heart rate and heart rate variability HRV are reported with regular and chronic alcohol use.
Although acute administration of drugs increases mesolimbic dopamine, regular and chronic use of abusive drugs and acute withdrawal states down regulate mesolimbic dopamine pathways with decreases in basal and stimulated dopamine reported in several preclinical studies. It is not entirely clear how long these changes persist or the extent to which there is recovery or normalization of these pathways and responses in related functional responses. Clinical symptoms of irritability, anxiety, emotional distress, sleep problems, dysphoria, aggressive behaviors, and drug craving are common during early abstinence from alcohol, cocaine, opiates, nicotine, and marijuana.
However, with chronic drug use, the term becomes associated with a physiological need, hunger, and strong intent to seek out the desired object, thereby representative of the more compulsive aspects of craving and drug seeking identified by addicted patients. Indeed some support for this idea comes from laboratory and imaging studies summarized below. In my laboratory, we have examined the effects of stress and drug-related cues on drug craving in alcoholics, cocaine-dependent individuals, and naltrexone-treated, opiate-dependent individuals in recovery. Drug craving and stress responses were assessed in treatment-engaged, abstinent, addicted individuals who were exposed to stressful and nonstressful drug-cue situations and neutral relaxing situations, using personalized guided imagery procedures as the induction method.
Biological and Psychological Mechanism
In addition, imagery of personal stressors produced significant increases in cocaine craving, while public speaking did not. In a more comprehensive assessment of the biological stress response in recently abstinent cocaine-addicted individuals, we reported that brief exposure to stress and to drug cues as compared to neutral relaxing cues activated the HPA axis with increases in ACTH, cortisol, and prolactin levels as well as the sympthoadrenomedullary systems, as measured by plasma norepinephrine and epinephrine levels.
Findings indicated that cocaine patients showed an enhanced sensitivity to emotional distress and physiological arousal and higher levels of drug craving to both stress and drug-cue exposure compared to controls. The recovering alcoholics at 4 weeks abstinence showed greater levels of basal heart rate and salivary cortisol levels compared to control drinkers.
Upon stress and alcohol-cue exposure, they showed persistently greater subjective distress, alcohol craving, and blood pressure responses, but a suppressed heart rate and cortisol response compared to controls. These data provide direct evidence of high drug craving and altered hedonic responses to both stress and drug cues in addicted individuals compared to social drinkers see Fig. They also indicate that alterations in physiological stress responses are associated with high levels of stress-induced and cue-induced craving and distress states.
The nature of the alterations are marked by increased emotional distress, heightened craving, altered basal responses, and blunted or suppressed physiological responses in abstinent addicted individuals compared to social drinkers. Mean and standard errors for peak craving and anxiety ratings during exposure to stress, drug cues, and neutral imagery conditions.
Detailed statistics provided in Fox et al. Many studies have also examined brain regions associated with craving in addicted individuals. Exposure to drug cues known to increase craving increases activity in the amygdala and regions of the frontal cortex, — with gender differences in amygdala activity and frontal cortex response in cocaine-dependent individuals.
As stress also increases drug craving, we examined brain activation during stress and neutral imagery in a functional magnetic resonance imaging fMRI study. Although healthy controls and cocaine-dependent individuals showed similar levels of distress and pulse changes during stress exposure, brain response to emotional stress in paralimbic regions such as the anterior cingulate cortex, hippocampus, and parahippocampal regions was greater in healthy controls during stress, while cocaine patients showed a striking absence of such activation. Recent PET studies have also shown significant positive correlations between the dorsal striatum and drug cue—induced cocaine craving.
While several efficacious behavioral and pharmacological therapies in the treatment of addiction exist, it is well known that relapse rates in addiction remain high. In the last decade, a substantial number of preclinical studies have shown that brain CRF, noradrenergic, and glutamatergic pathways contribute to reinstatement of drug seeking. These data are consistent with human findings reviewed in the previous section indicating that alterations in stress and dopaminergic pathways accompany high distress and craving states and blunted physiological and neural responses that are important in regulation of stress, craving, and impulse control.
Human research has also begun to identify markers of the stress and craving states that are predictive of relapse outcomes. To fully understand whether the increased distress and drug-craving state is predictive of relapse, we followed the inpatient treatment-engaged cocaine- and alcohol-dependent individuals in our studies described in previous sections after discharge from inpatient treatment for 90 days to assess relapse outcomes.
For the cocaine group, we found that stress-induced cocaine craving in the laboratory significantly predicted time to cocaine relapse. While stress-induced ACTH and cortisol responses were not associated with time to relapse, these responses were predictive of amounts of cocaine consumed during follow-up. These data suggest that at least in the case of cocaine dependence, stress and drug cue—induced distress states produce a similar compulsive drug-seeking state that is associated with relapse vulnerability. In alcoholics, negative mood, stress-induced alcohol craving, and blunted stress and cue-induced cortisol responses have been associated with alcohol relapse outcomes.
Findings from basic science and human laboratory and clinical outcome studies identify several pharmacological treatment targets to address stress-induced reinstatement of drug seeking and relapse susceptibility. Basic science data suggest CRF antagonists, alpha-2 adrenergic agonists, and glutamatergic agents could be promising in addressing stress-related relapse. Human laboratory studies are needed that will screen these agents to assess their promise with regard to intermediate markers of stress-related relapse susceptibility.
Such studies would target stress- and cue-induced drug craving, craving-related anxiety, HPA measures, and heart rate or heart rate variability as well as responses in specific brain regions. For example, mindfulness based stress reduction MBSR is efficacious in decreasing relapse to major depression, and adaptations of these strategies could be of benefit to address relapse risk in addiction.
This review focuses on the accumulating evidence from preclinical, clinical, and population studies that highly stressful situations and chronic stress increase addiction vulnerability, that is, both risk of developing addiction and risk of relapse. The types of stressors that increase addiction risk are identified in Table 1. The stressors tend to be highly emotionally, distressing events that are uncontrollable and unpredictable for both children and adults. The themes range from loss, violence, and aggression to poor support, interpersonal conflict, isolation, and trauma.
There is also evidence for a dose-dependent relationship between accumulated adversity and addiction risk—the greater the number of stressors an individual is exposed to, the higher the risk of developing addiction. Work-related stressors have weaker support, but individual-level variables such as trait negative emotionality and poor self-control possibly similar to poor executive function appear to also contribute uniquely to addiction risk.
Exposure to such stressors early in life and accumulation of stress chronicity result in neuroendocrine, physiological, behavioral, and subjective changes that tend to be long lasting and adversely affect development of brain systems involved in learning, motivation, and stress-related adaptive behaviors. Research that directly addresses stress-related neurobiological changes and their association with behavioral outcomes is sorely needed. Evidence to clarify the contribution of stress to alterations in mesolimbic dopamine activity and its association with drug use is also needed.
Figure 1 presents a schematic model of associations that have been supported in research, as well as remaining gaps. A review of evidence indicating the effects of drug use and abuse on stress responses and dopamine transmission is presented, along with altered emotional and motivational responses associated with craving and relapse to drug use. While substance abuse results in changes in stress and dopaminergic pathways involved in motivation, self control, and adaptive processes necessary for survival, evidence for whether such changes enhance drug seeking or craving and drug use behaviors is lacking.
For example, studies on whether prior exposure to licit and illicit drugs modifies the association between stress and drug self-administration are rare. While there are specific neuroadaptations in reward and associated regions, it is also important to examine which of these changes are involved in increasing drug intake and supportive of addictive processes such as progressive loss of control, persistence of craving, and escalating drug self-administration.
As stress also increases risk of mood and anxiety disorders that are highly comorbid with addiction, it is important to examine whether there are specific stress-related factors that contribute to risk for mood and anxiety disorders and addiction risk. That is, what are the resiliency factors that are protective for one set of illness but are vulnerabilities for the other. Exploration of gene—environment interactions could be particularly helpful in answering such questions.
A review of recent studies on stress-induced reinstatement to drug seeking, drug craving, and relapse susceptibility is also provided. Clinical implications include the development of new assessment procedures and markers that will be useful in identifying those who are at particular risk for stress-related relapse and testing of novel pharmacological therapies that target the link between stress and relapse risk. As shown in Figure 2 , addicted individuals show enhanced sensitivity to craving and greater anxiety in stress- and drug-related situations, but whether such altered responses represent transitions due to chronic drug use or chronic stress states needs to be further examined.
Research on the mechanisms by which chronic stress and drug use alter executive functions that are involved in adaptive behavioral responses is needed. Efficacious behavioral treatments focus on improving coping response. However, stress exposure and chronic distress decrease stress adaptive and coping mechanisms, and hence treatments that focus on enhancing coping may not be suitable for those with stress-related risk factors.
Development of new interventions that target self-control, especially in the context of stress is needed. Systematic research on these questions will lead to a greater understanding of how stress is associated with relapse. Furthermore, such research may be significant in developing new treatment targets to reduce relapse, both in the area of medication development and in developing behavioral treatments that specifically target the effects of stress on continued drug use and relapse in addicts.
National Center for Biotechnology Information , U. Ann N Y Acad Sci. Author manuscript; available in PMC Aug See other articles in PMC that cite the published article. Abstract Stress is a well-known risk factor in the development of addiction and in addiction relapse vulnerability. Introduction Stress has long been known to increase vulnerability to addiction. Stress and the Development of Addictive Behaviors There is a substantial literature on the significant association between acute and chronic stress and the motivation to abuse addictive substances see 30 for review.
Chronic Adversity and Increased Vulnerability to Drug Use There is considerable evidence from population-based and clinical studies supporting a positive association between psychosocial adversity, negative affect, and chronic distress and addiction vulnerability. Open in a separate window. Stress Exposure Increases Initiation and Escalation of Drug Self-Administration There is some evidence from animal studies to support the notion that acute exposure to stress increases initiation and escalation of drug use and abuse see 30 , 83 for reviews.
Possible Mechanisms Underlying Stress Effects on Addiction Vulnerability As evidence using diverse approaches has accumulated in support of a significant effect of stress on risk of addiction, this section examines research on neurobiological links between stress and reward pathways activated by abusive drugs. Stress Mechanisms Involved in Acquisition of Drug Self-Administration Research has also examined whether stress-related increases in acquisition of drug self-administration are mediated by corticosterone cortisol in humans.
Early Life and Chronic Stress, Dopamine Systems, and Drug Self-Administration There is growing evidence from basic science studies that early-life stress and chronic stress significantly affect the mesolimbic dopamine pathways and play a role in drug self-administration. Stress, Self-Control, and Addiction Vulnerability High emotional stress is associated with loss of control over impulses and an inability to inhibit inappropriate behaviors and to delay gratification.
Schematic Model of Stress Effects on Addiction Figure 1 presents a schematic model of stress effects on addiction.
Chronic Stress, Drug Use, and Vulnerability to Addiction
Drug Use and Abuse and Changes in Stress and Reward Pathways Acute and Chronic Drug Use and Changes in Stress Responses Acute administration of the most commonly abused drugs such as alcohol, nicotine, cocaine, amphetamines, and marijuana that activate brain reward pathways mesocorticolimbic dopaminergic systems also activate brain stress pathways CRF-HPA axis and the autonomic nervous system pathways with increases in plasma adrenocorticotropic hormone ACTH and corticosterone, changes in heart rate and blood pressure, and skin conductance responses.
Altered Stress Responses and Craving with Chronic Drug Abuse Clinical symptoms of irritability, anxiety, emotional distress, sleep problems, dysphoria, aggressive behaviors, and drug craving are common during early abstinence from alcohol, cocaine, opiates, nicotine, and marijuana. Stress-Induced Reinstatement of Drug Seeking and Relapse While several efficacious behavioral and pharmacological therapies in the treatment of addiction exist, it is well known that relapse rates in addiction remain high.
Summary and Future Directions This review focuses on the accumulating evidence from preclinical, clinical, and population studies that highly stressful situations and chronic stress increase addiction vulnerability, that is, both risk of developing addiction and risk of relapse. Footnotes Conflicts of Interest The author declares no conflicts of interest.
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Stress and Addiction
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Chronic Stress, Drug Use, and Vulnerability to Addiction
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Has Gender Always Been Binary? Must It Mean Fear and Danger? Stress and Addiction Biological and Psychological Mechanism. Browse book content About the book Search in this book. Browse this book By table of contents. Book description Stress is one of the most commonly reported precipitants of drug use and is considered the number one cause of relapse to drug abuse.
For the past several decades, there have been