Over time people form Schemas ( cognitive, emotional etc) and belief systems which are based upon a major stressful event in youth or an accumulation of stressful events over a long period of time. These form a vulnerability factor towards substance abuse, along with genetic predispositions. (See the works of people such as Aaron Beck). However should an individual not have a genetic vulnerability, and/or Schema/ belief system vulnerabilities these factors may buffer against substance abuse. The combination of different types of stressors/stressor in conjunction with genetic and cognitive vulnerabilities may determine who suffers with stress and the level of stress, and stress may be an outcome of a combination of the aforementioned factors. Another factor to consider is that psychological stress may have specific threshold dependent on the person's vulnerability factors. Thus, if cognitive resource allocation is dysfunctional due to ongoing attempts to keep at vulnerability factors at bay, or if physiological and psychological allostatic load has attenuated thresholds, high levels of psychological stress may occur due to meta cognitive awareness of the current internal state, and a belief/Schema that it may or may not be controllable.

Hope this helps!

I think it's also important to consider the use of substances as a response to psychological stressors. Emotion regulation strategies can be used to reduce an individual's psychological stress level. However, for some individuals, such as those with Borderline Personality Disorder (BPD), a disorder which revolves largely around difficulties with emotion regulation (see Linehan, 1993), emotion regulation may manifest itself in maladaptive behaviors. One of the common symptoms of BPD is self-damaging impulsivity, including behaviors such as substance abuse (see DSM-IV-TR). Thus, these individuals may be attempting to reduce their level of psychological stress through the means of abusing illicit drugs & alcohol (see Reitz et al., 2012).

To address your subsequent question, substance use is only one of a number of possible ways to regulate emotion and reduce the effect of stressors. For example, skills-based therapies such as Dialectical Behavior Therapy aim to develop strategies such as mindfulness to reduce psychological stress. Therefore, although many individuals face psychological stress daily, some may deal with it through other regulatory means than with substances. Perhaps, as Cheryl has pointed out, certain genetic vulnerabilities may explain the rift between individuals who use substances and other maladaptive emotion regulation strategies to deal with stress and those who find adaptive, beneficial means to the same end.

Genetics are most important here. And not all genetic influences impart risk. A modification in the promoter of the dynorphin gene leads to higher synthetic activity of this opioid peptide, which appears to confer protection against developing cocaine addiction. this would prevent experimentation and occasional use, which is so prevalent to develop into full addiction. But repeated use ultimately overcomes our finite adaptive ability. Also, early trauma, psychiatric risk, are all associated with a higher prevalence of substance abuse. So drug abuse can clearly be seen as an attempt at self regulation (at least this one working hypothesis) which ends up being mediocre at best if full dependence develops. If one can improve the state of aversiveness that cerain people feel as a result of life experience, or from the cumultion of drug addiction, one could I think achieve longer term recovery. This implies also, that we could better help non-addiction related source of pathological stress.

I agree with Cheryl's explanation and also with Benjamin and Wilfrid. The Cheryl's argument that stress makes an individual vulnerable to substance abuse but the actual engagement in use/abuse of substance depends on genetic and cognitive predispositions seems reasonable. The idea that individual differences in stress tolerance may also be a potential factor is also acceptable.

The Benjamin's idea is largely based on the self medication hypothesis of substance abuse which suggests that people use/abuse substance to cope with stress and/or emotional distress. Substantial support to this hypothesis is available in the existing literature. However, the contrary hypothesis that chronic substance abuse brings changes and bio-psycho-social level that may result in higher level of stress and psychopathology is also well documented. Both hypotheses, however, explain the comorbidity in substance abuse.

The role of genetic factors in substance abuse has also recieved substantial support and many researchers have presented evidence that this may be a third variable causing both - substance abuse and stress/psychopathology. And, thus the co-occurrence of stress and substance abuse may not be the reciprocal effect of each other rather it may be because of common genetic factors.

I do agree with all the aforesaid ideas and hypotheses, but would like to say that all of them give only a partial explanation why some stressed individuals engage in substance abuse and not the others. I would like to extend the aforesaid views by adding of the role of positive psychological factors.

I agree that stress forms a vulnerability towards substance abuse and also towards psychological disorders but it is the presence of other factors (predisposing and/or protective factors) that determines whether an individual will have the problem or not.

The same stress may lead to substance abuse in one and any specific psychopathology in the other depending on what are the other vulnerability or predisposing factors. The one having a genetic of substance abuse is likely to abuse substances to cope up with stress of life and the other with a genetic predisposition for depression is likely to be depressed in the similar stressful situation.

However, one may find several individuals facing highly stressful situation and also having genetic (or any other) predisposition for substance abuse but they do not engage in substance use/abuse. One reason may be that they might have other positive psychological resources and may be equipped with better behavioral/psychological skills to cope with life stress. Thus, such individuals are less likely to self-medicate with such substances that help them to protect from or reduce stress.

In my view, it is the balance between the pathogenic and protective psychological factors within an individual that determines whether one will engage in substance use/abuse or not. If pathogenic factors outweigh the protective factors during stressful encounters then it will enhance the likelihood of substance use/abuse whereas the reverse would be associated with reduced likelihood of substance abuse.

Even the Cheryl's speculation that differential threshold for stress tolerance is also one factor determining the chance of substance abuse, can also be explained in terms of the aforesaid hypothesis. The abundance of positive psychological resources may enhance the tolerance of stress and the lack of the same may result in an increase.

As far as the pathogenic (or vulnerability) factors and positive protective factors are concerned the list is long that includes psychological, biological (including nutritional factors), and social aspects of an individual. Such factors are well represented in the existing literature and therefore I am not naming them here.

Simple - diasthesis-stress models.

Cheryl indicated coping mechanisms for various personality prototypes and as others indicated susceptibility with biological aspects and environment.

There appear to be two possible vectors of co-morbidity: 1). it has long been known that populations of people who carry a diagnosis of "bipolar disorder" and manifest an unusually diminished activity of the mitochondrial monoamine oxidase (MAO) enzyme trait are virtually indistinguishable from populations identified as "alcoholic." Why this overlap exists remains unknown - since no one has bothered to investigate this presumptive anomaly. We cannot say if the relationship it etiologic or purely co-incidental, even though it is apparent that all of these people would present with high levels of emotional distress. 2). In a large population (over 200) chronic recidivistic addicts who were apparently refractory to the "usual" treatments, 70% were found to have electrophysioloc evidence of temporal lobe seizure activity and nearly 90% had a first degree relative with either panic disorder or agoraphobia. A very small subset also had greatly increased (as opposed to decreased) activity of the monoamine oxidase enzyme trait - making then present with "borderline" symptoms that remitted with they received an adequate does of an MAOI. Curiously, in this profoundly ill population the presence of decreased MAO was far less than expected for a population of addicts (see 1. above) who all had some morbid history of problems with drinking alcohol. Regardless of how well these people were or were not able to use cognitive treatments that mobilize higher cortical glutamate mediated inhibitory defenses against cravings, they only responded after full suppression of their temporal lobe foci and their panic disorders. In this population that would count as the "sickest" addicts, their use of alcohol and or benzodiazepines to suppress panic/agoraphobia, along with their insistence on using clonazepam - which was originally developed specifically for partial complex temporal lobe seizure disorders - their emotional disturbances were due to not primarily "caused" by abusing substances - they just didn't know how to regulate the dosage of the pharmacologic interventions that they had already found for their illnesses. By history, patients in this "sickest" population who manifested both temporal lobe pathology and panic/agoraphobia, had all improved dramatically when using heroin - which effectively suppressed the temporal lobe and the panic diatheses.. Inevitably they all had drifted to the bottom of the social structure and ultimately submitted to methadone maintenance to avoid the physical and political risks of using heroin. Apparently, methadone does not have the same blocking properties against temporal lobe and panic diatheses that they experienced from heroin. Thus they presented with severe social and emotional trauma, receiving methadone, and generally demanding both clonazepam and alprazolam in high doses. When their chosen regimes were stabilized and shifted to less stigmatized treatment with anticonvulsants, they became indifferent to opiates and alcohol -and had extremely good results from cognitive treatments alone with improved exercise and diet.