Depression Major depressive disorder (MDD) is highly comorbid with PTSD, with large epidemiological studies demonstrating a PTSD–MDD comorbidity rate of 48% to 55% (as reviewed in Price & van Stolk-Cooke, 2015; van Minnen et al., 2015). MDD is characterized by the following occurring for at least two weeks: Depressed mood (i.e., feeling sad or hopeless) more often than not, loss of interest or pleasure, sleeping and eating disturbances, diminished attention, feelings of worthlessness, and suicidal ideation (American Psychological Association [APA], 2013). Negative affect in particular has been shown to be a primary symptom that is associated with the overlap of PTSD and depression (Contractor et al., 2018; Price et al., 2019). The association between PTSD and MDD most commonly results from either a shared etiology or symptom overlap (Flory & Yehuda, 2022). Though depression may, at times, seem to come out of nowhere or result from a chemical imbalance, it can also be caused by traumatic life events. Exposure to traumatic events increases the risk for developing both PTSD and MDD (Price & van Stolk-Cooke, 2015). According to the shared etiology model of comorbidity, both PTSD and MDD may be caused by the same trauma. In the case of MDD, trouble managing painful experiences such as trauma can lead to depression (Hudenko et al., 2021, p. 1). For example, in addition to being traumatic, combat and war may also result in feelings of guilt, regret, and loss (Hudenko et al., 2021). Additionally, it is notable that there is considerable overlap in the DSM-5 criteria for PTSD and MDD, which may play a role in the high levels of comorbidity (Flory & Yehuda, 2022). The shared etiological relationship between depression and PTSD can be so strong that some researchers believe PTSD should be considered a subtype of MDD (Zhang et al., 2022), while others speculate there is a subtype of PTSD for some individuals who present with both diagnoses (Flory & Yehuda, 2022). Although the shared etiology model demonstrates that it is entirely possible to have both depression and PTSD at the same time, it is also possible that an individual can be misdiagnosed with either MDD or PTSD due to symptom overlap. According to a review by van Minnen and colleagues (2015), PTSD and MDD “share many diagnostic approximately half of individuals with a current diagnosis of substance use disorder (SUD) meeting criteria for PTSD (Berenz & Coffey, 2012; National Center for PTSD [NCPTSD], 2020). The presence of substance use among individuals with PTSD is higher for men than for women, and it is particularly pronounced in combat veterans (Roberts et al., 2015). Among the various forms of substance use disorder, alcohol use disorder is the most common PTSD comorbidity (Roberts et al., 2015). PTSD may exacerbate substance use disorder symptoms, lower general functioning, and stall recovery (Roberts et al., 2015). Individuals with comorbid PTSD and substance use disorder exhibit greater drug use severity, more intense cravings, and more frequent episodes of relapse; they also show poorer treatment outcomes than individuals with only one of the two disorders (Berenz & Coffey, 2012). Although for many people the challenges with substance use are initially targeted for therapy due to worry that deeper trauma processing may trigger relapse, several studies have shown that concurrent treatment to address PTSD and SUD does not lead to an increase in symptoms and is more effective than treating substance use alone (Back et al., 2019; Tripp et al., 2019). However, one study found that individuals who experienced trauma at an earlier age Substance Use Substance use often co-occurs with PTSD, with
symptoms, including anhedonia” (p. 4), attentional difficulties, sleep disturbances (insomnia or hypersomnia in depression; insomnia and recurring nightmares in PTSD), reduced pleasure in things previously enjoyed, disinterest in being around others, and increased irritability (APA, 2013; van Minnen et al., 2015). The disorders even exhibit similar biological changes, such as increased activation from the amygdala (the fear–response system of the brain; van Minnen et al., 2015). Differentiating whether an individual’s symptoms are primarily linked to the elevated arousal of PTSD or the persistent internal negative state of MDD may help in targeting interventions. Case Example Chris engaged in services primarily because he was experiencing a multitude of somatic symptoms. He was generally fatigued and unable to go to the gym or get through the workday without tiring. He was having difficulty describing his fatigue, suggesting that at times it felt like he was just worn down, in the same way he might be if he were sick. However, he also reported that his sleep patterns were erratic; at times he struggled to fall asleep and other times he would sleep 11 hours in a row. He was not eating much, and he was having difficulty concentrating at work. He also reported feeling down most of the day and unable to connect with his friends. The client’s symptom presentation suggested depression, but after some intake sessions that assessed childhood history, Chris disclosed that he had been sexually abused when he was a child. He had worked hard to suppress the memories, and although he was able to avoid thinking about his traumas during the day, intrusive memories would often creep into his dreams, impacting his sleep. Chris reported that he felt hyperarousal throughout the day, which was likely contributing to his fatigue; he stated, “my alarm system is on all day long, and just drains my battery.” Therapeutic work focused on acutely treating some of his somatic symptoms and then engaging in deeper traumatic processing. Chris was able to build up to the trauma narrative, slowly desensitizing himself rather than suppressing his emotions and memories, which reduced his hyperarousal and led to general symptom relief. showed less improvement in substance use as a result of treatment and may need additional specialized treatment (Fitzpatrick et al., 2020). The two primary causal models employed to explain PTSD and substance use comorbidity are the self-medication hypothesis (i.e., PTSD causes substance use) and the vulnerability hypothesis (i.e., substance use increases the risk for trauma). Research most strongly supports the self-medication hypothesis; however, there have been critiques raised as to the strength of studies that examine this model (Hawn et al., 2020). This theory suggests that individuals with PTSD rely on drugs or alcohol as a symptom management strategy in order to cope with psychiatric distress (e.g., intrusive traumatic memories) or to experience symptom relief through a numbing effect (Berenz & Coffey, 2012; Hawn et al., 2020; Roberts et al., 2015). Eventually, the PTSD and self-medication cause substance use disorder and/or chemical dependence. Multiple research studies have demonstrated that individuals with PTSD and co- occurring substance use experience increased cravings “in response to personalized trauma cues and PTSD symptoms” (Berenz & Coffey, 2012, p. 472). Another explanation for the relationship between substance use and PTSD is that preexisting substance use increases the risk for PTSD. One possibility is that substance use
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