Disorders related to stress and anxiety are on a rise and it is anticipated that the treatment of these disorders, such as PTSD and its comorbidities, will begin to present challenges within the healthcare system in the coming years. Multiple organ systems are impacted by PTSD and it increases the risk of developing things such as cardiovascular disease, arthritis, digestive disease, and cancer. This article discusses clinical data that links PTSD to cardiovascular disease via the renin-angiotensin system, inflammation, and autonomic dysfunction.
In this post, we will be discussing and summarizing the article, “Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease”
(Disclaimer: I am not a medical professional and all information provided in this post is from the article which is available in the “references” section at the bottom of the page. This post is meant only to provide a synopsis of the information covered in the original article.)
Introduction
Posttraumatic stress disorder (PTSD) is a psychiatric disorder characterized by persistent psychological and emotional stress following a traumatic event. PTSD presents with a wide array of symptoms such as nightmares, flashbacks, intrusive thoughts, hyperarousal, and avoidance of situations that bring back memories of the traumatic event.
A study examining the link between PTSD and heart failure demonstrated that veterans with PTSD were almost 50% more likely to develop heart failure compared to veterans without PTSD. These observations remained true even after factors such as military service, BMI, combat, diabetes, hypertension, hyperlipidemia, age, and sex were adjusted for. Furthermore, these observations hold true not just for veterans, but for civilians with PTSD as well.
Summary
PTSD is a psychiatric disorder characterized by persistent mental and emotional stress following a traumatic event and can present in many ways. Furthermore, it has been seen that those with PTSD are at a greater risk for cardiovascular disease and its related comorbidities
The Renin-Angiotensin System
The Renin-Angiotensin System (RAS) is crucial for electrolyte, blood pressure, and fluid homeostasis. However, this system is also activated in response to psychological stress and is responsible for cardiovascular injuries such as fibrosis and vasoconstriction. The presence of chronic stress (such as PTSD) causes the activation of the RAS, which leads to an increase in the synthesis of the hormone Angiotensin II (ANG II). Angiotensin is the main effector molecule within the RAS.
Some studies have also shown that an increase in the brain and circulating components of the RAS are associated with an increase in hypothalamic-pituitary-adrenal axis (HPA) stimulation as well as increased levels of the stress hormone called corticotropin-releasing hormone (CRH). Furthermore, chronic stress can result in a degeneration of the negative feedback system within the HPA axis over time. This degeneration promotes a reduction in CRH and cortisol which causes a significant long-term change in the psychological state of the affected individual.
Summary
The RAS is important for maintaining homeostasis within the body and is a crucial component of the stress response. Chronic stress causes an overactivation of the RAS which causes further mental and physical disruptions in a domino effect.
Autonomic Dysfunction in PTSD
It is well known that ANG II has sympathoexcitatory effects within the nervous system. In addition to this, previous human and animal studies have demonstrated that blocking the RAS improves baroreceptor sensitivity (BRS) and reduces sympathetic nervous system (SNS) activity. The hyperarousal that is often seen in PTSD is associated with an overactivation of the SNS. One potential cause of this overactivity is a reduced BRS. A decrease in BRS contributes to numerous conditions associated with SNS overactivity such as hypertension, heart failure, and obesity.
Additional evidence of PTSD-related autonomic dysfunction has come from studies that examined disrupted sleep patterns in PTSD. Observations of increased nighttime SNS activity and insomnia suggest that the sleep disturbances associated with PTSD may contribute to decreased BRS, increased CVD, and autonomic dysfunction.
Summary
The hyperarousal associated with PTSD is linked to the overactivity of the SNS. Overactivity of the SNS is connected to a decreased BRS, which is associated with a number of conditions such as hypertension, heart failure, and obesity. Furthermore, there is some evidence that sleep disruptions contribute to decreased BRS, increased CVD, and autonomic dysfunction.
Autonomic-Immune Dysfunction in PTSD
The ANS is highly innervated with the immune system. Therefore, immune system dysfunction resulting in inflammation is likely related to the autonomic dysfunction associated with PTSD. Furthermore, the dysregulation of the HPA axis may also contribute to higher levels of inflammation in those with PTSD. The combined impacts of these dysregulations may lead to immune dysfunction which then facilitates the development of inflammatory diseases and/or the progression of CVD.
Summary
Because of the immune system's close involvement with the ANS, it appears that autonomic and HPA axis dysregulation may lead to higher levels of inflammation within the bodies of those who have PTSD. These heightened levels of inflammation contribute to the progression of CVD and other inflammatory diseases.
Conclusion
There appear to be links between CVD and PTSD caused by the RAS, inflammation, and sympathetic overactivation. Furthermore, there is evidence that PTSD can cause autonomic dysfunction and contribute to the development of inflammatory diseases. These findings suggests that PTSD and it's comorbidities will begin to place greater strain on the healthcare system in the coming years.
References
Brudey, Chevelle, et al. “Autonomic and Inflammatory Consequences of Posttraumatic Stress Disorder and the Link to Cardiovascular Disease.” American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, U.S. National Library of Medicine, 15 Aug. 2015, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538229/.
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