Research suggests that post-traumatic stress disorder (PTSD) is associated with increased risks for chronic diseases, including cardiovascular disorders, rheumatoid arthritis, and other health conditions. The study by Ahmadi et al published in The American Journal of Cardiology adds to this research. This study, which was based on a sample of 637 veterans, goes beyond previous work; using coronary artery calcium scores, it suggests that PTSD is associated with the presence and severity of coronary atherosclerosis. In this study, PTSD also predicted future mortality independent of age, gender, and conventional risk factors, a finding reported several years earlier in a large national study. The question now is not so much if there is a link between PTSD and chronic disease but why this association is found, especially for cardiovascular disease. Another important question is whether these disease outcomes can be prevented.
Studies suggest that PTSD could result in inflammatory injuries through overactivation of the hypothalamic-pituitary-adrenal stress axis, subsequently followed by hypocortisolism related to molecular downregulation of these systems. Consistent with this, research suggests that systemic inflammatory activity appears common in patients with PTSD. This PTSD-disease link also could be related to health behaviors, such as cigarette smoking and substance misuse, related to self-regulation of aversive psychological states brought on by PTSD psychopathology. There are other variables that could also explain this association. At this time, no single causal pathway has been identified. Recently, our research indicated that FKBP5, COMT, and CHRNA5 genetic loci encompassing pathways associated with inflammation, addiction, sleep, and anxiety are associated with PTSD, suggesting that PTSD-related genes may be worthy of investigation related to these disease linkages. For example, researchers have reported that the CHRNA gene, which encodes components of the nicotinic acetylcholine receptor, were associated with lung cancer. This gene was also associated with cigarette smoking, nicotine dependence, opioid misuse, and PTSD. Thus, 1 pathway for lung cancer appears to include nicotine addiction associated with genetic variants of the CHRNA gene, without which there would be insufficient exposure to cigarette smoking to result in lung cancer in most cases. It is noteworthy that the CHRNA gene is associated not only with lung cancer but also with peripheral arterial disease. Cigarette smoking is also commonly associated with PTSD.
Similarly, other genetic components involved in PTSD onset, including the FKBP5, COMT, and CRH-R1 genes, may be associated with the pathophysiology of specific diseases after PTSD onset. The COMT gene has been associated with anxiety disorders, psychosis, depression, and other conditions involving catecholamine pathway regulation. The FKBP5 gene regulates glucocorticoid receptor sensitivity, is functionally involved in hypothalamic-pituitary-adrenal axis activity, and has been associated with PTSD. The CRH-R1 gene is involved in corticotropin-releasing hormone activity, a polypeptide hormone and neurotransmitter involved in the stress response. Studies have suggested that this gene also regulates hypothalamic-pituitary-adrenal axis function and is associated with the impact of traumatic stress exposure and PTSD onset. Thus, current PTSD-genetic findings are consistent with the cardiovascular disease links often reported for PTSD. Also noteworthy in this regard is that recent research suggests that trauma victims who received emergency counseling shortly after the traumatic event not only had better PTSD outcomes but also had improved outcomes in a number of clinical areas, including reductions in substance misuse. Evidence suggests that these early interventions may prevent PTSD memory consolidation. These PTSD findings may have implications for future cardiovascular disease prevention. Further research is advised.
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