Posttraumatic stress, heart rate variability, and the mediating role of behavioral health risks.

Acute stress has long been connected to cardiovascular risk (1). For individuals with posttraumatic stress disorder (PTSD), a disorder characterized by hyperarousal and frequent physiological symptoms related to anxiety and stress, dysregulation of the autonomic nervous system has been identified as an important precursor to cardiovascular disease, diabetes, and other health risks (2, 3). Indeed, a key indicator of autonomic functioning and cardiovascular health, heart-rate variability (HRV), is often depressed amongst individuals with PTSD (4). Although the link between PTSD and HRV is generally discussed as a purely psychosomatic phenomenon (5), a number of behavioral risk factors—namely smoking, alcohol misuse, obesity, and sleep disturbance—may account for this link. In this study, HRV was assessed amongst younger adults (18- to 39-years-old) with and without PTSD to determine whether autonomic dysfunction in individuals with PTSD is in part attributable to the higher rates of smoking, drinking, obesity, and sleep disturbance that often coincide with PTSD (6-9). Heart-Rate Variability Under normal circumstances, heart rate varies on a beat-to-beat basis due to the dynamic interplay of the sympathetic (SNS) and parasympathetic nervous system (PNS). The SNS stimulates excitation (e.g., increased heart rate and blood pressure) in response to unexpected changes in the body and/or environment through the release of catecholamines (10). The PNS restores cardiovascular activity to baseline levels via vagal innervation. When these two systems are in disequilibrium—either because the SNS is hyperactive or the PNS is hypoactive—HRV attenuates (3). Low HRV is both an indicator and a precursor of disease. It may signal some underlying irregularity, such as immune dysfunction resulting from diabetes, osteoporosis, arthritis, Alzheimer's disease, and some cancers (11). Reduced HRV may also stimulate deleterious effects on cardiovascular health. Lower HRV is a risk factor for arrhythmia and in turn is predictive of heart disease and cardiac arrest (12-14). Reduced HRV may also accelerate atherosclerosis (2) and result in increased variability in blood pressure, which is itself an independent risk factor for coronary artery disease (15). Psychophysiology of PTSD Exposure to psychological trauma increases the risk of developing PTSD, a disorder characterized by persistent re-experiencing of the traumatic event, avoidance of stimuli associated with the event, and increased arousal (16). These symptoms have long been known to convey autonomic dysregulation, such as elevated heart rate and increased blood pressure both at baseline (17) and in response to stressors (18). Even though the SNS is instrumental in the etiology of anxiety disorders, experimental evidence suggests that the PNS may be responsible for the maintenance of elevated physiology in psychopathology (15). For instance, the administration of catecholamine (SNS) antagonists prior to induced panic attacks does little to reduce heart rate, suggesting that the SNS plays a minor role in such attacks (19). However, lactate, which is a known suppressor of vagal (PNS) activity, accumulates during panic attacks (20), and is even administered in laboratory studies to induce panic attacks (21) and stimulate PTSD symptoms (22). Thus, suppressed PNS activity and consequently reduced HRV are implied in individuals with anxiety or trauma-related disorders such as PTSD. Indeed, individuals with PTSD exhibit reduced HRV in both short-term laboratory-based measurements of HRV (5, 23-26) and 24-hour ambulatory measures (4, 27). In turn, individuals with PTSD are more likely than those without PTSD to develop cardiovascular disease (28) and face an increased risk of cardiac death (29). Although reduced HRV in PTSD is primarily attributed to the direct impact of psychological hyperarousal and anxiety on the autonomic nervous system (5), behavioral risk factors could partially account for that association. Individuals with PTSD are more likely than individuals without PTSD to smoke and do so heavily (6), abuse alcohol (7), be obese (8), and suffer from sleep disturbance stemming from flashbacks and nightmares (9). Each of these risk factors are independently associated with reduced HRV (30-33), suggesting that the relationship between PTSD and HRV may in part be due to the behavioral health risks that frequently accompany PTSD. Current Study In the present study, the prediction that the link between PTSD and HRV is partially mediated by smoking, lifetime alcohol dependency, abdominal obesity, and sleep disturbance was tested amongst a sample of younger adults (i.e., under 40 years of age) with and without PTSD. Younger adults were targeted to quantify the early health risks posed by PTSD and associated psychopathology. Latent variable modeling was used to model HRV via a combination of long- and short-term measures of autonomic functioning to minimize the impact of measurement error on that construct. Three sets of hypotheses were tested: 1) PTSD symptoms would be associated with lower HRV; 2) PTSD symptoms would be associated with greater smoking, higher rates of lifetime alcohol dependence, higher rates of abdominal obesity, and more sleep disturbance; and 3) each of these behavioral risk factors would partially mediate the association between PTSD symptoms and HRV. That is, accounting for each of these behavioral health risks would attenuate the association of PTSD symptoms with HRV.