Heart rate variability in preadolescents with familial risk for depression

Heart rate variability in preadolescents with a familial risk for depression Abstract Background: Depression is characterized by dysfunctions in emotional, cognitive and physiological responses. Previous research showed autonomic nervous system dysregulation – high sympathetic and/or low parasympathetic nervous system activity – in people with major depression. Specifically, reduced heart rate variability (HRV), an index of sympathetic and parasympathetic cardiac modulation reflecting emotional processing and regulation, has been found in depression. However, while evidence robustly supports reduced vagal tone in individuals with current depressive symptoms, it remains unclear whether vagal dysregulation also represents a predisposing factor that can be detected before the onset of the disorder. Therefore, the main aim of the present study was to investigate the role of cardiac vagal tone, indexed by reduced HRV, as a measure of depression vulnerability. To this end, the study was focused on preadolescents with familial risk for depression because they are at higher risk to develop depressive symptoms or a full-blown depressive episode than preadolescents without a familial risk for depression. Methods: A total of 32 healthy preadolescents took part in the study (21 F, mean age 11.9, SD ± 0.77), 16 with a family history for depression and 16 without a family history for depression. To obtain a measure of cardiac vagal tone, resting-state ECG signal was continuously recorded for 3 minutes from which HRV indexes in the time and frequency domains were derived. T-tests were conducted to examine the differences between the two groups in vagally-mediated HRV (SDNN, RMSSD, HF power). Results: No significant difference emerged in vagally-mediated HRV measures between the two groups (SDNN, RMSSD, HF power; all ps > 0.05). Discussion: These results suggest that reduced vagal tone may not yet be evident in early stages of vulnerability or that it may emerge later as the risk translates into clinical symptoms. Also, it is possible that disruptions in cardiac vagal function emerge later in development, perhaps in response to cumulative stress exposure, the onset of affective symptoms, or critical developmental transitions such as adolescence. Given the importance of early identification of biological risk markers, future research should adopt longitudinal designs to clarify whether alterations in cardiac vagal function develop over time in at-risk youth and contribute to the onset of depressive symptoms.