Key result
Genetic variations affecting serotonin and dopamine systems modulate the expression of fear-induced bradycardia, suggesting caution when using it as a clinical biomarker for psychiatric disorders.
Why the study?
Fear-induced bradycardia is underemployed and potentially subtended by genetic interindividual differences, suggesting precaution when recommending its use in clinical psychiatry.
Individual genetic differences in neurotransmitter systems mediate fear-induced bradycardia, highlighting the need for caution before using it as a psychiatric biomarker.
Urges caution against using fear-induced bradycardia as a psychiatric biomarker; leaves open its validity without genetic stratification.
Fear-induced bradycardia, a transient heartbeat deceleration following exposure to threat, is a physiological index observable in humans, especially in fear conditioning experiments. While gaining interest in recent years, it is still currently underemployed in neuroscientific research compared to more popular physiological indices. Besides its use in research, it could also constitute a valuable resource in a clinical psychiatry setting, as many disorders are also characterized by altered heart rate responses. However, differences in fear-induced bradycardia may also be subtended by genetic interindividual differences, thus suggesting precaution when recommending its use in the clinical setting. Here, we discussed the first endeavors that aimed at clarifying the genetic underpinnings of heart rate variations, which suggest that individual genetic differences have a role in defining the characteristics of heart rate responses. Given this, translating heart rate measurements in the clinical setting must be implemented with caution. Future endeavors in this field will aim at identifying these differences even further, thus allowing for more precise clinical interventions.
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Battaglia et al. (2024) conducted a review in Fear-induced bradycardia. Genetic variations in serotonin and dopamine systems was evaluated. Genetic variations affecting serotonin and dopamine systems modulate the expression of fear-induced bradycardia, suggesting caution when using it as a clinical biomarker for psychiatric disorders.
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