Heritability of startle reactivity and affect modified startle

Abstract

Startle reflex and affect-modified startle reflex are used as indicators of defensive reactivity and emotional processing, respectively. The present study investigated the heritability of both the startle blink reflex and affect modification of this reflex in a community sample of 772 twins ages 14–15 years old. Subjects were shown affective picture slides falling in three valence categories: negative, positive and neutral; crossed with two arousal categories: high arousal and low arousal. Some of these slides were accompanied with a loud startling noise. Results suggested sex differences in mean levels of startle reflex as well as in proportions of variance explained by genetic and environmental factors. Females had higher mean startle blink amplitudes for each valence-arousal slide category, indicating greater baseline defensive reactivity compared to males. Startle blink reflex in males was significantly heritable (49%), whereas in females, variance was explained primarily by shared environmental factors (53%) and non-shared environmental factors (41%). Heritability of affect modified startle (AMS) was found to be negligible in both males and females. These results suggest sex differences in the etiology of startle reactivity, while questioning the utility of the startle paradigm for understanding the genetic basis of emotional processing.

Fear‐potentiated startle response as an endophenotype: Evaluating metrics and methods for genetic applications

“…The current findings are in line with those of two previous twin studies (Anokhin et al, ; Dhamija et al, ), which concluded that a common pathway model with a single set of genetic and environmental factors was the driving force behind startle response to neutral, positive, and negative affective stimuli. Another study (Vaidyanathan et al, ) found that overall raw SR, but not modulated startle, was moderately heritable.…”

“…Some aspects of the SR have been found to be heritable; for a thorough review, see Savage, Sawyers, Roberson-Nay, and Hettema (2017). Briefly, studies have found the overall SR (not FPS) to have a heritability of 37-67% (Anokhin, Golosheykin, & Heath, 2007;Dhamija, Tuvblad, Dawson, Raine, & Baker, 2017;Vaidyanathan, Malone, Miller, McGue, & Iacono, 2014). These same studies, using negative/positive affective imagery to alter SR, found no genetic contribution to the affective modulation of startle in humans.…”

“…A potential limitation of the methodology of existing heritability studies is that FPS has been characterized by subtracting SR during a neutral or positive affect condition (e.g., baseline) from SR during a fear/negative affect condition and estimating heritability based on the raw residuals (Anokhin et al, ) or percent change from neutral (Dhamija et al, ). Further, some studies have first conducted a within‐person standardization of the SR prior to calculating difference scores (e.g., Vaidyanathan et al, ).…”

“…Multivariate twin models that simultaneously include the raw, unstandardized, baseline startle response magnitudes in addition to FPS may provide more accurate estimates of the heritability of both baseline SR and FPS, akin to the statistical improvement achieved by using polynomial regression methods instead of difference scores (e.g., Edwards, ). The studies of Anokhin et al () and Dhamaji et al () have indirectly (and incidentally) found such an effect through their use of a “common pathway” multivariate model for evaluating genetic and environmental influences of overall startle, a composite measure comprised of raw SR values under neutral, positive, and negative affect conditions; however, they treated affect‐modulated startle as a separate univariate outcome. A systematic investigation into the impact of these measurement issues on biometrical heritability estimates has yet to be conducted.…”

“…A systematic investigation into the impact of these measurement issues on biometrical heritability estimates has yet to be conducted. Further, existing studies have focused on adult or adolescent samples (mean age of 15: Dhamaji et al, , 18: Vaidyanathan et al, , or range of 18–29: Anokhin et al, ). Previous work has shown that FPS manifests similarly throughout development from childhood to adulthood, though the magnitude of SR increases from early to late childhood (Quevedo, Smith, Donzella, Schunk, & Gunnar, ).…”