## 3 Emotional Regulation, Dysregulation, and Twin Studies
### Twin Studies on Emotional Dysregulation  
To date, only a limited number of studies have employed twin study methodologies to investigate the genetic underpinnings of ED. Consequently, its etiology remains poorly understood from a quantitative genetics' perspective. The absence of a widely accepted definition of ED further contributes to inconsistencies across studies, leading to substantial variability in its conceptualization and phenotypic characterization [7]. [PERSON] et al. [39] investigated the genetic and environmental factors contributing to Affect Intensity and Affect Lability. Affect Intensity is defined as the predisposition to experience emotions with high magnitude, while Affect Lability refers to the tendency to undergo rapid and unpredictable emotional shifts. To explore these constructs, the authors administered the Affective Lability Scale (ALS) [40] and the Affect Intensity Measure (AIM) [41] to 182 MZ and 119 DZ male twins from the Vietnam Era Twin Registry. Model-fitting analyses were subsequently conducted to portion the variance into genetic and environmental components. Their findings highlight that additive genetic factors accounted for 40% of the variance in Affect Intensity and 25% of the variance in the ALS subscale assessing mood shifts between anxiety and depression [39]. Additionally, non-additive genetic influences were identified for ALS subscales measuring shifts from normal mood to depression (29%) and from normal mood to anger (27%) [39]. Evidence for shared environmental influences on affect-related measures was negligible, while non-shared environmental factors accounted for between 52% and 74% of the variance across all the scales [39]. Therefore, these results suggest that individual variability in Affective Lability and Affective Instability is primarily attributable to additive genetics influences and unique personal experiences, rather than shared environmental factors [39]. Further research has focused on exploring the genetic and environmental influences on ER strategies, such as Cognitive Reappraisal and Suppression, in a sample of 448 MZ and 295 DZ twin pairs [42]. Their findings suggest that non-shared environmental factors seem to play a significant role in explaining most of the variance in Cognitive Reappraisal (80%) and Suppression (65%), while additive genetic factors accounted for 20% and 35% of the variance, respectively. Consistent with the findings of [PERSON] et al. [39], shared environmental factors were found to have a negligible effect on these phenotypes in their sample [42]. More specifically, Reappraisal was found to be less heritable than Suppression and was primarily influenced by non-shared environmental factors, highlighting the importance of context in shaping functional ER strategies [42]. Moreover, this study examined the covariance between these variables through a Cholesky Decomposition, highlighting an overlap between the non-shared environmental factors influencing Reappraisal and the broader construct of adaptive emotional functioning, as measured by the Brief Risk-Resilience Index for Screening (BRISC) [43]. In examining the role of ED in psychopathology, [PERSON] et al. [44] investigated the genetic and environmental factors underlying the mediating role of ER in the comorbidity between Internalizing Disorders and Disordered Eating in a sample of 688 adult female twins. The analyses revealed significant genetic overlap between Internalizing Disorders and ED, with approximately 50% of the genetic variance in internalizing symptoms attributable to ER difficulties, and 17% of the genetic variance in Disordered Eating also linked to these challenges [44]. Notably, while internalizing symptoms shared substantial genetic influences with ER, Disordered Eating showed a distinct genetic contribution that did not overlap with either internalizing symptoms or ER difficulties [44].