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Page 109 De Francesco et al. J Transl Genet Genom 2024;8:102-18 https://dx.doi.org/10.20517/jtgg.2023.51

depression becomes notably higher in females compared to males and remains stable in middle
[32]
adulthood .
Overall, it can be stated that AMAB people are more at risk of developing EXT disorders, whereas INT
[30]
symptoms are more prevalent in AFAB individuals . The reasons for this distinction are not well
understood yet. There seems to be a possible biological explanation related to the greater predisposition of
[33]
AFAB individuals to develop INT disorders ; however, social factors underlying this distinction are
certainly not to be overlooked. For example, within Western cultural contexts, a significant discrepancy can
be observed in the ways emotions are allowed to be expressed by these two genders: AFAB individuals are
encouraged from a young age to externalize emotions such as sadness and to experience them in a more
introspective manner, while AMAB individuals are expected from childhood to primarily express emotions
[33]
related to anger and markedly EXT symptomatology . Regarding the incidence of disorders, in the last
decade, there has been an increase in INT symptoms, especially during adolescence, in AFAB individuals .
[34]
More recent data also estimate a worsening of the mental health of AFAB adolescents following the
COVID-19 pandemic: the social withdrawal resulting from infection prevention measures seems to have
exacerbated latent INT symptoms, leading to an increase in symptomatic experiences among adolescents .
[35]
In particular, the World Health Organization indicated that the COVID-19 pandemic resulted in a global
rise of approximately 27.6% in cases of major depressive disorder and a 25.6% increase in cases of anxiety
[36]
disorders .
The contribution of twin studies in the analysis of developmental trajectories
Twin studies have been used to address the developmental trajectories of INT-EXT disorders and the latent
[37]
factors responsible for symptoms’ stability or changes through time. For example, Haberstick et al. have
implemented a longitudinal study through which they examined a sample of 382 twin pairs, aged between 7
and 12 years old, by observing annually the development of INT-EXT symptomatology . By applying the
[37]
Cholesky model, they were able to determine the extent to which shared genetic and environmental
influences contributed to the modification of the symptoms in the transition between childhood and
[37]
adolescence . While EXT symptoms seemed to remain stable during the development of the subjects, the
INT symptomatology tended to fluctuate significantly over time because of non-shared environmental
experiences. Symptom stability within both INT and EXT disorders was mainly influenced by additive
[37]
genetic factors transmitted from infancy to adolescence .
[38]
These results were confirmed by Hatoum et al. through a longitudinal study that involved 408 twin pairs
[38]
aged between 7 and 16 years . To examine the temporal patterns of symptomatic manifestations, the
authors applied a Latent Growth Model to the data . This model includes the presence of two latent
[38]
variables, namely the intercept (I) and the slope (S); the former represents the mean value of the phenotype
under study, while the latter indicates its rate of change . Each observed score at each measurement point
[39]
is thus a linear function of these two parameters, along with the contribution of random error. In a sample
from which genetic information can be derived, such as a twin sample, it is also possible to decompose the
[39]
variance of variables I and S into genetic and environmental latent factors . Through the application of this
latest version of the Latent Growth Model, Hatoum et al. were able to observe that the intercept values,
indicative of the stability of the curve over time, were highly heritable . Genetic influences explained
[38]
[38]
approximately 86% of the variance for INT symptoms and about 72% for EXT symptoms . As for the
variance values related to S, they found that the change in the trajectory of symptoms over time was not
only due to unique environmental components (thus replicating the results of the previous study), but also
to specific genetic factors linked to age .
[38]