This model is supported by several studies demonstrating the

This model is supported by several studies demonstrating the impact of alexithymia on socio-cognitive ability, particularly in the affective domain, in both typical and atypical populations. A large body of research demonstrates that alexithymia impairs emotion recognition from both facial (Grynberg et al., 2012) and vocal (Heaton et al., 2012) stimuli in typical individuals, while further studies suggest it GDC0199 is also responsible for the atypical emotion expression, recognition, empathy, and eye-fixation seen in some individuals with autism (Bird et al., 2010a 2011; Cook et al., 2013; Heaton et al., 2012; Oakley et al., 2016; Trevisan et al., 2016) and Feeding and Eating Disorders (Brewer et al., 2015b). If it is the case that alexithymia represents a general impairment in the interoceptive domain, these findings suggest that intact interoceptive abilities are crucial for successful socio-emotional functioning. Together, research on the importance of interoception for the development of typical cognition (in the emotional, learning and decision-making, sensory, and social domains) and its potential role in the aetiology and/or symptomatology of a number of psychiatric conditions, make understanding the development of interoceptive ability, and the relationship between interoception and alexithymia, across the lifespan an urgent research goal. If, as we propose, interoception does represent the ‘p-factor’, understanding why heightened and impaired interoception is associated with distinct pathologies (e.g., anxiety, depression) may shed light on the mechanism by which interoception confers risk and resilience to pathology. In addition, identifying periods of significant developmental change in interoceptive ability may explain periods of enhanced risk for the development of psychopathology, and why some individuals develop symptoms despite prior typical development.
Interoception across the lifespan Research on the development of interoception is not plentiful, but where it exists we provide an overview below. Where research is completely lacking, such as in infancy, we outline the measures that could be used to make progress, and the issues surrounding their use. Where data are available that rely upon measures of alexithymia rather than explicit tests of interoceptive ability, we incorporate this evidence in order to provide a more comprehensive review of the existing evidence subject to the assumptions detailed in Section 2. Identifying the gaps in our understanding of the development of interoception will, we hope, lead to these gaps being addressed, and to an understanding of the causal mechanisms by which interoception contributes to the development of higher-order cognition.
Conclusions and future directions
Funding JM was supported by a doctoral studentship from the Economic and Social Research Council [1599941; ES/J500057/1]. GB was supported by the Baily Thomas Charitable Trust.
Introduction Although reading is a complex cognitive function, 90–95% of all children master it without notable problems. However, children suffering from developmental dyslexia never attain fluent reading skills despite adequate intellectual abilities and educational opportunities (Blomert, 2005; Lyon et al., 2003). Among the reading-related deficits of developmental dyslexia, reading dysfluency poses the most pronounced and long lasting hurdle (Shaywitz et al., 2008), especially in relatively transparent orthographies, such as Dutch or German (Blomert, 2011; Wimmer and Schurz, 2010). At the same time, dyslexics show substantial inter-individual variability in their level of reading (dys)fluency (Katzir et al., 2008; Leinonen et al., 2001). One of the neurobiological signatures of dyslexia is an abnormal pattern of functional and/or anatomical connectivity within the brain’s reading network (Geschwind, 1965; Paulesu et al., 1996; Vandermosten et al., 2012; Wimmer and Schurz, 2010). Impaired connectivity could disrupt decoding or orthographic–phonological integration at word (Wimmer and Schurz, 2010), syllable and/or phoneme level (Blomert, 2011), causing slower and less accurate reading in dyslexics. In the present study we investigate whether atypical neural connectivity scales with differences in the level of reading (dys)fluency in dyslexic children.