Scientific literature does not provide conclusive data on the correlations between Eating Disorders (ED) and Neurodevelopmental Disorders (NDD). Different neuroscience research centres have recently been trying to characterize a spectrum of cognitive dysfunctions in ED. For example, in 2017 Chen and collaborators have proposed an interesting neurophysiological model, which they describe as a “core eating network” model [1]. This network consists of two main pathways – the dorsal control pathway and the ventral reward pathway. According to Chen and collaborators, the balance between these two pathways is a key factor in food intake management. In line with this theory, ED spectrum could be the result of executive function impairments, ranging from the over-control/rigidness of Anorexia Nervosa (AN) to the under-control/disinhibition of Binge Eating Disorder (BED). Executive functions in ED have also been examined in other relevant studies [2–3], which describe different test performances in the various ED [4].
Focusing on the cognitive aspects of the single ED, AN seems to have an impact on central coherence, which could explain patients’ typically rigid focus on body details while they overlook global health conditions [5]. Cognitive flexibility and decision-making also appear to be affected [6], possibly impaired by a defective equilibrium between the ventral limbic and dorsal executive circuit activities. These two circuits are involved in wide cognitive functioning such as decision-making and the inhibitory control and reward systems [7]. Dysfunctions in this cognitive functioning could explain such typical aspects of AN as the pathological relationship between food, inhibition, and reward. Consistent with these studies, relevant research on AN patients has evidenced dysfunctions in different cognitive fields unrelated to their Body Mass Index (BMI) [8]. According to these findings, AN patients show dysfunctional behaviour in information processing and memory performance, especially the working, visual and verbal memory. The authors concluded that neuropsychological impairments in AN may not be a consequence of the mental disorder; instead, cognitive dysfunctions may be a risk factor for AN. Comparing the various effects of ED on cognitive performances, it appears that compared with Bulimia Nervosa (BN) patients and healthy controls (HCs), AN patients perform poorer executive functions [4].
On the other hand, BN patients exhibit deficient inhibition controls [9] and poorer decision-making ability when compared to HCs [10]. An fMRI study compared selected brain activities in BN patients and HCs [11]. BN patients showed a hyperactivation of the parieto-occipital regions and a reduced deactivation of default-mode-network (DMN) areas during alerting.
These dysfunctions correlated with the severity of the ED, and were thought to be connected with the typical food and body-shape concerns. Furthermore, compared to HCs, BN patients presented a weaker activity of the anterior cingulate regions, the parahippocampus and the temporo-parietal junction, during specific attention tasks (i.e., reorienting and executive control of attention) [11]. This hypoactivity could explain other typical BN features such as impulsive behaviour, inattention, and dysfunctional emotion regulation [11].
With regard to the cognitive performances of Binge Eating Disorder (BED) patients, these appear to be in line with AN patients’ results as examinations show deficiency in central coherence, decision-making, and cognitive flexibility. Decision-making and cognitive flexibility in BED appear even more damaged than in AN patients [6]. Typically, in BED patients, the reward system appears dysfunctional [12]. This has been demonstrated in an MRI study, focused on rewarding system networks in both the anticipatory and outcome phases. The MRI shows that there is an inefficient recruitment of ventral striatum and the inferior frontal gyrus during the anticipatory phase, whereas there is a decreased activity of the medial prefrontal cortex in the outcome phase [13]. Furthermore, the corticostriatal circuits also appear dysfunctional, thus contributing to the motivation/reward and impulsivity dysfunctions [14].
BED is frequently associated with overweight (OW) or obesity (OB) [12]. Different neurocognitive patterns have been found in OW/OB patients related to the presence/absence of BED. The presence of BED in OW/OB patients is associated with a weaker working memory, worse self-regulatory control, and reduced planning skills [15]. Furthermore, BED OW/OB patients appear to be more vulnerable to food related impulsivity [16].
MRI shows that BED OW/OB patients, when exposed to visual/auditory high calorie food cues, present a stronger activity of the dorsal anterior cingulate cortex and a weaker function of the prefrontal cortex, probably related to the loss of control over the feeding choice [16–17].
Following these neurodevelopmental models, scientific research is trying to address the substantial comorbidities between ED and either mental or behavioural disorders, such as Mood Disorders, Anxiety Disorders, Obsessive-Compulsive Disorder, Personality Disorders, Autism Spectrum Disorder, Complex Refusal Syndromes [12, 18–22]. In 2019, Wentz and collaborators published a paper in which they presumed a common neurodevelopmental origin in ED and different psychiatric conditions [23].
In Specific Learning Disorders (SLD), a neurobiological origin of the neuropsychological deficits has been repeatedly argued for, even if the cause is still unknown [12]. As mentioned for ED, genetic predisposition could be responsible for altered SLD neurodevelopmental patterns. Studies on twins, which show a common genetic neurodevelopmental root in reading and mathematics ability, support these theories [24].
Furthermore, upon comparing cognitive performances in patients with reading disabilities and patients with math disabilities, it was observed that both groups manifest common weaknesses in working memory, processing speed, and verbal comprehension, which supports a multiple-deficit neuropsychological model of SLD [25].
In accordance with these findings, several research groups have looked for overlaps and psychiatrics comorbidities of the most common neurodevelopmental disorders like SLD, Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) [26–28].
If the literature concerning ED and general neurodevelopmental disorders is not extensive, scientific publications on ED and SLD are almost non-existent. Our Italian study, which aims to assess the prevalence of SLD in an ED population of children and adolescents, is a first step toward filling a significant gap in this area.