Dear colleagues,
It is my great pleasure to introduce to you the fourth issue of 2016 featuring up-to-date research on eating disorders and pathophysiological factors of psychiatric disorders.
At the outset, a review by Solmi and colleagues discusses the association between the 5-HTTLPR polymorphism and eating disorders (ED). Using genotype information from a biobank consisting of 735 ED patients and 241 healthy controls they did not find any differences between ED patients and controls. Thus they conclude that 5-HTTLPR is not associated with ED in general or anorexia nervosa or bulimia nervosa in particular. They propose that future studies should focus on the role of ethnicity and psychiatric comorbidities as the possible source of bias.
Lang and associates investigated the neuropsychological processing style of unaffected mothers of offsprings with anorexia nervosa (AN) using neuropsychological measures. They detected significant differences between unaffected mothers compared to the control group as they displayed more inflexible thinking style in addition to showing lower levels of global processing. Their results support the idea of familiar nature of cognitive styles in AN.
Paszynska and colleagues measured stress responses as a possible factor in the pathogenesis in anorexia nervosa (AN). They measured the salivary free cortisol, salivary alpha-amylase (sAA) and correlated it to secretory IgA (sIgA) in AN patients compared to controls. It emerged that AN patients displayed disturbances in sAA secretion, with increased cortisol and sIgA levels. There was a distinct correlation between those parameters suggesting that the effect of stress responses can be reliably assessed in saliva in AN patients.
Paulukat and co-workers assessed whether memory functions correlate with 17β -estradiol (E2) plasma levels in an activity-based anorexia rat model (ABA). Measuring acute and chronic starvation in rats, they found that starvation reduces the E2 levels which are also associated with memory deficits. They conclude that this effect may explain the reduced memory capacity in AN patients and the potentially limited effectiveness of psychotherapeutic interventions while in this state.
Introducing our second topic, Ramyead and associates investigated whether abnormal neural oscillations can be used as predictors of psychosis in high-risk patients. By assessing patterns of beta and gamma oscillations they did indeed find differences. They found that the left superior temporal gyrus, the left inferior parietal lobe and the precuneus most strongly contributed to the prediction of psychosis. Their results indicate that using resting state EEG may advance the prediction of psychosis on a single-subject level.
Using resting-state EEG, Ramyead and colleagues examined the neural oscillations in antipsychotic naïve first episode psychosis (FEP) patients in comparison to healthy controls. They detected altered oscillations in the frontal regions in FEP patients. They conclude that these altered synchronized neural oscillations may suggest disruptions in cortico-cortical communications.
In a brief report, Rivero and associates investigated the α2CDel322-325-AR gene polymorphism and its association with suicide completion and related psychiatric disorders. Extracting post-mortem brain DNA, the authors did not detect any differences between suicide and non-suicide victims as well as between depressed and schizophrenic patients. They did however detect an association with opiate abuse and dependence, and thus conclude that the polymorphism may play a role in its pathophysiology.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor