Diet and nutrition against inflammatory bowel disease: Trick or treat(ment)?

Even if the relationships between nutrition and inflammatory bowel disease (IBD) remain underexplored, the current literature is providing, day by day, much more evidence on the effects of various diets in both prevention and treatment of such illnesses. Wrong dietary habits, together with other environmental factors such as pollution, breastfeeding, smoke, and/or antibiotics, are among the theoretical pathogenetic causes of IBD, whose multifactorial aetiology has been already confirmed. While some of these risk factors are potentially reversible, some others cannot be avoided, and efficient treatments become necessary to prevent IBD spread or recurrence. Furthermore, the drugs currently available for treatment of such disease provide low-to-no effect against the symptoms, making the illnesses still strongly disabling. Whether nutrition and specific diets will prove to effectively interrupt the course of IBD has still to be clarified and, in this sense, further research concerning the applications of such dietary interventions is still needed.     

Idiopathic Headache as a Possible Risk Factor for Phantom Tooth Pain

Following tooth pulp extirpation, some subjects suffer from persistent pain which affects edentate sites in absence of any local pathology. As regards this peculiar pain, called phantom tooth pain (PTP), what is puzzling is the fact there is a low prevalence of PTP in a very large population showing identical conditions of tooth pulp extirpation. The present investigation indicates that PTP mainly affects migraine (M) and cluster headache (CH) sufferers, whereas it does not affect subjects who have a negative personal and family history for idiopathic headache (IH). These results circumscribe the presence of PTP to a specific section of the population. The present results, besides indicating that PTP may be the result of a peculiar neuronal predisposition relating to IH pathogenesis, suggests some practical therapeutic hints. In fact, successful anti- M and anti-CH prophylactic treatment greatly improve PTP syndrome.     

Altered excitatory and inhibitory amino acid receptor binding in hippocampus of patients with temporal lobe epilepsy.

We examined binding to excitatory amino acid and inhibitory amino acid receptors in frozen hippocampal sections prepared from surgical specimens resected from 8 individuals with medically refractory temporal lobe epilepsy. The excitatory receptors studied included N-methyl-D-aspartate (NMDA), strychnine-insensitive glycine, phencyclidine, and quisqualate. The inhibitory receptors studied were gamma-aminobutyric acid type A (GABAA) and benzodiazepine. Excitatory and inhibitory amino acid receptor binding were differentially altered in the patients with temporal lobe epilepsy in comparison to 8 age-comparable autopsy control subjects, and changes in receptor binding were regionally selective in four areas. Binding to phencyclidine receptors associated with the NMDA channel was reduced by 35 to 70% in all regions in the hippocampi of the patients. In contrast, binding to the NMDA recognition site and its associated glycine modulatory site was elevated by 20 to 110% in the cornu ammonis (CA) 1 area and dentate gyrus of the hippocampus of the patients. Binding to these sites was unaffected in area CA4. Binding to the quisqualate-type excitatory amino acid receptor was unchanged in all regions except the stratum lacunosum moleculare CA1, where it was increased by 63%. GABAA and benzodiazepine receptor binding was reduced by 20 to 60% in CA1 and CA4, but unchanged in dentate gyrus. The data indicate that excitatory and inhibitory amino acid receptors are altered in the hippocampus of patients with temporal lobe epilepsy.     

Erratum: Serotonin reuptake inhibitors in pregnancy and the risk of major malformations: a systematic review

Hum Psychopharmacol 2007; 22 : 121–128. DOI: 10.1002/hup.836 It has come to our attention that there was an error contained in the above article within the abstracts heading relating to Methods. The article stated that: ‘A literature search was conducted within PsychoINFO’. This should have been published as: ‘A literature search was conducted within PsycINFO’. We apologise for this anomaly.