Postprandial lipid and vascular responses following consumption of a commercially-relevant interesterified palmitic acid-rich spread in comparison to functionally-equivalent non-interesterified spread and spreadable butter: a randomised controlled trial in healthy adults.

Background: Interesterification is an industrial processing technique used widely where hard fats are essential for functionality and consumer acceptability, e.g. margarines and lower fat spreads. Objective: The aim of this study was to compare acute cardiovascular effects of functionally equivalent spreads (similar solid fat content) made with interesterified (IE) or non-IE palm-based fats, or spreadable butter. Methods: A randomised, controlled, 4-armed crossover, double-blind study (25 men, 25 women; 35-75 years; healthy; mean BMI 24.5, SD 3.8), compared effects of mixed nutrient meals containing 50 g fat from functionally equivalent products [IE spread, non-IE spread and spreadable butter (SB), with rapeseed oil (RO) as a reference treatment: with 16.7%, 27.9%, 19.3% and 4% palmitic acid, respectively] on 8 h postprandial changes in plasma triacylglycerol (TAG) and endothelial dysfunction (flow-mediated dilatation; FMD). Circulating reactive oxygen species (estimated using a neutrophil oxidative burst assay), glucose, insulin, NEFA, lipoprotein particle profiles, inflammatory markers (glycoprotein acetylation (Glyc-A) and IL-6), and biomarkers of endotoxemia were measured. Results: Postprandial plasma TAG concentrations after test meals were similar. However following RO versus the 3 spreads, there were significantly higher postprandial apolipoprotein B concentrations, and small HDL and LDL particle concentrations, and lower postprandial extra-large, large, and medium HDL particle concentrations, as well as smaller average HDL and LDL particle sizes. There were no differences following IE compared to the other spreads. Postprandial FMD% did not decrease after high-fat test meals, and there were no differences between treatments. Postprandial serum IL-6 increased similarly after test meals, but RO provoked a greater increase in postprandial concentrations of glycoprotein acetyls (GlycA), as well as 8 h sCD14, an endotoxemia marker. All other postprandial outcomes were not different between treatments. Conclusions: In healthy adults, a commercially-available IE-based spread did not evoke a different postprandial triacylglycerol, lipoprotein subclass, oxidative stress, inflammatory or endotoxemic response to functionally-equivalent, but compositionally-distinct alternative spreads. Clinical trial registry number: NCT03438084 (https://ClinicalTrials.gov).

An Open Science MRI Database of over 100 Synaesthetic Brains and Accompanying Deep Phenotypic Information.

We provide a neuroimaging database consisting of 102 synaesthetic brains using state-of-the-art 3 T MRI protocols from the Human Connectome Project (HCP) which is freely available to researchers. This database consists of structural (T1- and T2-weighted) images together with approximately 24 minutes of resting state data per participant. These protocols are designed to be inter-operable and reproducible so that others can add to the dataset or directly compare it against other normative or special samples. In addition, we provide a 'deep phenotype' of our sample which includes detailed information about each participant's synaesthesia together with associated clinical and cognitive measures. This behavioural dataset, which also includes data from (N = 109) non-synaesthetes, is of importance in its own right and is openly available.

A symptom network model of misophonia: From heightened sensory sensitivity to clinical comorbidity.

OBJECTIVES: Misophonia-an unusually strong intolerance of certain sounds-can cause significant distress and disruption to those who have it but is an enigma in terms of our scientific understanding. A key challenge for explaining misophonia is that, as with other disorders, it is likely to emerge from an interaction of traits that also occur in the general population (e.g., sensory sensitivity and anxiety) and that are transdiagnostic in nature (i.e., shared with other disorders). METHODS: In this preregistered study with a large sample of participants (N = 1430), we performed a cluster analysis (based on responses to questions relating to misophonia) and identified two misophonia subgroups differing in severity, as well as a third group without misophonia. A subset of this sample (N = 419) then completed a battery of measures designed to assess sensory sensitivity and clinical comorbidities. RESULTS: Clinical symptoms were limited to the most severe group of misophonics (including autistic traits, migraine with visual aura, anxiety sensitivity, obsessive-compulsive traits). Both the moderate and severe groups showed elevated attention-to-detail and hypersensitivity (across multiple senses). A novel symptom network model of the data shows the presence of a central hub linking misophonia to sensory sensitivity which, in turn, connects to other symptoms in the network (relating to autism, anxiety, etc.). CONCLUSION: The core features of misophonia are sensory-attentional in nature with severity linked strongly to comorbidities.

A phenomenological cartography of misophonia and other forms of sound intolerance.

People with misophonia have strong aversive reactions to specific "trigger" sounds. Here we challenge this key idea of specificity. Machine learning was used to identify a misophonic profile from a multivariate sound-response pattern. Misophonia could be classified from most sounds (traditional triggers and non-triggers) and, moreover, cross-classification showed that the profile was largely transferable across sounds (rather than idiosyncratic for each sound). By splitting our participants in other ways, we were able to show-using the same approach-a differential diagnostic profile factoring in potential co-morbidities (autism, hyperacusis, ASMR). The broad autism phenotype was classified via aversions to repetitive sounds rather than the eating sounds most easily classified in misophonia. Within misophonia, the presence of hyperacusis and sound-induced pain had widespread effects across all sounds. Overall, we show that misophonia is characterized by a distinctive reaction to most sounds that ultimately becomes most noticeable for a sub-set of those sounds.