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Low protein intake may accelerate age-related loss of lean mass and physical function. We investigated the prevalence of low protein intake (<1·0 g/kg/day) and the associations between dietary patterns, modifiable risk factors and low protein intake in self-reliant community-dwelling adults ≥ 80 years. This cross-sectional study consisted of two home visits. Data collection consisted of physical measurements (e.g. physical function, physical activity) and self-report of nutritional intake (4-d food records), appetite, eating symptoms and medical conditions. Binary analyses were performed to compare participants with low and normal protein intake. Multiple logistic regression analyses were performed to investigate associations between low protein intake, dietary patterns and modifiable risk factors adjusted for age, sex, BMI categories and diseases. One hundred twenty-six were included in the study. Prevalence of low protein intake was 54 %. A greater day-to-day variation in protein intake was associated with low protein intake (adjusted OR 2·5; 95 % CI 1·14, 5·48). Participants with low protein intake had a higher prevalence of nausea, diarrhoea and mouth dryness. Reduced appetite, mouth dryness and pain increased odds of low protein intake (adjusted OR 3·06, 95 % CI 1·23, 7·63; OR 3·41, 95 % CI 1·51, 7·7; OR 1·54, 95 % CI 1·00, 2·36, respectively). There was a high prevalence of low protein intake in community-dwelling adults aged ≥ 80 years. Day-to-day variability, appetite, mouth dryness and pain may be potentially modifiable risk factors. Targeting dietary patterns and risk factors in primary prevention strategies may potentially improve intake of protein and minimise risk of physical frailty.
To develop a fully automated algorithm using data from the Veterans’ Affairs (VA) electrical medical record (EMR) to identify deep-incisional surgical site infections (SSIs) after cardiac surgeries and total joint arthroplasties (TJAs) to be used for research studies.
Retrospective cohort study.
This study was conducted in 11 VA hospitals.
Patients who underwent coronary artery bypass grafting or valve replacement between January 1, 2010, and March 31, 2018 (cardiac cohort) and patients who underwent total hip arthroplasty or total knee arthroplasty between January 1, 2007, and March 31, 2018 (TJA cohort).
Relevant clinical information and administrative code data were extracted from the EMR. The outcomes of interest were mediastinitis, endocarditis, or deep-incisional or organ-space SSI within 30 days after surgery. Multiple logistic regression analysis with a repeated regular bootstrap procedure was used to select variables and to assign points in the models. Sensitivities, specificities, positive predictive values (PPVs) and negative predictive values were calculated with comparison to outcomes collected by the Veterans’ Affairs Surgical Quality Improvement Program (VASQIP).
Overall, 49 (0.5%) of the 13,341 cardiac surgeries were classified as mediastinitis or endocarditis, and 83 (0.6%) of the 12,992 TJAs were classified as deep-incisional or organ-space SSIs. With at least 60% sensitivity, the PPVs of the SSI detection algorithms after cardiac surgeries and TJAs were 52.5% and 62.0%, respectively.
Considering the low prevalence rate of SSIs, our algorithms were successful in identifying a majority of patients with a true SSI while simultaneously reducing false-positive cases. As a next step, validation of these algorithms in different hospital systems with EMR will be needed.
Diet quality indices are a practical, cost-effective method to evaluate dietary patterns, yet few have investigated diet quality in athletes. This study describes the relative validity and reliability of the recently developed Athlete Diet Index (ADI). Participants completed the electronic ADI on two occasions, 2 weeks apart, followed by a 4-d estimated food record (4-dFR). Relative validity was evaluated by directly comparing mean scores of the two administrations (mAdm) against scores derived from 4-dFR using Spearman’s rank correlation coefficient and Bland–Altman (B–A) plots. Construct validity was investigated by comparing mAdm scores and 4-dFR-derived nutrient intakes using Spearman’s coefficient and independent t test. Test–retest reliability was assessed using paired t test, intraclass correlation coefficients (ICC) and B–A plots. Sixty-eight elite athletes (18·8 (sd 4·2) years) from an Australian sporting institute completed the ADI on both occasions. Mean score was 84·1 (sd 15·2; range 42·5–114·0). The ADI had good reliability (ICC = 0·80, 95 % CI 0·69, 0·87; P < 0·001), and B–A plots (mean 1·9; level of agreement −17·8, 21·7) showed no indication of systematic bias (y = 4·57–0·03 × x) (95 % CI −0·2, 0·1; P = 0·70). Relative validity was evaluated in fifty athletes who completed all study phases. Comparison of mAdm scores with 4-dFR-derived scores was moderate (rs 0·69; P < 0·001) with no systematic bias between methods of measurement (y = 6·90–0·04 × x) (95 % CI −0·3, 0·2; P = 0·73). Higher scores were associated with higher absolute nutrient intake consistent with a healthy dietary pattern. The ADI is a reliable tool with moderate validity, demonstrating its potential for application to investigate the diet quality of athletes.
Heavy alcohol consumption is associated with poorer cognitive function in older adults. Although understudied in middle-aged adults, the relationship between alcohol and cognition may also be influenced by genetics such as the apolipoprotein (ApoE) ε4 allele, a risk factor for Alzheimer’s disease. We examined the relationship between alcohol consumption, ApoE genotype, and cognition in middle-aged adults and hypothesized that light and/or moderate drinkers (≤2 drinks per day) would show better cognitive performance than heavy drinkers or non-drinkers. Additionally, we hypothesized that the association between alcohol use and cognitive function would differ by ApoE genotype (ε4+ vs. ε4−).
Participants were 1266 men from the Vietnam Era Twin Study of Aging (VETSA; M age = 56; range 51–60) who completed a neuropsychological battery assessing seven cognitive abilities: general cognitive ability (GCA), episodic memory, processing speed, executive function, abstract reasoning, verbal fluency, and visuospatial ability. Alcohol consumption was categorized into five groups: never, former, light, moderate, and heavy.
In fully adjusted models, there was no significant main effect of alcohol consumption on cognitive functions. However, there was a significant interaction between alcohol consumption and ApoE ε4 status for GCA and episodic memory, such that the relationship of alcohol consumption and cognition was stronger in ε4 carriers. The ε4+ heavy drinking subgroup had the poorest GCA and episodic memory.
Presence of the ε4 allele may increase vulnerability to the deleterious effects of heavy alcohol consumption. Beneficial effects of light or moderate alcohol consumption were not observed.
Introduction: Trauma care is highly complex and prone to medical errors. Accordingly, several studies have identified adverse events and conditions leading to potentially preventable or preventable deaths. Depending on the availability of specialized trauma care and the trauma system organization, between 10 and 30% of trauma-related deaths worldwide could be preventable if optimal care was promptly delivered. This narrative review aims to identify the main determinants and areas for improvements associated with potentially preventable trauma mortality. Methods: A literature review was performed using Medline, Embase and Cochrane Central Register of Controlled Trials from 1990 to a maximum of 6 months before submission for publication. Experimental or observational studies that have assessed determinants and areas for improvements that are associated with trauma death preventability were considered for inclusion. Two researchers independently selected eligible studies and extracted the relevant data. The main areas for improvements were classified using the Joint Commission on Accreditation of Healthcare Organizations patient event taxonomy. No statistical analyses were performed given the data heterogeneity. Results: From the 3647 individual titles obtained by the search strategy, a total of 37 studies were included. Each study included between 72 and 35311 trauma patients who had sustained mostly blunt trauma, frequently following a fall or a motor vehicle accident. Preventability assessment was performed for 17 to 2081 patients using either a single expert assessment (n = 2, 5,4%) or an expert panel review (n = 35, 94.6%). The definition of preventability and the taxonomy used varied greatly between the studies. The rate of potentially preventable or preventable death ranged from 2.4% to 76.5%. The most frequently reported areas for improvement were treatment delay, diagnosis accuracy to avoid missed or incorrect diagnosis and adverse events associated with the initial procedures performed. The risk of bias of the included studies was high for 32 studies because of the retrospective design and the panel review preventability assessment. Conclusion: Deaths occurring after a trauma remain often preventable. Included studies have used unstandardized definitions of a preventable death and various methodologies to perform the preventability assessment. The proportion of preventable or potentially preventable death reported in each study ranged from 2.4% to 76.5%. Delayed treatment, missed or incorrect initial diagnosis and adverse events following a procedure were commonly associated with preventable trauma deaths and could be targeted to develop quality improvement and monitoring projects.
The presentation aims at summarizing current knowledge about sleep in children and adolescents and at describing possible factors influencing their sleep.
For preschoolers, there is evidence that objectively assessed (sleep-EEG, actigraphy) poor sleep is associated with increased endocrine activity; this is to say, with increased morning cortisol secretion, an associative pattern observed so far only in adults. Furthermore, poor sleep and increased cortisol secretion are associated with emotional and behavioral difficulties.
During life span, notable changes occur with respect to sleep quantity and quality. Compared to childhood, in adolescence, three prominent changes occur: First, sleep quantity declines from about 10 hours at 10 years of age to between 6.5 and 8.5 hours in older adolescents. Second, a marked shift towards a longer sleep duration and later bed time from school nights to weekend nights is observable. Third, daytime sleepiness (20%) and insomnia symptoms (25%) are common among adolescents.
Among a variety of factors affecting adolescents’ sleep, we could show that negative parenting styles unfavorably influenced adolescents’ sleep quality, suggesting that even 18 years old adolescents may be far away from been emotionally independent from their parents. Furthermore, the so-called weekend-shift was correlated with increased sleepiness during the week, suggesting that irregular sleep schedules may negatively influence sleep quality and daytime functioning.
Last, if compared to healthy controls, children and adolescents after cleft lip and palate (CLP) repair were not at risk reporting sleep difficulties; rather, irrespective of the presence of CLP, sleep was affected by psychological strain.
Fluid intelligence expresses the capacity for interpretation of novel stimuli and flexible behavioral adaptation to such cues. Phasic dopamine firing closely matches a temporal difference prediction error (PE) signal important for learning and rapid behavioral adaptation. Both fluid intelligence and dopaminergic neurotransmission decline with age. So far, no study investigated the relationship between fluid IQ, PE signal and direct measures of dopaminergic neurotransmission. Here we used a multimodal imaging approach that combines positron emission tomography and functional magnetic resonance imaging.
A group of healthy controls was investigated with both 6-[18F]FluoroDOPA PET and functional MRI with a probabilistic reversal task. The task required a constant behavioral adaptation to changes in reward contingencies, while choosing between two abstract stimuli. A reinforcement learning algorithm was used to compute a trial-by-trial prediction error, which was the used as a regressor in the fMRI data analysis with SPM8.
The prediction error signal was associated with functional activation in the basal ganglia including the ventral striatum and putamen. Fluid intelligence was associated with the PE signal in the ventral striatum, which correlated with age-related changes in dopamine synthesis capacity in the prefrontal cortex.
These findings provide insight into the role of age-related changes in dopaminergic neurotransmission on behavioral adaptation. The multimodal imaging approach allows the characterization of interactions between dopamine metabolism and learning-related neuronal activation and may thus be a useful tool to clarify mechanisms underlying learning and plasticity in old age, which are crucial to our understanding of successful aging.
In alcoholism, one relevant mechanism contributing to relapse is the exposure to stimuli that are associated with alcohol intake. Such conditioned cues can elicit conditioned responses like alcohol craving and consumption. In the last decade, considerable progress has been made in identifying basic neuronal mechanisms that underlie cue-induced alcohol craving.
We explored whether functional brain activation during exposure to alcohol-associated stimuli is related to the prospective relapse risk in detoxified alcohol-dependent patients.
46 alcohol-dependent and 46 healthy volunteers participated in a fMRI study using a cue reactivity paradigm, in which visual alcohol-related and control stimuli were presented. Patients were followed for 3 months. Afterwards data was analysed regarding the subsequent relapse, resulting in 16 abstainers and 30 relapsers.
Alcohol-related versus neutral stimuli activated a frontocortical-limbic network including inferior, medial and middle frontal gyrus as well as putamen in the group of patients relative to healthy controls. Moreover, abstainers showed a stronger activation in orbitofrontal cortex as well as midbrain during the presentation of alcohol-related cues whereas relapsers revealed a stronger activation of cingulate gyrus.
This study suggests that cue-induced activation of orbitofrontal cortex and dopaminergic innervated midbrain is negatively associated with the prospective relapse risk in alcohol-dependent patients. This could indicate a more pronounced and conscious processing of alcohol cues which might serve as a warning signal and a behavioural controlling function. In contrast, prospective relapsers showed a stronger activation of cingulate gyrus, a region involved in the attribution of motivational value.
Sleep regulation is closely associated to HPA activity. Alterations in both systems may be precursors of psychiatric disorders like depression even at an early stage of development. So far the impact of microstructure in sleep regulation like sleep spindles is unknown. In recent studies, sleep spindles have been linked to efficient cortical-subcortical connectivity and cognitive abilities especially during neurodevelopment.
Sleep spindles in kindergarten children were analyzed and related to sleep regulation and HPA axis functioning.
Patients and Methods: Nine five-year old kindergarten children were enrolled in a cross-sectional examination of HPA system activity assessed by saliva cortisol measurements (morning cortisol after awakening) and sleep regulation investigated by sleep EEG-monitoring. Sleep EEG spindles were visually scored and were put into relation to macrostructural sleep and HPA activity parameters.
Sleep spindles were correlated to basal morning cortisol secretion (AUC basal) (curvilinear r = .83, p = .01), though were negatively correlated to cortisol increase (AUC netto) after awakening (r = -.77, p < .05). Though not statistically significant but by trend, spindle density (i.e. number of spindles per hour of stage 2 -sleep) is negatively correlated to REM density (r = - .57, p = .11), as increase of awakening cortisol was associated to REM density by trend (r = .63, p = .07).
Not only sleep continuation parameters as reported before but also sleep microstructure reflected by sleep spindles may be associated to sleep regulation and HPA system functioning.
Studies investigating indicators of recovery from schizophrenia yielded two concepts of recovery. The first is the reduction of psychiatric symptoms and functional disabilities (‘clinical recovery’), while the second describes the individual adaptation process to the threat posed to the individual sense of self by the disorder and its negative consequences (‘personal recovery’). Evidence suggests that both perceptions contribute substantially to the understanding of recovery and require specific assessment and therapy. While current reviews of measures of clinical recovery exist, measures of personal recovery have yet to be investigated. Considering the steadily growing literature on recovery, this article gives an update about existing measures assessing personal recovery.
A literature search for instruments was performed using Medline, Embase, PsycINFO&PSYNDEXPlus, ISI Web of Knowledge, and Cochrane Library. Inclusion criteria were: (1) quantitative self-report measures; (2) specifically developed for adults with schizophrenia or schizoaffective disorder or at least applied to individuals suffering from severe mental illness; (3) empirically tested psychometric properties and/or published in a peer-reviewed, English-language journal. Instruments were evaluated with regard to psychometric properties (validity and reliability) and issues of application (user and administrator friendliness, translations).
Thirteen instruments met the inclusion criteria. They were individually described and finally summarized in a table reflecting the pros and cons of each instrument. This may enable the reader to make an evidence-based choice for a questionnaire for a specific application.
The Recovery Assessment Scale is possibly the best currently available measure of personal recovery when all evaluation criteria are included. However, the ratings listed in the current paper depended on the availability of information and the quality of available reports of previous assessment of the measurement properties. Considering the significant amount of information lacking and inconsistent findings, further research on the reviewed measures is perhaps more important than the development of new measures of personal recovery.
Frowning expresses negative emotions like anger, fear, and sadness. According to the facial feedback hypothesis, suppression of frowning will also diminish the corresponding negative emotions. Hence, mood improvement has been observed in patients who underwent treatment of glabellar frown lines with botulinum neurotoxin. This observation suggests the possibility that the intervention may be employed for the management of psychiatric disorders associated with negative emotions. Preliminary data from an open case series indicate that the intervention might improve the symptoms of depression.
Aims & objectives
To test whether an onabotulinumtoxinA injection into the glabellar region is benefical as an adjunctive treatment of major depression within a clinical trial.
We used a randomized, double-blinded, placebo-controlled study design (n = 30; ClinicalTrials.gov, number, NCT00934687).
We show that a single onabotulinumtoxinA treatment shortly leads to a strong and sustained improvement in partly chronic major depression that did not respond sufficiently to previous treatment. As for the primary end-point, Hamilton Depression Rating Scale (HAM-D17) six weeks after treatment compared to baseline, scores of onabotulinumtoxinA recipients showed 37.9% (8.34 points) more improvement than those of placebo-treated participants (F = 12.30, p = 0.002, η2 = 0.31, d = 1.28).
Our findings support the concept that the facial musculature not only expresses, but also regulates, mood states. As it stands, treatment of glabellar frown lines with botulinum neurotoxin can be considered for depressed patients with the objective of inducing mood-lifting effects.
There is a lack of evidence for the efficacy of stimulant pharmacotherapy in patients with substance dependence and comorbid attention deficit hyperactivity disorder (ADHD).
The aim of the present trial was to test the efficacy and safety of 180 mg extended release methylphenidate for treating ADHD in patients with amphetamine dependence.
54 incarcerated men, mean age 42 years, meeting the DSM-IV criteria for amphetamine dependence and ADHD were randomized to methylphenidate or placebo in a 24-week randomized double-blind, placebo-controlled trial, with parallel groups design. The medication started within 14 days before release from prison and continued in outpatient care with twice weekly visits including once weekly cognitive behaviour therapy. The primary end point was relapse to any drug use measured by urine toxicology. Secondary endpoints included relapse to amphetamine use, retention to treatment, and change in selfrated ADHD symptoms.
The methylphenidate group had significantly fewer drug positive urines compared to the placebo group (95% CI -0.31 to -0.05, P=.034), fewer amphetamine positive urines, (95% CI -0.36 to -0.07, P=.019) and better retention to treatment (95% CI 15.64 to 78.58, P=.001). Compared to the placebo group, the methylphenidate group also significantly reduced their selfrated ADHD symptoms (95% CI -21.09 to -3.37, P=.008) during the 24-week treatment.
This is the first randomized clinical trial to demonstrate the efficacy of a stimulant treatment for substance dependent individuals with ADHD. The treatment with MPH led to reduction in drug use and a clinically relevant improvement of ADHD symptoms.
A dimensional approach in psychiatry strives to identify neurobiological signatures of core (dys)functions such as responses to emotional stimuli across nosological boundaries.
We compared responses to emotional stimuli between major psychiatric disorders and investigated whether there is a psychopathological correlate irrespective of diagnostic group.
We used functional magnetic resonance imaging (fMRI) to assess the functional correlates of responses to unexpected pleasant and aversive emotional pictures in n=175 subjects suffering from alcohol dependence (n=29), schizophrenia (n=37), major depressive disorder (MDD; n=25), bipolar disorder (acute manic episode; n=12), panic disorder (n=12) or attention deficit/hyperactivity disorder (ADHD; n=20) and in healthy controls (n=40). The level of anxiety was measured in all diagnostic groups with the State-Trait Anxiety Inventory, and severity of depressive mood was measured with Beck's depressions inventory in all diagnostic groups with the exception of bipolar patients.
Over all diagnostic groups, a significant activation of BA10 was observed during the presentation of unexpected pleasant pictures, whereas a significant activation of the left amygdala and left insula was found during the presentation of unexpected aversive pictures. We did not find significant effects of group, nor a correlation of neuronal activation with depressed mood or anxiety.
In spite of reported alterations in emotion processing in different psychiatric diseases, responses to emotional pictures did not differ across nosological boundaries in our study. However, a dimensional approach that targets e.g. personality traits or basic learning mechanisms and their neuropsychological correlates across traditional disease categories may be more promising.
Alcohol addiction is assumed to reflect the endpoint of a series of transitions: from initial alcohol intake that causes hedonic feelings, through loss of control over this behaviour, such that it becomes compulsive. Alcohol dependent patients are dominated by their addiction despite the negative consequences and experience other stimuli as providing little reward. Still, some patients manage to abstain from alcohol, whereas others relapse quiet often. Two recent studies (Beck et al., 2012; Charlet et al., 2013) could show that relapsers not only display greater atrophy in limbic and prefrontal areas, but also seem to have attenuated functional connectivity of these areas during cue-reactivity and emotional tasks. It has been proposed that habitual stimulus-triggered responses result in the compulsive nature of alcohol consumption (Everitt and Robbins, 2005), the formation of these inflexible stimulus-response associations being described as habit-based learning which is commonly seen as the counterpart of outcome-directed actions, so called goal-directed learning. Our current research project therefore aims to comprehensively assess how learning alterations might contribute to the assignment of aberrantly high value in the development and recurrence of alcoholism. The project compares alcohol-dependent patients to healthy controls on a battery of tasks assessing Pavlovian, habitual and goal-directed reward-dependent learning behaviourally and with functional MRI. We are going to report preliminary results of our ongoing research.
Despite the large scientific debate concerning potentially stigmatizing effects of informing an individual about being in an at-risk mental state (ARMS) for psychosis, studies investigating this topic are rare and quantitative assessment of this kind of stigmatization does not exist so far.
This study presents first results regarding potentially helpful or stigmatizing effects of being informed about an ARMS assessed with a newly developed quantitative self-rating (FePsy-Stigma questionnaire).
Forty ARMS patients participating in the prospective Basel Early Detection of Psychosis (FePsy) study as well as patients clinically assessed in the early detection service of the Psychiatric Services of Solothurn, completed the FePsy-Stigma questionnaire during their follow-up assessments at least six months after they had been informed about their increased risk of developing psychosis. The questionnaire was constructed based on a previous qualitative study and on adapted versions of formerly used instruments for assessing stigma in mental health (Internalized Stigma of Mental Illness Scale, Personal Beliefs and Experiences Questionnaire).
Stigmatization appeared to be low overall except for social withdrawal due to suspected stigma. Stigma resistance, stereotype awareness and expected discrimination scored considerably higher than actually experienced discrimination, alienation and stereotype endorsement.
The results suggest that early detection services help individuals cope with symptoms and build certain resilience toward potential stigmatization, rather than enhancing or causing the latter. In line with previous studies, our results indicate that there is a considerable difference between expected and actually experienced discrimination as well as between stereotype awareness and stereotype endorsement.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
The development and maintenance of an alcohol addiction is a complex interaction between genetic and environmental factors. Genetic effects seem to contribute substantially to the risk of developing an addiction, but also to its course and patients’ responses to different treatments. Recent studies identified associations between polymorphisms in the genes of glutamate and μ-opioid receptors and addiction risk. Those receptors are of special interest, because they are targets of therapeutic agents, such as acamprosate and topiramate.
Objectives and aims
Several studies were conducted, in order to further determine the effects of genetic polymorphisms in glutamate and opioid receptor genes on addictive behavior, neural response to alcohol cues and relapse risk.
Genetic effects were investigated in samples of alcohol-dependent patients using functional imaging techniques, neuropsychological tests and follow-up investigation after standard clinical treatment. Data on clinical parameters, neuronal response to alcohol cues, functional neuronal connectivity and relapse risk were collected and analyzed.
Results demonstrate effects of genetic polymorphisms in glutamate and opioid receptors on neuronal response to alcohol cues in frontal and mesolimbic brain areas, subjective craving and time to first relapse. Current findings will be discussed in the light of existing evidence on the contribution of genetic effects to treatment outcome and patient stratification.
The investigation of genetic risk factors and mechanisms by which they affect addiction related phenotypes seems to be a promising tool to identify molecular treatment targets and predictors for successful treatment strategies.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
22q11.2 deletion syndrome (22q11DS) is a genetic disorder caused by a microdeletion on chromosome 22q11.2 and associated with an increased risk for psychosis. A dysfunctional motivational reward system is thought to be one of the salient features in psychosis caused by abnormal dopamine functioning. It is unknown whether patients with 22q11DS have a dysfunctional reward system.
This study aims to investigate reward learning in 22q11DS. The study included 10 adults with 22q11DS (age: 33.1 years, 60% female) and 10 age-gender-matched healthy controls (HC, age: 39.7 years, 60% female). A single infusion 18F-fallypride PET scan was acquired during which all subjects performed a version of the learning phase of the Probabilistic Stimulus Selection Task for reward learning (RL), modified to deliver social feedback.
IQ-scores were significantly lower in the 22q11DS group (P < .001) compared to HC. The 22q11DS group both earned significantly less money (P < .05) and performed worse during the RL-task (P < .05) than HC. However, the learning curve for the RL-task was the same for both groups. IQ-scores were a significant positive predictor for earnings (P < .05) and performance (P < .05), but not for the learning curve.
These preliminary results indicate that people with 22q11DS are capable of learning at the same speed as HC, however they are less susceptible for reward than HC because their overall performance during RL is worse than HC. This lower reward sensitivity could be a result of haplo-insufficiency of COMT in 22q11DS and consequently abnormal prefrontal dopamine functioning.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Alcohol relapse is often occurring to regulate negative affect during withdrawal. On the neurobiological level, alcoholism is associated with gray matter (GM) abnormalities in regions that regulate emotional experience such as the orbitofrontal cortex (OFC). However, no study to our knowledge has investigated the neurobiological unpinning of affect in alcoholism at early withdrawal and the associations of OFC volume with long-term relapse risk.
One hundred and eighty-two participants were included, 95 recently detoxified alcohol dependent patients (ADP) and 87 healthy controls (HC). We measured affective states using the positive and negative affect schedule (PANAS). We collected T1-weighted brain structural images and performed Voxel-based morphometry (VBM).
Findings revealed GM volume decrease in alcoholics in the prefrontal cortex (including medial OFC), anterior cingulate gyrus, and insula. GM volume in the medial OFC was positively associated with NA in the ADP group. Cox regression analysis predicted that risk to heavy relapse at 6 months increases with decreased GM volume in the medial OFC.
Negative affect during alcohol withdrawal was positively associated with OFC volume. What is more, increased GM volume in the OFC also moderated risk to heavy relapse at 6 months. Reduced GM in the OFC poses as risk to recovery from alcohol dependence and provides valuable insights into transient negative affect states during withdrawal that can trigger relapse. Implications exist for therapeutic interventions signifying the OFC as a neurobiological marker to relapse and could explain the inability of ADP to regulate internal negative affective states.
The protein brain derived neurotrophic factor (BDNF) is a major contributor to neuronal plasticity. There is numerous evidence that BDNF expression is decreased by experiencing psychological stress and that accordingly a lack of neurotrophic support causes depression. The use of serum BDNF concentration as a potential indicator of brain alteration is justified through extensive evidence. Recently, we reported, for the first time, a relationship between BDNF and insomnia, since we could show that reduced levels of serum BDNF are correlated with sleep impairment in control subjects, while partial sleep deprivation was able to induce a fast increase in serum BDNF levels in depressed patients. Using a bi-directional stress model as an explanation approach, we propose the hypothesis that chronic stress might induce a deregulation of the HPA system leading in the long term to sleep disturbance and decreased BDNF levels, whereas acute sleep deprivation, can be used as therapeutical intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial sleep deprivation (PSD) induced a very fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Moreover, we revealed that stress experience and subjective sleep perception interact with each other and affect serum BDNF levels. We identified sleep as a mediator of the association between stress experience and serum BDNF levels.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
To explore associations of whole grain and cereal fibre intake to CVD risk factors in Australian adults.
Cross-sectional analysis. Intakes of whole grain and cereal fibre were examined in association to BMI, waist circumference (WC), blood pressure (BP), serum lipid concentrations, C-reactive protein, systolic BP, fasting glucose and HbA1c.
Australian Health Survey 2011–2013.
A population-representative sample of 7665 participants over 18 years old.
Highest whole grain consumers (T3) had lower BMI (T0 26·8 kg/m2, T3 26·0 kg/m2, P < 0·0001) and WC (T0 92·2 cm, T3 90·0 cm, P = 0·0005) compared with non-consumers (T0), although only WC remained significant after adjusting for dietary and lifestyle factors, including cereal fibre intake (P = 0·03). Whole grain intake was marginally inversely associated with fasting glucose (P = 0·048) and HbA1c (P = 0·03) after adjusting for dietary and lifestyle factors, including cereal fibre intake. Cereal fibre intake was inversely associated with BMI (P < 0·0001) and WC (P < 0·0008) and tended to be inversely associated with total cholesterol, LDL-cholesterol and apo-B concentrations, although associations were attenuated after further adjusting for BMI and lipid-lowering medication use.
The extent to which cereal fibre is responsible for the CVD-protective associations of whole grains may vary depending on the mediators involved. Longer-term intervention studies directly comparing whole grain and non-whole grain diets of similar cereal fibre contents (such as through the use of bran or added-fibre refined grain products) are needed to confirm independent effects.