There is an ongoing scientific debate about whether unhealthy, highly processed foods are addictive and whether this contributes to overeating and obesity. Through this debate series, we identified ...numerous points of consensus, including that 1) addictive-like eating exists, 2) mechanisms implicated in substance-related and addictive disorders contribute to overeating and obesity, and 3) food industry practices are also a key contributor to this phenomenon. We also agree that obesity, a multifaceted condition, is not synonymous with addictive-like eating and that further research is needed to clarify the understanding of addictive-like eating. Disagreements remain regarding the strength of evidence that highly processed foods are addictive, the appropriate framework for conceptualizing addictive-like eating, and the societal implications of identifying unhealthy, highly processed foods as addictive. Finally, we highlight future research needed to address existing gaps in the scientific literature that underlie continuing controversies, most notably the need for scientific consensus about what measures should be used to evaluate whether highly processed foods are addictive.
"Food addiction" has become a focus of interest for researchers attempting to explain certain processes and/or behaviors that may contribute to the development of obesity. Although the scientific ...discussion on "food addiction" is in its nascent stage, it has potentially important implications for treatment and prevention strategies. As such, it is important to critically reflect on the appropriateness of the term "food addiction", which combines the concepts of "substance-based" and behavioral addiction. The currently available evidence for a substance-based food addiction is poor, partly because systematic clinical and translational studies are still at an early stage. We do however view both animal and existing human data as consistent with the existence of addictive eating behavior. Accordingly, we stress that similar to other behaviors eating can become an addiction in thus predisposed individuals under specific environmental circumstances. Here, we introduce current diagnostic and neurobiological concepts of substance-related and non-substance-related addictive disorders, and highlight the similarities and dissimilarities between addiction and overeating. We conclude that "food addiction" is a misnomer because of the ambiguous connotation of a substance-related phenomenon. We instead propose the term "eating addiction" to underscore the behavioral addiction to eating; future research should attempt to define the diagnostic criteria for an eating addiction, for which DSM-5 now offers an umbrella via the introduction on Non-Substance-Related Disorders within the category Substance-Related and Addictive Disorders.
Does it matter what we eat for our mental health? Accumulating data suggests that this may indeed be the case and that diet and nutrition are not only critical for human physiology and body ...composition, but also have significant effects on mood and mental wellbeing. While the determining factors of mental health are complex, increasing evidence indicates a strong association between a poor diet and the exacerbation of mood disorders, including anxiety and depression, as well as other neuropsychiatric conditions. There are common beliefs about the health effects of certain foods that are not supported by solid evidence and the scientific evidence demonstrating the unequivocal link between nutrition and mental health is only beginning to emerge. Current epidemiological data on nutrition and mental health do not provide information about causality or underlying mechanisms. Future studies should focus on elucidating mechanism. Randomized controlled trials should be of high quality, adequately powered and geared towards the advancement of knowledge from population-based observations towards personalized nutrition. Here, we provide an overview of the emerging field of nutritional psychiatry, exploring the scientific evidence exemplifying the importance of a well-balanced diet for mental health. We conclude that an experimental medicine approach and a mechanistic understanding is required to provide solid evidence on which future policies on diet and nutrition for mental health can be based.
•Epidemiological data highlight the association between nutrition and mental health but do not provide information about causality or underlying mechanism.•Emerging findings from intervention studies suggest that diet (often combined with lifestyle) modification has potential in the prevention and treatment of mental health and may modify drug treatment effects.•Dietary intervention studies are informative but often limited methodologically due to: heterogeneity in population characteristics, lack of biomarkers to adequately stratify within and across populations, small sample sizes, lack of blinding of participants to treatment allocation and/or lack of blinded observers.•Progress will require mechanistic insight into the impact of different diets and dietary components at various levels: metabolic and cellular processes, neural circuits, core cognitive and emotional processes, whole organism and disease (models).•Genetic background can be used to strengthen hypotheses on the effects of specific nutrients on mental disorders, which can subsequently be tested in randomized controlled trials.•High quality and adequately powered experimental medicine studies will enable the identification of interventions that have a higher probability of succeeding when tested in large randomized controlled trials.•Sensitivity to mental health issues vary across the lifespan and between individuals and is influenced by genetic background, cultural setting and the environment. Nutritional needs also differ across the lifespan. To provide dietary recommendations for improving mental health, a major challenge is to advance knowledge from population-based observations towards personalized nutrition.
School attendance problems (SAPs) become manifest in many ways and are associated with multiple risk factors, calling for comprehensive assessment methods. This study documents the development of the ...inventory of school attendance problems (ISAP), which assesses both the quality and the function of a broad spectrum of SAPs by first asking students with SAPs to rate the intensity of symptoms prior to or at school and then to rate their impact on school attendance. An empirically generated pool of 124 items was analyzed (explorative factor analysis) using a clinical sample of
N
= 245 students with SAPs (53.5% male;
M
age
: 14.4). The Youth Self Report (YSR), a German version of the School Refusal Assessment Scale (SRAS), and the extent of school absenteeism were used to determine construct validity. The resulting 48 items loaded on 13 factors. The 13 scales assess internalizing and externalizing symptoms (Depression, Social Anxiety, Performance Anxiety, Agoraphobia/Panic, Separation Anxiety, Somatic Complaints, Aggression, School Aversion/Attractive Alternatives) as well as emotional distress due to problems in the school or family context (Problems with Teachers, Dislike of the Specific School, Problems with Peers, Problems Within the Family, Problems with Parents). All scales showed good internal consistencies. Their correlations with the YSR and the SRAS indicated convergent and discriminant validity. Positive associations between most of the scales and the extent of school absenteeism were obtained. Although preliminary, these results support the usefulness of the ISAP for a comprehensive assessment of SAPs in clinical settings.
Attention-deficit/hyperactivity disorder (ADHD) shows substantial heritability and is two to seven times more common in male individuals than in female individuals. We examined two putative genetic ...mechanisms underlying this sex bias: sex-specific heterogeneity and higher burden of risk in female cases.
We analyzed genome-wide autosomal common variants from the Psychiatric Genomics Consortium and iPSYCH Project (n = 20,183 cases, n = 35,191 controls) and Swedish population register data (n = 77,905 cases, n = 1,874,637 population controls).
Genetic correlation analyses using two methods suggested near complete sharing of common variant effects across sexes, with rg estimates close to 1. Analyses of population data, however, indicated that female individuals with ADHD may be at especially high risk for certain comorbid developmental conditions (i.e., autism spectrum disorder and congenital malformations), potentially indicating some clinical and etiological heterogeneity. Polygenic risk score analysis did not support a higher burden of ADHD common risk variants in female cases (odds ratio confidence interval = 1.02 0.98–1.06, p = .28). In contrast, epidemiological sibling analyses revealed that the siblings of female individuals with ADHD are at higher familial risk for ADHD than the siblings of affected male individuals (odds ratio confidence interval = 1.14 1.11–1.18, p = 1.5E-15).
Overall, this study supports a greater familial burden of risk in female individuals with ADHD and some clinical and etiological heterogeneity, based on epidemiological analyses. However, molecular genetic analyses suggest that autosomal common variants largely do not explain the sex bias in ADHD prevalence.
Author Affiliation: (1) Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Essen, University of Duisburg-Essen, Essen, Germany (a) ...Franziska.Degenhardt@lvr.de Article History: Registration Date: 03/16/2021 Online Date: 03/27/2021 Byline:
Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes. Several G-protein-coupled receptors have been identified as ...free-fatty-acid receptors important in physiology as well as in several diseases. GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference. Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Purpose
While observational studies revealed inverse associations between serum vitamin D levels 25(OH)D and depression, randomized controlled trials (RCT) in children and adolescents are lacking. ...This RCT examined the effect of an untreated vitamin D deficiency compared to an immediate vitamin D
3
supplementation on depression scores in children and adolescents during standard day and in-patient psychiatric treatment.
Methods
Patients with vitamin D deficiency 25(OH)D ≤ 30 nmol/l and at least mild depression Beck Depression Inventory II (BDI-II) > 13 (
n
= 113) were 1:1 randomized into verum (VG; 2640 IU vitamin D
3
/d) or placebo group (PG) in a double-blind manner. During the intervention period of 28 days, both groups additionally received treatment as usual. BDI-II scores were assessed as primary outcome, DISYPS-II (Diagnostic System for Mental Disorders in Childhood and Adolescence, Self- and Parent Rating) and serum total 25(OH)D were secondary outcomes.
Results
At admission, 49.3% of the screened patients (
n
= 280) had vitamin D deficiency. Although the intervention led to a higher increase of 25(OH)D levels in the VG than in the PG (treatment difference: + 14 ng/ml; 95% CI 4.86–23.77;
p
= 0.003), the change in BDI-II scores did not differ (+ 1.3; 95% CI − 2.22 to 4.81;
p
= 0.466). In contrast, DISYPS parental ratings revealed pronounced improvements of depressive symptoms in the VG (− 0.68; 95% CI − 1.23 to − 0.13;
p
= 0.016).
Conclusion
Whereas this study failed to show a vitamin D supplementation effect on self-rated depression in adolescent in- or daycare patients, parents reported less depressive symptoms in VG at the end of our study. Future trials should consider clinician-rated depressive symptoms as primary outcome.
Trial registration
“German Clinical Trials Register” (
https://www.drks.de
), registration number: DRKS00009758
Tourette syndrome (TS) is a model neuropsychiatric disorder thought to arise from abnormal development and/or maintenance of cortico-striato-thalamo-cortical circuits. TS is highly heritable, but its ...underlying genetic causes are still elusive, and no genome-wide significant loci have been discovered to date. We analyzed a European ancestry sample of 2,434 TS cases and 4,093 ancestry-matched controls for rare (< 1% frequency) copy-number variants (CNVs) using SNP microarray data. We observed an enrichment of global CNV burden that was prominent for large (> 1 Mb), singleton events (OR = 2.28, 95% CI 1.39–3.79, p = 1.2 × 10−3) and known, pathogenic CNVs (OR = 3.03 1.85–5.07, p = 1.5 × 10−5). We also identified two individual, genome-wide significant loci, each conferring a substantial increase in TS risk (NRXN1 deletions, OR = 20.3, 95% CI 2.6–156.2; CNTN6 duplications, OR = 10.1, 95% CI 2.3–45.4). Approximately 1% of TS cases carry one of these CNVs, indicating that rare structural variation contributes significantly to the genetic architecture of TS.
•Rare structural variants contribute significantly to the genetic architecture of TS.•Increased global CNV burden is driven by large, rare, clinically relevant events.•NRXN1 deletions and CNTN6 duplications confer a substantial increase in TS risk.
Tourette syndrome is highly genetic, but identifying definitive disease susceptibility genes has been challenging. Huang et al. report two genome-wide, significant, recurrent, rare copy-number variants (NRXN1 deletions and CNTN6 duplications), each conferring a substantial increase in TS risk.
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