Anorexia nervosa (AN) is a debilitating and often refractory eating disorder that is unique among psychiatric disorders insofar as nutrition is key to recovery. Treatment options and efficacy are limited with no approved medications for AN. Genetic studies are clarifying the etiology of AN, with the goal of eventually informing the development of innovative personalized pharmacologic, nutritional, microbial, and behavioral interventions. We present the current state of genome-wide and epigenome-wide association studies, gut microbiome research, and functional genomics investigations and discuss translating this knowledge into clinical practice.

In this review, we explore the biomarkers of different psychiatric disorders, such as major depressive disorder, generalized anxiety disorder, schizophrenia, and bipolar disorder. Moreover, we show the interplay between genetic and environmental factors. Novel techniques such as genome-wide association studies (GWASs) have identified numerous risk loci and single-nucleotide polymorphisms (SNPs) implicated in these conditions, contributing to a better understanding of their mechanisms. Moreover, the impact of genetic variations on drug metabolisms, particularly through cytochrome P450 (CYP450) enzymes, highlights the importance of pharmacogenomics in optimizing psychiatric treatment. This review also explores the role of neurotransmitter regulation, immune system interactions, and metabolic pathways in psychiatric disorders. As the technology advances, integrating genetic markers into clinical practice will be crucial in advancing precision psychiatry, improving diagnostic accuracy and therapeutic interventions for individual patients.

Anxiety sensitivity may be associated with both anxiety and eating disorder symptoms, which could contribute to the frequent comorbidity of both syndromes. This study examined the common (i.e., correlated) genetic and environmental contributions to anxiety sensitivity, cognitive symptoms of eating disorder severity, and anxiety symptoms to understand their co-occurrence in adolescence. This study analyzed data from the Twins Early Development Study. When twins were 16 years old (N = 5,111 pairs), they self-reported anxiety sensitivity via the Child Anxiety Sensitivity Index and cognitive symptoms of eating disorder severity via four items from the Eating Disorder Diagnostic Scale. Parents reported adolescent anxiety symptoms via the Anxiety Related Behaviour Questionnaire. Common genetic and non-shared environmental factors contributed to phenotypic correlations among cognitive symptoms of eating disorders. Genetic and nonshared environmental influences contributed to anxiety sensitivity and a latent variable of cognitive symptoms of eating disorder severity. Genetic, shared-, and nonshared- environmental influences contributed to anxiety symptoms. Common genetic and nonshared environmental influences contributed to anxiety sensitivity and anxiety symptoms, as well as anxiety sensitivity and cognitive symptoms of eating disorder severity. However, there was no evidence of common genetic or environmental contributions to anxiety symptoms and cognitive symptoms of eating disorder severity. This study implicates anxiety sensitivity as a potential cognitive process associated with both anxiety symptoms and cognitive symptoms of eating disorders.

Anorexia nervosa (AN) is a serious and complex psychiatric disorder yet treatment results are suboptimal. Insight into the etiology of this illness is much needed. Research highlights the implication of anxiety-related traits in the development and maintenance of AN. This study investigates firstly, behavioural inhibition and intolerance for uncertainty (IU) in adolescents with and without AN, and secondly relations between these traits.

In a cross-sectional study, 165 adolescent girls (AN = 94, HC = 71) completed questionnaires measuring behavioural inhibition, IU and trait anxiety. ANOVAs tested differences between AN and HC groups, and mediation models with IU as a mediator between behavioural inhibition and trait anxiety were run.

AN adolescents reported significantly higher levels of behavioural inhibition, IU and trait anxiety compared to their peers. In both AN and HC, a direct and a total effect of behavioural inhibition on trait anxiety was found. However, only in the AN group IU partially mediated the relation between behavioural inhibition and trait anxiety.

Data is cross-sectional and longitudinal studies are required. A mean illness duration of nearly 2 years may mean early effects of malnourishment and habituation and future studies should include patients with shorter illness duration.

Results highlight that behavioural inhibition and IU may contribute to anxiety in AN whilst their peers may have developed better executive and social-emotional skills to manage uncertainty. Adolescents with AN may benefit from interventions targeting behavioural inhibition and IU.

Maladaptation in balancing internal energy needs and external threat cues may result in eating disorders. However, brain mechanisms underlying such maladaptations remain elusive. Here, we identified that the basal forebrain (BF) sends glutamatergic projections to glutamatergic neurons in the ventral tegmental area (VTA) in mice. Glutamatergic neurons in both regions displayed correlated responses to various stressors. Notably, in vivo manipulation of BF terminals in the VTA revealed that the glutamatergic BF → VTA circuit reduces appetite, increases locomotion, and elicits avoidance. Consistently, activation of VTA glutamatergic neurons reduced body weight, blunted food motivation, and caused hyperactivity with behavioral signs of anxiety, all hallmarks of typical anorexia symptoms. Importantly, activation of BF glutamatergic terminals in the VTA reduced dopamine release in the nucleus accumbens. Collectively, our results point to overactivation of the glutamatergic BF → VTA circuit as a potential cause of anorexia-like phenotypes involving reduced dopamine release.

Eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) are a heterogeneous class of complex illnesses marked by weight and appetite dysregulation coupled with distinctive behavioral and psychological features. Our understanding of their genetics and neurobiology is evolving thanks to global cooperation on genome-wide association studies, neuroimaging, and animal models. Until now, however, these approaches have advanced the field in parallel, with inadequate cross-talk. This review covers overlapping advances in these key domains and encourages greater integration of hypotheses and findings to create a more unified science of eating disorders. We highlight ongoing and future work designed to identify implicated biological pathways that will inform staging models based on biology as well as targeted prevention and tailored intervention, and will galvanize interest in the development of pharmacologic agents that target the core biology of the illnesses, for which we currently have few effective pharmacotherapeutics.

Identifying risk factors that contribute to the development of anorexia nervosa (AN) is critical for the implementation of early intervention strategies. Anxiety, obsessive-compulsive behavior, and immune dysfunction may be involved in the development of AN; however, their direct influence on susceptibility to the condition remains unclear. Here, we used the activity-based anorexia (ABA) model to examine whether activity, anxiety-like behavior, compulsive behavior, and circulating immune markers predict the subsequent development of pathological weight loss.

Female Sprague-Dawley rats (n = 44) underwent behavioral testing before exposure to ABA conditions after which they were separated into susceptible and resistant subpopulations. Blood was sampled before behavioral testing and after recovery from ABA to screen for proinflammatory cytokines.

Rats that were vulnerable to pathological weight loss differed significantly from resistant rats on all key ABA parameters. While the primary measures of anxiety-like or compulsive behavior were not shown to predict vulnerability to ABA, increased locomotion and anxiety-like behavior were both associated with the extent of weight loss in susceptible but not resistant animals. Moreover, the change in expression of proinflammatory markers IL-4 and IL-6 evoked by ABA was associated with discrete vulnerability factors. Intriguingly, behavior related to risk assessment was shown to predict vulnerability to ABA.

We did not find undisputable behavioral or immune predictors of susceptibility to pathological weight loss in the ABA rat model. Future research should examine the role of cognition in the development of ABA, dysfunction of which may represent an endophenotype linking anorectic, anxiety-like and compulsive behavior.

Anorexia nervosa (AN) has among the highest mortality rates of all psychiatric disorders and treatment options remain limited in their efficacy. Understanding what types of risk factors contribute to the development of AN is essential for implementing early intervention strategies. This study describes how some of the most common psychological features of AN could be used to predict susceptibility to pathological weight loss in a well-established animal model.

Background: Sleep problems and eating disorders (EDs) are both serious public health concerns often seen in young adults. Yet, the underlying mechanisms for such associations are largely unknown. This study aims to examine potential serial multiple mediation effects of problematic smartphone use (PSU) and psychological distress (i.e., depressive and anxiety symptoms) in the relationship between sleep quality and disordered eating behaviors/attitudes (DEBs). Methods: A total of 4,325 students from two Tibet universities in China (2,657 females and 1,668 males) completed an online survey that included the following measurements: Eating Attitude Test-26 for disordered eating behaviors/attitudes, the Chinese Version of Pittsburgh Sleep Quality Index (CPSQI), Smartphone Addiction Scale-Short Version (SAS-SV) for problematic smartphone use, Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) for psychological distress. Results: While the direct path linking sleep quality and DEBs was not found to be significant (Standardized β = 0.006, 95% CI = -0.0667~0.0970), both PSU (Standardized β = 0.016, 95% CI = 0.0256~0.0591) and anxiety symptoms (Standardized β = 0.014, 95% CI = 0.0203~0.0526) may mediate a link between sleep quality and DEBs; serial multiple mediation analysis revealed that a serial indirect pathway of "sleep quality -> PSU -> anxiety symptoms -> DEBs" existed(Standardized β = 0.001, 95% CI = 0.0002~0.0012). Similarly, while the direct path linking sleep quality and DEBs was not found to be significant (Standardized β = 0.006, 95% CI = -0.0667~0.0970), both PSU (Standardized β = 0.020, 95% CI = 0.0337~0.0692) and depressive symptoms (Standardized β = 0.015, 95% CI = 0.0139~0.0652) may mediate a link between sleep quality and DEBs; serial multiple mediation analysis revealed that a serial indirect pathway of "sleep quality -> PSU -> depressive symptoms -> DEBs" existed (Standardized β = 0.001, 95% CI = 0.0006~0.0038). Conclusions: Psychological and behavioral factors may comprehensively work together, leading to flow-on effects from sleep problems to disordered eating behaviors among university students. Appropriate interventions that target problematic smartphone use could thus potentially reduce anxiety and depression levels, which in turn will provide a buffer against the negative impact of poor sleep quality on eating disorder symptoms.

Evidence from observational studies suggests an association between anxiety disorders and anorexia nervosa (AN), but causal inference is complicated by the potential for confounding in these studies. We triangulate evidence across a longitudinal study and a Mendelian randomization (MR) study, to evaluate whether there is support for anxiety disorder phenotypes exerting a causal effect on AN risk.

Study One assessed longitudinal associations of childhood worry and anxiety disorders with lifetime AN in the Avon Longitudinal Study of Parents and Children cohort. Study Two used two-sample MR to evaluate: causal effects of worry, and genetic liability to anxiety disorders, on AN risk; causal effects of genetic liability to AN on anxiety outcomes; and the causal influence of worry on anxiety disorder development. The independence of effects of worry, relative to depressed affect, on AN and anxiety disorder outcomes, was explored using multivariable MR. Analyses were completed using summary statistics from recent genome-wide association studies.

Study One did not support an association between worry and subsequent AN, but there was strong evidence for anxiety disorders predicting increased risk of AN. Study Two outcomes supported worry causally increasing AN risk, but did not support a causal effect of anxiety disorders on AN development, or of AN on anxiety disorders/worry. Findings also indicated that worry causally influences anxiety disorder development. Multivariable analysis estimates suggested the influence of worry on both AN and anxiety disorders was independent of depressed affect.

Overall our results provide mixed evidence regarding the causal role of anxiety exposures in AN aetiology. The inconsistency between outcomes of Studies One and Two may be explained by limitations surrounding worry assessment in Study One, confounding of the anxiety disorder and AN association in observational research, and low power in MR analyses probing causal effects of genetic liability to anxiety disorders. The evidence for worry acting as a causal risk factor for anxiety disorders and AN supports targeting worry for prevention of both outcomes. Further research should clarify how a tendency to worry translates into AN risk, and whether anxiety disorder pathology exerts any causal effect on AN.

Despite established comorbidity between anxiety and disordered eating (DE), and a plethora of research using various methodologies to examine this overlap, use of twin modeling to expose whether a shared genetic liability underpins these conditions remains rare.

Data from a longitudinal sample of female twins were selected: measures of risk for DE from Wave 1 (N = 699, 351 pairs, aged 12-15 years), and the Eating Disorder Examination (EDE) and Children's Anxiety Sensitivity Index (CASI) from Wave 2 (N = 669, 338 pairs, aged 16-19 years). At this time, they also completed Children's Anxiety Sensitivity Index (CASI). Bivariate Cholesky decomposition models adjusting for age and body mass index centile investigated the covariance structure between the CASI and EDE.

Modeling both genetic and nonshared environmental influences parsimoniously fit these data. All paths were significant. Additive genetic influences were notable for CASI and EDE phenotypes; 14% of the heritable variance was contributed by CASI to the expression of EDE. There was also a smaller but significant contribution of nonshared environmental influences. A multinomial logistic regression indicated body dissatisfaction (RRR = 1.53; 95% CI = 1.07-2.18) differentiated groups with highest EDE scores from the highest CASI scores.

Shared genetic and environmental influences appear to underpin the relationship, and potentially the observed comorbidity, between anxiety sensitivity and DE. The age of onset is typically earlier for anxiety than DE, suggesting a significant opportunity for early intervention work to reduce the likelihood of subsequent development of DE.

To determine whether anxiety disorders are prospectively associated with fasting for weight-loss/to avoid weight-gain, a behaviour that precedes and is typical of anorexia nervosa (AN), during adolescence.

Participants were 2,406 female adolescents of the Avon Longitudinal Study of Parents and Children. Anxiety disorders were assessed when participants were aged 13-14 and 15-16; fasting was measured approximately 2 years after each anxiety assessment. Generalised estimating equation models examined whether anxiety disorders predicted later fasting, across the two longitudinal waves of data. To probe the moderating effect of time, data were stratified by wave and binary logistic regression analyses completed.

Across longitudinal waves, anxiety disorder presence predicted increased risk of later fasting. Evidence from wave-stratified analyses supported a positive association between anxiety disorder presence at wave 15-16 and fasting at wave 17-18, however did not indicate an association between anxiety disorders at wave 13-14 and fasting at wave 15-16.

Anxiety disorder presence in mid-late, but not early, adolescence predicted increased likelihood of later fasting. The differential association could be explained by anxiety being parent-reported at wave 13-14. Findings highlight anxiety disorder pathology as a possible eating disorder prevention target, though the nature of association observed requires clarification.

To assess gender-specific genetic and environmental correlations between depressive and anxiety symptoms, and concurrent and follow-up eating behavior in Korean twins and their family members.

Center for Epidemiological Studies Depression Scale and State-Trait Anxiety Inventory were used to measure depressive and anxiety symptoms in subjects. To assess concurrent and follow-up relationships of the symptoms with eating behavior domains (restrained, emotional, and external eating), the Dutch Eating Behavior Questionnaire was administered to 2359 subjects at baseline (men, 48.5%; 42.0 ± 12.7 years; monozygotic twins, 33.7%) and to 1169 subjects at follow-up (men, 45.9%; 44.9 ± 11.6 years; monozygotic twins, 41.0%). A mixed linear model and bivariate analysis were applied.

After adjusting for age, twin and family effects, income, education, smoking status, alcohol use, exercise, and body mass index, depressive and anxiety symptoms were positively associated with concurrent and follow-up emotional and external eating, but not with restrained eating. The effect size of association with emotional eating increased in men in men over time, but decreased in women. Common genetic and environmental correlations showed a difference between genders, and their strength changed with time. Nevertheless, common genetic correlations were found between depressive and anxiety symptoms, and concurrent emotional eating, in both genders. There were common environmental correlations between anxiety symptoms, and concurrent restrained and emotional as well as follow-up emotional eating, in both genders.

There are similarities and differences in genetic and environmental relationships between depressive and anxiety symptoms and eating behaviors, based on gender and time of assessment.

Level III, cohort study.

Perfectionism is a transdiagnostic factor across eating disorders, anxiety, and depression. Previous research has shown anxiety mediates the relationship between perfectionism and eating disorders in adults. The aim of this study was to investigate the relationships between anxiety/depression, perfectionism and eating disorder symptoms in children and adolescents with eating disorders.

Structural equation modeling was used to investigate three models in a clinical sample of children and adolescents (N = 231, M age = 14.5, 100% female): (1) anxiety and depression as mediators of the relationship between perfectionism and eating disorder symptoms, (2) eating disorder symptoms as a mediator of the relationship between perfectionism and anxiety and/or depression, and (3) perfectionism as a mediator of the relationship between anxiety/depression and eating disorders.

Results indicated that both models 1 and 2 fit the data well, while model 3 provided a poor fit. These findings suggest that in clinical populations of children and adolescents, anxiety and depression mediate the relationship between perfectionism and eating disorder symptoms, and there is also a reciprocal relationship whereby eating disorders mediate the association between perfectionism, and anxiety and/or depression.

The results highlight the importance of further research to determine whether targeting perfectionism is helpful in the treatment of eating disorders and comorbid anxiety and depression in young people. It would be useful for clinicians to consider assessing for and treating perfectionism directly when it is elevated in children and adolescents with eating disorders.

This review serves as a systematic guide to the genetics of generalized anxiety disorder (GAD) and further focuses on anxiety-relevant endophenotypes, such as pathological worry fear of uncertainty, and neuroticism. We inspect clinical genetic evidence for the familialityl heritability of GAD and cross-disorder phenotypes based on family and twin studies. Recent advances of linkage studies, genome-wide association studies, and candidate gene studies (eg, 5-HTT, 5-HT1A, MAOA, BDNF) are outlined. Functional and structural neuroimaging and neurophysiological readouts relating to peripheral stress markers and psychophysiology are further integrated, building a multilevel disease framework. We explore etiologic factors in gene-environment interaction approaches investigating childhood trauma, environmental adversity, and stressful life events in relation to selected candidate genes (5-HTT, NPSR1, COMT, MAOA, CRHR1, RGS2), Additionally, the pharmacogenetics of selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor treatment are summarized (5-HTT, 5-HT2A, COMT, CRHR1). Finally, GAD and trait anxiety research challenges and perspectives in the field of genetics, including epigenetics, are discussed.

Biomarkers are defined as anatomical, biochemical or physiological traits that are specific to certain disorders or syndromes. The objective of this paper is to summarise the current knowledge of biomarkers for anxiety disorders, obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD).

Findings in biomarker research were reviewed by a task force of international experts in the field, consisting of members of the World Federation of Societies for Biological Psychiatry Task Force on Biological Markers and of the European College of Neuropsychopharmacology Anxiety Disorders Research Network.

The present article (Part I) summarises findings on potential biomarkers in neuroimaging studies, including structural brain morphology, functional magnetic resonance imaging and techniques for measuring metabolic changes, including positron emission tomography and others. Furthermore, this review reports on the clinical and molecular genetic findings of family, twin, linkage, association and genome-wide association studies. Part II of the review focuses on neurochemistry, neurophysiology and neurocognition.

Although at present, none of the putative biomarkers is sufficient and specific as a diagnostic tool, an abundance of high-quality research has accumulated that will improve our understanding of the neurobiological causes of anxiety disorders, OCD and PTSD.

Individuals with anorexia nervosa (AN) restrict eating and become emaciated. They tend to have an aversion to foods rich in fat. Because epoxide hydrolase 2 (EPHX2) was identified as a novel AN susceptibility gene, and because its protein product, soluble epoxide hydrolase (sEH), converts bioactive epoxides of polyunsaturated fatty acid (PUFA) to the corresponding diols, lipidomic and metabolomic targets of EPHX2 were assessed to evaluate the biological functions of EPHX2 and their role in AN. Epoxide substrates of sEH and associated oxylipins were measured in ill AN, recovered AN and gender- and race-matched controls. PUFA and oxylipin markers were tested as potential biomarkers for AN. Oxylipin ratios were calculated as proxy markers of in vivo sEH activity. Several free- and total PUFAs were associated with AN diagnosis and with AN recovery. AN displayed elevated n-3 PUFAs and may differ from controls in PUFA elongation and desaturation processes. Cytochrome P450 pathway oxylipins from arachidonic acid, linoleic acid, alpha-linolenic acid and docosahexaenoic acid PUFAs are associated with AN diagnosis. The diol:epoxide ratios suggest the sEH activity is higher in AN compared with controls. Multivariate analysis illustrates normalization of lipidomic profiles in recovered ANs. EPHX2 influences AN risk through in vivo interaction with dietary PUFAs. PUFA composition and concentrations as well as sEH activity may contribute to the pathogenesis and prognosis of AN. Our data support the involvement of EPHX2-associated lipidomic and oxylipin dysregulations in AN, and reveal their potential as biomarkers to assess responsiveness to future intervention or treatment.

Disordered eating is prevalent among college student populations, and Orthorexia nervosa (ON) is being explored as a new type of eating disorder. There is currently no standardized ON diagnostic tool, and the majority of ON research has been conducted among European populations. The present study explored the Bratman Orthorexia Test (BOT) for ON diagnosis, and its relationship to validated tools for assessing disordered eating, body dysmorphic, and obsessive-compulsive tendencies among college students attending a western university. A convenience sample of 448 college students with a mean age of 22 years was recruited to complete an online survey that included the BOT, Eating Attitudes Test-26 (EAT-26), Body Dysmorphic Disorder Questionnaire (BDDQ), Obsessive Compulsive Inventory, Revised (OCI-R) and demographics. Spearman correlation, Mann-Whitney U, Kruskal-Wallis, chi-square, and multiple linear regressions were used for analyses. The average BOT score was 4.71, near the "health fanatic" range, with Hispanic/Latino subjects and overweight/obese students having significantly higher median BOT scores. Gender, age, and college major were not significantly associated with BOT score. Significant positive correlations were observed between total BOT and EAT-26 scores (r = .47, p < 0.01), BOT and BDDQ scores (r = .25, p < 0.01), and BOT and OCI-R scores (r = .19, p < 0.01). ON tendencies may exist among college students and Hispanic/Latino and overweight/obese students may be at increased risk. Further research is needed to determine ON risk factors among diverse student populations in order to inform prevention and treatment approaches on college campuses.

Anxiety disorders are a category of mental disorders characterized by feelings of anxiety and fear, which include generalized anxiety disorder (GAD). Obsessive-Compulsive Disorder (OCD) used to be categorized as anxiety disorder in DSM-IV. However OCD was no longer included in anxiety disorders and came into its own category titled as Obsessive-Compulsive and Related Disorders (OCRD) in DSM-5. It will be interesting to explore is there any different biological characteristics between OCD and anxiety disorders. Brain-derived neurotrophic factor (BDNF) was a potential candidate gene in both OCD and GAD. The results of genetic association studies between BDNF and OCD have been inconsistent. BDNF plasma/serum levels in OCD have been found lower than those in healthy controls. However the heritable reason of the lowered BDNF levels was not well elucidated. The amount of studies about BDNF and GAD were relatively small. The aims of this study were to determine whether single nucleotide polymorphism Val66Met of BDNF was associated with OCD and GAD, to examine BDNF plasma levels in OCD and GAD, and to explore whether Val66Met variation influences BDNF plasma levels.

We genotyped Val66Met variation in 148 OCD patients, 108 GAD patients and 99 healthy controls. Within the same sample, BDNF plasma levels were determined in 113 OCD patients, 102 GAD patients and 63 healthy controls.

Val66Met variation was not associated with OCD or GAD. BDNF plasma levels in OCD and GAD patients were significant lower than those in healthy controls. Val66Met variation had no influence on BDNF plasma levels. No difference was found between OCD and GAD. Results do not change no matter taking OCD and GAD as one group or separated two.

First, the sample size for genotyping was relatively small, which leaded to a low statistical power of the genetic part in this study. Second, we genotyped just one SNP in BDNF gene. Third, parts of the participants did not be assayed for BDNF plasma levels.

Our findings support the hypothesis that BDNF is involved in the pathophysiology of mental disorders, not only OCD but also GAD. OCD and GAD patients both show lower BDNF plasma levels compared to healthy controls. The BDNF plasma levels are not associated with Val66Met variation.

The heritability of eating disorders has been estimated to range from 22% to over 62%.The aim of this study is to determine the relative influence of genetics and environment that contribute to the drive for thinness, body dissatisfaction, perfectionism, and ineffectiveness, by evaluating sex differences in a sample of adolescent twins from Valencia, Spain.

Five hundred eighty-four pairs of adolescent twins between 13 and 18 years of age completed the study. To determine zygosity, teachers responded to a questionnaire on physical similarity. Psychological traits of eating disorders were assessed with four sub-scales of the Eating Disorder Inventory (EDI); drive for thinness, body dissatisfaction, perfectionism, and ineffectiveness. Twin models were used to assess genetic and environmental (common and unique) factors affecting these four psychological traits.

All four traits showed significant genetic contributions among girls, with heritability estimates of 37.7% for ineffectiveness, 42.8% for perfectionism, 56.9% for drive for thinness, and 65.5% for body dissatisfaction. Among boys, body dissatisfaction showed no additive genetic contributions, indicating significant shared and individual specific environment effects. The three other traits in boys showed significant additive genetic contributions, but were lower than in girls.

With the exception of body dissatisfaction in boys, psychological traits of eating disorders show heritability patterns that differ according to sex.

Anorexia nervosa is a serious psychiatric disorder characterized by restricted eating, a pursuit of thinness, and altered perceptions of body shape and size. Neuroimaging in anorexia nervosa has revealed morphological and functional alterations in the brain. A better understanding of physiological changes in anorexia nervosa could provide a brain-specific health marker relevant to treatment and outcomes. In this study, we applied several advanced magnetic resonance imaging (MRI) techniques to quantify regional and global cerebral blood flow (CBF) in 25 healthy women (HC), 23 patients currently with anorexia (AN-C) and 19 patients in long-term weight recovery following anorexia (AN-WR). Specifically, CBF was measured with pseudo-continuous arterial spin labeling (pCASL) MRI and then verified by a different technique, phase contrast (PC) MRI. Venous T2 values were determined by T2 relaxation under spin tagging (TRUST) MRI, and were used to corroborate the CBF results. These novel techniques were implemented on a standard 3T MRI scanner without any exogenous tracers, and the total scan duration was less than 10min. Voxel-wise comparison revealed that the AN-WR group showed lower CBF in bilateral temporal and frontal lobes than the AN-C group. Compared with the HC group, the AN-C group also showed higher CBF in the right temporal lobe. Whole-brain-averaged CBF was significantly decreased in the AN-WR group compared with the AN-C group, consistent with the PC-MRI results. Venous T2 values were lower in the AN-WR group than in the AN-C group, consistent with the CBF results. A review of prior work examining CBF in anorexia nervosa is included in the discussion. This study identifies several differences in the cerebral physiological alterations in anorexia nervosa, and finds specific differences relevant to the current state of the disorder.

To depict the processes through which animals and human beings engage their environment in continuously evolving states of conflict and cooperation.

Descriptive literature review.

Life history outcomes are more relative than they are absolute. Genetic variations play a crucial role, but heavily influencing behavioral outcomes, psychopathology included, are external cues that epigenetically remodel DNA along experience-dependent signaling pathways. The result is phenotypes that either optimize adjustment, or constrain it.

Knowledge of epigenetic mechanisms may help shed new light on the origin of maturational phenotypes underlying eating disorders and why adjusting treatments to these realities warrants our attention.

Over the past century, the definition and classification of psychiatric disorders has evolved through a combination of historical trends, clinical observations, and empirical research. The current nosology, instantiated in the DSM-5 and ICD-10, rests on descriptive criteria agreed upon by a consensus of experts. While the development of explicit criteria has enhanced the reliability of diagnosis, the validity of the current diagnostic categories has been the subject of debate and controversy. Genetic studies have long been regarded as a key resource for validating the boundaries among diagnostic categories. Genetic epidemiologic studies have documented the familiality and heritability of clinically defined psychiatric disorders and molecular genetic studies have begun to identify specific susceptibility variants. At the same time, there is growing evidence from family, twin and genomic studies that genetic influences on psychiatric disorders transcend clinical boundaries. Here I review this evidence for cross-disorder genetic effects and discuss the implications of these findings for psychiatric nosology. Psychiatric genetic research can inform a bottom-up reappraisal of psychopathology that may help the field move beyond a purely descriptive classification and toward an etiology-based nosology.

Previous studies examined caffeine use and caffeine dependence and risk for the symptoms, or diagnosis, of psychiatric disorders. The current study aimed to determine if generalized anxiety disorder (GAD), panic disorder, phobias, major depressive disorder (MDD), anorexia nervosa (AN), or bulimia nervosa (BN) shared common genetic or environmental factors with caffeine use, caffeine tolerance, or caffeine withdrawal.

Using 2,270 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, bivariate Cholesky decomposition models were used to determine if any of the psychiatric disorders shared genetic or environmental factors with caffeine use phenotypes.

GAD, phobias, and MDD shared genetic factors with caffeine use, with genetic correlations estimated to be 0.48, 0.25, and 0.38, respectively. Removal of the shared genetic and environmental parameter for phobias and caffeine use resulted in a significantly worse fitting model. MDD shared unique environmental factors (environmental correlation=0.23) with caffeine tolerance; the genetic correlation between AN and caffeine tolerance and BN and caffeine tolerance were 0.64 and 0.49, respectively. Removal of the genetic and environmental correlation parameters resulted in significantly worse fitting models for GAD, phobias, MDD, AN, and BN, which suggested that there was significant shared liability between each of these phenotypes and caffeine tolerance. GAD had modest genetic correlations with caffeine tolerance, 0.24, and caffeine withdrawal, 0.35.

There was suggestive evidence of shared genetic and environmental liability between psychiatric disorders and caffeine phenotypes. This might inform us about the etiology of the comorbidity between these phenotypes.