Worse glycemic control, higher rates of diabetic ketoacidosis, and more hospitalizations in children, adolescents, and young adults with type 1 diabetes and anxiety disorders.

The aim of the study was to explore the metabolic characteristics and outcome parameters in youth with type 1 diabetes and anxiety disorders. HbA1c levels, rates of severe hypoglycemia, diabetic ketoacidosis (DKA), and hospital admission in children, adolescents, and young adults with type 1 diabetes and an anxiety disorder from 431 diabetes-care-centers participating in the nationwide German/Austrian/Swiss/Luxembourgian diabetes survey DPV were analyzed and compared with youth without anxiety disorders. Children, adolescents, and young adults with type 1 diabetes and anxiety disorders (n = 1325) had significantly higher HbA1c (8.5% vs. 8.2%), higher rates of DKA (4.2 vs. 2.5 per 100 patient-years), and higher hospital admission rates (63.6 vs. 40.0 per 100 patient-years) than youth without anxiety disorders (all p < 0.001). Rates of severe hypoglycemia did not differ. Individuals with anxiety disorders other than needle phobia (n = 771) had higher rates of DKA compared to those without anxiety disorders (4.2 vs. 2.5 per 100 patient-years, p = 0.003) whereas the rate of DKA in individuals with needle phobia (n = 555) was not significantly different compared to those without anxiety disorders. Children, adolescents, and young adults with anxiety disorders other than needle phobia had higher hospitalization rates (73.7 vs. 51.4 per 100 patient-years) and more inpatient days (13.2 vs. 10.1 days) compared to those with needle phobia (all p < 0.001). Children, adolescents, and young adults with type 1 diabetes and anxiety disorders had worse glycemic control, higher rates of DKA, and more hospitalizations compared to those without anxiety disorders. Because of the considerable consequences, clinicians should screen for comorbid anxiety disorders in youth with type 1 diabetes.

Fear of cancer recurrence among breast cancer survivors could be controlled by prudent dietary modification with polyunsaturated fatty acids.

BACKGROUND: The pathophysiology of fear of cancer recurrence (FCR), the leading unmet psychological need of cancer survivors, may involve the dysfunctional processing of fear memory. n-3 polyunsaturated fatty acids (PUFAs) have beneficial effects on psychiatric disorders, including depressive disorder and anxiety disorders, and are involved in fear memory processing. We hypothesized that n-3 PUFA composition is associated with FCR in cancer survivors. METHODS: We conducted a cross-sectional study to examine the relationship between n-3 PUFAs and FCR among breast cancer survivors. Adults who had been diagnosed with invasive breast cancer and were not undergoing chemotherapy were asked to participate. Blood PUFA composition was evaluated by using capillary blood. We directly administered the Concerns About Recurrence Scale (CARS) to assess the grade of FCR. RESULTS: Among 126 participants used for the analysis, the mean age (SD) was 58 (11) years and 47% had stage I cancer. Multiple regression analysis controlling for possible confounders, depressive symptoms, and post-traumatic stress disorder (PTSD) symptoms revealed that the alpha-linolenic acid (ALA) level was significantly inversely associated with the average score on the CARS overall fear index (beta = -0.165, p = 0.04). No significant associations were found for other PUFAs. LIMITATIONS: Our findings were obtained from a cross-sectional study in a single institute. CONCLUSION: These findings provide the first evidence of a beneficial effect of ALA on FCR and indicate the need for prospective study of this association. FCR among breast cancer survivors might be controllable by prudent selection of ALA-containing cooking oil.

Graduated exposure to treat fear of hypoglycemia in a young adult with type 1 diabetes: A case study.

Hypoglycemia is a common and dangerous complication of type 1 diabetes (T1D). Although some worry about hypoglycemia is adaptive, some individuals develop severe and impairing anxiety symptoms about hypoglycemic episodes. This presentation, known as severe fear of hypoglycemia (FOH), is similar to a specific phobia, and becomes problematic when it interferes with one's quality of life or T1D management. Although FOH is common, there have not yet been any treatment studies to address severe and impairing levels of FOH in the T1D population. The purpose of the following case report is to: (a) describe the presentation of a severe case of FOH in a young adult with T1D; (b) demonstrate the effectiveness of graduated exposure therapy for treatment of severe FOH; and (c) provide implications for clinical practice. A previously developed conceptual model for FOH management guided treatment. Treatment using graduated exposure therapy for FOH resulted in reduced worry about low blood glucose (BG) and significant reduction in behaviors to maintain high BG levels. Assessment of FOH and the risk and benefits of using a continuous glucose monitor among individuals with T1D and their families are discussed.

Prospective association of depression and phobic anxiety with changes in telomere lengths over 11 years.

BACKGROUND: Although depression and anxiety have been associated with shorter telomeres in cross-sectional studies, the data regarding the prospective relations of depression and anxiety to accelerated telomere length shortening are limited and findings are mixed. We prospectively examined relations of baseline depression and phobic anxiety to subsequent 11-year change in relative leukocyte telomere lengths (LTLs). METHODS: We selected 1,250 women from a subcohort of the Nurses' Health Study who provided blood specimens at both blood collections (1989-1990 and 2000-2001). Depression was defined by self-reported regular antidepressant use or presence of severe depressive symptoms; anxiety symptoms were assessed using the Crown-Crisp Experiential Index. Using quantitative real-time polymerase chain reaction assay, LTLs were measured as the copy number ratio of telomere repeat to a single control gene. Changes in LTLs were defined in three ways: absolute change, symmetrized percent change, and decile shift. RESULTS: Overall, there were no statistically significant associations of depression or phobic anxiety to subsequent 11-year LTL shortening, despite a point estimates in the direction of greater telomere shortening among participants with versus without depression, across all three metrics of telomere change. The strongest predictor of LTL change was baseline telomere length, and regression-to-the-mean was observed. CONCLUSION: Baseline depression and phobic anxiety were not significantly associated with 11-year attrition in LTLs among 1,250 mid-life and older women. However, a suggestion of depression and greater subsequent LTL attrition, while not statistically significant, may warrant further inquiry, particularly in prospective studies with larger sample sizes and broader windows of the lifespan.

Associations between severity of anxiety and clinical and biological features of major affective disorders.

Patients with major affective disorders (MAFD) with comorbid anxiety show a greater functional impairment than those without anxiety. The aim of this study is to delineate the associations between severity of anxiety in MAFD, namely bipolar disorder (BD) and major depression (MDD), and MAFD characteristics and serum high-density lipoprotein (HDL)-cholesterol levels. Recruited were 82 participants with anxiety disoders and 83 without anxiety disoders, including 101 MAFD patients and 51 healthy controls. We used the Hamilton Anxiety Rating Scale (HAM-A) to measure severity of anxiety and made the diagnoses of posttraumatic stress disorder (PTSD), obsessive compulsive disorder (OCD), panic disorder (PD), generalized anxiety disorder (GAD) and phobias. The HAM-A score is significantly predicted by higher number of depressive episodes, GAD and phobias, childhood trauma, tobacco use disorder, metabolic syndrome and lowered HDL-cholesterol. Increased HAM-A scores are, independently from severity of depression, associated with lowered quality of life, increased disabilities and suicidal ideation. Lithium treatment significantly lowers HAM-A scores. It is concluded that severity of anxiety significantly worsens the phenomenology of MAFD. Therefore, treatments of MAFD should target increased severity of anxiety and its risk factors including low HDL-cholesterol, metabolic syndrome, childhood trauma and tobacco use disorder.

Reactivity to 35% carbon dioxide in bulimia nervosa and panic disorder.

The inhalation of 35% carbon dioxide (CO2) induces panic and anxiety in people with panic disorder (PD) and in people with various other psychiatric disorders. The anxiogenic effect of CO2 in people with eating disorders has received sparse attention despite the fact that PD and bulimia nervosa (BN) have several common psychological and neurobiological features. This study compared CO2-reactivity across three groups of participants: females with BN, females with PD, and female controls without known risk factors for enhanced CO2-reactivity (e.g., social anxiety disorder, first degree relatives with PD). Reactivity was measured by self-reported ratings of panic symptomatology and subjective anxiety, analyzed as both continuous variables (change from room-air to CO2) and dichotomous variables (positive versus negative responses to CO2). Analyses of each outcome measure demonstrated that CO2-reactivity was similar across the BN and PD groups, and reactivity within each of these two groups was significantly stronger than that in the control group. This is the first study to demonstrate CO2-hyperreactivity in individuals with BN, supporting the hypothesis that reactivity to this biological paradigm is not specific to PD. Further research would benefit from examining transdiagnostic mechanisms in CO2-hyperreactivity, such as anxiety sensitivity, which may account for this study's results.

Discovery of serum biomarkers predicting development of a subsequent depressive episode in social anxiety disorder.

Although social anxiety disorder (SAD) is strongly associated with the subsequent development of a depressive disorder (major depressive disorder or dysthymia), no underlying biological risk factors are known. We aimed to identify biomarkers which predict depressive episodes in SAD patients over a 2-year follow-up period. One hundred sixty-five multiplexed immunoassay analytes were investigated in blood serum of 143 SAD patients without co-morbid depressive disorders, recruited within the Netherlands Study of Depression and Anxiety (NESDA). Predictive performance of identified biomarkers, clinical variables and self-report inventories was assessed using receiver operating characteristics curves (ROC) and represented by the area under the ROC curve (AUC). Stepwise logistic regression resulted in the selection of four serum analytes (AXL receptor tyrosine kinase, vascular cell adhesion molecule 1, vitronectin, collagen IV) and four additional variables (Inventory of Depressive Symptomatology, Beck Anxiety Inventory somatic subscale, depressive disorder lifetime diagnosis, BMI) as optimal set of patient parameters. When combined, an AUC of 0.86 was achieved for the identification of SAD individuals who later developed a depressive disorder. Throughout our analyses, biomarkers yielded superior discriminative performance compared to clinical variables and self-report inventories alone. We report the discovery of a serum marker panel with good predictive performance to identify SAD individuals prone to develop subsequent depressive episodes in a naturalistic cohort design. Furthermore, we emphasise the importance to combine biological markers, clinical variables and self-report inventories for disease course predictions in psychiatry. Following replication in independent cohorts, validated biomarkers could help to identify SAD patients at risk of developing a depressive disorder, thus facilitating early intervention.

Do genetic risk scores for body mass index predict risk of phobic anxiety? Evidence for a shared genetic risk factor.

BACKGROUND: Obesity and anxiety are often linked but the direction of effects is not clear. METHOD: Using genetic instrumental variable (IV) analyses in 5911 female participants from the Nurses' Health Study (NHS, initiated 1976) and 3697 male participants from the Health Professional Follow-up Study (HPFS, initiated 1986), we aimed to determine whether obesity increases symptoms of phobic anxiety. As instrumental variables we used the fat mass and obesity-associated (FTO) gene, the melanocortin 4 receptor (MC4R) gene and a genetic risk score (GRS) based on 32 single nucleotide polymorphisms (SNPs) that significantly predict body mass index (BMI). 'Functional' GRSs corresponding with specific biological pathways that shape BMI (adipogenesis, appetite and cardiopulmonary) were considered. The main outcome was phobic anxiety measured by the Crown Crisp Index (CCI) in 2004 in the NHS and in 2000 in the HPFS. RESULTS: In observational analysis, a 1-unit higher BMI was associated with higher phobic anxiety symptoms [women: ß = 0.05, 95% confidence interval (CI) 0.030-0.068; men: ß = 0.04, 95% CI 0.016-0.071). IV analyses showed that BMI was associated with higher phobic anxiety symptoms in the FTO-instrumented analysis (p = 0.005) but not in the GRS-instrumented analysis (p = 0.256). Functional GRSs showed heterogeneous, non-significant effects of BMI on phobic anxiety symptoms. CONCLUSIONS: Our findings do not provide conclusive evidence in favor of the hypothesis that higher BMI leads to higher levels of phobic anxiety, but rather suggest that genes that influence obesity, in particular FTO, may have direct effects on phobic anxiety, and hence that obesity and phobic anxiety may share common genetic determinants.

The reaction to social stress in social phobia: discordance between physiological and subjective parameters.

BACKGROUND: Research on the biopsychological background of social phobia (SP) is scarce and inconsistent. We investigated endocrine and autonomic markers along with subjective responses to a standardized stress situation (Trier Social Stress Test, TSST) in SP patients and healthy controls (HC). METHODS: We examined 88 patients with the primary diagnosis of SP as well as 78 age and sex comparable HCs with the TSST. Blood and saliva samples were obtained before and after the TSST for the assessment of salivary cortisol, plasma cortisol, salivary alpha-amylase (sAA), and prolactin. Heart rate (HR) and heart rate variability (HRV) were recorded continuously. Scalp-near hair samples were collected for the assessment of long-term cortisol secretion. The self-reported stress response was measured with different state and trait scales. RESULTS: While self-reported anxiety was elevated in SP before, during, immediately after, and one week after the TSST, no significant differences in biological stress responses were observed between SP and HC. There was a trend for SP to show higher baseline stress markers. Also long-term cortisol deposition in hair remained unaltered. CONCLUSIONS: Our results suggest that the excessive self-reported stress in SP is not reflected by a respective biological stress response. Patients with SP apparently show neither an extreme form of focused fear reactivity nor excessive defensive impairment.

Endogenous cortisol levels influence exposure therapy in spider phobia.

Previous research in patients with phobia showed that the administration of glucocorticoids reduces fear in phobic situations and enhances exposure therapy. Glucocorticoids underlie a daily cycle with a peak in the morning and low levels during the evening and night. The aim of the present study was to investigate whether exposure is more effective when conducted in the morning when endogenous cortisol levels are high. Sixty patients meeting DSM IV criteria for specific phobia (animal type) were randomly assigned to one-session exposure treatment either at 08.00 a.m. (high cortisol group) or at 06.00 p.m. (low cortisol group). Participants returned for a posttreatment assessment one week after therapy and a follow-up assessment three months after therapy. Both groups showed good outcome, but patients treated in the morning exhibited significantly less fear of spiders in the behavioral approach test (BAT) and a trend for lower scores on the Fear of Spiders Questionnaire (FSQ) than patients treated in the evening. This effect was present at posttreatment and follow-up. Our findings indicate that exposure therapy is more effective in the morning than in the evening. We suggest that this may be due to higher endogenous cortisol levels in the morning group that enhance extinction memory.

Glucocorticoids enhance in vivo exposure-based therapy of spider phobia.

BACKGROUND: Preclinical and clinical studies indicate that the administration of glucocorticoids may promote fear extinction processes. In particular, it has been shown that glucocorticoids enhance virtual reality based exposure therapy of fear of heights. Here, we investigate whether glucocorticoids enhance the outcome of in vivo exposure-based group therapy of spider phobia. METHODS: In a double blind, block-randomized, placebo-controlled, between-subject study design, 22 patients with specific phobia of spiders were treated with two sessions of in vivo exposure-based group therapy. Cortisol (20 mg) or placebo was orally administered 1 hr before each therapy session. Patients returned for a follow-up assessment one month after therapy. RESULTS: Exposure-based group therapy led to a significant decrease in phobic symptoms as assessed with the Fear of Spiders Questionnaire (FSQ) from pretreatment to immediate posttreatment and to follow-up. The administration of cortisol to exposure therapy resulted in increased salivary cortisol concentrations and a significantly greater reduction in fear of spiders (FSQ) as compared to placebo at follow-up, but not immediately posttreatment. Furthermore, cortisol-treated patients reported significantly less anxiety during standardized exposure to living spiders at follow-up than placebo-treated subjects. Notably, groups did not differ in phobia-unrelated state-anxiety before and after the exposure sessions and at follow-up. CONCLUSIONS: These findings indicate that adding cortisol to in vivo exposure-based group therapy of spider phobia enhances treatment outcome.

Functional effects of chronic paroxetine versus placebo on the fear, stress and anxiety brain circuit in Social Anxiety Disorder: initial validation of an imaging protocol for drug discovery.

Recent studies suggest that pharmacologic effects of anxiolytic agents can be mapped as functional changes in the fear, stress and anxiety brain circuit. In this work we investigated the effects of a standard treatment, paroxetine (20mg/day), in subjects with Social Anxiety Disorder (SAD) versus placebo using different fMRI paradigms. The fMRI sessions, performed before and after the treatment, consisted of a public exposition of recorded performance task (PERPT), an emotional face processing task (EFPT) and a 6-min resting state followed by an off-scanner public speaking test. Paroxetine significantly improved the clinical conditions of SAD patients (n=17) vs. placebo (n=16) as measured with Clinical Global Inventory - Improvement (CGI-I) while no change was seen when using Liebowitz Social Anxiety Scale, as expected given the small size of the study population. Paroxetine reduced the activation of insula, thalamus and subgenual/anterior cingulate cortex (ACC) in PERPT. Resting-state fMRI assessment using Independent Component Analysis indicated that paroxetine reduced functional connectivity in insula, thalamus and ACC when compared with placebo. Both paradigms showed significant correlation with CGI-I in rostral prefrontal cortex. Conversely, paroxetine compared to placebo produced activation of right amygdala and bilateral insula and no effects in ACC when tested with EFPT. No treatment effects on distress scores were observed in the off-scanner Public Speaking Test. Overall this study supports the use of fMRI as sensitive approach to explore the neurobiological substrate of the effects of pharmacologic treatments and, in particular, of resting state fMRI given its simplicity and task independence.

Anxiety disorders and inflammation in a large adult cohort.

Although anxiety disorders, like depression, are increasingly being associated with metabolic and cardiovascular burden, in contrast with depression, the role of inflammation in anxiety has sparsely been examined. This large cohort study examines the association between anxiety disorders and anxiety characteristics with several inflammatory markers. For this purpose, persons (18-65 years) with a current (N=1273) or remitted (N=459) anxiety disorder (generalized anxiety disorder, social phobia, panic disorder, agoraphobia) according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and healthy controls (N=556) were selected from the Netherlands Study of Depression and Anxiety. In addition, severity, duration, age of onset, anxiety subtype and co-morbid depression were assessed. Inflammatory markers included C-reactive protein (CRP), interleukin (IL)-6 and tumor-necrosis factor (TNF)-α. Results show that after adjustment for sociodemographics, lifestyle and disease, elevated levels of CRP were found in men, but not in women, with a current anxiety disorder compared with controls (1.18 (s.e.=1.05) versus 0.98 (s.e.=1.07) mg l(-1), P=0.04, Cohen's d=0.18). No associations were found with IL-6 or TNF-α. Among persons with a current anxiety disorder, those with social phobia, in particular women, had lower levels of CRP and IL-6, whereas highest CRP levels were found in those with an older age of anxiety disorder onset. Especially in persons with an age of onset after 50 years, CRP levels were increased compared with controls (1.95 (s.e.=1.18) versus 1.27 (s.e.=1.05) mg l(-1), P=0.01, Cohen's d=0.37). In conclusion, elevated inflammation is present in men with current anxiety disorders. Immune dysregulation is especially found in persons with a late-onset anxiety disorder, suggesting the existence of a specific late-onset anxiety subtype with a distinct etiology, which could possibly benefit from alternative treatments.

Brain-derived neurotrophic factor in generalized anxiety disorder: results from a duloxetine clinical trial.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of depression and anxiety, but has not been examined systematically in generalized anxiety disorder (GAD). The objective of this study was to examine the relationship between baseline BDNF level and treatment response in patients with GAD. METHODS: Patients (N=168) were from China, met criteria for DSM-IV GAD, had a Hospital Anxiety and Depression Rating Anxiety (HADS-A) subscale score ≥10, and a Sheehan Disability Scale (SDS) global functioning total score ≥12 at baseline. Study design was double-blind therapy for 15 weeks with duloxetine 60-120 mg or placebo. Efficacy measures included the HADS-A and Hamilton Anxiety Rating Scale (HAMA) total score. Change from baseline to endpoint for BDNF by treatment group was analyzed using ANCOVA models with baseline BDNF level as a covariate. RESULTS: No significant association was found between baseline plasma BDNF levels and anxiety illness severity. Patients who received duloxetine (n=88) had a significantly greater mean increase in plasma BDNF level (957.80 picograms/ml) compared with patients who received placebo (n=80; 469.93 pg/mL) (P=.007). Patients who met response and remission criteria (with either treatment) had greater mean increases in BDNF at endpoint from baseline (P≤.05) but when compared with nonresponders and nonremitters, respectively, the differences in mean increase were not statistically significant between groups. CONCLUSIONS: BDNF levels significantly increased with duloxetine treatment for GAD, but response and remission outcomes were not clearly related to an increase in plasma BDNF level.

Internal sensations as a source of fear: exploring a link between hypoxia and flight phobia.

Although flight phobia is very common in the general population, knowledge of the underlying mechanisms is limited. The aim of the current study is to determine whether hypoxia is selectively associated with flight anxiety. We wanted to explore levels of oxygen saturation (SpO2) and the associated subjective somatic sensations in flight phobics and controls. The data collected in this study were obtained from 103 participants: 54 had flight phobia, 49 were controls. SpO2 as well as a subjective report of somatic sensations and anxiety were measured during short haul flights, both at ground level and at cruising altitude. Results indicated that both flight phobics and controls showed a comparable clinical significant decrease in SpO2 from sea level to cruising altitude. Next, at ground level the flight phobic group reported more somatic sensations, most likely due to the elevated levels of anxiety at that point. However, at cruising altitude the flight phobic group still reported more somatic sensations while the level of anxiety was no longer significantly different from controls. This finding points to altered symptom perception in flight phobia and stresses the importance of somatic sensations in this particular phobia.

[The prognostic significance of brain-derived neurotrophic factor (BDNF) for phobic anxiety disorders, vegetative and cognitive impairments during conservative treatment including adaptol of some functional and organic diseases of nervous system].

We have studied the efficacy of adaptol in the treatment of 45 patients with somatoform dysfunction of the autonomic nervous system and 30 patients with closed head injury. The condition of patients during the treatment was evaluated with clinical and neuropsychological scales. The serum level of BDNF before and after the treatment has been studied as well. Adaptol has been shown to enhance the production of BDNF, reduce significantly the intensity of anxiety, autonomic disorders and improve intellectual processes. The dose-dependent effect of the drug has been demonstrated. In conclusion, adaptol can be recommended for treatment of diseases that demand stimulation of neuroplasticity in the CNS.

Salivary cortisol in pregnant women suffering from blood and injection phobia.

Stress and/or anxiety during pregnancy affect maternal and fetal well-being and can cause premature delivery and postnatal pathology in the child. Women suffering from phobias related to blood and injections are prone to high levels of stress, including anxiety and sometimes panic attacks, during pregnancy. Cortisol is amongst the mediators through which the neurohormonal expressions of maternal psychological factors may be transduced to the fetus. The aim of this study was to investigate whether pregnant women suffering from blood and injection phobia have raised cortisol levels or are characterized by unusual diurnal salivary cortisol profiles compared with healthy controls. The sample consisted of 110 pregnant women with blood and injection phobia and 110 pregnant healthy controls. Both groups provided morning and evening saliva samples in weeks 25 and 36 for the assay of cortisol. In gestational week 25, when blood was drawn for the mandatory blood testing, extra blood was taken to analyze corticotrophin-releasing factor, adrenocorticotropic hormone, and cortisol in serum. The diurnal decline in salivary cortisol as well as increased cortisol levels were observed during pregnancy. Pregnant women suffering from blood and injection phobia had a higher output of cortisol compared with women without the phobia (F = 6.25, df = 1, p = 0.014), but no marked difference in the diurnal cortisol rhythm was found between groups. Our findings indicate that untreated blood and injection phobia during pregnancy increases cortisol concentrations. Blood and injection phobia is treatable, and cognitive behavioral therapy can be used. Women with blood and injection phobia during pregnancy therefore need to be recognized and offered treatment without delay in early pregnancy.

Co-involvement of psychological and neurological abnormalities in infertility with polycystic ovarian syndrome.

OBJECTIVE: To investigate psychological distress, serum levels of monoamine neurotransmitters and their metabolites, as well as their correlation with polycystic ovarian syndrome (PCOS). METHODS: Thirty infertility patients with PCOS were assigned as the experimental group and 30 infertility patients without PCOS were assigned as the control group. Psychological distress was self-evaluated in all patients with Symptom Checklist 90 (SCL-90). Serum concentrations of norepinephrine (NE) and its metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA) and its metabolites homovanillic acid (HVA) and dihydroxy-phenyl acetic acid (DOPAC) were measured by high-performance liquid chromatography. RESULTS: The anxious and depressive subscales of SCL-90 were significantly higher in infertility patients with PCOS than those without PCOS (p < 0.05). The serum concentrations of 5-HT, 5-HIAA and HVA were significantly lower in infertility patients with PCOS than those without PCOS (p < 0.05). Importantly, the phobia subscale scores of SCL-90 positively correlated with serum MHPG level (p < 0.05), while the hostility subscale's scores negatively correlated with serum DOPAC level (p < 0.05). CONCLUSION: Psychological and neurological factors play a crucial role in PCOS.

The endocrinology of exclusion: rejection elicits motivationally tuned changes in progesterone.

Social exclusion can have profound effects on a vast array of motivated psychological processes, from social withdrawal and aggression to prosocial behavior and social affiliation. The current studies examined motivationally tuned endocrinological consequences of exclusion by measuring the release of progesterone, a hormone that reflects an individual's level of social-affiliative motivation. Results from two experiments indicate that release of progesterone following social exclusion depends on people's levels of social anxiety and rejection sensitivity. Individuals high in social anxiety displayed a drop in progesterone in response to exclusion, a pattern consistent with a lack of affiliative motivation. In contrast, individuals high in rejection sensitivity displayed an increase in progesterone when given an opportunity to reaffiliate, a change consistent with a desire for compensatory social contact. These findings provide new insight into the immediate biological changes precipitated by social exclusion--changes that could initiate a range of motivated social responses.

Phobic anxiety is associated with higher serum concentrations of adipokines and cytokines in women with diabetes.

OBJECTIVE: Phobic anxiety has been associated with increased risk of cardiovascular disease (CVD), but the underlying mechanisms are poorly understood. We aimed to determine whether associations of phobic anxiety with several known markers of CVD might be contributors. RESEARCH DESIGN AND METHODS: We used a 16-point validated index (Crown-Crisp) measured in 1988 to categorize 984 women with type 2 diabetes from the Nurses' Health Study as having low, moderate, or high phobic anxiety. Groups were then compared for differences in adipokines (adiponectin and leptin), inflammatory markers (C-reactive protein and tumor necrosis factor [TNF]-alpha receptor II), and markers of endothelial function (sE-selectin, soluble intercellular adhesion molecule [sICAM]-1) measured on blood samples provided between 1989 and 1990. RESULTS: Higher levels of phobic anxiety were associated with higher BMI and lower education. Higher levels of phobic anxiety were also associated with higher leptin and soluble TNF-alpha receptor II in both crude analyses and after adjustment for potential confounders. sICAM and sE-selectin were higher in the highest tertile compared with the middle tertile, but there was no significant trend across tertiles. We found no association between phobic anxiety and adiponectin. CONCLUSIONS: High levels of phobic anxiety are associated with increased levels of leptin and inflammatory markers, which may in part explain the previously observed relationship between anxiety and other psychosocial disorders with CVD.