Investigation of the relationships between eating attitudes, body image and depression among Turkish university students.

INTRODUCTION: Eating disorders are one of the most prevalent psychiatric disorders and have become a growing problem nowadays. Research shows that eating disorders are mostly widespread in industrialized societies where beauty is associated with thinness. This study investigates the relationships between eating attitudes, body image and depression among Turkish university students aged 18 to 25. MATERIALS AND METHODS: The sample comprised of 221 female and 80 male university students from four different universities located in Istanbul and Ankara. Demographic Information Form, Body Image Scale, Eating Attitude Test (EAT-40) and Beck Depression Inventory were used to collect data. Height and weight of the participants were also collected to measure Body Mass Index (BMI) of the individuals. RESULTS: This study found that 55 (18.3%) students had abnormal eating attitudes, 115 (38.2%) students had negative body image and 102 (33.9%) students showed moderate and severe levels of depression. Body image was negatively correlated with eating attitude and depression in underweight individuals when grouped according to their BMI. Being underweight was significantly higher in females. Females also had more negative body image and higher depression levels. Individuals with abnormal eating attitudes had higher depression levels. BMI and gender did not lead to any significant difference in the eating attitudes of the students. CONCLUSION: This study has contributed to the literature on the relationships between eating attitudes, body image and depression among Turkish university students between the ages of 18 and 25. It has further drawn attention to the importance of eating disorders in Turkey and being aware of the relationships among eating attitudes, body image, depression, and BMI. Results of the study are discussed in detail and in consideration of cultural context.

Aminoacyl-tRNA synthetase deficiencies in search of common themes.

PURPOSE: Pathogenic variations in genes encoding aminoacyl-tRNA synthetases (ARSs) are increasingly associated with human disease. Clinical features of autosomal recessive ARS deficiencies appear very diverse and without apparent logic. We searched for common clinical patterns to improve disease recognition, insight into pathophysiology, and clinical care. METHODS: Symptoms were analyzed in all patients with recessive ARS deficiencies reported in literature, supplemented with unreported patients evaluated in our hospital. RESULTS: In literature, we identified 107 patients with AARS, DARS, GARS, HARS, IARS, KARS, LARS, MARS, RARS, SARS, VARS, YARS, and QARS deficiencies. Common symptoms (defined as present in ≥4/13 ARS deficiencies) included abnormalities of the central nervous system and/or senses (13/13), failure to thrive, gastrointestinal symptoms, dysmaturity, liver disease, and facial dysmorphisms. Deep phenotyping of 5 additional patients with unreported compound heterozygous pathogenic variations in IARS, LARS, KARS, and QARS extended the common phenotype with lung disease, hypoalbuminemia, anemia, and renal tubulopathy. CONCLUSION: We propose a common clinical phenotype for recessive ARS deficiencies, resulting from insufficient aminoacylation activity to meet translational demand in specific organs or periods of life. Assuming residual ARS activity, adequate protein/amino acid supply seems essential instead of the traditional replacement of protein by glucose in patients with metabolic diseases.

Investigation of differential HDAC4 methylation patterns in eating disorders.

The objective of this study was to investigate the relationship between methylation patterns of the histone deacetylase 4 gene and eating disorders in a site previously associated with anorexia nervosa (AN). Women with AN (N=28) or bulimia nervosa (BN) (N=19) were age-matched and sex-matched to controls (N=45). We obtained saliva-derived DNA and use bisulfite pyrosequencing to examine region-specific methylation differences between cases and controls. The region assayed includes 15 CpGs. We found no significant association between the previously implicated CpG and either AN or BN. We found that three CpGs were nominally associated with AN (P=0.02-0.03); the largest difference was a 9% hypermethylation in AN. One CpG was nominally associated with BN (P=0.04), with 4% hypomethylation. None of these results remained significant after correction for multiple testing. We did not replicate previous findings, though through expanded coverage, we identified additional CpGs that were nominally associated with eating disorders.

Catechol-O-methyltransferase activity in erythrocytes from patients with eating disorders.

PURPOSE: Abnormal feeding has been linked to disruptions in brain dopaminergic activity and recent studies have assessed the role of catechol-O-methyltransferase (COMT) in eating disorders. This is the first study to quantify the soluble catechol-O-methyltransferase (S-COMT) activity in erythrocytes from patients with anorexia nervosa (AN), bulimia nervosa (BN) and binge-eating disorder (BED) and the first study at all to evaluate the COMT on patients with BED. METHODS: Forty blood samples from patients with AN, BN and BED and healthy controls were drawn to evaluate S-COMT activity in erythrocytes by high-performance liquid chromatography and mass spectrometry. Since several patients were being treated with fluoxetine 20 mg, they were included in a different group (BN MED and BED MED). Liver homogenates from rats were used to evaluate baseline S-COMT activity in the presence of fluoxetine by the same in vitro procedures and assays. RESULTS: Erythrocyte S-COMT activity (pmol/mg prt/h) was significantly increased in patients with BN and BED (41.3 ± 6.8 and 41.4 ± 14, respectively) compared to control group (25.3 ± 9.7). In fluoxetine-treated patients with BN, S-COMT activity (15.9 ± 8.8) was decreased compared to the other BN group; however, in BED group, the difference between BED MED and BED was not observed. In patients with AN, no significant difference was found compared to controls. CONCLUSION: Patients with BN and BED presented higher S-COMT activity in erythrocytes, which is in agreement with previous studies on the literature addressing the high-activity COMT allele, Val158, as risk factor for eating disorders. Although in fluoxetine-treated patients with BN the activity of S-COMT was similar to the controls, this is not explained by a direct interaction between fluoxetine and S-COMT as verified in in vitro assays.

Associations between liver enzymes, psychopathological and clinical features in eating disorders.

Elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels are frequently reported in patients with anorexia nervosa (AN) and in subjects who are overweight or with hyperlipidemia, which can be found to be associated with binge eating disorder (BED) and bulimia nervosa (BN). Liver functioning and psychopathological features have been evaluated in 43 patients with AN, 33 with BN, and 32 with BED. Body mass index was found to be inversely associated with AST and ALT in AN, and directly associated with AST and ALT in BED. A positive association between ALT and AST and body shape concern in AN was observed. Liver enzymes could be considered as an index of severity in AN and BED patients.

Transient hyperphosphatasemia in children revisited.

OBJECTIVE: Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH. METHODS: We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003-08. One hundred and twenty-two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO-PAL and Hydragel 15 ISO-PAL kits were used for the identification and quantification of ALP isoenzymes in human serum. RESULTS: The ALP levels of the study group were 805-8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one-third of the patients, and showed that the bone isoenzyme was elevated in most. Forty-three (71%) subjects were diagnosed in the second half of the calendar year. CONCLUSIONS: We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.

Cholinesterase and other serum liver enzymes in underweight outpatients with eating disorders.

OBJECTIVE: The present study aimed to evaluate serum liver enzymes in underweight outpatients with anorexia nervosa (A-NERV) or eating disorders not otherwise specified (EDNOS). METHOD: Serum alanine amino transferase (ALT), aspartate amino transferase (AST), lactic dehydrogenase (LDH), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and cholinesterase (CHE) were determined in 97 patients with A-NERV, 66 patients with EDNOS, and 56 controls. RESULTS: In the A-NERV group AST, LDH, and GGT were higher, as compared with controls, and inversely related to weight, while ALP and CHE were lower. AST and GGT increased and CHE decreased in patients with EDNOS. Hypertransaminasemia occurred in 14.4 and 15.2%, and low CHE in 29.9% of the A-NERV group and 13.6% and EDNOS group, respectively. Three or more abnormalities were found in 9.3% of patients with A-NERV and 7.5% of those with EDNOS. CONCLUSION: Abnormalities in serum liver enzymes are common in outpatients with eating disorders plus underweight. CHE might be considered as a marker of the effects of primary malnutrition on liver function.

Psychological traits and platelet monoamine oxidase activity in eating disorder patients: their relationship and stability.

Self-reported behavior and attitudes towards eating [Eating Disorder Inventory-2; Garner DM (1991). Eating Disorder Inventory-2: Professional Manual. Odessa, Fl.: Psychological Assessment Resources; Estonian version Podar I, Hannus A, Allik J (1999). Personality and Affectivity Characteristics Associated With Eating Disorders: a Comparison of Eating Disordered, Weight-Preoccupied, and Normal Samples. J Pers Assess; 73(1), 133-147] and the activity of platelet monoamine oxidase (MAO) was studied in 11 patients with anorexia nervosa (AN), 43 patients with bulimia nervosa (BN) and a healthy control group (n=138). Nineteen patients filled in the EDI-2 questionnaire and donated blood samples three times with three month intervals in order to determine platelet MAO activity. Eating disordered (ED) patients scored higher on all EDI-2 subscales and had lower MAO activity compared to the control group. They also scored higher than the control group on the Neuroticism domain but lower on the Extraversion, Openness, and Conscientiousness domains of the NEO-PI-R questionnaire. The average stability of MAO on different occasions (r=.56) was slightly smaller than the stability of the EDI-2 scores (r=.70). The lack of correlations between personality dispositions and MAO activity indicates that they have independent influence on eating disorders. A possible relationship between neurochemical mechanisms and psychological symptoms of eating disordered behavior is discussed.

Reduced ingestion of sweetened milk induced by interleukin-1 and lipopolysaccharide is associated with induction of cyclooxygenase-2 in brain endothelia.

UNLABELLED: Previous studies have shown that interleukin-1 (IL-1) and lipopolysaccharide (LPS) administration to animals induces behavioral changes, including a reduction in feeding. These effects of IL-1 and LPS have been shown to be sensitive to inhibitors of cyclooxygenase (COX). OBJECTIVES: To determine the relationships between induction of COX-2 in the brain with IL-1beta- and LPS-induced changes in body temperature, plasma corticosterone and feeding. METHODS: Mice were injected with intraperitoneal doses of IL-1beta and LPS that decreased feeding. The induction of COX-2 was studied immunocytochemically in the brain, in parallel with core body temperature, the drinking of sweetened milk, and plasma concentrations of corticosterone. RESULTS: COX-2 immunoreactivity (ir) was sparse in the brains of the untreated mice, but IL-1beta and LPS both increased its expression. This COX-2 induction appeared to be confined to blood vessels, and was not markedly region specific. Induction was evident 30 min after IL-1 or LPS, and was greater at 90 than at 30 min. COX-2-ir in the parenchyma did not change significantly. Thus induction of COX-2 occurred in brain endothelia in parallel with the reduction in feeding. This is consistent with the previously determined sensitivity of IL-1-induced changes in feeding to selective COX-2 inhibitors, and the responses to IL-1 in COX-2-deficient mice. The time courses of the IL-1- and LPS-induced increases in plasma corticosterone paralleled those in the reduction in milk drinking, however, the changes in body temperature appeared later. CONCLUSIONS: Endothelial COX-2 may be involved in IL-1- and LPS-induced decreases in milk drinking, and possibly in the HPA axis activation. The decreased milk drinking may occur when IL-1 and LPS bind to receptors on brain endothelial cells subsequently inducing COX-2 and the production of prostanoids which elicit the reductions in milk drinking. Thus the behavioral effects of peripherally administered IL-1 and LPS appear to be mediated by multiple mechanisms, including endothelial COX-2, and vagal afferents.

Association of catecholamine-O-methyltransferase and 5-HTTLPR genotype with eating disorder-related behavior and attitudes in females with eating disorders.

OBJECTIVE: There is growing evidence, that genetic variants contribute to the pathogenesis of anorexia nervosa and bulimia nervosa. Genetic studies have revealed candidate genes, but no satisfactory associations with the disorders have been found so far. The aim of the present study was to evaluate, whether behavioral and attitudinal traits of the disorders can serve as phenotypes with a possible association with two common functional polymorphisms of the monoaminergic pathways. METHOD: Forty-five female in-patients of a specialized hospital for eating disorders were included into the study. Eating disorder symptomatology was assessed using the Eating Disorder Inventory-2. The functional catecholamine-O-methyltransferase (COMT) 158 Val-->Met polymorphism and the deletion/insertion polymorphism of the serotonin transporter promoter 5-HTTLPR were determined. RESULTS: Carriers of at least one Met-allele of the COMT gene had significantly higher total scores of the Eating Disorder Inventory-2, as well as significantly higher scores on the subscales bulimia, ineffectiveness, interoceptive awareness, maturity fears and impulse regulation. Carriers of the deletion of the 5-HTTLPR had significantly higher scores on the subscales drive for thinness and body dissatisfaction. CONCLUSION: We found associations between the COMT and the 5-HTTLPR polymorphisms and specific clinical, behavioral and attitudinal traits of eating disorders. These polymorphisms may predispose their carriers to exhibit certain symptoms of eating disorders or confer a general risk for more severe forms of these disorders.

Increased nitric oxide production in eating disorders.

Animal studies showed that nitric oxide (NO)/cyclic-GMP (cGMP) pathway is involved in the modulation of eating behavior. To address its role in eating disorders (ED), plasma nitrite and cGMP levels were studied in 50 ED patients (25 with Anorexia Nervosa, AN; 25 with Bulimia Nervosa, BN) and 20 sex- and age-matched controls (C). Nitrites (nmol/mg protein, mean+/-S.E.M.: any ED 1.01+/-0.29; AN 1.15+/-0.47; BN 0.88+/-0.36; C 0.25+/-0.07; p<0.01) and cGMP (nmol/ml plasma, mean+/-S.E.M.: any ED 2.58+/-0.60; AN 2.81+/-1.10; BN 2.41+/-0.70; C 0.11+/-0.05; p<0.01) were significantly higher in ED patients than in C. Nitrite and cGMP levels inversely correlated with BMI in AN patients (nitrites: r=-0.62 p<0.01; cGMP r=-0.45 p<0.05) but not in BN patients (nitrites: r=-0.15 p=0.49; cGMP: r=-0.05 p=0.13) or in control subjects (nitrites: r=0.11 p=0.98; cGMP r=0.37 p=0.32). Significant correlations were also present in bulimic patients between nitrite levels, frequency of binges and several psychopathological dimensions, as assessed through the EDE. This is the first evidence of an alteration of the NO pathway in ED patients. Further studies are needed to ascertain whether an increase in NO levels plays a possible role in the pathogenesis of ED.

Eating disorders: a role for dipeptidyl peptidase IV in nutritional control.

Dipeptidyl peptidase IV (DPP IV), a serine protease with broad tissue distribution and known activity in serum, has been postulated to modulate nutrition control by modification or inactivation of peptide hormones operating in the enteroinsular axis. We hypothesized that changes of DPP IV activity in serum are related to the nutrition status of patients with eating disorders. Serum DPP IV activity was measured in 52 patients (28 with anorexia nervosa and 24 with bulimia nervosa) in four consecutive weekly analyses. Simultaneously, the number of CD26 (DPP IV)-positive peripheral blood lymphocytes was counted. The same analyses were carried out in 28 healthy female volunteers. In week 1 and throughout the observation period, DPP IV activity in the sera of patients with anorexia nervosa and, to a lesser extent, those with bulimia nervosa was elevated in comparison to that of healthy controls (week 1: means = 92.8 U/L for anorexia-nervosa patients and 89.3 U/L for bulimia-nervosa patients versus 74.7 U/L for healthy control subjects, P = 0.014; weeks 1-4: 91.8 U/L for anorexia-nervosa patients and 86.2 U/L for bulimia-nervosa patients versus 77.6 U/L for healthy controls, P < 0.001). We assume that the increase in DPP IV serum activity will increase the turnover of distinct peptide hormones with known effects on nutrition control and susceptibility to degradation by DPP IV. The potential impact of an increase in DPP IV activity in serum on satiety and nutrition control contributes to previously reported implications for immune function.

Alterations in expression and in serum activity of dipeptidyl peptidase IV (DPP IV, CD26) in patients with hyporectic eating disorders.

The notion that patients with eating disorders maintain a functional immunosurveillance in spite of severe malnutrition has attracted researchers for years. Dipeptidyl peptidase IV (DPP IV), a serine protease with broad tissue distribution and known activity in serum, operates in the cascade of immune responses. Membrane-bound DPP IV expressed on lymphocytes, also known as the leucocyte antigen CD26, is considered to participate in T-cell activation. We hypothesized that the activity of DPP IV in serum and expression of CD26 in lymphocytes may be altered in patients with eating disorders. Serum DPP IV activity and the number of CD26 (DPP IV)-positive peripheral blood lymphocytes were measured in 34 patients [anorexia nervosa (AN): n = 11, bulimia (B): n = 23] in four consecutive weekly analyses. In addition, the expression of CD25 (interleukin-2 receptor alpha chain) was evaluated to estimate the degree of T-cell activation. The same analyses were carried out in healthy female volunteers (HC, n = 20). CD2-CD26-positive cells were reduced in patients compared with healthy controls [mean 40.2% (AN) and 41.1% (B) versus 47.4% (HC), P < 0.01], while the DPP IV activity in serum was elevated [mean 108.4 U/l (AN) versus 91.1 U/l (B) and 80.3 U/l (HC), P < 0.01]. The potential implications of our observations on, and beyond, immune function are discussed.

Pancreatic pseudocyst associated with eating disorder.

We describe a patient with an eating disorder and hyperamylasemia originating from the salivary glands, who developed pancreatitis with a huge pancreatic pseudocyst. A 40-year-old woman was referred for the treatment of an eating disorder that had persisted for 9 years. She was admitted with abdominal pain, diarrhea, and nausea. She had bilateral parotid enlargement with marked elevation of total serum amylase level (3288 IU/l; normal range, 60-220) and an isolated increase of salivary isoamylase activity. After her symptoms resolved, oral intake of food was commenced. She subsequently complained of abdominal pain; this was associated with a slight elevation of serum pancreatic isoamylase and lipase levels, and a huge pancreatic pseudocyst was detected. Percutaneous drainage of the pseudocyst was successful. Endoscopic retrograde cholangiopancreatography demonstrated irregularity of the pancreatic duct. Based on these findings, the final diagnosis was parotid enlargement and acute exacerbation of chronic pancreatitis associated with a pancreatic pseudocyst in a patient with an eating disorder.

Abnormal liver enzymes in outpatients with eating disorders.

OBJECTIVE: This study was undertaken to screen a large series of outpatients with anorexia or bulimia for liver enzyme abnormalities, examining their frequency and their clinical correlates. METHOD: Eight hundred seventy-nine eating-disordered outpatients presenting at a suburban clinic constituted the subject population. Serum glutamic oxalacetic transaminase, serum glutamic pyruvate transaminase, and gamma glutamyl transpeptidase (SGOT, SGPT, and GGTP, respectively) were drawn at intake. Medical charts were reviewed to obtain further clinical data on all patients with an enzyme elevation. RESULTS: Liver enzymes were abnormally high in 36 patients (4.1%). Elevated SGPT was the most frequent enzyme abnormality and was correlated with lower current and past weight and body mass index (BMI). DISCUSSION: Hepatic dysfunction in eating-disordered outpatients is neither specific nor common. Low weight alone can cause liver damage, yet elevated liver chemistries in patients with anorexia and especially bulima are often not due to their eating disorder.

[ALDH phenotype in eating disorders with and without alcoholism].

Individuals who have inactive low Km aldehyde dehydrogenase (ALDH2) are much less likely to develop alcoholism than those who have active ALDH2. On the other hand, frequent alcoholism has been reported in eating disorder patients. Whether inactive ALDH2 works as an inhibitory factor for alcoholism in these patients is not known. We compared the ALDH2 phenotype in eating disorder patients with and without alcoholism. Among the 25 subjects (4 with anorexia nervosa, 6 with anorexia nervosa and bulimia nervosa, 13 with bulimia nervosa and 2 with eating disorder not otherwise specified according to the DSM-III-R), 13 were alcoholics and 12 were non-alcoholics. Isoelectric focusing of hair roots samples demonstrated that 8% of the alcoholic subjects had the inactive ALDH2, while 58% of the non-alcoholic subjects had this variant form of the isozyme (p < 0.01). The results suggest inactive ALDH2 has a similar inhibitory effect for alcoholism as in eating disorder patients as has been reported in normal populations.

Duodenal toxicity of dietary Phaseolus vulgaris lectins in the rat: an integrative assay.

It is now generally admitted that phytohemagglutinin (PHA) constitutes the main factor responsible for the dietary toxicity of raw kidney beans. In the growing rat, an impairment of growth is the unique expression of a malnutrition syndrome. The aim of this work was to precise to what extent the intestinal injuries may account for this malnutrition. PHA was administered for 9 days to growing rats at levels ranging from 0.0025 to 0.25% of food dry matter. One group of controls was fed ad libitum and other groups were restrained. In such conditions, PHA reduced the food intake when offered at a level higher than 0.04% as a linear function of the logarithm of lectin rate. Intestinal injuries were also dose-dependent: blebbing of microvilli and loss of alkaline phosphatase occurred at the smallest dose of PHA, cell loss occurred at higher doses. A compensatory hyperplasia was observed as a consequence of both intestinal injury and reduced food intake. Our main results are that, whatever may be the damages caused to the duodenal mucosa, the observed growth impairment was quasi-totally imputable to the reduction of food intake.