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    Complementary and Alternative Medical Lab Testing Part 18: Psychiatry
    Complementary and Alternative Medical Lab Testing Part 18: Psychiatry
    Complementary and Alternative Medical Lab Testing Part 18: Psychiatry
    Ebook287 pages3 hours

    Complementary and Alternative Medical Lab Testing Part 18: Psychiatry

    By Ronald Steriti

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    About this ebook

    Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.

    CAM Labs 18 – Psychiatry

    1. Anorexia Nervosa
    2. Anxiety
    3. Attention Deficit Hyperactivity Disorder
    4. Bipolar Affective Disorder
    5. Depression
    6. Obsessive Compulsive Disorder
    7. Post-Traumatic Stress Disorder
    8. Schizophrenia
    9. Seasonal Affective Disorder

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 4, 2016
    ISBN9781310913365
    Complementary and Alternative Medical Lab Testing Part 18: Psychiatry
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Book preview

      Complementary and Alternative Medical Lab Testing Part 18 - Ronald Steriti

      Complementary and Alternative

      Medical Lab Testing

      Part 18: Psychiatry

      By Ronald Steriti, ND, PhD

      ©

      Complementary and Alternative Medical Lab Testing Clinician’s Guide Part 18: Psychiatry

      By Ronald Steriti, ND, PhD

      Copyright © 2016

      All rights reserved. No part of this book may be reproduced in any form or by any means, including photocopying, including in a web site, or stored in a retrieval system, or transmitted in any form by any means, without expressed, written permission of the copyright owner.

      The contents of this document are the sole property of the author.

      Disclaimer

      This book has not been evaluated by the FDA and is not intended to diagnose, treat, cure or prevent any disease.

      The information contained in this book is for educational purposes only, and should not be construed as medical advice or instruction. No action should be taken based solely on the contents of this book. Readers should consult appropriate health officials.

      While extensive efforts have been made to ensure the accuracy of the information contained, the possibility of errors, omissions, and misinterpretations cannot be ruled out. The reader is advised to consult the original references for verification and clarification.

      Foreward

      This book is a summary the published research on lab tests, primarily from PubMed. The studies are limited to those with trials on humans. As such, some labs may be excluded due to the lack of published research. That is simply a reflection of the current state of research - much more work is needed!

      Although this book may be useful for differential diagnosis, lab tests are can also be used to identify inderlying causes and associated conditions.

      The sections on conventional lab tests are purposefully brief. These tests are typically used to confirm a diagnosis. There are other more comprehensive sources of information on conventional medical lab testing.

      Table of Contents

      1. Anorexia Nervosa

      2. Anxiety

      3. Attention Deficit Hyperactivity Disorder

      4. Bipolar Affective Disorder

      5. Depression

      6. Obsessive Compulsive Disorder

      7. Post-Traumatic Stress Disorder

      8. Schizophrenia

      9. Seasonal Affective Disorder

      Chapter 1. Anorexia Nervosa

      Conventional Lab Tests

      CBC and Chemistries

      Thyroid panel: TSH and T3

      Fasting glucose

      Additional Lab Tests

      Fasting Glucose, Hemoglobin A1C

      Of 208 young women with insulin dependent diabetes, 15 (7%) had a clinically apparent eating disorder (anorexia nervosa or bulimia), a much higher prevalence than reported in non-diabetic women. Most, but not all, of these patients had a long history of poor glycemic control. In contrast with previous suggestions, control did not deteriorate after the onset of the eating disorder. There was a high incidence and an early onset of diabetic complications. Eleven of the 15 patients had retinopathy, six with proliferative changes; six had nephropathy; and six neuropathy. Most strikingly, four patients with anorexia nervosa developed acute painful polyneuropathy. In each case pain started when the eating disorder developed, almost coinciding with the peak of weight reduction. Remission of pain occurred as weight was regained. The symptoms were accompanied by abnormalities in peripheral nerve electrophysiology and autonomic nerve function, some improvements in which accompanied weight recovery. (Steel et al., 1987)

      To assess the prevalence of anorexia nervosa and bulimia among young diabetic women, a questionnaire was sent to 264 young women with insulin-dependent diabetes mellitus in two clinical settings. Among the women who responded (30%), none reported a history of anorexia nervosa, but 28 (35%) reported a history of bulimia. These results suggest that bulimia represents a common problem among young women with diabetes. (Hudson et al., 1985)

      Insulin Resistance, Metabolic Syndrome

      We examined 21 women with anorexia nervosa (AN) and 24 healthy normal-weight female controls. Euglycemic hyperinsulinemic clamp, indirect calorimetry, and the measurement of serum adiponectin concentration were performed in all the subjects. There were no differences in insulin sensitivity, oxidative and nonoxidative glucose metabolism in insulin-stimulated conditions, and metabolic flexibility between AN and control subjects. Serum adiponectin was higher in AN women in comparison with control group (P = .002). Women with AN have normal insulin sensitivity because of the preserved response of glucose oxidation, nonoxidative glucose metabolism in response to insulin, and normal metabolic flexibility. High adiponectin concentration and normal insulin sensitivity in anorectic women suggest that in AN the adipocytes are still capable of functioning at the level that is sufficient to prevent the metabolic consequences. (Karczewska-Kupczewska et al., 2010)

      A study measured fasting plasma levels of adiponectin, leptin, resistin, insulin and glucose in 10 women with a restrictive type of AN and in 12 healthy women (C). Insulin sensitivity was determined according to homeostasis model assessment of insulin resistance (HOMA-R). Plasma resistin, leptin and insulin levels were significantly decreased, whereas plasma adiponectin levels were significantly increased in patients with AN compared to the C. HOMA-R was significantly decreased in patients with AN compared to the C group. Plasma adiponectin and leptin concentrations negatively and positively correlated with the body mass index and percentage body fat in both groups. Plasma adiponectin levels were negatively related to plasma insulin levels in the AN group only. In conclusion, we demonstrated that AN is associated with significantly decreased plasma leptin and resistin levels, markedly increased plasma adiponectin levels and increased insulin sensitivity. Plasma leptin and adiponectin levels were related to the body size and adiposity. Hyperadiponectinemia could play a role in increased insulin sensitivity of patients with AN. Neither body size and adiposity nor insulin sensitivity are the major determinants of plasma resistin levels in AN. (Dostalova et al., 2007)

      A study included 18 females recovered from AN and 18 female controls and measures included plasma insulin, leptin, glucose and beta-hydroxybutyrate (beta-HBA) concentrations together with desire to eat. Fasting glucose concentrations were normal in both groups, but fasting insulin concentrations were significantly lower and the fasting glucose/insulin ratio significantly higher in the recovered subjects. The glucose concentration was significantly higher at the end of the meal period in the recovered group. The peak increase of insulin during the meal was significantly less in the recovered group and in response to the meal, glucose/insulin ratios were significantly higher for the first 45 minutes indicating a delayed insulin response. Fasting beta-HBA concentrations were not significantly different between groups, but postmeal decreases were significant and larger in the recovered AN group. Fasting and meal-related leptin concentrations were not significantly different between the groups and in both groups were correlated with BMI. In controls, but not in recovered subjects, the reported desire to eat was correlated with plasma glucose and leptin concentrations. The insulin, glucose and beta-HBA data indicated the presence of insulin hypersensitivity in the recovered subjects. As the insulin response to the meal was blunted and apparently delayed, there may be a persistent alteration in pancreatic function as a long-term pathological consequence of the anorexia. Alternatively, these data indicate a possible trait marker for AN. (Brown et al., 2003)

      Insulin sensitivity, kinetics, and metabolic effects were measured using the euglycemic clamp in nine females with AN (age 25.2 +/- 1.9 years and 70.6 +/- 2.2% ideal body weight), and the results compared with seven female normal controls (NC) (age 23.6 +/- 1.0 years and 92.7 +/- 2.5% ideal body weight). Fasting plasma glucose (FPG), immunoreactive insulin (IRI), and C-peptide were significantly lower in AN as compared to NC (84.3 +/- 1.5 v 91.5 +/- 1.7 mg dL-1, 9.3 +/- 1.0 v 13.5 +/- 1.4 microU mL-1, and 0.26 +/- 0.03 v 0.41 +/- 0.02 pmol mL-1) (P less than 0.05). During the glucose clamp, the glucose metabolized (M), the metabolic clearance rate of glucose (MCRg), and the glucose metabolized per unit of insulin (M/I ratio) were all higher in AN as compared to NC (M, 8.7 +/- 1.2 v 6.9 +/- 0.6 mg min-1 kg-1; MCRg, 9.9 +/- 1.5 v 7.4 +/- 0.6 mL min-1 kg-1; M/I ratio, 8.6 +/- 1.6 v 5.0 +/- 0.3 mg min-1 kg-1/microU mL-1 X 100), but only the M/I ratio attained statistical significance (P less than 0.05). (Zuniga-Guajardo et al., 1986)

      Obestatin

      Fasting plasma obestatin, acyl-ghrelin, desacyl-ghrelin, leptin, glucose serum adiponectin, and insulin were measured in 10 obese subjects, 11 restricting-type anorexics, and 11 control subjects. Obese group had significantly lower levels of obestatin (p < .01), while anorexic group had significantly higher levels (p < .01). Obestatin was negatively correlated with body mass index (BMI) (r = -.74), glucose (r = -.56), insulin (r = -.55), leptin (r = -.66), and also with the homeostasis model assessment of insulin resistance (HOMA-R) (r = -.49) and was positively correlated with acyl-ghrelin (r = .65) and desacyl-ghrelin (r = .60). No correlation was seen between obestatin and adiponectin, but the latter was negatively correlated with both acyl-ghrelin and desacyl-ghrelin. Desacyl-ghrelin to acyl-ghrelin ratio was significantly different between anorexic and control groups (p < .05), while no difference was seen between obese and control groups. Both obestatin and ghrelin are increased in anorexic and decreased in obesity. Obestatin may be useful as a nutritional marker reflecting body adiposity and insulin resistance. (Nakahara et al., 2008)

      Resistin

      Serum RES (ELISA) and fT4, TSH, ACTH, LH, FSH, estradiol and testosterone (ECLIA) concentrations have been assayed in 195 adolescent girls: 87 with restrictive AN, 17 with not otherwise specified eating disorders (NOS), 30 with simple obesity (OB) and 61 healthy (H) subjects. Mean serum FT4, LH and estradiol concentrations were significantly lower (p=0.015; p<0.0001; p<0.0001, respectively) in AN than in OB group, and cortisol increased (p<0.001) compared to OB and H subjects. In all examined subjects BMI correlated positively (p<0.0001) with LH (r=0.61) and estradiol (r=0.30), and negatively with cortisol (r=-0.35; p=0.008). Also the significant positive relationship between serum RES and FT4 (r=0.34), LH (r=0.57) as well as estradiol (r=0.28) was observed, whereas serum cortisol correlated negatively with RES (r=-0.40). Changes in resistin serum concentrations in eating disorders may be involved in the altered regulation of hypothalamic-pituitary-adrenal, thyroid and gonadal axes. (Ziora et al., 2011)

      Digestive Assessments

      Celiac Disease

      Ten severely malnourished AN women were studied at hospital admittance (body mass index = 11.44-16.16 kg/m(2)) and after weight recovery with artificial nutrition (body mass index >/= 20 kg/m(2)). In nine patients, (13)C-labelled triglycerides digestion tests and the facal elastase and d-xylose tests were normal both before and after weight recovery. In one patient, the results were abnormal, and they led to the detection of a previously undiagnosed celiac disease in addition to her AN. (Martinez-Olmos et al., 2013)

      A study was conducted at the Neuropsychiatry Unit of Bambino Gesu Children's Hospital in Rome from January 2005 to December 2010. All patients with diagnosis of AN according to the Diagnostic and Statistical Manual of Mental Disorders 4th edition criteria were screened for CD. One hundred and seventy-seven patients (33 males and 144 females) were enrolled. Only one patient was found to be affected with CD as confirmed by intestinal biopsy. The overall prevalence of CD in AN patients was 0.6 % which is similar to that observed in the general population. In conclusion, AN patients do not seem to require a regular screening program for CD. The screening for CD may be useful in selected AN patients in which the symptoms are only partially responding to psychiatric interventions. (Basso et al., 2013)

      Cause-and-effect relationships between anorexia nervosa and celiac disease are unclear, and celiac disease may lead to confusion in the differential diagnosis of anorexia nervosa. Particularly in atypical cases, and in cases where nausea and bloating are prominent complaints, workup for celiac sprue may reveal the presence of this condition. I (Yucel et al., 2006)

      A study reported two cases of women suffering from AN and celiac disease. The former received the diagnosis of celiac disease before the onset of the eating disorder. For the latter, the diagnosis of celiac disease followed that of AN. Authors discuss the complex relationships between celiac disease and AN. In the first case the dietary restriction could act as a trigger for the eating disorder, whereas in the second case, the onset of celiac disease could have exacerbated the clinical symptoms of AN. (Ricca et al., 2000)

      Intestinal Permeability

      A study assessed IP in 14 drug-free anorexic women and 19 drug-free age-matched healthy women by means of the lactulose/mannitol (LA/MA) test. IP, as expressed by the 5-h LA/MA excretion ratio, was significantly decreased in anorexic women because of a lower urinary recovery of lactulose. Moreover, in patients, the time course of lactulose excretion significantly differs from healthy controls. These results do not confirm our hypothesis of increased IP in anorexia nervosa. Since IP reflects the anatomical-functional status of intestinal mucosa, the present findings support the idea that changes in the anatomical-physiology of intestinal mucosa occur in anorexia nervosa. (Monteleone et al., 2004)

      Comprehensive Sex Steroid Panel

      Estradiol, T3 and T4

      Blood samples and anthropometry were taken from patients with AN on admission (N=30) and matched controls (N=30). Twenty-one patients were re-tested after four months of treatment. Total cholesterol, LDL, Apo B and fibrinogen concentrations were elevated in patients on admission compared with controls, while retinol and tocopherol were decreased. Low levels of T3, T4 and estradiol were correlated with increased cholesterol values. After treatment there was a tendency for most of the abnormal markers to normalize. However, HDL levels decreased leaving patients with an undesirable lipid profile. (Matzkin et al., 2007)

      A study investigated serum levels of receptor activator of nuclear factor kappaB ligand (RANKL), osteoprotegerin (OPG), and bone turnover markers of 26 Japanese young female AN patients and 7 age-matched healthy women. Mean serum levels of E2, IGF-I, T3 and leptin in AN patients were significantly lower than those of controls (p<0.05). Serum levels of OPG in AN patients were significantly higher than those in controls and negatively correlated with body mass index (BMI), E2, IGF-I or leptin. Serum levels of free RANKL could not be detected except for only one healthy control in both groups. These results suggest that serum OPG levels may be increased by a compensatory mechanism for malnutrition and estrogen deficiency, which induces an increase in bone resorption. (Ohwada et al., 2007)

      Testosterone

      72 females in the active phase of AN were evaluated. 52 healthy women constituted the control group. The concentrations of leptin, insulin, IGF-1, triiodothyronine, LH, FSH, estradiol, and testosterone were significantly lower and those of cortisol and growth hormone significantly higher in the AN than the control group. No hormonal differences between restrictive and binge-purging AN subtypes were found. Leptin, IGF-1, gonadotropins, and sex steroids correlated significantly negatively; and growth hormone positively with total reduction of body weight or the degree of undernutrition. Associations were also found between lower insulin concentration and family violence, lower cortisol and psychiatric diseases in the family, higher testosterone and patient's alcohol or drug abuse. The changed activity of the somatotropin-somatomedin, gonadal, and corticotrophin axes corresponds to the clinical stage of AN. Plasma IGF-1 seems to be the most sensitive and useful independent hormonal marker of cachexia. (Smiarowska et al., 2014)

      32 women participated in the study: 11 women with anorexia nervosa (AN), 11 normal-weight women, and 10 obese women of comparable mean age. Free testosterone was higher in obese women and lower in women with AN than in normal-weight women, and was the only independent (and positive) predictor of IGF1 levels, accounting for 14% of the variability (P=0.032) in the group as a whole. This relationship was stronger when obese women were excluded, with free testosterone accounting for 36% of the variability (P=0.003). Trunk fat accounted for 49% of the variability (P<0.0001) of GH, with an additional 7% of the variability attributable to E(2) (P=0.042) in the group as a whole, but was not a significant determinant of GH secretion when obese women were excluded. Free testosterone is a significant determinant of IGF1 levels in women across the body weight spectrum. In contrast, GH secretion is differentially regulated at the extremes of the weight spectrum. (Brick et al., 2010)

      In order to elucidate the mechanism of disturbances of gonadal hormones secretion in anorexia nervosa 14 female patients were investigated. A control group also consisted of 14 women of the same age. In patients with anorexia nervosa the serum testosterone and estriol concentrations were dramatically elevated, whereas LH, progesterone and estrone + estradiol were decreased as compared with the control group. Considerable weight gain induced by cyproheptadine treatment caused a normalization of the serum testosterone and estriol concentrations in all the patients. A negative correlation between the testosterone level and the deficit in body weight was observed. (Baranowska and Zgliczynski, 1979)

      SHBG

      SHBG was assayed in children with protein-energy malnutrition (29 children with kwashiorkor and 28 with marasmus), in 29 anorectic girls (before and after refeeding), and in age- and sex-matched control subjects. Mean (+/-SE) serum SHBG concentrations were higher in the children with kwashiorkor (0.18 +/- 0.07 micromol/L) than in the children with marasmus (0.11 +/- 0.05 micromol/L, P < 0.0001) or the control subjects (0.11 +/- 0.03 micromol/L, P < 0.0005). In the children with anorexia nervosa before weight gain, serum SHBG concentrations were significantly higher (0.10 +/- 0.04 micromol/L) than in the age-matched control subjects (0.06 +/- 0.03 micromol/L, P < 0.001) and decreased significantly after 30 d of refeeding (0.04 +/- 0.01 micromol/L, P < 0.0001). This decrease was negatively correlated with insulin-like growth factor I but not with insulin. Mean serum SHBG concentrations were influenced neither by inflammation, as indicated when C-reactive protein was used as a marker (0.27 +/- 0.27, 0.34 +/- 0.42, and <0.04 micromol/L in the children with marasmus, kwashiorkor, and anorexia nervosa, respectively), nor by glomerular filtration, as indicated when cystatin-C was used as a marker (68.46 +/- 23.08, 66.90 +/- 43.08, and 49.23 +/- 7.69 micromol/L, respectively). The high SHBG concentration observed in anorexia nervosa and kwashiorkor seems to be of multifactorial origin. For these 2 diseases, SHBG is a reliable marker of nutritional status, is unrelated to either C-reactive protein or cystatin-C, and may be helpful in distinguishing kwashiorkor from marasmus and as a follow-up marker after refeeding. (Pascal et al., 2002)

      A study included 19 women with anorexia nervosa. Seven healthy women with normal weight and regular menstrual cycles served as controls. The serum concentrations of SHBG in patients with anorexia nervosa (165.27 +/- 63.5 nmol/l) were significantly higher (p < 0.01) than those in the control group (96.21 +/- 38.04 nmol/l), but the levels of estradiol, testosterone, free triiodothyronine and the ratio of testosterone to SHBG were significantly lower. An inverse correlation between SHBG and body weight (r = -0.761) was found in the patients. The alterations in SHBG concentrations were not associated with the changes in testosterone, gonadotropins, thyroid hormones and biochemical parameters. These findings suggest that body weight is one of the more important factors influencing the SHBG concentrations in women with anorexia nervosa. (Tomova et al., 1995)

      Serum sex-hormone-binding globulin (SHBG), transferrin, prealbumin, retinol-binding protein, and ceruloplasmin concentrations were evaluated in 12 women with anorexia nervosa before and after weight gain and in 12 healthy women with normal weight. The serum SHBG concentrations were higher in patients with anorexia nervosa before weight gain than in control subjects and they returned to the normal range after weight gain. The changes of SHBG concentrations were not associated with any change in plasma testosterone, estradiol, or free thyroxin concentrations. The body mass index in our patients after weight gain was lower than in control subjects. Prealbumin, retinol-binding protein, ceruloplasmin, and transferrin in anorectic patients before weight gain did not differ from those of

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