Nutrition_Management_of_Thyroid_Disease.pdf

Nutrition
Management
of Thyroid
Disease
NICOLE ANZIANI, MS, RD, CDN, CDCES
with FRANCESCO S. CELI, MD, MHSc
THE HEALTH PROFESSIONAL’S GUIDE TO

Nutrition
Management
THE HEALTH PROFESSIONAL’S GUIDE TO
of Thyroid
Disease
NICOLE ANZIANI, MS, RD, CDN, CDCES
With Introduction and Medical Review by
FRANCESCO CELI, MD, MHSC

Academy of Nutrition and Dietetics
120 S. Riverside Plaza, Suite 2190
Chicago, IL 60606
The Health Professional’s Guide to Nutrition Management of Thyroid Disease
978-0-88091-019-4 (print)
978-0-88091-022-4 (eBook)
Catalog Number 019420 (print)
Catalog Number 019420e (eBook)
Copyright © 2020, Academy of Nutrition and Dietetics. All rights reserved. Except for brief quotations embodied in
critical articles or reviews, no part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any
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positions of the Academy of Nutrition and Dietetics. Mention of product names in this publication does not constitute
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Library of Congress Cataloging-in-Publication Data
Names: Anziani, Nicole, author.
Title: The health professional’s guide to nutrition management of thyroid disease / Nicole Anziani, MS, RD, CDN, CDE ;
with introduction and medical review by Francesco Celi, MD, MHSC.
Description: Chicago, IL : Academy of Nutrition and Dietetics, [2020] | Includes bibliographical references and index. |
Summary: “This comprehensive reference provides guidance for dietitians, physicians, and other allied care professionals
working with patients with thyroid disease. Using the most current evidence based guidelines from the American Thyroid
Association, the American Association of Clinical Endocrinologists, and available research, this guide addresses: Thyroid
function, weight regulation, and the role of iodine Energy and nutrient requirements in thyroid disease Diagnosis, medical
management, and applying the Nutrition Care Process to provide patient centered nutrition care of hypothyroidism,
hyperthyroidism, and thyroid cancer Awareness of additional interventions, including alternative treatments Working
with special populations, related conditions and issues, and prevention strategies Useful appendix materials include sample
food plans, low iodine diet guidelines, list of goitrogens, monitoring recommendations, suggested resources, and more”--
Provided by publisher.
Identifiers: LCCN 2020003212 (print) | LCCN 2020003213 (ebook) | ISBN 9780880910194 (paperback) | ISBN
9780880910224 (ebook)
Subjects: LCSH: Thyroid gland--Diseases--Diet therapy.
Classification: LCC RC655 .A58 2020 (print) | LCC RC655 (ebook) | DDC 616.4/40654--dc23
LC record available at https://lccn.loc.gov/2020003212
LC ebook record available at https://lccn.loc.gov/2020003213

List of Boxes, Tables, and Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
Frequently Used Terms and Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Reviewers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xvii
About the Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xix
Special Note . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xxi
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xxiii
SECTION 1
Introduction to Thyroid
Disorders
Chapter 1 Overview of the Thyroid and Its Function . . . . . . . . . . . . . . . . . . . . . . . 2
Chapter 2 Thyroid and Weight Regulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Chapter 3 Energy and Nutrient Requirements in Thyroid Disease . . . . . . . . . . . 29
Chapter 4 Iodine and Its Role in Thyroid Management . . . . . . . . . . . . . . . . . . . . 36
SECTION 2
Hypothyroidism
Chapter 5 Signs and Symptoms, Risk Factors, and Etiology of
Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
Chapter 6 Medical Management of Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . 48
Chapter 7 Medical Nutrition Therapy and Nutrition Recommendations for
Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Chapter 8 Alternative Treatments for Hypothyroidism . . . . . . . . . . . . . . . . . . . . . 87
SECTION 3
Hyperthyroidism
Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
Chapter 10 Medical Management of Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . 99
Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
Chapter 12 Alternative Treatments for Hyperthyroidism . . . . . . . . . . . . . . . . . . . 131
SECTION 4
Thyroid Cancer
Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
Chapter 14 Medical Management of Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . 139
Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
Chapter 16 Alternative Treatments for Thyroid Cancer . . . . . . . . . . . . . . . . . . . . 166
Contents

Appendix A Web, Print, and Other Resources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
Appendix B Drugs, Foods, Supplements, and Conditions Affecting Thyroid
Medication Absorption and Thyroid Function Tests . . . . . . . . . . . . . 214
Appendix C Goitrogens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
Appendix D Low-Iodine Diet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216
Appendix E Sample Food Plans (Low-Glycemic, Gluten-Free, Anti-
Inflamatory, Autoimmune Paleo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
Appendix F Self-Check of the Neck . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
Appendix G Quick Guide to Follow-Up Cadence and Monitoring
Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
Continuing Professional Education . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
SECTION 6
Appendixes
SECTION 5
Additional Information for
Health Professionals Working
with Thyroid Patients
Chapter 17 Special Populations: Prepregnancy, Prenatal, Postpartum/
Lactation, Elderly, and Pediatric . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
Chapter 18 Managing Additional Concerns and Conditions . . . . . . . . . . . . . . . . 189
Chapter 19 Prevention of Thyroid Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
iv
CONTENTS

List of Boxes, Tables, and
Figures
BOXES Box 1.1 Potential Challenges to Treatment Based on Thyroid-Stimulating
Hormone Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Box 1.2 Additional Information Regarding Thyroid Hormone Levels . . . . . . . . 7
Box 1.3 Lab Definitions and Interpretation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Box 1.4 The Nutrition Care Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Box 2.1 Research on Thyroid Medications and Weight Management . . . . . . . 19
Box 2.2 Optimization of Diet for Weight Management with
Thyroid Imbalance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
Box 2.3 Optimization of Physical Activity for Weight Management in
Thyroid Imbalance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
Box 2.4 Physical Activity Strategies for Weight Loss and Prevention of
Weight Regain for Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
Box 4.1 Dietary Allowances and Tolerable Upper Intake Level for Iodine . . . 37
Box 4.2 How Iodine Levels May Present in Thyroid Patients . . . . . . . . . . . . . . 37
Box 5.1 Signs and Symptoms of Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . . . 42
Box 6.1 Conditions that Warrant Thyroid-Stimulating Hormone Screening . . 48
Box 6.2 Complications of Untreated or Undertreated Hypothyroidism . . . . . . 49
Box 7.1 Food- or Nutrition-Related History and Hypothyroidism,
Hashimoto Disease, and Endemic Goiter . . . . . . . . . . . . . . . . . . . . . . . 62
Box 7.2 Sample Laboratory Data for Hypothyroid Patients . . . . . . . . . . . . . . . 66
Box 7.3 Hypothyroid Nutrition-Related Intake Diagnoses and
PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68
Box 7.4 Hypothyroid Nutrition-Related Clinical Diagnoses and
PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
Box 7.5 Hypothyroid Nutrition-Related Behavioral–Environmental
Diagnoses and PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
Box 7.6 Nutrition Intervention Goals for Hypothyroidism . . . . . . . . . . . . . . . . . 73
Box 7.7 Medical Nutrition Therapy for Intestinal Permeability in
Hashimoto Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
Box 7.8 Sample Nutrition Prescriptions in Hypothyroidism,
Hashimoto Disease, and Endemic Goiter . . . . . . . . . . . . . . . . . . . . . . . 80
Box 7.9 Nutrition Monitoring and Evaluation of Adult
Hypothyroid Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
Box 8.1 Supplements Common to Hypothyroidism . . . . . . . . . . . . . . . . . . . . . . 88
Box 9.1 Signs and Symptoms of Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . . 93
v

Box 10.1 Complications of Untreated Hyperthyroidism . . . . . . . . . . . . . . . . . . 101
Box 10.2 Medications for Hyperthyroidism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
Box 10.3 Monitoring of Medical Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
Box 11.1 Food- or Nutrition-Related History for Hyperthyroidism and
Graves Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
Box 11.2 Sample Laboratory Data for Hyperthyroid Patients . . . . . . . . . . . . . . 114
Box 11.3 Hyperthyroid Nutrition-Related Intake Diagnoses and
PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
Box 11.4 Hyperthyroid Nutrition-Related Clinical Diagnoses and
PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
Box 11.5 Hyperthyroid Nutrition-Related Behavioral–Environmental
Diagnoses and PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120
Box 11.6 Nutrition Intervention Steps for Hyperthyroidism . . . . . . . . . . . . . . . 121
Box 11.7 Sample Nutrition Prescriptions in Hyperthyroidism and
Graves Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
Box 11.8 Nutrition Monitoring and Evaluation of Adult Hyperthyroid
Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
Box 14.1 Risk Stratification of Death from Thyroid Cancer . . . . . . . . . . . . . . . . 140
Box 15.1 Food- or Nutrition-Related History for Nodules and
Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Box 15.2 Sample Laboratory Snapshot with Clinical History/Assessment
Criteria for Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
Box 15.3 Thyroid Cancer Nutrition-Related Intake Diagnoses
and PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
Box 15.4 Thyroid Cancer Nutrition-Related Clinical Diagnosis
and PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
Box 15.5 Thyroid Cancer Nutrition-Related Behavioral–Environmental
Diagnoses and PES Statements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154
Box 15.6 Foods to Avoid on a Low-Iodine Diet . . . . . . . . . . . . . . . . . . . . . . . . . . 157
Box 15.7 Potential Complications of Radioactive Iodine and Nutritional
Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158
Box 15.8 Sample Nutrition Prescriptions for Thyroid Nodules and
Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 160
Box 15.9 Nutrition Monitoring and Evaluation of Adult Patients with
Thyroid Nodules and Thyroid Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . 163
Box 17.1 Concerns for Treatment Options Used for Graves Disease in
Pediatric Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182
Box 17.2 Thyroid Cancer Types and Follow-Up Recommendations in
Pediatric Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
Box 19.1 Food and Lifestyle Practices to Promote Thyroid Health and
Prevent Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
vi
LIST Of BOxES, TaBLES, aNd fIgurES

Table 1.1 Level of Thyroid-Stimulating Hormone with Interpretation and
Expected Hormonal Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Table 1.2 Typical vs Other Lab Ranges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Table 2.1 Hormones, Weight Regulation, and Relationship to the Thyroid . . . . 16
Table 3.1 Activity and Stress/Injury Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Table 3.2 Quick Estimations for Energy Needs . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Table 3.3 Daily Protein Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
Table 3.4 Dietary Reference Intake Method of Estimating Fluid
Requirements for Healthy Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
Table 3.5 Selected Recommended Dietary Allowances/Adequate Intake
and Tolerable Upper Intake Levels of Nutrients, and
How They May Present in Thyroid Patients . . . . . . . . . . . . . . . . . . . . . . 33
Table 4.1 Recommended Intake of Iodine in Different Populations . . . . . . . . . 39
Table 6.1 Medication Options for Treating Hypothyroidism . . . . . . . . . . . . . . . . . 50
Table 6.2 Thyroid Conditions and Medication Dosing . . . . . . . . . . . . . . . . . . . . . . 55
Table 6.3 Conversion of Thyroid Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
Table 7.1 Lab Ranges to Test for Hypothyroidism and
Hashimoto Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64
Table 7.2 Hemoglobin Values and Interpretation for Anemia . . . . . . . . . . . . . . . 65
Table 11.1 Optimal Lab Ranges to Test for Hyperthyroidism and
Graves Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Table 17.1 American Thyroid Association Trimester-Specific
Thyroid-Stimulating Hormone Guidelines . . . . . . . . . . . . . . . . . . . . . . 172
Table 17.2 Recommended Intake of Iodine in Different Populations . . . . . . . . 178
Table 17.3 Urinary Iodine Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178
Table 17.4 Levothyroxine Needs Based on Age . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
Table 17.5 Dosing of Methimazole in Pediatric Patients . . . . . . . . . . . . . . . . . . . . 182
TaBLES
fIgurES Figure 1.1 Thyroid Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Figure 1.2 Hormonal Interplay Among the Hypothalamus,
Pituitary Gland, and Thyroid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
vii
List of Boxes, Tables, and figures

Frequently Used Terms
and Abbreviations
AACE American Association of Clinical Endocrinologists
AAFP American Academy of Family Physicians
ACE angiotensin converting enzyme
ACTH adrenocorticotropic hormone
ADH antidiuretic hormone
AI Adequate Intake
AICR American Institute for Cancer Research
AITD autoimmune thyroiditis
AJCC American Joint Committee on Cancer
AN anorexia nervosa
ASPEN American Society for Parenteral and Enteral Nutrition
ATA American Thyroid Association
ATD antithyroid drugs
BEE basal energy expenditure
BIA bioelectrical impedance analysis
BMI body mass index
BN bulimia nervosa
BPA bisphenol-A
CEA carcinoembryonic antigen
CH congenital hypothyroidism
CI EBNPG Critical Illness Evidence-Based Nutrition Practice Guidelines
CLA conjugated linoleic acid
CLT chronic lymphocytic thyroiditis
CPK creatine phosphokinase
CRP C-reactive protein test
D3 type 3 iodothyronine deiodinase
DEXA dual energy x-ray absorptiometry
DKA diabetic ketoacidosis
DRIs Dietary Reference Intakes
DTC differentiated thyroid cancer
DTE desiccated thyroid extract
DV Daily Value
ix

EDNOS eating disorder not otherwise specified
EGCG epigallocatechin gallate
FDA US Food and Drug Administration
FNA fine needle aspiration (biopsy)
FODMAPs fermentable oligosaccharides, disaccharides , and
monosaccharides and polyols
FSH follicle-stimulating hormone
FT3 free triiodothyronine (T3)
FT4 free thyroxine (T4)
GD Graves disease
GFR glomerular filtration rate
GH growth hormone
GI gastrointestinal
GO Graves ophthalmopathy
H/H hemoglobin/hematocrit
HBE Harris-Benedict equation
hCG human chorionic gonadotropin
HCTZ hydrochlorothiazide
HIIT high-intensity interval training
HPA hypothalamic-pituitary-adrenal
HPT hypothalamic-pituitary-thyroid
HRT hormone replacement therapy
HSL hormone-sensitive lipase
IBS irritable bowel syndrome
IgE immunoglobulin E
IgG immunoglobulin G
IIH iodine-induced hyperthyroidism
LBM lean body mass
LC-MS/MS liquid chromatography–tandem mass spectrometry
LDN low-dose naltrexone
LH luteinizing hormone
LLLT low-level laser therapy
LPL lipoprotein lipase
L-T3 liothyronine
L-T4 levothyroxine
MCTs medium-chain triglycerides
MCV mean corpuscular volume
MI myo-inositol
MMA methylmalonic acid
MMI methimazole
x
frEquENTLy uSEd TErmS aNd aBBrEvIaTIONS

MMP matrix metalloproteinase
MNT medical nutrition therapy
MTC medullary thyroid cancer/carcinoma
MTHFR methylenetetrahydrofolate reductase
NAC N-acetylcysteine
NCP Nutrition Care Process
NIH National Institutes of Health
OH overt hypothyroidism
PCOS polycystic ovary syndrome
PES problem, etiology, signs and symptoms statements
PFASs perfluoroalkyl and polyfluoroalkyl substances
PTH parathyroid hormone
PTU propylthiouracil
RAI radioactive iodine
RCT randomized controlled trial
RDA Recommended Dietary Allowance
RDW red blood cell distribution width
rhTSH recombinant human TSH
RMR resting metabolic rate
RT3 reverse triiodothyronine (T3)
RxWBS post-treatment whole body scan
SCH subclinical hypothyroidism
SH subclinical hyperthyroidism
SHBG sex hormone binding globulin
SIBO small intestinal bacterial overgrowth
SSKI potassium iodide
T1 monoiodothyronine
T2 diiodothyronine
T3 triiodothyronine
T4 thyroxine
TA toxic adenoma
TAb thyroid antibody
TBG thyroxine-binding globulin
TBII thyrotropin-binding inhibitory immunoglobulin
TEE total energy expenditure
TFT thyroid function test
Tg thyroglobulin
TgAb thyroglobulin antibody
TIBC total iron binding capacity
TMNG toxic multinodular goiter
xi
frequently used Terms and abbreviations

TPO thyroid peroxidase/thyroperoxidase
TPOAb thyroid peroxidase antibody
TRAb thyroid stimulating hormone receptor antibody
TRH thyrotropin-releasing hormone
TSH thyroid-stimulating hormone
TSI thyroid stimulating immunoglobulin
TT total thyroidectomy
TT3 total triiodothyronine (T3)
TT4 total thyroxine (T4)
TTR transthyretin
UBW usual body weight
UICC Union for International Cancer Control
UL Tolerable Upper Intake Level
US ultrasound
WBS whole body scan
xii
frEquENTLy uSEd TErmS aNd aBBrEvIaTIONS

Reviewers
Sheila dean, DSc, RDN, LDN, IFMCP
Co-founder, Integrative and Functional Nutrition Academy
Palm Harbor, FL
Lori Enriquez, MPH, RDN, LDN, CHES, FAND
Nutrition and Health Consultant, Eat Fit Health, LLC
King of Prussia, PA
Nicole german morgan, RDN, LD, CLT
Registered Dietitian Nutritionist, Nicole’s Nutrition, LLC dba Thyroid Dietitian
Bradenton, FL
Cheryl Harris, MPH, RD
Owner, Harris Whole Health
Fairfax, VA
Nancy Jolliffe, RD, CSO, LD
Clinical Dietitian II, Hall-Perrine Cancer Center
Cedar Rapids, IA
Lisa markley, MS, RDN
Registered Dietitian Nutritionist, Nourish Yourself Nutrition & Wellness
Lenexa, KS
Clara Schneider, MS, RD, RN, LDN, CDE
Diabetes Educator
Corolla, NC, and Alameda, CA
xiii

Preface
This book is intended mainly for the health care professional and, in that vein, is
written using scientific and medical language. I would ask health professionals
using this book to approach the nutrition care of thyroid patients with an open
mind. Thyroid care is nuanced—no two patients are the same, and each person
will present with a different set of clinical parameters and reported symptoms.
This book, which contains a wealth of available evidence-based practices and
potential interventions at the time of writing, provides guidance for health care
practitioners such as physicians, dietitians, and all other allied care professionals
working with patients with thyroid disease. My hope is that once a patient has
tried “everything” yet still doesn’t feel “right,” this book will help us as provid-
ers to determine additional options to better help them. This book is intended as
both a time-saver and a guide, matching nutrition care with medical care, but
with the understanding that research will continue to refine and improve recom-
mendations over time.
Throughout the writing and revision phases, I have tried to provide a bal-
anced account of the available research, citing evidence-based guidelines from
the American Thyroid Association (ATA) and the American Association of
Clinical Endocrinologists (AACE), as well as citing numerous other research
studies. I have based the framework of nutrition care on the Academy of Nutri-
tion and Dietetics Nutrition Care Process (NCP). You will also find informa-
tion from several evidence-based integrative and functional medicine resources
included within. Peer reviewers weighed in to help ensure that content was rele-
vant, up-to-date, and useful for practitioners.
Although evidence will continue to evolve from ongoing research, we must
remember that our patients are people, not study subjects. There may not yet be
robust research to demonstrate every potential benefit that practitioners might
see for each intervention. My hope is that this book helps provide a fluid set
of recommendations that are subject to change based on the available research.
There is controversy in the subject of thyroid care; therefore, there are times
where a provider may need to use clinical judgment to supersede the overarching
recommendations and use innovative interventions, though keeping a patient’s
safety in mind is of primary importance in any of these decisions.
The main premise I wish to urge is that we focus on patient-centered care—
listening closely to our patients, taking time and giving the attention needed to
find the best course of action for each patient, one thyroid at a time.
Nicole Anziani, MS, RD, CDN, CDCES
Brooklyn, New York
xv

Acknowledgments
I dedicate this work to my parents.
I wish to thank:
Debbie—my mother and the only person in my family to buy a book about
thyroid when I was struggling, who called me to say, “I’m on page 108. I know all
about you now. Oy … the hormones!” In 2015, while I was writing this book, my
mother had a stroke. Much of this manuscript was written in her hospital room
over a period of months. She constantly encouraged me to write, even when I was
her caretaker. Thank you, Bella, for calling me your author.
Raul, my father and first editor—you’ve always encouraged me and believed
in my abilities more than I did. You’ve shared in every triumph and struggle in
my life. You were the first person I saw when I opened my eyes after surgery and
the only one who offered to make me soup. I have endless appreciation for you
and hope this makes you proud.
Grandma Mickey—along with my parents, you jumped around your kitchen
doorway when the proposal for this book was approved. Thank you for being.
My paternal grandma, Elba Anziani, Mamita—you watched from the spirit
realm as I wrote each word.
My brother Reuben “Madhu”—for providing me with healing (and a BioMat
to write on) when my stress level was high.
My cousins J. Javier Anziani, JD, and Andre Anziani, JD, LLM, who pro-
vided contract expertise and advice.
Vanessa Alvarez, MS, RD—one of the best dietitians (and people) I know,
whose empathy is unparalleled. You are part of the reason I am a dietitian today.
Love you, my sister.
Jamillah Hoy Rosas, MPH, RD, CDCES—you were my first registered
dietitian nutritionist boss and advisor in academic research at New York Uni-
versity. You always had faith in me, offering so many professional opportunities
throughout my career. I will always look up to you as a mentor in the field.
Heather Perillo, MS, RD, CDN—you were a prime example of what a dieti-
tian should aspire to be, first as my preceptor and later my colleague. Your train-
ing shaped my work and I thank you for having been my reference all these years.
All other instrumental mentors or dietitians in my academic life—including,
but not limited to: Robert Fabini; Joan Cone; Christopher Dolder; Joan Thomp-
son, PhD, MPH, RD, CDCES; Mary Mead, MEd, RD, CDCES; Nancy
Hudson, PhD (Hon), MS, RD; Domingo Piñero, PhD; Antionette Franklin,
MS, RD, CDN; Lisa Garback Garner, MS, RD, CDN; Mary Ellen Kelly, MS,
RDN, CSSD, LDN; Pamela Purcell, MS, RD, CNSC, LDN; Eileen Ostrander,
MS, RD, CDN; Cynthia Floyd, MS, RD, CDN, CDCES; Valerie L. Thomas,
MS, RD, CDN; and Cindy Sizemore, MS, RD, LD.
The reviewers of this publication—thank you so much for your meticulous
work and valuable comments that have made this publication a quality one.
xvii

Francesco Celi, MD, MHSc—your time and expertise as medical reviewer
of this work is tremendously appreciated. Thank you for your contribution to thy-
roid research and for making this project stronger in so many ways.
The Academy of Nutrition and Dietetics—for taking on this project, and
for your willingness to bring controversial information to light for the benefit of
health professionals and patients alike.
Arlene Bregman, DrPh—for your organization of the local ThyCa meetings
in NYC.
Yan Qi, PhD, and Liza Wong—for your suggestions and sharing conference
notes.
Jaime Schehr, ND, RD—for pointing me to Dietitians in Integrative and
Functional Medicine and the Natural Medicines Database for evidence-based
research on dietary supplements.
Jennifer Trevillian and April Conlon, PharmD—for sharing resources and
your personal journeys with me.
Anne Eller, PhD—for helping me understand the review process and sitting
with me as I read the first set of reviews. Thanks for your expert insight!
Mally—you were one of the first to congratulate me on this project and sent
motivational raps for the writing process. Thank you!
The B-School focus group who helped inspire the proposal for this book—
Christine Gutierrez, LMHC; Tatiana Dellepiane; Dominick Quartuccio; Ber-
tina Lee; Jennifer Spivak; Michelle Shemilt; and the memory of Jamie Lauren
Zimmerman.
My friends and former coworkers at 185th Street, who made me feel like a
rock star when they found out about this book—namely, Kimone Gilphilin, MS,
RN; Lisa Calandra, DPM; Marlene Velez; and Danny Vairo.
All my colleagues at Cecelia Health—for your daily support.
The doctors who have helped me in my personal thyroid experience—Marc A.
Cohen, MD, MPH; Arthur Spokojny, MD (RIP), and his medical staff (Sher-
ine Smith); Naina Marballi, BASM; Alla Khalfin, DO; Maurice Beer, MD;
Robin Berzin, MD; Lilli Link, MD; and Rekha Kumar, MD, MS. Each of you,
in your own way, saved my life. How can I possibly thank you?
The most inspirational thought leaders I’ve encountered on my personal jour-
ney with thyroid cancer—Kris Carr; Terri Cole, LCSW; Sara Gottfried, MD;
and Alan Christianson, ND—your work and vision have all contributed to my
work. You’ve given me a reason to get up in the morning, permission to live with-
out fear, and a fire to learn and hope for a better future.
Jancarlo—at the start of this project, your work ethic inspired mine; as the
project continued, your laughter medicine became just as vital as my thyroid
medicine. Thank you for your partnership and love.
All the souls I’ve had the privilege to work with, share time with, and learn
from, and my community of friends and family—thank you for encouraging my
medical and writing journeys. Your support has kept me truly alive.
xviii
aCkNOwLEdgmENTS

About the Authors
Nicole Anziani, MS, RD, CDN, CDCES, received her bachelor’s degree in
nutrition and dietetics from the University of California at Berkeley and com-
pleted her dietetic internship at the James J. Peters VA Medical Center in the
Bronx, NY, coordinated with a master of science in clinical dietetics from New
York University. She is a registered dietitian licensed in New York, a certified
diabetes care and education specialist, and certified as a personal trainer, group
fitness instructor, Ayurvedic wellness counselor, and reiki practitioner. As a thy-
roid cancer survivor, Anziani’s passion and mission is to make nutrition care
information for thyroid conditions easily accessible to practitioners and patients.
Born and raised in Richmond, CA, Anziani now lives and works remotely via
Brooklyn, NY.
Introduction and Medical Review
Francesco S. Celi, MD, MHSc, is the William G. Blackard Professor of Med-
icine and Chair of the Division of Endocrinology Diabetes and Metabolism at
Virginia Commonwealth University in Richmond. Prior to joining the faculty of
Virginia Commonwealth University, Celi worked for 10 years as clinical inves-
tigator at the National Institute of Diabetes, Digestive, and Kidney Diseases in
Bethesda, MD. Celi is a graduate of the University of Rome “La Sapienza,” and
a diplomate of the Board of Internal Medicine, with subspecialty in endocrinol-
ogy, diabetes, and metabolism. He was awarded the master’s in health sciences by
Duke University in Durham, NC. Celi conducts both clinical and translational
research and his scientific interest is focused on the physiology and pathophysi-
ology of thyroid hormone action as it relates to energy metabolism. Another area
of research is in the mechanisms of adipose tissue differentiation and on the role
of hormonal signaling (including thyroid hormone) on promoting differentiation
of adipose tissue depots in thermogenic fat and its ability to dissipate energy. Celi
has published more than 80 peer-reviewed manuscripts and has been invited to
lecture at various institutions across the United States and Europe. Celi’s clin-
ical interests are thyroid disease, management of thyroid cancer, and treatment
of diabetes.
xix

Special Note
The Academy of Nutrition and Dietetics has adopted the increasingly common
practice of dropping possessive apostrophes from the names of diseases and dis-
orders. In alignment with the Endocrine Society, the American Medical Associ-
ation, the 32nd edition of Dorland’s Illustrated Medical Dictionary, and new mate-
rial from National Institutes of Health, the Health Professional’s Guide to Nutrition
Management of Thyroid Disease spells terms such as Graves disease without an
apostrophe. Other organizations and older publications may still maintain an
apostrophe, but there is no difference in meaning between Graves disease and
Graves’ disease or Hashimoto thyroiditis and Hashimoto’s thyroiditis.
xxi

Introduction
Francesco S. Celi, MD, MHSc
The action of thyroid hormone affects virtually all tissues of an organism, and
it plays a critical role in the modulation of energy metabolism. Indeed, the dra-
matic effects of overt thyroid disease—particularly hyperthyroidism—on body
weight and composition are valuable examples of the critical role hormones play
in the regulation of metabolism. Aside from energy metabolism, thyroid hor-
mone action affects other critical systems in an organism: first and foremost, the
central nervous system, both during development and throughout adult life. Thy-
roid hormone action is also particularly important for bone growth and remod-
eling, as well for skeletal muscle development and function. Collectively, the
action of thyroid hormone is pervasive, and its regulation is crucial for mainte-
nance of body functions.
Disorders affecting the thyroid gland—both function and tumors—are very
common in the general population and are disproportionally frequent in women.
Although the symptomatology associated with overt thyroid dysfunction is quite
characteristic and easily recognizable, most patients with thyroid disorders are
affected by mild forms of thyroid dysfunction, with symptoms and signs that
are often vague and aspecific. As individuals age, the prevalence of thyroid dys-
function can be as high as 12%, and population studies indicate that thyroid
nodules are also very common. Increasing availability of sophisticated diagnos-
tic tools and more widespread use of thyroid ultrasound has contributed to the
increased frequency of diagnoses of thyroid dysfunction, nodules, and cancer in
recent years.
This increase in diagnoses of thyroid pathology has been mirrored by an
increase in awareness among the general public of the role (whether real or per-
ceived) that thyroid function plays regarding an individual’s sense of well-being.
This has progressed to the point that assessment of thyroid function is one of the
first steps providers undertake while evaluating symptomatology that is not clear
and that may have overlap with other chronic conditions. As a consequence, thy-
roid disease and dysfunction are very common concerns among patients and pro-
viders, and, quite often, both parties share the notion that subclincal or unrec-
ognized thyroid dysfunction may be the root cause of otherwise unexplained
symptoms. As a consequence, modulation of thyroid function, via either therapy
or dietary supplements, is often employed to address a variety of conditions, par-
ticularly those involving weight gain, low energy, chronic fatigue, and depression.
Against this background of increased awareness and, in some cases, perhaps
excessive expectations, it’s important to consider that the thyroid gland and its
function is heavily affected by nutrition and adequate delivery of oligo-elements:
in particular, iodine and selenium. In fact, iodine deficiency represents the most
common preventable cause of intellectual disabilities worldwide. Although
the United States is considered an iodine-sufficient area, some conditions and
dietary habits can significantly impact iodine intake, resulting in iodine defi-
ciency. Thyroid pathology itself, in either the acute or recovery phase of disease,
xxiii

often requires nutritional intervention to optimize the healing process and to
prevent additional morbidity.
Some lay literature and a substantial number of practitioners—particularly
in the fields of alternative and complementary medicine—strongly support using
nutritional supplements and modification of diet to optimize thyroid function,
either by addressing nutritional deficiencies or stimulating immune function.
Although the empirical evidence of this in humans is marginal and of limited
quality, it is important to note that in vitro experiments and mechanistic studies
carried out in laboratory animal or cell culture systems have indicated that nutri-
tion and oligo-element supplementation play roles in the pathophysiology of the
thyroid. While this is important, it’s also important to recognize the knowledge
gap between findings in experimental models and clinical relevance in patients.
The Health Professional’s Guide to Nutrition Management of Thyroid Disease
takes a unique course by defining the role of nutrition and dietary supplemen-
tation in thyroid physiology and pathology. By systematically defining the vari-
ous physiologic states and pathologic conditions affecting the thyroid, this book
provides relevant information on the potential roles of nutrition intervention and
use of dietary supplements. It strives to define the mechanistic rationale for such
interventions; whenever possible, it provides references to relevant human stud-
ies. It provides references to guidelines of leading professional organizations that
are dedicated to the study and care of thyroid disease, and it recognizes the gaps
in knowledge of the effects of nutritional interventions and dietary supplementa-
tion that exist in relation to thyroid disorders.
This book’s systematic approach to the topic and its extensive references to
high-quality published research make it a useful reference for nutritionists and
practitioners alike. At the same time, each chapter’s introduction provides a good
framework of the problem presented, which enables a nonmedical audience to
better understand the roles nutrition and dietary supplementation can serve in
the amelioration of thyroid disease, all while maintaining realistic expectations.
Finally, the extensive references and resources herein provide a comprehensive
tool set to help readers further deepen their knowledge of the interactions among
nutrition, dietary supplementation, and thyroid function.
xxiv
INTrOduCTION

SECTION 1
Introduction to
Thyroid Disorders
CHaPTEr 1
2
CHaPTEr 2
15
CHaPTEr 3
29
CHaPTEr 4
36
Overview of the Thyroid and Its Function
Thyroid and Weight Regulation
Energy and Nutrient Requirements in Thyroid Disease
Iodine and Its Role in Thyroid Management

1 The thyroid is a butterfly-shaped endocrine gland weighing less than 1 ounce
(28 g) in healthy adults and children. It is located in the middle of the lower neck,
in front of the trachea (see Figure 1.1).1
Thyroid hormones regulate the body’s
metabolism and affect nearly every action of every cell, including such vital func-
tions as heart rate and energy level.2,3
The thyroid works in conjunction with the pituitary gland and the hypothal-
amus. The hypothalamus, located in the lower central area of the brain, produces
thyrotropin-releasing hormone (TRH) in response to external factors and stress-
ors.4
TRH travels to the pituitary gland at the base of the brain. There, thyrotropin/
thyroid-stimulating hormone (TSH) is produced. TSH is sent to the thyroid gland
to regulate thyroid hormone storage, production, and release. Figure 1.2 illustrates
the feedback mechanisms of the hypothalamic-pituitary-thyroid (HPT) axis.
Overview of the Thyroid
and Its Function
FIGURE 1.1
THYROID ANATOMY
INTRODUCTION
Larynx
Right thyroid gland
Trachea
Isthmus
Left thyroid gland
2

The two primary hormones produced by the thyroid are thyroxine (T4) and
triiodothyronine (T3). T4 contains four iodine atoms; it is converted to the bio-
logically active thyroid hormone T3 by losing one iodine atom via a process
called monodeiodination.5
A healthy thyroid produces about 80% to 90% T4,3,4
or about 85 µg/d,4,5
and 10% to 20% T3.3,5
Normal total daily T3 produced in a
healthy male is 33 µg/d. About 26 µg (~80%) of this is derived from conversion of
T4 in peripheral tissues, mostly within the liver and kidneys1
; only 6.5 µg (~20%),
is secreted directly by the thyroid.6
Nearly 70% of T4 produced in the peripheral tissues is deiodinated and
then converted to T3 or reverse triiodothyronine (RT3) or eliminated.1
RT3
is a metabolite of T4 created by selective deiodination of an iodine atom in the
inner ring of T4.7
This conversion has long been established to occur in times of
acute and chronic stress resulting from nonthyroidal illness, thus decreasing the
pool of circulating T3.8,9
The thyroid also produces a small amount of the thy-
roid hormones diiodothyronine (T2), which has two iodine atoms, and mono-
iodothyronine (T1), which has only one iodine atom.10,11
Preliminary studies
show that T2 may play a role in metabolism and fat burning processes and may
also help with conversion of T4 to T3.12
Further research is needed. T1 has no
known function to date.10
FIGURE 1.2
HORMONAL
INTERPLAY AMONG
THE HYPOTHALAMUS,
PITUITARY GLAND,
AND THYROID
(+) positive feedback stimulation,
(−) negative feedback inhibition
CHaPTEr 1: OvErvIEw Of THE THyrOId aNd ITS fuNCTION
3

According to the American Thyroid Association (ATA), more than 12% of the
US population will develop a thyroid condition during their lifetime. Women are
five to eight times more likely than men to have thyroid problems; one in eight
women will develop a thyroid disorder in her lifetime.3
In regions where nutritional iodine is sufficient, the causes of thyroid prob-
lems are largely unknown.13
Several areas have been implicated in the develop-
ment of both biological and nonbiological thyroid imbalances, including nutri-
ent deficiencies; increased thyroid binding proteins; over- or under-conversion of
the inactive thyroid hormone to the active hormone; autoimmunity; or problems
with the anterior pituitary.1
There is a strong genetic component to the develop-
ment of thyroid dysfunction.14
Each chapter in this book is condition-specific
and will discuss potential etiologies in more detail. However, in general:
• In hypothyroidism, or “slow thyroid,” where the body requires more
thyroid hormone to function properly,TSH levels will elevate in an
attempt to signal the thyroid to produce more thyroid hormone.
• In hyperthyroidism, or “fast thyroid,” where there is an excess of thyroid
hormone in the body,TSH levels will decrease, signaling the thyroid to
produce less hormone.
Generally, TSH has an inverse relationship with thyroid function—when it
is lower than the range, the thyroid is typically overactive; when it is higher than
the range, the thyroid is prompted by the pituitary gland to produce more thy-
roid hormone because it is underactive.
DEFINITIONS AND
CAUSES OF THYROID
DISORDERS
Thyroid Disorders and
Health Impact
Because thyroid hormone influences nearly every cell, thyroid disorders can affect
multiple systems in the body and have a wide variety of effects and symptoms.
The thyroid plays a key role in calcium balance; maintenance of the rate at which
the body utilizes fat and carbohydrate; the body’s temperature control; regulation
of the production of protein; the oxygen consumption of cells; heart rate; over-
all hormone balance; and mood. Some research has shown that the thyroid also
affects the metabolism of folate and homocysteine.15
Genes in many cells, including hepatocytes; cardiac and skeletal myocytes;
kidney cells; lung endothelial cells; and brain cells, are highly sensitive to thy-
roid hormone.13
Thyroid conditions can increase the risk of cardiovascular dis-
ease, osteoporosis, infertility, miscarriage, and preterm births, as well as severe
developmental problems in children born to mothers with underactive thyroids.3
Thyroid disease also has many implications in the realm of mental disorders, such
as depression and anxiety.13
Disorders of the thyroid tend to last the duration of
one’s life and require medical management.3
UNDERSTANDING
DIAGNOSTIC
CRITERIA
Traditionally, TSH levels are monitored to assess thyroid disease. Elevated TSH
would indicate hypothyroidism, whereas TSH below the range may indicate
hyperthyroidism. There is debate in the medical world, however, as to what the
acceptable normal reference range for TSH really is. Many medical facilities list
the TSH reference range as 0.45 to 4.5 mIU/L, but in January 2003, the Amer-
ican Association of Clinical Endocrinologists (AACE) issued an announcement
recommending treatment of patients based on a more narrow range for TSH of
0.3 to 3.0 mIU/L.16
The statement noted that in the future, it is likely that the
“limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L
because less than 95% of rigorously screened normal euthyroid volunteers have
serum TSH values between 0.4 and 2.5 mIU/L.… A serum TSH result between
0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard
levothyroxine (L-T4) replacement dose for primary hypothyroidism.”10
The ref-
4
SECTION 1: INTrOduCTION TO THyrOId dISOrdErS

erence ranges, though time-consuming to develop, are created by studying levels
in people who have both normal and abnormal thyroid levels, which creates a
non-normal distribution. This narrower TSH range has not been widely adopted
into practice, however, and these recommendations are not included in the ATA/
AACE 2012 Clinical Practice Guidelines for Hypothyroidism in Adults or the
2014 Guidelines.5
Table 1.1 provides information on how TSH levels can be used to under-
stand, assess, and monitor thyroid disease.17-19
Some experts suggest that an upper limit of 1.5 mIU/L for TSH might be
advised, and that treating some patients within the upper range of the normal
TSH reference range can improve comorbidities and symptoms of subclinical
hypothyroidism (SCH) that are related to the non-normal distribution of TSH
in the currently used reference range.20,21
TABLE 1.1 LEVEL OF THYROID-STIMULATING HORMONE WITH
INTERPRETATION AND EXPECTED HORMONAL PROFILE17,18,19
Thyroid-Stimulating
Hormone (TSH) Interpretation Expected Hormonal Profile
20 mIU/L Moderate to severe hypothyroidism Low free triiodothyronine (FT3),
low free thyroxine (FT4)
>10 mIU/L Overt hypothyroidism Low FT4
4.5-10 mIU/L Subclinical hypothyroidism Normal FT3 and FT4
2.5-4.5 mIU/L Normal, but may indicate hypothyroidism if symptoms are
present; some practitioners consider TSH at 2.5 or above to be
indicative of subclinical hypothyroidism (SCH)
Normal FT3 and FT4 (may be
low, but rarely would this TSH
range warrant testing, even if
requested by a patient)
0.4-2.5 mIU/L Normal Normal FT3 and FT4
0.1-0.39 mIU/L Gray zone for too much thyroid hormone, subclinical
hyperthyroidism (SH), or pituitary dysfunction; some
practitioners consider hyperthyroidism when TSH is below 0.3
Normal FT3 or FT4
<0.1 mIU/L Hyperthyroidism, pituitary problem, or TSH suppression due to
medications (note: TSH suppression due to thyroid medications
does not always produce elevated thyroid hormones)
High FT3 or FT4
Concerns When Using
Thyroid-Stimulating
Hormones to Assess
Thyroid Status
While TSH is generally the first, and often the only, test ordered to assess thy-
roid disease, using this test alone to assess thyroid health can raise concerns.
Additionally, the health professional should be aware of some potential concerns
with narrowing the TSH range and treating at subclinical levels. See Boxes 1.1
and 1.2 (pages 6 and 7).
5

BOX 1.1 POTENTIAL CHALLENGES TO TREATMENT BASED ON
THYROID-STIMULATING HORMONE LEVELS
Controversy in Diagnosing
Hypothyroidism and
Hyperthyroidism
The health professional should be aware that guidelines of different professional
societies recognize areas where further research is needed and that some dis-
agreement exists as to treatment recommendations and as to which tests should
be ordered.33
Prior to thyroid hormone blood tests becoming available, diagno-
ses to indirectly assess thyroid function were commonly made based on basal
temperature (low in hypothyroidism); serum cholesterol (low in hyperthyroidism
and high in hypothyroidism); iodine levels (typically low in hypothyroidism and
high in hyperthyroidism); and Achilles reflex time (slower in hypothyroidism
and quicker in hyperthyroidism). Some practitioners treat underactive thyroid
based on symptoms alone without ordering blood work, while others base treat-
ment plans on biochemical values alone without taking clinical symptomology
into account. It is important to be aware of these polarities.
UNDERSTANDING
THYROID HORMONES
AND LABORATORY
MEASURES
Measuring free thyroxine (FT4), free triiodothyronine (FT3), total thyroxine
(TT4), and total triiodothyronine (TT3) can provide more information as to
the severity of thyroid conditions. Thyroid hormone is bound to carrying pro-
teins, such as thyroxine-binding globulin (TBG), in the blood stream. TBG is
produced in the liver and can be affected by illness, liver disease, and some med-
ications, including estrogen.13
More than 99% of thyroid hormone in the blood
is bound to carrying proteins; TT4 and TT3 can be high or low when there are
varying levels of these proteins. High and low TT4 and TT3 levels do not nec-
essarily reflect a thyroid problem. A T3 uptake test to estimate the amount of
TBG present can be ordered, revealing an estimate of biologically active thyroid
hormone in the body when combined with TT4 or T3 readings, but this test is
not presently in frequent use.
See Box 1.3 for definitions of laboratory values and Table 1.2 on page 10 for
optimal lab values.
Ordering a thyroid-stimulating hormone (TSH) level test as the
sole diagnostic criteria for hypo/hyperthyroidism would not
uncover an autoimmune thyroid condition or aberrations in
thyroid hormone levels.
One study showed that more than 50% of women who test
positive for antithyroid antibodies had a TSH between 2 and
4.5 mIU/L, which is considered within the normal range.22
There are concerns that narrowing the TSH normal reference
range may lead to over-diagnosis, increased risk of
overtreatment, and a financial burden to society.23,24
There is some evidence that levels of thyroid hormone in tissues
differ from pituitary thyroid hormone levels, and therefore
would not be reflected in the TSH.13
Research on animals has shown that different tissues may have
differing levels of triiodothyronine (T3), reflecting inconsistent
thyroid status from tissue to tissue.13
TSH may be normal in some hypothyroid patients treated with
the most common thyroid hormone replacement medicine,
levothyroxine (L-T4), with a high thyroxine (T4):T3 ratio even
when T3 levels are lower than the normal range.13
A study found that as L-T4 doses were increased, TSH levels
further decreased, and the drug became progressively less
effective at maintaining free T3 (FT3) levels. The lowered TSH
levels presumably led to an inability to maintain FT3 levels in
the normal range.13
The researchers of this study suggested that
for this reason, T3 levels should be considered in addition to
those of TSH.13,25
It has been shown that TSH levels fluctuate, even within the
course of a single day.5
6

BOX 1.3 LAB DEFINITIONS AND INTERPRETATION15,34
Total Thyroxine, Total T4,
Serum Thyroxine (TT4)
The total amount of serum thyroxin, including what is bound
to proteins. Bound thyroxine does not affect tissue function in
the body.
BOX 1.2 ADDITIONAL INFORMATION REGARDING
THYROID HORMONE LEVELS
continued on next page
It is not known if all tissues in the body can maintain
uniform levels of thyroid hormone when the thyroxine
(T4):triiodothyronine (T3) ratio is altered—namely, when T3
is low—due to different tissue deiodinases, transporters, and
thyroid receptors (TRs).13
The clinical significance of T3 serum concentrations fluctuating
within and below the normal range is unknown.13
T4 can be continuously converted to reverse triiodothyronine
(RT3).8,9
Some practitioners consider an elevated RT3 to signify
a problem with conversion of T4 to T315
; however, RT3 can
elevate for many reasons, most unrelated to the thyroid.
When the body is under physical or emotional stress, such
as acute/chronic illness, high cortisol levels, selenium/iron
deficiency, trauma, surgery, medical conditions/medications,
aging/inflammation, and circumstances in which it must
conserve energy for prioritized use in another function, it
increases conversion to RT3, which causes T3 levels to
decrease, so patients may theoretically feel the symptoms of
hypothyroidism due to the decreased effect of active T3.8,9,15
Decreased levels of serum iron, iron saturation, and ferritin,
which lead to low hemoglobin and red blood cells, are all
common in thyroid disease.
The stresses of hypothyroidism, including suboptimal treatment,
can lead to high cortisol production by the adrenal glands.
Excess cortisol prevents conversion of T4 to T3, causing further
production of RT3 and perpetuating the problem.15,26,27,28
Some practitioners consider RT3 levels over 15 ng/dL (with
a normal reference range of 8 to 25 ng/dL) to be indicative of
inadequate cellular T3.29,30
The ratio of free triiodothyronine (FT3):RT3 or total
triiodothyronine (TT3):RT3 can be checked to assess thyroid
tissue status. Some practitioners recommend that the FT3:RT3
ratio be greater than 20 for adequate thyroid hormone in the
tissues; if TT3 is used, the ratio should be at 10 or above.31
These ratios, which are more commonly used by some
integrative medicine practitioners, may help the patient, but
they are not supported by the professional societies in the area
of thyroid due to a lack of research validating this calculation.
However, it has recently been suggested that the T3:RT3 ratio is
significantly higher in instances of insulin resistance.32
Free Thyroxine, Free T4 (FT4)
The amount of unbound T4 in the blood; >1% of T4 is
unattached. Free thyroxine affects tissue function in the body.
Most tests are affected by the carrier protein concentration in
the serum.
INTERPRETATION
Low levels may indicate hypothyroidism.
Low T4 with an elevated TSH implicates the thyroid as the cause.
Low T4 with normal or low TSH may indicate secondary (central)
hypothyroidism or thyroid binding deficiency.
TT4 may appear high during pregnancy, during estrogen replacement
therapy, or with the use of oral contraception, but this may not indicate
hyperthyroidism.
INTERPRETATION
High FT4 may indicate hyperthyroidism.
Low FT4 suggests hypothyroidism.
Note that measurement of free thyroid hormones is usually
performed on analog assays and not by equilibrium dialysis or
mass spectroscopy; in that case, the result is an estimate rather
than an actual measure.
7

Serum Triiodothyronine, Serum T3,
Total T3 (TT3)
The total amount of serum triiodothyronine, including what is
bound to proteins.
BOX 1.3 LAB DEFINITIONS AND INTERPRETATION (continued)15,34
INTERPRETATION
High T3 may indicate hyperthyroidism.
Low T3 may indicate hypothyroidism.
Free Triiodothyronine, Free T3 (FT3)
The amount of free, unbound T3 in the blood; >1% of T3 is
unattached. T3 has a greater effect on the body’s utilization of
energy than T4.
INTERPRETATION
High FT3 may indicate hyperthyroidism.
Low FT3 may indicate hypothyroidism.
The test is not considered particularly precise because of very
low concentrations of the analyte; for this reason, the American
Thyroid Association does not advocate for routine testing of FT3.
T3 Resin Uptake (T3 Uptake)a
Test seldom used to assess whether abnormal T4 and T3 levels
are due to thyroid imbalance or due to hormone binding in the
bloodstream, as it indirectly measures the thyroid hormone
capacity of the serum.
INTERPRETATION
High T4 and high free thyroxine index (FTI) would indicate
hyperthyroidism.
Low T4 and low FTI would indicate hypothyroidism.
High T4 and low T3 resin uptake would indicatehigh TBG.
Low T4 and high T3 resin uptake would indicate low TBG.
Thyroglobulin (Tg)
A protein produced by the thyroid; its serum concentration is
proportional to the thyroid tissue mass.
INTERPRETATION
Low or normal in normal thyroid.
May be elevated when inflammation is present, such as in large
goiters or in thyroiditis, which causes a release of this protein.
In thyroid cancer, the burden of tissue causes an increase
in thyroglobulin level, and Tg can be used as a marker of
recurrence.
Reverse T3 (RT3)
Created from T4 when the body is under stress (instead of T4
converting into T3).
INTERPRETATION
Considered an inactive form of T3; used to conserve energy
versus thyroid converting to active T3.
Thyroid Microsomal Antibodies/
Antimicrosomal Antibodies (Thyroid
Antimicrosomal Antibody, Antimicrosomal
Antibody, Microsomal Antibody, Thyroid
Peroxidase Antibody)
Seen in Hashimoto thyroiditisb
and granulomatous thyroiditis;
indicates an autoimmune process.
INTERPRETATION
More than 80% of people with Hashimoto thyroiditis have
elevated levels.
8

BOX 1.3 LAB DEFINITIONS AND INTERPRETATION(continued) 15,34
a
Sometimes referred to as the free thyroxine index (FTI) test when performed with T3 and T4
b
The Academy of Nutrition and Dietetics has adopted the increasingly common practice of dropping possessive apostrophes from the names of
diseases and disorders . Please see Special Note on page xxi for more information .
Thyroid Peroxidase Antibodies (TPOAbs)
Antibodies to an enzyme related to thyroid.
INTERPRETATION
May indicate Hashimoto thyroiditis; less commonly seen in Graves
disease.b
If not present, Hashimoto disease is not ruled out.
Thyroglobulin Antibodies (TgAbs)
Used to identify autoimmune thyroiditis and related conditions
and as part of the thyroglobulin tumor
marker panel.
INTERPRETATION
May be present in Hashimoto disease.
Occasionally present in the normal population.
May be elevated in thyroid cancer monitoring if a recurrence is
present.
Thyroid Stimulating Immunoglobulin (TSI)
Antibodies
Binds to and activates the TSH receptor, causing the production
of excess thyroid hormones.
INTERPRETATION
Presence indicates Graves disease is the primary cause.
Thyroid Stimulating Hormone Receptor
Antibody (TRAb)
Used to investigate the possible diagnosis of Graves disease.
INTERPRETATION
May be elevated in Graves disease.
Thyroxine-Binding Globulin (TBG)
Made in the liver; binds to T3 and T4, preventing the kidneys
from removing these hormones from the blood; hormones are
released when needed in the body.
INTERPRETATION
Low TBG may be congenital.
High TBG may indicate hypothyroidism or liver problems.
Increased levels may be seen when estrogens are used, such as
when taking oral contraception or during pregnancy.
Decreased levels can be caused by prednisone, androgens, and
high doses of aspirin.
9

TABLE 1.2 TYPICAL VS OTHER LAB RANGES35-44
Test Name Typical Lab range Other ranges in use by Integrative medicine Practitioners
Thyroid-stimulating hormone
(TSH)
0.4-4.5 mIU/L 0.3-2.0 mIU/L
Free thyroxine (FT4) 0.8-1.8 ng/dL or
9-23 pmol/L
1.1-1.8 ng/dL or 15-23 pmol/L
Free triiodothyronine (FT3) 2.3-4.2 pg/mL or
3-7 pmol/L
Some practitioners recommend more narrow ranges within
the normal range (such as 5-7 pmol/L)
Thyroid peroxidase antibodies
(TPOAbs)
<35 IU/mL Some practitioners prefer this to be <9.0 IU/mL or even as low
as <2 IU/mL
Thyroglobulin antibodies (TgAbs) <20 IU/mL Some practitioners prefer this to be as low as <2 IU/mL
Reverse triiodothyronine (RT3) 8-25 ng/dL 11-18 ng/dL
Thyroid stimulating
immunoglobulin (TSI)
<140% activity Some labs use the reference range <125%; the higher the
percentage, the higher the likelihood of autoimmune activity
NUTRITION CARE
AND THYROID
DISEASE
Many patients with thyroid disorders experience unintended weight changes.
Because nutrition is so integral to weight management, a proper nutrition plan
can play a powerful role in a thyroid disease patient’s quest to lose, gain, or stabi-
lize weight, but practitioners must take the hormonal profile into account. A diet
or exercise program may prove to be unsuccessful without medical management
to treat the underlying hormonal dysfunction.
Thyroid treatment, including nutritional approaches to optimize thyroid con-
ditions, relies on understanding the unique concerns of patients with thyroid prob-
lems and also each thyroid-specific condition. The registered dietitian nutritionist
(RDN), along with other health professionals, can help clients achieve their nutri-
tional goals and improve their health. Additionally, the RDN’s work with patients
with thyroid conditions can help improve autoimmune conditions, address the
physical stressors caused by thyroid disease, and augment management of each
specific thyroid disorder while simultaneously examining their root cause.
Interacting with these patients provides the opportunity to raise awareness
of key nutritional factors involved in medical management for optimal thyroid
function; this may include a recommendation for a referral to an endocrinolo-
gist or another physician specializing in thyroid disorders to oversee a patient’s
care. Most patients with thyroid disorders are treated by their primary care phy-
sician. Endocrinologists, physicians who have specialized training in the hor-
monal system and treatment of endocrine diseases, may also treat these patients.
Other practitioners working with these patients may include complementary and
alternative practitioners; naturopaths; and integrative or functional medicine
physicians. Patients with thyroid dysfunction also require nutrition counseling
10

provided with sensitivity, informative nutrition education, and assurances of and
advocacy for adequate medical care.
While this professional resource provides guidance for nutritional manage-
ment of thyroid disorders utilizing the Nutrition Care Process (NCP; described
below in Box 1.4 and in further detail in the appendixes), research on optimal
thyroid management and treatment is ongoing. Conflict exists among the med-
ical and alternative medicine communities as to the best methods for treating
thyroid diseases. At present, there are no official guidelines specific to the role of
nutrition in the treatment of thyroid disorders.
BOX 1.4 THE NUTRITION CARE PROCESS45,46
Step Domains
Nutrition assessment Food- or nutrition-related history
Anthropometric measurements
Biochemical data, medical tests, and procedures
Nutrition-focused physical findings
Patient/client history
Nutrition diagnosis Intake
Clinical
Behavioral-environmental
Nutrition intervention Food or nutrient delivery
Nutrition education
Nutrition counseling
Coordination of nutrition care
Nutrition monitoring and evaluation Food-/nutrition-related history
Anthropometric measurements
Biochemical data, medical tests, and procedures
Nutrition-focused physical findings
Regardless of treatment plan, it is important for nutrition professionals to:
• evaluate the patient’s eating and lifestyle habits;
• create individualized healthy eating and lifestyle patterns addressing
nutrition concerns and physical needs;
• assist patients in establishing a healthy eating program in regard to
medication and condition-specific needs;
• understand that typical weight loss projections based on energy intake
may not be appropriate for a person with thyroid disease47
;
• assess and determine the need for micronutrient supplementation, as
vitamin and mineral deficiencies often occur with certain thyroid disorders,
11

and proper supplementation or dietary intervention may improve outcomes;
• discuss food–drug and herb–drug interactions and be aware of signs and
symptoms of residual disease; and
• discuss ideal timing of medications in relation to intake of food and
supplements.
The Nutrition Care Process The NCP developed by the Academy of Nutrition and Dietetics is a systematic
approach to providing high-quality nutrition care. The NCP provides a frame-
work for the nutrition practitioner to individualize care, taking into account the
patient’s needs and values and using the best evidence available to make nutrition
care recommendations. The NCP delineates four steps, including (1) nutrition
assessment; (2) nutrition diagnosis; (3) nutrition intervention; and (4) nutrition
monitoring and evaluation.45,46
Box 1.4 delineates the domains (or categories)
within each of the NCP’s steps. Screening is not an official part of the NCP,
but awareness of signs and symptoms of thyroid disease may allow a dietitian or
other health professional to identify the potential need for further medical inves-
tigation of a potential thyroid condition.
Chapters 7, 11, and 15 explore the roles that the NCP can play in treating
patients with hypothyroidism, hyperthyroidism, and thyroid cancer, respectively.
ADVICE FOR HEALTH
PRACTITIONERS
WORKING
WITH PATIENTS
WITH THYROID
CONDITIONS
In addition to having a thorough understanding of the thyroid’s function and
possible treatment options for thyroid conditions (both through medication and
medical nutrition therapy), the health professional has additional concerns when
working with patients with thyroid conditions. Health professionals should
strive to follow the actions discussed below.
Express understanding and empathy. Some patients may turn to holistic and
naturopathic practitioners after perceiving that their symptoms have not been
adequately addressed by conventional medicine.
Stay abreast of the current research. A thorough working knowledge of med-
ications, lab interpretation, food–drug interactions, timing of medications for
optimal absorption, and dietary strategies to overcome weight loss resistance and
other weight-related challenges are integral to effective nutrition diagnoses and
interventions.
Understand not only the physical but also the mental implications of thyroid
disease. Both underactive and overactive thyroid conditions can affect mood,
depression, anxiety, and the ability to adhere to a food and lifestyle plan. Helping
patients address and manage stress can be a good starting place because of the
connection between thyroid health and adrenal imbalances.
Be aware of the other practitioners who treat patients with thyroid disease
and be willing to work with them in the interest of providing the patient with
the best level of care. These may include general practitioners, endocrinologists,
functional medicine practitioners, naturopaths, and even nuclear medicine doc-
tors who work with Graves disease and thyroid cancer patients. At times, oncol-
ogists and otolaryngologists (ENTs) are involved in the care of patients with
thyroid cancer.
Encourage regular monitoring and have an understanding of ideal medical
follow-up schedules. Thyroid lab values can fluctuate from season to season,48
in the progression of the thyroid disease, or due to the thyroid itself (for example,
during a flare-up of Hashimoto thyroiditis).49
A patient may benefit from testing
12

more frequently than once a year. If a patient is taking medications, it is import-
ant to follow up with blood tests to avoid hormone excesses and deficiencies.
Understand challenges to treatment. Being diagnosed with and treated for thy-
roid imbalance may be a relief, and benefits may be noticeable, at least initially,
but for some patients, a diagnosis is just the beginning of a journey toward opti-
mal treatment and thyroid management. Once patients begin treatment, they
may also encounter residual symptoms, including emotional effects, and weight
gained during a thyroid imbalance is often difficult to lose.13,50
The health pro-
fessional can work with the patient to optimize dietary and lifestyle recommen-
dations.
Understand that not all patients with thyroid disease should be managed the
same way. Thyroid management usually depends on the approach of the physi-
cian treating the patient as well as the patient’s individual circumstances, includ-
ing past medical history, age, severity of the imbalance, and other concerns. If
difficulties arise during treatment, the patient should be referred to an endocri-
nologist.13
Keep an open mind and be prepared to revise a patient’s care plan. Anecdotally,
some patients report that they are unable to lose weight unless they try unconven-
tional measures, such as giving up grains (especially gluten-containing grains) or
considerably reducing carbohydrates. In these cases, it is important not to dismiss
the patient. When weight loss resistance arises in patients with thyroid conditions,
it can be challenging to successfully navigate potential options for weight loss and
maintenance. Hormonal effects on weight management are discussed in depth in
Chapter 2.
The remaining chapters in this book will delve into each thyroid condition
in detail. This information will assist the health professional in choosing a treat-
ment plan by understanding the causes and etiology, medical management, nutri-
tional management, and alternative and lifestyle management for each condition.
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20. Wartofsky L, Dickey RA. The evidence for
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23. Garber JR. Clinical Practice Guidelines for
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25. Hoermann R, Midgley JE, Larisch R, Dietrich
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27. Brtko J, Macejová D, Knopp J, Kvetnanský
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28. Hidal JT, Kaplan MM. Inhibition of thyroxine
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29. Chopra IJ. A study of extrathyroidal
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30. van den Beld AW, Visser TJ, Feelders RA,
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32. Ruhla S, Arafat AM, Weickert MO, et
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33. Nainggolan L. Endocrine societies at odds over
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14

A common complaint associated with hypothyroidism is weight gain,1
as a signif-
icant decrease in thyroid levels can disrupt hormonal function and slow metabo-
lism by 15% to 40%.2
Weight changes in hypothyroid patients have been investi-
gated in two retrospective studies discussed in the American Thyroid Association
(ATA) Guidelines for the Treatment of Hypothyroidism.3
One showed no sig-
nificant weight changes among participants receiving either replacement levels or
thyroid-stimulating hormone (TSH)-suppressive levels of levothyroxine (L-T4)
after total thyroidectomy.4
The other study looked at weight changes over a year
in four groups of patients; it found those with hypothyroidism gained more
weight than those who were euthyroid (meaning that they had normal thyroid
levels).5
Weight gain was greatest in patients with recent thyroidectomies, fol-
lowed by patients with preexisting hypothyroidism, and last in patients with a
preexisting thyroid cancer diagnosis.3,5
While hypothyroidism is the condition most often associated with weight
gain, in some cases, hyperthyroidism may result in weight gain as well.6
This
may occur because hypermetabolism can lead to hyperphagia and other hor-
monal effects. Free radical accumulation7
and insulin resistance can develop in
hyperthyroidism,8
causing even further weight gain. Similarly, in hypothyroid-
ism, there is a combination of increased ghrelin and insulin levels, leptin resis-
tance, and higher visceral fat—all of which can contribute to weight gain.9,10
Leptin, also known as the satiety hormone, is produced by adipose cells and plays
a role in the regulation of long-term energy balance by decreasing appetite and
food intake, thus leading to weight loss. Conversely, ghrelin, the hunger hor-
mone, acts quickly to increase hunger and prompt food consumption.10
The enzyme lipoprotein lipase (LPL) regulates fat storage, while hormone-
sensitive lipase (HSL) controls how fat is released.11
Both enzymes are directly
affected by insulin, cortisol, and the catecholamines epinephrine and norepi-
nephrine; they are indirectly affected by estrogen, progesterone, and testosterone.
All of these hormones—but especially insulin, cortisol, and the catecholamines
—are affected by thyroid hormone, which highlights the thyroid’s key role in the
potential for weight loss or gain.12
Even subclinical or borderline thyroid deficiency can be associated with sig-
nificant difficulty in achieving weight loss.13
Treating the hormonal imbalance is
the first priority, but many patients are unable to lose weight through this treat-
ment alone.14,15,16
For most people, adequate medical management will help make
weight loss attainable but will not cause it to occur spontaneously.
Thyroid and Weight
Regulation
HORMONES
INVOLVED IN WEIGHT
REGULATION
Other Mechanisms Involved
in Weight Regulation
Endocrine imbalances can contribute to increased adiposity, decreased lean body
mass, and slowed metabolism. As hormones regulate biochemical processes in
the body, they play a primary role in weight regulation.
2
15

The amount of heat generated by mitochondria is increased by the effects of
leptin, thyroid hormone, and certain amino acids but is decreased by ghrelin.17
This is sensed by the hypothalamus, which is responsible for activating the auto-
nomic nervous system and regulating many hormones involved in metabolism,
such as thyroid hormone, growth hormone (GH), and cortisol levels. Cortisol,
leptin, ghrelin, and thyroid also affect the hypothalamus and, therefore, they
affect food choices and appetite; sugary foods activate the pleasure center in the
brain. It is important to minimize lifestyle factors the hypothalamus perceives as
threats—including stress, lack of sleep, and hunger—to prevent fat storage and
excessive impulses to eat.18
Excess consumption of fat and sugar causes inflammation in the appetite cen-
ters of the hypothalamus, affecting food choices and increasing hunger and energy
intake due to decreased leptin sensitivity.19,20
Conversely, dietary protein can cause
mitochondria to produce more heat and thus can increase caloric burn.21,22
See Table 2.1 for a summary of several hormones involved in weight regula-
tion and their relationship to the thyroid.
TABLE 2.1 HORMONES, WEIGHT REGULATION, AND
RELATIONSHIP TO THE THYROID
Hormone Production and function Effect on weight regulation relationship to Thyroid
Leptin Produced by adipose tissue.
Highest between midnight and
early morning.23
Decreases appetite and food
intake.
Known as the “fullness
hormone.”
Women have 2-3 times as much
leptin as men due to higher
body fat percentage.24
Subcutaneous fat produces
more leptin than visceral fat.25
Production increases with increased body fat.
Excess levels lead to leptin resistance, further
weight gain, and slowed metabolism.26
Dramatic caloric restriction significantly
decreases leptin levels, increasing appetite and
slowing metabolism.
Reducing dietary fructose27
and eating a
moderate amount of healthy fats (such as
monounsaturated fats found in olive oil and
avocado) can help induce weight loss via leptin
sensitization. A high-fat diet (defined as 60% fat)
has been shown to reduce 24-hour leptin, leading
to weight gain, while a low-fat diet (defined as
20% fat) did not.23
A high-protein diet has been shown to help reduce
body weight despite leptin concentration.28
It promotes production of
thyroid hormones.
It signals cellular
conversion of thyroxine
(T4) to triiodothyronine
(T3).
Blunted signal of leptin
leads to decreased
thyroid hormone
efficiency at the cellular
level.29
Leptin becomes less
efficient in the presence
of excess thyroid
hormone, leading to
increased appetite and
food consumption.
Ghrelin Produced mainly in the stomach
with small contributions from
the pituitary, pancreas, brain,
and testicles.
Known as the “hunger
hormone.”
Rises before a meal to signal
one to eat and lowers once
eating has stopped to send the
signal of satiety; other factors,
such as quantity of intake, play
a role in secretion.10
It increases appetite, slows metabolism, and
leads to fat storage.
It remains high when caloric intake is decreased
to encourage eating.
Eating a high-protein meal decreases the desire
to eat.28,30
It slows the thyroid when
elevated.
Some practitioners
suggest eating at regular
intervals to avoid the rise
of ghrelin prior to a meal
and recommend including
high-fiber foods and
protein at each meal to
blunt hunger.
16

Thyroid
(active T3)
Affects the appetite centers of
the hypothalamus controlling
food choices and fat burn.
Involved with almost all
chemicals that regulate
metabolism, including leptin,
ghrelin, and growth hormone
(GH), while increasing energy
burn and improving mood.31
Thyroid hormone deficiency promotes leptin
resistance, further decreasing metabolism and
leading to weight gain.29,31
Low thyroid hormone increases ghrelin,
increasing appetite.32
Thyroid hormone stimulates mitochondria to produce
heat, regulating temperature and metabolism.
It regulates abdominal adiposity, insulin sensitivity,
cardiovascular function, blood lipid levels, blood
pressure, and neurotransmitters affecting mood,
satiety, appetite, food choices, and taste.33
Overweight status is associated with a relative
increase in T3 levels (within normal range). It is
not clear whether this state is associated with a
state of relative resistance to the T3 action.
It is the center of
metabolic regulation.
Dramatic caloric restriction
causes the thyroid to slow
metabolism by converting
more T4 to reverse T3.
Obesity is related to
hypothyroidism. Body mass
index is related to increasing
thyroid-stimulating
hormone (TSH).34
Obesity is associated with
both a mild increase in
TSH and T3, potentially
suggesting a compensatory
activation of the thyroid axis.
Insulin Regulates glucose and fat
metabolism.
After eating, glucose enters the
bloodstream and triggers the
release of insulin, which then
signals cells in the liver, muscle,
and fat to uptake glucose.
Consumption of excess carbohydrates will cause
the excess glucose to be converted into fat in a
process called lipogenesis. This can also lead to in-
sulin resistance and cause weight gain, further
insulin resistance, and depletion of adiponectin.
Adiponectin is a hormone produced solely by
adipocytes and is a regulator of glucose and
energy homeostasis. It has been shown to exert
anti-inflammatory and antiatherogenic effects and
to reverse insulin resistance in rodents primarily
by increasing hepatic insulin sensitivity.35
The higher the blood sugar level is, the higher the
levels of systemic inflammation will be, making
metabolism less efficient, leading to leptin
resistance, and affecting the hypothalamus and
appetite control center.36,37
Insulin stimulates the production of the enzyme
11-beta-hydroxysteroid dehydrogenase (11 beta
HSD), which creates its own cortisol and is found
at high levels in visceral fat.38
It enhances activity of lipoprotein lipase (LPL)
and suppresses hormone-sensitive lipase (HSL),
making fat storage more likely in the presence of
excess energy intake; it decreases energy burn
with caloric restriction.12
It works in concert with cortisol to promote
central adiposity.12
Thyroid hormone can
either be insulin agonistic
or antagonistic in
different tissues.39
In hyperthyroidism, free
radical accumulation and
insulin resistance can
develop, causing weight
gain.
In hypothyroidism,
insulin resistance may
be due to dysfunction in
mitochondrial oxidative
metabolism.39
Growth
hormone
Released during REM sleep; helps
increase metabolism and break
down fats; l-arginine signals the
pituitary to release GH.40
Increases muscle mass and
bone mineralization and plays
a role in protein synthesis and
cellular growth.41
It works in congruence with cortisol and
adrenaline to oxidize fat and build muscle when
hormones are in balance.
Low levels lead to muscle breakdown, decreased
energy and libido, increased adiposity, and
insulin resistance, and can cause emotional
instability.41,42
In GH deficiency,
treatment with GH
increases circulating T3.
Plays a role in the
physiological regulation
of thyroid function and
in peripheral conversion
of T4.43
RELATIONSHIP TO THE THYROID (continued)
CHaPTEr 2: THyrOId aNd wEIgHT rEguLaTION
17

Cortisol Produced by the adrenal glands.
In a normal pattern, it is highest
in the morning, encouraging the
release of blood glucose upon
awakening to fuel activity.
There are over 400% more
cortisol receptors in visceral
fat than subcutaneous fat,44,45
which implicates cortisol in
the accumulation of intra-
abdominal fat deposits.12,46
Compared to subcutaneous fat,
visceral fat is more sensitive to
cortisol, is less sensitive to insulin,
has a greater blood supply, and is
richer in beta-receptors.12
It is involved in both fat release and fat storage,
as it enhances LPL and HSL.
Its effects on HSL are decreased and its effects
on LPL are increased when in the presence of
insulin.12
High levels may promote accumulation of visceral
fat due to effects in the body and brain.13
It affects neuropeptide-Y (NPY), corticotropin-
releasing hormone (CRH), and leptin, which are
all involved in the regulation of appetite. For
this reason, when cortisol is high, people crave
palatable, unhealthy foods and are driven to eat
them more often.46,47
Stress can be a factor in
thyroid autoimmunity.48
Low thyroid is often
secondary to adrenal
insufficiency or cortisol
dysregulation.49
Chronic activation of the
hypothalamic-pituitary-
adrenal (HPA) axis
decreases conversion of
T4 to T3.
Sex
hormones
Adipose tissue has receptors
for sex hormones, which affect
the metabolism of fat.12
Progesterone and estrogen help control visceral
fat.
Estrogen decreases insulin and cortisol’s effects
on visceral fat, while progesterone suppresses
cortisol’s effects.
Testosterone at high levels in women and at
low levels in men can precipitate abdominal fat
storage.12
Hypothyroidism in women
promotes low estrogen,
low progesterone, and
cessation of ovulation.50
Testosterone is higher
and estrogen is normal or
decreased in hyperthyroid
women.51
In men, hypothyroidism
decreases testosterone52
and may increase female
sex hormones.53
THYROID-SPECIFIC
WEIGHT LOSS
TECHNIQUES
Weight management is one of the most frequent reasons why people visit a dieti-
tian. Practitioners specializing in the treatment of patients with thyroid disorders
have found some specific measures to be helpful in weight management counsel-
ing for this patient population.
The thyroid controls metabolism, so if either hyperthyroidism or hypothy-
roidism is present, all physiologic processes will be affected, including the ability
to promote weight change. The underlying medical causes should be treated as
top priority. The five biomarkers commonly tested (often referred to as “thyroid
function tests”) are as follows:
1. TSH
2. levothyroxine (T4) (free or total)
3. triiodothyronine (T3) (free or total)
4. anti-thyroperoxidase (TPO) and anti-thyroglobulin antibodies (TgAbs) for
hypothyroidism
5. thyroid stimulating immunoglobulin (TSI) antibodies for hyperthyroidism
There is a sixth and less commonly tested biomarker: reverse triiodothyronine (RT3).
Professional organization guidelines suggest the use of TSH as a screening test
RELATIONSHIP TO THE THYROID (continued)
18

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