Treatment of Thyroid Autoimmune Disease · •Week one: 12.5 mcg T3 •Week two: 12.5 mcg T3 BID...

Treatment of Thyroid Autoimmune Disease

Michaël Friedman ND

Executive Director- AARM

Treatment Protocols

Can Maximize Thyroid Recovery Rates in Low Thyroid

1) Patients who currently are on T4

2) Patients who have autoimmune Hashimotos, recently diagnosed

3) Patients who have autoimmune Hashimotos, longstanding for over a year

4) Patients who have no primary thyroid disease, but hypothyroid symptoms

American Thyroid Association Guidelines (2014)

Guidelines for Treatment of HypothyroidismJonklaas, J. & Bianco, A.C., Bauer, A.J., Burman, K.D., Cappola, A.R., Celi, F.S., Cooper, D.S., Kim, B.W., Rosenthal, M.S., Sawka, A.M.

7b. Does levothyroxine therapy that returns the TSH levels of hypothyroid patients to the reference range also result in normalization of their T3 levels?

Summary statementPatients with hypothyroidism treated with levothyroxine to achieve normal TSH values often have T3 concentrations that are at the lower end of the reference range, or even below the reference range. The clinical significance of this is unknown.

© 2013 BLab

Patients who currently are on T4

• If not feeling well and body temp under 98.6, then switch to T3

• 75% patients need to stay around 25 MCG BID T3

• 25% need to go higher

• Different Dosing Strategies

-Cunningham MD

-Wilson MD

Cunningham’s Protocol

Cycle by taking:

• Week one: 12.5 mcg T3

• Week two: 12.5 mcg T3 BID

• Week three: 25 MCG T3 AM and 12.5 MCG PM

• Week Four: 25 MCG T3 BID

Wilson’s Protocol

• Increase 7.5 MCG SR –T3 BID daily

• Cycle until 75 MCG SR-T3 BID or temp reaches 98.6 F, then wean every two days until off for 2 days, and cycle again

Example of T4 Saturation

• In patients with destroyed Thyroid Tissue due to Ablation (RAI, Surgery in Graves Patients)

Friedman Protocol:

• Gradually Lower T4 by 25% a day, while increasing T3 by 7.5 MCG SR-T3 BID

• Plateau at a dose where patient feels well, typically 75 MCG SR T3 BID

Synergistic Supplements

Synergistic Hormones• Hydrocortisone• DHEA

Synergistic Nutritionals• Iodine/Diiodotyrosine• Selenium

Synergistic BotanicalsAdaptogens: Rhodiola, Ashwagandha, EtcAntiinflammatory Resins: Guggul, Boswellia

• Rosmarinic Acid Containing Herbs: Melissa officinalis, Lycopus spp

Integrating Restorative Protocols

In patients with and Fatigue and Normal TSH

Use Nutrition:

– Iodine/Dioiodotyrosine

– Adaptogens –( Help with mitochondria)

– Thyroid Herbs

– Low Dose Cortisol ( if blood pressure low)

– Licorice

• T3 (different dosing)

Conventional Treatment of Hypothyroidism

• 50-100 mcg of T4 irrespective of TSH level, and irrespective of patient response

• Disordered sleep

• Hormone Deficiencies

• Nutritional deficiencies

• Infections

• Mitochondrial dysfunction

• Coagulation defect

• Gastrointestinal dysfunction

10

Common Associated Dysfunctions/CFS

Conventional Treatment of Hyperthyroidim

• Thionamide methimazole is the primary drug used to treat Graves' hyperthyroidism at 10 mg a day

• Then RAI Ablation Therapy

• Treat the adrenergic response: 40 to 120 mg propanolol or 25 to 50 mg atenolol daily until their serum T3 and serum T4 concentrations are normal

Conventional Treatment of Hyperthyroidim

• The thionamide methimazole is the primary drug used to treat Graves' hyperthyroidism at 10 mg a day

• Then RAI Ablation Therapy

Treat the Adrenergic Reponse

40 to 120 mg propanolol or 25 to 50 mg atenolol

daily until their serum T3 and serum T4

concentrations are normal

• Reproductive cancers, especially breast cancer are associated with hypothyroidism.

• Iodine and Selenium are hypothesized to provide antioxidant and action and offer chemoprevention effect on the breasts and thyroid.

Biofactors. 2003;19(3-4):121-30. Role of iodine in antioxidant defence in thyroid and breast disease. Smyth PP.

Cancer Causes Control. 2000 Feb;11(2):121-7. Hypothesis: iodine, selenium and the development of breast cancer. Cann SA, van Netten JP, van Netten C.

IODINE, SELENIUM AND BREAST CANCER

14

Conventional Thoughts on AIT

• Don’t take iodine

– Will cause/worsen AIT

• Don’t take desiccated thyroid

– Will cause/worsen AIT

Leo Tolstoy

“I know that most men, including those at ease with problems of the

greatest complexity, can seldom accept even the simplest and most

obvious truth if it would oblige them to admit to the falsity of

conclusions they have delighted in explaining to their colleagues.”

How Much Iodine Stored In The Body?

• Approximately 1.5-2gm stored in body at sufficiency

– Fat tissue: 700mg

– Striated tissue: 650mg

– Thyroid: 50mg

Every organ and all tissues contain iodine

Iodine Transport

These numbers are impossible to reach at the RDA (150µg/day) for iodine!

To achieve the maximum transport of iodine ≈600µg/day across the cell membrane,

there must be sufficient iodine in the serum:

≈10-5-10-6 M

However, 50mg/day iodine/iodide can reach a 10-5 M!

Where is Iodine Found in the Body?

• Every cell in the body contains and utilizes iodine

– WBC’s cannot effectively guard against infection without adequate amounts of iodine

• Concentrated in the glandular system

– Thyroid gland contains the largest amount of iodine

– Breasts, ovaries, salivary glands, parotid glands, pancreas, cerebrospinal fluid, brain, stomach, skin, lacrimal glands, etc.

In Thyroid, What Happens to Iodine After Absorption?

I-NIS

I-

TSH

Oxidation (H202+

TPO) Organificatio

n

δ –Iodolactone

and other

iodinated lipids

Horm. Metab. Res. 1994;26:465

However, organification of lipids will only

occur with iodine intake in excess of the RDA.

100x

RDA

I2

MIT, DIT, T3, T4

RDATG

Iodolactone

Iodine + arachidonic acid δ-iodolactone

TPO

δ-iodolactone is a key regulator of apoptosis and cellular proliferation in the thyroid. It

inhibits Epidermal Growth Factor from thyroid follicles. δ-iodolactone is not detected in

human tissue when iodine deficiency is present, but is present with iodine administration

at 100x the RDA.

Eur. J. of Endocrin. 132. 735-43, 1995

Horm. Metab. Res. 26. 465-69. 1994

Hormnes. 2010. 9(1) 60-66

DHA and EPA- Iodolactone

Iodine + DHA (C22:6, ω-3) 5-iodo-γ-lactone (DHA-γ-IL)

Iodine + EPA (C20:5, ω-3) EPA-δ-IL

Without adequate iodine levels, it is impossible for EPA/DHA to be converted into IL. LP

is expressed in breast cancer cells.

Hormones. 2010. 9(1):60-66

J. Mammory Gland Biol. Neoplasia. 10. 189-96. 2005

Mol. Cell. Endocrinol. 31:49-57. 2005

LPO+H20

2

LPO+H20

2

Low Iodine and δ-Iodolactone

• Methyl-nitrosourea (MNU) induced tumors contain 4x more AA than normal mammary glands

– I2 supplementation is accompanied by a 10x higher δ-iodolactone content in tumors

– Same research shows that δ-iodolactone and iodine have antiproliferative and apoptotic properties.

Prostaglandins. Med. 1. 31-38. 1978

Endocr. Relat. Cancer. 13; 1147-58. 2006

Organified Iodine

• Regulates the cell cycle in thyroid gland by inducing apoptosis

G0,1: growth and preparation of the chromosomes for

replication

S:synthesis of DNA

G2: Preparation for Mitosis

(G1 and G2)

Endocrin. 126. 984-92

http://en.wikipedia.org/wiki/Image:Cell_Cycle_2.png

I-NIS

I-

TSH

Oxidation (H202+

TPO)

T

G

Organificatio

n

MIT, DIT, T3, T4

NADPH-Oxydase

SystemIodinated

LipidsCalciu

m

Basolateral membrane

δ -

Iodolactone

I2

In Thyroid, What Happens to Iodine After Absorption?(2)

In Thyroid, What May Happen If Iodine Levels Are Too Low? AIT

I-NIS

I-

TS

H

Oxidation H202+

TPO

T

G

Organificatio

n

MIT, DIT, T3, T4

NADPH-Oxydase

SystemIodinated

LipidsCalciu

m

Apical membrane

δ -

Iodolactone

I2

Anti TPO

Anti TG

Early

Treatment: Iodine, Magnesium, B2 and B3, Selenium, Vitamin C,

as well as Antioxidants

Does Iodine Cause Autoimmune Thyroiditis?

• Results of study:

– KI in solution of 30mM and higher found to inhibit the normal growth curve of thyroid cells

• Arrested cell cycle at G0/G1 and G2/M after 72 hours of treatment

• Did not induce apoptosis or necrosis of thyroid cells

Thyroid. Vol. 19. N.3. 2009

“

This study showed that iodine excess inhibited human primary thyroid proliferation…in

the presence of low dose IFN, KI…could induce lymphocytic infiltration in the thyroid

gland and secretion of proinflammatory cytokines. …{This} could explain the

development of hypothyroidism after adding iodide in a diet of persons that already have

lymphocytic infiltration and/or mild inflammation of the thyroid gland.”


• What amount of KI do you need to ingest to achieve a serum level of:

• 10uM KI:

• 100uM KI:

• 10mM KI:

• 30mM KI:

• 100mM KI:



• 1mM of KI = 127mg/L

• The renal clearance of I is approx. 42.5L/day

• So:

– 1mM of KI=127mg/L x 42.5L/day =5,398mg/day




• 10uM KI: 54mg/day


• 10mM KI: 54000mg/day

• 30mM KI: 161,000mg/day

• 100mM KI: 540,000mg/day



Conclusions of article:

“Normal human thyroid cell proliferation is inhibited

in a dose-dependant manner by iodine

concentrations over 10mM

{REMEMBER: 161gm/day).”

MEDICAL

IODOPOBIA!Thyroid. Vol. 19. N.3. 2009


• Real conclusion:

• Iodine doses up to 161gm/day did not cause changes in normal human thyroid cell proliferation. Iodine is not associated with autoimmune thyroid illness unless it was given in large doses along with a goitrogen such as IFN.



• In vitro studies with purified fractions of calf thyroid glands showed 10-5 molar I protects TPO against oxidative damage

To achieve 10-5 molar iodide, a human adult needs to take in

50-100mg I per day.

Endocrin. 1965;76:632-45

Does Iodine Prevent Autoimmune Thyroid Disorders?

• In-Vitro study of thyroid cells containing TSH receptor mutation

• Different amounts of NaI:

– Control

– 1mM NaI (5.4g/day)

– 10mM NaI (54g/day)


Genomics. 97 (2011):94-100


• 1mM NaI (5.4g/day) inhibited cell proliferation from 43-83%

• Iodine promoted apoptosis of mutant cells

Genomics. 97 (2011):94-100

“Importantly, despite a constitutive TSHR activation, iodide still causes down regulation

of proliferation and function in early stage autonomy.”

Alex 1.12

Alex 9.12

Alex 1.12 Alex 9.12

Iodine Deficiency

• Iodine deficiency was seen more in cases with hypothyroidism

• Iodine status was a strong predictor of the thyroid status

Ergür AT, Evliyaoğlu O, Şıklar Z, Bilir P, Öcal G, Berberoğlu M. Evaluation of thyroid functions with respect to iodine status and TRH test in chronic autoimmune thyroiditis. J Clin Res Pediatr Endocrinol. 2011;3(1):18-21. Epub 2011 Feb 23.

Iodine Therapy

• Six mg iodine or more is given daily to a person who has Graves' disease and is not already receiving iodine, within the succeeding 7 or 10 days there will be an amelioration in symptoms, and the FTI level will fall in parallel.

• If iodine administration is then stopped, the signs and symptoms quickly return to their previous state

• Iodine alone as a definitive form of treatment has been used in the past, but is not used today because its benefits may be transient or incomplete

• Saturated solution of KI (SSKI) is typically given orally in adult doses of about 250 mg iodide several times a day (5 drops of SSKI assumed to be ⅓ ml) for thyroid blockade (to prevent the thyroid from excreting thyroid hormone)

• As adjunctive therapy with antithyroid drug therapy in Graves’ disease – Low dose (50 mg) potassium iodide tablets added to methimazole results in normal free T4 levels by two weeks in 54 and 59 percent of patients treated with 15 or 30 mg methimazole, respectively, compared with 27 and 29 percent of patients treated with 15 or 30 mg methimazole alone.

“Small”doses are in the range of a few mg

“Large”doses are in the range of 500 mg

IODINE AND THYROID FUNCTION

• Usually small doses of Iodine :

• Stimulate thyroid function

• Induce the iodinase enzymes and

• Induce thyroxine synthesis

• Larger doses of Iodine:

• May Suppress Thyroid Function

• However larger doses of Iodine are not typically given to purposefully suppress thyroid function.

42

• Excess iodine can be more cytotoxic in the presence of selenium deficiency. Iodine supplementation in selenium-deficient populations is theoretically problematic, partly for this reason.

Smyth, PP (2003). "Role of iodine in antioxidant defence in thyroid and breast disease". BioFactors (Oxford, England) 19 (3–4): 121–30.doi:10.

Excess Iodine

https://en.wikipedia.org/wiki/Digital_object_identifier





• 10mM KI: 54000mg/day

• 30mM KI: 161,000mg/day

• 100mM KI: 540,000mg/day



Conclusions of article:

“Normal human thyroid cell proliferation is inhibited

in a dose-dependant manner by iodine

concentrations over 10mM

{REMEMBER: 161gm/day).”

MEDICAL

IODOPOBIA!Thyroid. Vol. 19. N.3. 2009


• Real conclusion:

• Iodine doses up to 161gm/day did not cause changes in normal human thyroid cell proliferation. Iodine is not associated with autoimmune thyroid illness unless it was given in large doses along with a goitrogen such as IFN.



• In vitro studies with purified fractions of calf thyroid glands showed 10-5 molar I protects TPO against oxidative damage

To achieve 10-5 molar iodide, a human adult needs to take in

50-100mg I per day.

Endocrin. 1965;76:632-45


• In-Vitro study of thyroid cells containing TSH receptor mutation

• Different amounts of NaI:

– Control

– 1mM NaI (5.4g/day)



Genomics. 97 (2011):94-100


• 1mM NaI (5.4g/day) inhibited cell proliferation from 43-83%

• Iodine promoted apoptosis of mutant cells

Genomics. 97 (2011):94-100

“Importantly, despite a constitutive TSHR activation, iodide still causes down regulation

of proliferation and function in early stage autonomy.”

Suppression of thyroid-stimulating hormone (TSH) secretion in normal subjects by the administration of thyroid hormone results in thyroid atrophy.

Although the pathogenesis of thyroid nodules and sporadic nontoxic multinodulargoiters is poorly understood, TSH is presumed to be necessary if not sufficient and, therefore, suppression of TSH secretion might be expected to result in a decrease in nodule or goiter size or at least prevent further enlargement.

The clinical importance of the thyroid nodule evaluation is primarily related to the need to exclude thyroid cancer, which is present in 4.0 to 6.5 percent of thyroid nodules.

Thyroid Nodules

AUTOIMMUNE DISEASES:

•Offer Immune Modulating Herbs such as Adaptogens

•Eat a Hypoallergenic, Chemical Free Diet

•Make an Earnest Effort to Remove all Chemicals from the home, workplace, and places visited possible.

•Consider Detoxification Protocols

•Optimize Digestion and Gut Health

•Supplement Antioxidants, Fish Oils and Vitamin D

BASIC THERAPIES FOR AUTOIMMUNE DZ

51

1/3 of small molecules in human blood

• Metabolites produced by gut bacteria can enter the bloodstream by absorption,enterohepaticcirculation or impaired gut barrier function

• Up to one-third of the small molecules in human blood can be derived from gut bacteria

52

Wikoff, W. R. et al. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proc.

Natl Acad. Sci. USA 106, 3698–3703 (2009).

Hood, L. Tackling the microbiome. Science 336, 1209 (2012).

Endotoxins Up-Regulate Inflammation, Etc.

53http://medical-dictionary.thefreedictionary.com/endotoxin

Selenium and Rosmarinic Acid

• Selenium– Thyroid Autoimmunity

– Hashimoto’s Thyroiditis

– Grave’s Disease

• Rosmarinic Acid– Thyroid Autoimmunity

– Hashimoto’s Thyroiditis

– Grave’s Disease

• Probiotics and prebiotics can be used to manipulate cytokines

• Some probiotics preferentially stimulate a Treg/Th3 cytokine profile

• Some probiotics stimulate a Th1 profile

Probiotics Can Suppress T Cells

Cytokines Probiotics

Increase Th1 (IFN gamma) Lactobacillus rhamnosus GG (LGG)

Increase Treg/Th3 (TGF beta and/or IL-10)

L. Reuteri DSM 17938Bifidobacterium infantisBifidobacterium adolescentisBifidobacterium lactisBifidobacterium breveLactobacillus rhamnosus GG

Decrease Th1 Lactobacillus plantarum Lactobacillus gasseri

Decrease Th2 Bifidobacterium lactisLactobacillus plantarumLactobacillus casei ShirotaLactobacillus reuteri

Decrease pro-inflammatory cytokines (IL-1, IL-6, IL-8, and TNFa)

Lactobacillus delbruekiiLactobacillus fermentumLactobacillus gasseri

Ther Adv Gastroenterol (2010) 3(5307319

Thyroid Autoimmunity

• Selenium deficiency confers increased risk.

• Selenium deficiency increases duration and severityof disease.

• Selenium supplementation decreases markers of autoimmune thyroid conditions, specifically anti-TPO and thyroglobulin levels.

Saranac L, Zivanovic S, Bjelakovic B, Stamenkovic H, Novak M, Kamenov B. Why is the thyroid so prone to autoimmune disease? Horm Res Paediatr. 2011;75(3):157–65.

Hashimoto’s and Selenium

• Selenium supplementation in individuals with Hashimoto’s reduces oxidative stress through glutathione peroxidase and lowers hydrogen peroxide levels.

• A study demonstrated a significant reduction in anti-TPO in the intervention group (n=36, 200 μg of selenium selenite and L-T(4)) versus those in a control group treated with L-T(4) only.

• Those with anti-TPO levels over 1200 IU/mL experienced a mean reduction of 40%, while those under 1200 IU/mLexperienced a mean reduction of 10%.

Gartner R, Gasnier BC, Dietrich J, Krebs B, Angstwurm M. Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J Clin Endocrinol Metab. 2002;87(4):1687–91

Hashimoto’s and Selenium

• 4 studies included in a 2013 Cochrane Review demonstrated significant decreases in anti-TPO levels, with one study reporting subjective improvements in quality of life.

• Reviewers concluded insufficient evidence for clinical application due to unclear blinding strategies, and the absence of health-related quality of life scores.

Ej VZ, Ay A, Fedorowicz Z, Carter B, Pijl H. Seleniumsupplementation for Hashimoto’s thyroiditis (Review).Cochrane Database Syst Rev. 2014;3(1):25–31

Grave’s Disease and Selenium

• There are a number of possible mechanisms through which selenium may positively influence the course of Grave’s Disease. As an important component of both GPx , selenium may influence the regulation of T3 levels.

• Selenium helps to decrease inflammatory cytokines via NF-kappa-B inhibition, thereby attenuating the inflammatory

• there is an ongoing double-blind placebo controlled clinical trial, the Graves’ Disease Selenium Supplementation trial (GRASS), which aims to establish the clinical role of selenium in the treatment of Grave’s.

Watt T, Cramon P, Bjorner J, Bonnema S, Feldt- Rasmussen U, Gludd C. Selenium supplementation for patients with Graves’ hyperthyroidism (the GRASS trial): study protocol for a randomized controlled trial. Trials. 2013;14:119

Selenium and Graves Opthalmopathy

• Case-control data has demonstrated that selenium levels are significantly lower in GO patients that develop GO, compared to those with GO alone, suggesting selenium deficiency may be an independent risk factor for GO development in GO

• A 2011 double blind RCT demonstrated that supplementation with 200mcg of selenium per day significantly decreased GO, improved quality of life, and decreased worsening of disease

Marcocci C, Kahaly G, Krassas GE, et

al. Selenium and the Course of Mild

Graves’ Orbitopathy. N Engl J Med.

2011.

Emerging Research

• Currently, a multi-centred RCT is underway to assess the impact of 12 months of selenium supplementation in patients with autoimmune thyroiditis treated with levothyroxine.

• The CATALYST study (the chronic autoimmune thyroiditis quality of life selenium trial) is taking place across four clinic sites in Denmark involving 472 participants, and will be the first to assess quality of life as a primary outcome.

Winther KH, Watt T, Bjorner JB, Cramon P, Feldt- Rasmussen U, Gluud C, et al. The chronic autoimmune thyroiditis quality of life selenium trial (CATALYST): study protocol for a randomized controlled trial. Trials. 2014;15:115

Rosmarinic Acid and Thyroid Antibodies

• Botanicals containing Rosmarinic Acid– Lowers Thyroid Stimulating

Immunoglobulin levels

– Lowers Thyroid Antibodies

Pharmaceutical Biology 1986, Vol. 24, No. 2, Pages 53-63 , Effects of Lithospermum officinale and Related Plants on Hypophyseal and Thyroid Hormones in the Rat H.Sourgens,H.Winterhoff,HG. Gumbinger and FH. Kemper

Rosmarinus officinalis

Rosmarinic acid is a phenolic compound derived the following plants including:

Melissa officianalis (Lemon Balm)

Lycopus europeas (Gypsywort)

Lycopus virginia (Bugleweed)

Lithospermum officianalis (Stoneseed or Gromwell) • All have been traditionally used for thyroid

Rosmarinic Acid for Hyperthyroidism

64

Food Science and Technology, Volume 41, Issue 3, April 2008, Pages 391-400 Chemical composition and in vitro antioxidative activity of a lemon balm (Melissa officinalis L.) extract Keyvan Dastmalchi, H.J. Damien Dorman, Päivi P. Oinonen, Yusrida Darwis, Into Laakso, Raimo Hiltunen

Pharmaceutica Acta Helvetiae, Volume 72, Issue 5, January 1998, Pages 301-305 The aromatic and polyphenoliccomposition of lemon balm (Melissa officinalis L. subsp. officinalis) tea A. P. Carnat, A. Carnat, D. Fraisse, J. L. Lamaison

• Melissa has been shown to decrease TSI antibody to promote intracellular cyclic AMP responses

• Lycopus:• Binds with TSI, dose dependent• 905 patients, 87% improved

• No side effects noted • Officially recognized in Germany as a prescription

Harvey, R. Lycopus europaeus L. And Lycopus virginicus L.: A review of scientific research. British journal of Phytotherapy 4 (20, 55-65) 1995

ROSMARINIC ACID AND GRAVE’S ANTIBODIES

65

In Japan,

1.2 mg/day to as high as 13 mg/day from seaweed consumption

66

Thyroid. 2008 Jun;18(6):667-8. The average of dietary iodine intake due to the ingestion of seaweeds is 1.2 mg/day in Japan. Nagataki S.

Thyroid Research 2011 Oct 5:4(1):14 Assessment of Japaneses iodine intake based on seaweekconsumption in Japan: A literature-based analysis. Ava TT, Zava DT

SEAWEED

• Guggul and Boswellia tree resins that are anti inflammatory

Commiphora mukulGuggul Burseraceae Family

67

Beta Blockers

• hyperthyroidism is associated with an increased number of beta-adrenergic receptors

• decreases serum triiodothyronine (T3) concentrations by as much as 30 percent , via inhibition of the 5'-monodeiodinase

Rauwolfia

• Depletes tissue stores of catecholamines (EPI, NE)

Rand MJ, Jurevics H. The pharmacology of rauwolfia alkaloids. In: gross F, ed. Antihypertensive agents new York, Springer-Verlag, 1977, 77-159

Vitamin D 3 and Hashimoto’s Disease

• 1,25 Vitamin D levels are lower in individuals with Hashimoto’s disease

• Supplementation with Vitamin D 3 in animal models prevents the development of autoimmune thyroiditis

Iodine Transport Problems

• When problems develop with iodine use, think detoxification– Vitamin C

– Salt

– Water

– Liver and kidney support

– Exercise

– Clean Diet

Hashimoto’s Disease

• Impossible to experimentally induce Hashimoto’s disease in laboratory animals by administering iodine

• Only by the use of anti-thyroid drugs (i.e., goitrogens) can you induce Hashimoto’s disease in laboratory animals

Goitrogens induce not only hyperplasia they cause iodine deficiency!

Radioactive Iodine

• Half-life of 131I:

– Graves’ disease: 5.4 days

– Nontoxic goiter: 6.4 days

– Uninodular adenoma: 5.7 days

Nuclear Medicine Comm. 2010;31:201-5

Where Does Radioactive Iodine Go?

10-32% Thyroid– Ovaries

– Testicles

– Parathyroids

– Adrenals

– Breasts

– Eyes

– Intestine

• Salivary glands

• Pituitary glands

• Muscles

• Bones

• Skin

• Gallbladder

• Kidneys.

68-90% Extra-Thyroidal

Radioactive Iodine

“Radioactive iodine is effective, safe and relatively inexpensive.”

Werner and Ingbar’s The Thyroid. 2000

Radioactive Iodine: Effective?

• If the goal is to destroy the thyroid, then it is effective

– Only if the cause of autoimmune thyroid disorders is too much thyroid tissue that needs to be destroyed

HOWEVER: Excess thyroid tissue is not the cause; it is the consequence of the illness.

Radioactive Iodine: Safe?

• Radioactive iodine will bind to all tissues where iodine is bound

– Glands• Breasts, prostate, ovaries, etc

All tissues of the body utilize iodine.

Radioactive Iodine: Safe?

• 6,841 patients with thyroid cancer

• Received an average dose of 162mCi of *I

• Dose dependant increase in cancer of:

– Salivary gland, bone, soft tissue and colorectum

• Increased risk of primary malignancy of 27%

Br. J. Ca. 2003:89:1638-44

FP News: 2.1.07

Iodine Transport Problems

• When problems develop with iodine use, think detoxification– Vitamin C

– Salt

– Water

– Liver and kidney support

– Exercise

– Clean Diet

Radioactive Iodine

• Half-life of 131I:

– Graves’ disease: 5.4 days

– Nontoxic goiter: 6.4 days

– Uninodular adenoma: 5.7 days

Nuclear Medicine Comm. 2010;31:201-5

Hashimoto’s Disease

• Initial

15 year old boy

TSH

After 5 years

0

20

40

60

80

Initial After 5 years

TPO AB

0

5

10

15

20

Hashimoto’s Thyroiditis

• Initial

0

5

10

15

20

After 3 months

0

50

100

150

200

Initial After 3 months

27 year old female

TSH T3

TSH: 5.1

Tx: Nt 1/2gn

Iodine

25mg/d

Tx: Nt 1gn

Iodine

37.5mg/d

Tx: Nt 1gn

Iodine

37.5mg/d

Tx: Nt 1.5gn

Iodoral

50mg/d

Case Study-2

• 55 Year Old woman with severe Hyperthyroidism, anxiety, heart palpitations, temp 99 for over 3 years, BP 160/100

• MD ‘I need something which will work within 5 days or she will need to get irradiated’

Botanicals Prescribed

• Symptoms normalized within 5 days

Case Study-3

• 50 Year Old woman with severe Hyperthyroidism, anxiety, heart palpitations, temp 99 for over 4 years, BP 230/110

• Refused conventional treatment

• Total T3 levels 350 ng/dl (ref 60 -181 ng/dl)

Case Study-3 cont’d.

• One month later 160/100, loose stools,

Total T3 350 ng/dl no change

• 3 months later

BP 150/90, loose stools, no heart palpitations

Total T3 360 ng/dl


– 6 months later-BP 160/90, diarrhea, dizziness-Total T3 300 ng/dl

– 9 months later-BP 160/90-Total T3 300 ng/dl

– 12 months later-BP 160/90, diarrhea, dizziness-Total T3 250 ng/dl (ref 60 -181 ng/dl)


– 16 months later

-BP 120/90, got divorced

-Total T3 200 ng/dl (ref 60 -181 ng/dl)

– Since then Total T3 fluctuates, no palpitations, BP fluctuates between mild to moderate hypertension. Does not need irradiation.

Hyperthyroid Lab Report




Case Study-1

• Jan 2004, 12 year old with DM type 1

• diagnosed with Graves’

• Recommended Thyroidectomy or Irradiation

• Instead took Botanicals, symptoms normalized within three months blood tests improved but not cured

• No longer needed irradiation

Toxic Multi Nodular Goiter

After 3 months

TSH Reference Values (.35-5 mIU/ml)

Total T3 Reference Values (60-181 ng/dl)

Total T3

0

50

100

150

200

250

37 year old male

Initial

Graves Disease

Initial

TSI Reference Values (under 130)

TSI

0

50

100

150

200

250

40 year old woman

After 2 months

Hyperthyroid FAQ’s

• Dosage

• Drug Interaction

• Blood test monitoring

• Interpreting low TSH values, when all other blood tests normalized, and symptoms normalized

• Cases in which it doesn’t work well

In Summary, safe, natural remedies for Hyperthyroidism include:

• Iodine 2-5 mg/day

• Selenium 200 mcg twice a day

• Rosmarinic Acid containing plants (200-400 mg of RM daily)

• Adaptogens and Adrenal Supportive Herbs

• Herbal Specifics for Individual Presentations

• Higher the dose, the better the result with herbs and Hyperthyroidism.

• However even at a low dose, its is possible to have complete normalization of TSI levels.

HYPERTHYROIDISM SUMMARY

101

*Jillian Stansbury, ND*Joseph Pizzorno, ND

David Brownstein MDEdwin Cunningham MD

• Acknowledgements

Date post:	24-May-2020
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Treatment of Thyroid Autoimmune Disease · •Week one: 12.5 mcg T3 •Week two: 12.5 mcg T3 BID...

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