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SUBCLINICAL SUBCLINICAL HYPOTHYROID HYPOTHYROID MANAGING PATIENTS USING RESTING METABOLIC RATE AND BRACHIORADIALIS REFLEXOMETRY Dr. Konrad Kail 480-905-9200 [email protected]
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SUBCLINICAL HYPOTHYROID

Feb 06, 2016

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SUBCLINICAL HYPOTHYROID. MANAGING PATIENTS USING RESTING METABOLIC RATE AND BRACHIORADIALIS REFLEXOMETRY Dr. Konrad Kail 480-905-9200 [email protected]. GENERAL CONSIDERATIONS. MUST WORK FOR HUMANS TO FUNCTION ABSORPTION AND ASSIMILATION DETOXIFICATION AND ELIMINATION REGULATION - PowerPoint PPT Presentation
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Page 1: SUBCLINICAL HYPOTHYROID

SUBCLINICAL SUBCLINICAL HYPOTHYROIDHYPOTHYROID

MANAGING PATIENTS USING RESTING METABOLIC RATE

AND BRACHIORADIALIS REFLEXOMETRY

Dr. Konrad Kail [email protected]

Page 2: SUBCLINICAL HYPOTHYROID

GENERAL CONSIDERATIONSGENERAL CONSIDERATIONS MUST WORK FOR HUMANS TO FUNCTION

– ABSORPTION AND ASSIMILATION– DETOXIFICATION AND ELIMINATION– REGULATION

STRESS IMPACTS ALL OF THESE BUT THE MOST PROFOUND AND IMMEDIATE EFFECT IS ON REGULATION– ADRENAL AND THYROID GLANDS ARE THE MOST STRESS LABILE

ADRENAL AND THYROID INTERACT IN REGULATING– WEIGHT– ENERGY– BLOOD SUGAR– BLOOD FATS– NEUROTRANSMITTERS– SEX HORMONES– INFLAMMATION– IMMUNE FUNCTION

Page 3: SUBCLINICAL HYPOTHYROID

ORGAN RESERVEORGAN RESERVE

ORGANRESERVE

STRESSORS

SUPPORT

Degeneration

Page 4: SUBCLINICAL HYPOTHYROID

Thyroid Feedback RegulationThyroid Feedback Regulation The production of thyroid

hormone is controlled by a feedback loop. When there is not enough receptor site activity in the hypothalamus, TRH is elaborated which stimulates the anterior pituitary to make TSH, which then stimulates the thyroid to make more T3 and T4.

The thyroid gland uses L-Tyrosine and Iodine to

make T4, the storage form of thyroid hormone and T3 the active form

Page 5: SUBCLINICAL HYPOTHYROID

SUBCLINICAL HYPOTHYROIDSUBCLINICAL HYPOTHYROID SYMPTOMS COMPATIBLE WITH

HYPOTHYROID (> 12 on Symptom Survey) LOW BBT (< 97.5o F axillary) SLOW REFLEXES (> 137 msecs) LOWER RMR NORMAL TO SLIGHTLY HIGH TSH NORMAL FREE T3, FREE T4 NORMAL T3U, T4, T7 PREVALENCE UNKNOWN (8-30%)

Page 6: SUBCLINICAL HYPOTHYROID

CARDIOVASCULARCARDIOVASCULARRISKRISK

INCREASED– SERUM LIPIDS– HOMOCYSTEINE– C-REACTIVE PROTEIN– CORONARY HEART DISEASE– HYPERTENSION– ISCHEMIC HEART DISEASE– ENDOTHELIAL DAMAGE– COAGUABILITY– PERIPHERAL ARTERY DISEASE

DECREASED– STROKE VOLUME– CARDIAC OUTPUT

MARKERS OF SUDDEN DEATHRISK

Page 7: SUBCLINICAL HYPOTHYROID

DIABETES RISKDIABETES RISK DISRUPTION OF GLP-1 SIGNALLING DECREASED THYROID FUNCTION UP TO

18 HOURS AFTER HYPOGLYCEMIC EPISODES

ASSOCIATED WITH INSULIN RESISTANCEINCREASED HOMA AND TRIG/HDL DYSGLYCEMIA OBESITY

Page 8: SUBCLINICAL HYPOTHYROID

ARTHRITIS & INFLAMMATIONARTHRITIS & INFLAMMATION

INCREASED RATES OF HASHIMOTO’S INCREASED EUTHYROID SICK RISK RA PATIENTS WITH SUBCLINICAL

HYPOTHYROID HAD DYSFUNCTIONS OF GLUCOSE METABOLISM AND INSULIN RESISTANCE

Page 9: SUBCLINICAL HYPOTHYROID

NEURO-PSYCHOLOGICAL RISKNEURO-PSYCHOLOGICAL RISKINCREASED HOFFMAN’S SYNDROME

– WEAKNESS AND STIFFNESS DUPUYTREN’S CONTRACTURE CARPAL TUNNEL SYNDROME POLYMYOSITIS-LIKE SYNDROME PARKINSONS HEARING LOSS ANXIETY AND DEPRESSION 1.97 RELATIVE RISK OF COGNITIVE DECLINE

(ALZHEIMER’S)

Page 10: SUBCLINICAL HYPOTHYROID

BONE RISKBONE RISKINCREASED BONE RESORPTION IN HYPERTHYROID

– URINARY PYRIDINOLINE– URINARY DEOXYPYRIDINOLINE– URINARY CALCIUM– SERUM TELOPEPTIDES

NO CALCIUM METABOLISM PROBLEMS IN HYPOTHYROID– CALCIUM BINDS THYROID

(TAKE THYROID AT LEAST 45 MINS AWAY FROM CALCIUM)

Page 11: SUBCLINICAL HYPOTHYROID

PREGNANCYPREGNANCY FERTILITY ISSUES 3 FOLD INCREASE IN PLACENTA

PREVIA 2 FOLD INCREASE IN PREMATURE

DELIVERY MAY AFFECT MENTATION IN

OFFSPRING– NOT WELL STUDIED

Page 12: SUBCLINICAL HYPOTHYROID

FACTORS AFFECTING FACTORS AFFECTING THYROID FUNCTIONTHYROID FUNCTION

PERIPHERAL CONVERSION OF T4 TO T3– HEPATIC, RENAL, MITOCHONDRIAL FUNCTION – DECREASED 5’D-1

INHIBITED BY IL-1, IL-6 TOXIC MATERIALS

– LEAD, MERCURY– PCB– FUNGICIDES, ORGANO-CHLORINE INSECTICIDES

DRUGS AMIODORONE, ANTI-CONVULSANTS, SALSALATE, LITHIUM

MITOCHONDRIAL PROTEIN LEAKAGE– UNCOUPLING PROTEIN 3

CYTOKINES– NF-KAPPA-B– TNF-ALPHA– IL-1 ALPHA/BETA

EUTHYROID SICK SYNDROME IMPAIRS FUNCTION UP TO 60 DAYS FOLLOWING ACUTE SEVERE ILLNESS

Page 13: SUBCLINICAL HYPOTHYROID

DISTRIBUTION DISTRIBUTION OF THYROIDOF THYROID

Page 14: SUBCLINICAL HYPOTHYROID

DECREASED CONVERSIONDECREASED CONVERSION

Page 15: SUBCLINICAL HYPOTHYROID

REVERSE T3 (RT3)REVERSE T3 (RT3)

Page 16: SUBCLINICAL HYPOTHYROID

Vasoactive Intestinal Peptide and Vasoactive Intestinal Peptide and Thyroid FunctionThyroid Function

VIP exerts action through 2 receptors VPAC1 and VPAC2– VPAC1 receptors are in liver, breast, kidney, prostate, ureter,

bladder, pancreatic ducts, GI mucosa, lung, thyroid, adipose tissue, lymphoid tissue, and adrenal medulla.

– VPAC2 receptors are in blood vessels, smooth muscles, the basal part of mucosal epithelium in colon, lung, and vasculature of kidney, adrenal medulla and retina. Also present in thyroid follicular cells and acinar cells of the pancreas.

In hypothyroid, there was a 2-fold increase in all peptides derived from VIP, found in the gastric fundus

In hypothyroid significant increases of pituitary VIP VIP modulates T3 and T4 (decreases) in any inflammation

Page 17: SUBCLINICAL HYPOTHYROID

DE-IODINASESDE-IODINASES

TypeTissues Site Substrate

PreferenceInhibitors

D1 Liver, Kidneys, Thyroid

Plasma membra rT3, T4, T3 PTU, T4+,

IL1, IL6, TNFα

D2 Thyrotrophs, Hypothalamus, Skeletal Muscle, Heart, Thyroid

Endo. Retic

T4, rT3 Iopanoate, T4+, T3+

D3 Brain, Placenta, Pregnant Uterus, Skin

SubPlasmaMemb

T3, T4 Iopanoate, Dexamethasone

Bianco AC, Salvatore D, et al. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002Feb;23(1):38-89.

T4 to T3 CONVERSION

ACTION ON METABOLISM

Page 18: SUBCLINICAL HYPOTHYROID

Thyroid Receptor PhenotypesThyroid Receptor Phenotypes

TYPE TISSUES

TRβ2 Pituitary Thyrotrophs

TRβ1 Liver, Kidney

TRα1 Skin, Muscle, HeartBrown Fat

TRα2 BrainHypothalamus (inhibitory)

Alkemade A, Vujist CL, et al. Thyroid hormone receptor expression in the humanhypothalamus and anterior pituitary. J Clin Endocrinol Metab. 2005 Feb;90(2):904-12.

T4 to T3 Conversion

Action on Metabolism

Page 19: SUBCLINICAL HYPOTHYROID

TSH- REGULATIONTSH- REGULATION

TISSUE ACTION RECEPTOR DE-IODINASE

HYPOTHALAMUSBRAIN (action on metabolism)

TRH TR-α2 D2, D3

THYROTROPHS(Pituitary)

TSH TR-β2 D2

THYROID(T4, T3 production)

T4, T3 TR-β2 ? D1, D2

LIVERKIDNEYS (T4 to T3 conversion)

T3 TR-β1 D1

SKELETAL MUSCLESHEART TR-α1 D2

MAY NOT REPRESENT METABOLIC DEMAND

Page 20: SUBCLINICAL HYPOTHYROID

NUTRIENTS AND THYROIDNUTRIENTS AND THYROID SELENIUM

– IMPROVES FUNCTION DECREASES RECOVERY TIME IN EUTHYROID SICK SYNDROME

IRON AND ZINC – INCREASE THYROID FUNCTION IN IRON/ZINC DEFICIENT – NO EFFECT IN IRON/ZINC SUFFICIENT

CALCIUM– INHIBITS ABSORPTION

ALPHA-TOCOPHEROL – NO EFFECT

KELP AND ALL IODINE – HELPFUL IN IODINE DEFICIENT– DOSE DEPENDENT DECREASE IN THYROID FUNCTION IF IODINE

SUFFICIENT L-CARNITINE DECREASES THYROID FUNCTION

– PREVENTS THYROID HORMONE ENTRY INTO NUCLEUS OF CELLS High Soy intake inhibits thyroid function

– Ipriflavone helps bone resorption but does not increase cancer risk

Page 21: SUBCLINICAL HYPOTHYROID

Lithium and Thyroid FunctionLithium and Thyroid Function Enters thyrocyte via the Na+/I- Symporter Concentrated in thyroid gland to 3-4 times serum

levels Increases intra-thyroidal iodine content Inhibits coupling of iodotyrosine residues Decreases colloid droplet formation Inhibits microtubule formation Inhibits thyroid hormone secretion Blocks iodine release from thyroid gland Treats hyperthyroid in people allergic to iodine

Page 22: SUBCLINICAL HYPOTHYROID

Iodine Uptake and RetentionIodine Uptake and Retention

Thyroid peroxidase H

2 O2

I- I- I-

Iodinated TG

TGProteolysisT4 T3

T4 T3

Colloid Resorption

ECF Colloid

TSH Iodine

(trapping)

SymporterIodine, Lithium

(Retention)

ATP mitochondria

Page 23: SUBCLINICAL HYPOTHYROID

HPA AXIS HPT AXIS

HYPOTHALAMUS

HYPOTHALAMUSHYPO HYPER

PITUITARY PITUITARY

ADRENAL CORTEX

MEDULLA

THYROID

CRH CRH

ACTH ACTH

SNS

GLUCOCORTICOIDS(CORTISOL)

GLUCOCORTICOIDS(CORTISOL)

CATECHOLAMINES(EPINEPHRINE, NOREPINEPHRINE, ALDOSTERONE)

TRH

TSH

T4

T3

RT3

5’DEIODINASEINHIBITS

INHIBITS

INHIBITS

Hypercortisolemia Inhibits Thyroid Function

SELENIUM, ZINC, VIT E,ASWAGANDA

SELENIUM, VIT DIODINE +/-

ZINC

Page 24: SUBCLINICAL HYPOTHYROID

Influence of Other Hormones Influence of Other Hormones on Thyroid Activity on Thyroid Activity

STRONGTHYROID STIMULATORS

MILDTHYROIDSTIMULATORS

STRONGTHYROID INHIBITORS

MILD THYROID INHIBITORS

Growth Hormone IGF-1 TestosteroneOther Androgens

DHEAAndrostenedioneMelatoninProgesteroneCortisol at physiologic doses

ORAL ESTROGENS OF ANY TYPE

Transdermal or injectable Estradiol, Cortisol in small doses

InsulinIn patients with insulin deficiency

Erythropoietin(hypothetical)

Cortisol and otherGlucocorticoids at high dose

InsulinIn patients with insulin resistance

HERTOGHE, T; The Hormone Handbook. International Medical BooksSurrey, UK, 2006, p88.

Page 25: SUBCLINICAL HYPOTHYROID

Hypothyroid Causes Hypothyroid Causes Adrenal DysfunctionAdrenal Dysfunction

Results in hypersecretion of CRH and AVP from hypothalamus

Significantly increased pituitary content of VIP ↓ Adrenal weight, ↓ Corticosterone ACTH, CRH, AVP Tohei A. Studies on the functional relationship

between thyroid, adrenal and gonadal hormones. J Reprod Dev 2004 Feb;50(1):9-20.

Page 26: SUBCLINICAL HYPOTHYROID

MEASUREMENTSMEASUREMENTS OF THYROID FUNCTION OF THYROID FUNCTION

SERUM MEASUREMENTS What’s on the shelves at the pharmacy TSH INSENSITIVE WHEN APPROACHING NORMAL

PHYSIOLOGIC MEASUREMENTS What you took home from the pharmacy

BODY MASS INDEX– CORRELATION WITH RESTING METABOLIC RATE

BASAL BODY TEMPERATURES– IDENTIFY SUBCLINICAL HYPOTHYROID– TOO SLOW TO RESPOND TO TREATMENT

RESTING METABOLIC RATE– SOME ARTIFACTS

CONGESTION REACTIVE AIRWAY DISEASE ASTHMA OR OTHER COPD

REFLEXES– ACHILLES, BRACHIORADIALIS, STAPEDIAL– NO ARTIFACTS UNLESS NERVE DAMAGE

Page 27: SUBCLINICAL HYPOTHYROID

METHODOLOGYMETHODOLOGY ENTRY CRITERIA

– BBT<97.50 F AXILLARY AVERAGE (BRODA BARNES) BASELINE MEASUREMENT AND THIRTY DAY

TREATMENT INTERVALS– SYMPTOM SURVEY– BODY MASS INDEX– RESTING METABOLIC RATE (oxygen consumption)– BRACHIORADIALIS REFLEXOMETRY (mean of 4)– TSH,T3U, T4, T7

ADDED FREE T3, FREE T4 SOME HAD

– MICROSOMAL (TPO) AB– THYROGLOBULIN AB– REVERSE T3– THYROTROPIN RELEASING HORMONE

– LIPIDS CHOLESTEROL LDL HDL TRIGLYCERIDES

Page 28: SUBCLINICAL HYPOTHYROID

RESTING METABOLIC RATEMEASUREMENT VIA OXYGENCONSUMPTION

Page 29: SUBCLINICAL HYPOTHYROID

PROTO-TYPE BRACHIORADIALIS REFLEXOMETRY SYSTEM

Page 30: SUBCLINICAL HYPOTHYROID

Hammer

Inclinator

Link

INCLUDESCOMPUTER

Page 31: SUBCLINICAL HYPOTHYROID

Pre-fireInterval

FireInterval

Euthyroid

Hammer Strike

Page 32: SUBCLINICAL HYPOTHYROID

Pre-Fire Fire

HYPOTHYROID

Page 33: SUBCLINICAL HYPOTHYROID

Prefire Interval Fire Interval

Hyperthyroid

Page 34: SUBCLINICAL HYPOTHYROID

Analyzed Signal

0

-50

50

Inclinometer, deg

0.5 1.0 1.5 2.0 2.5 3.0 3.50.0 4.0s

Periods 1...2... 3 Fir... 4 End 0.3 5...6 Fi... 7 End 1.3 8... 9 Fir... 10 End 2.3 1... 12 ... 13 End 3.3 1...

Pre-Fire: Duration of Each Period Mean, s

0.118 0.094 0.107 0.105

0.05

0.00

0.10

0.106

Inclinometer, s

1 2 3 4PeriodsFire: Duration of Each Period Mean, s

0.204 0.193 0.231 0.182

0.100.15

0.00

0.25

0.202

Inclinometer, s

1 2 3 4PeriodsFire Minus Pre-Fire of Each Period Mean, s

0.086 0.099 0.124 0.077

0.05

0.00

0.10

0.096

Inclinometer, s

1 2 3 4Periods

NORMAL

NORMAL = .052 to 0.137 SECS

Page 35: SUBCLINICAL HYPOTHYROID

Analyzed Signal

0

-50

50

Inclinometer, deg

0.5 1.0 1.5 2.0 2.5 3.0 3.50.0 4.0s

Periods 1...2... 3 Fire... 4 End 0.4 5... 6 Fire... 7 End 1.4 8...9 Fir... 10 End 2.3 1... 12 Fir... 13 End 3.4 1...

Pre-Fire: Duration of Each Period Mean, s

0.123 0.115 0.091 0.110

0.05

0.00

0.10

0.110

Inclinometer, s

1 2 3 4Periods

Fire: Duration of Each Period Mean, s

0.247 0.252 0.231 0.252

0.100.150.20

0.00

0.25

0.246

Inclinometer, s

1 2 3 4Periods Fire Minus Pre-Fire of Each Period Mean, s

0.124 0.137 0.140 0.142

0.05

0.10

0.00

0.15

0.136

Inclinometer, s

1 2 3 4Periods

Borderline

NORMAL = .052 to 0.137 SECS

Page 36: SUBCLINICAL HYPOTHYROID
Page 37: SUBCLINICAL HYPOTHYROID
Page 38: SUBCLINICAL HYPOTHYROID
Page 39: SUBCLINICAL HYPOTHYROID

KAIL-WATERS EQUATIONKAIL-WATERS EQUATION

RMR = 2307.62 + [-7.53(CM)] + [27.09(KG)] + [-42.59(BMI)] + [-45.47(PREFIRE)] + [45.85(FIRE)] +

[-46.27(FIRE-PREFIRE)]

Page 40: SUBCLINICAL HYPOTHYROID

PREDICTED vs MEASURED RMRPREDICTED vs MEASURED RMR

1442.84

1919.16

1499.89

1874.721948.43

1442.78

2040.7 1926.13

0

500

1000

1500

2000

2500

ENTIRE NO MEDS AT TARGET

RMR-HBRMRRMR-KW

Page 41: SUBCLINICAL HYPOTHYROID

WORST TO BESTWORST TO BEST11stst Cohort Cohort

18.47

25.96

96.46110.27

217.56

104.13

16.5

25.79

96.74

113.73

180.28

66.45

0

50

100

150

200

250

WORST BEST

SymptomsBMIBBTPrefireFireFire-Prefire

Page 42: SUBCLINICAL HYPOTHYROID

WHY TSH DOES NOT IDENTIFY WHY TSH DOES NOT IDENTIFY THOSE AT RISK !!!THOSE AT RISK !!!

138.62

382.57

050

100150200250300350400

CHANGE IN RMR

N=100

TSH <0.3 FIRE-PREFIRE<66

Patients that became normal by reflexes and symptoms had a mean RMR increase of about 400 kcals

TSH gets too low before adequate effect (RMR)

Page 43: SUBCLINICAL HYPOTHYROID

<0.3 n = 1090.3-0.5 n = 50.5-4.5 n = 146>4.5 n = 22

Page 44: SUBCLINICAL HYPOTHYROID

PREDICTABILITY OF PREDICTABILITY OF BRACHIORADIALIS REFLEX BRACHIORADIALIS REFLEX

TESTINGTESTING179 in Subpopulation on No Medication

Normals Hypothyroid (+)

Euthyroid (-)

RestingMetabolicRate

> 2000 kcals.

117 58

Brachio-RadialisReflex

Fire-Prefire< 66 msecs.

123 57

Page 45: SUBCLINICAL HYPOTHYROID

PREDICTABILITY OF PREDICTABILITY OF BRACHIORADIALIS REFLEX TESTINGBRACHIORADIALIS REFLEX TESTING

Gold StandardRMR (+)

Gold StandardRMR (-)

BR Test (+) True Positives(117)

False Positives(6)

BR Test (-) False Negatives(1)

True Negatives(58)

Page 46: SUBCLINICAL HYPOTHYROID

SENSITIVITYSENSITIVITY Sensitivity is the proportion of those that are

hypothyroid that are correctly diagnosed. It is expressed as:

________True Positives_______ = __117__ = 0.992True Positives + False Negatives 117 + 1

Page 47: SUBCLINICAL HYPOTHYROID

SPECIFICITYSPECIFICITY Specificity is the proportion of those that are

euthyroid that were correctly identified. It is expressed as:

________True Negatives_______ = ___58___ = 0.906True Negatives + False Positives 58 + 6

Page 48: SUBCLINICAL HYPOTHYROID

PREDICTIVE VALUEPREDICTIVE VALUEof POSITIVE TESTof POSITIVE TEST

Predictive Value of a Positive Test is the proportion of those with a positive test that are hypothyroid. It is expressed as:

________True Positives_______ = ___117__= 0.951

True positives + False Positives 117+6

Page 49: SUBCLINICAL HYPOTHYROID

PREDICTIVE VALUEPREDICTIVE VALUEof NEGATIVE TESTof NEGATIVE TEST

Predictive Value of a Negative Test is considered the proportion of those with a negative test who are euthyroid: It is expressed as:

_______True Negatives_______ = ___58____= 0.983False Negatives + True Negatives 1 + 58

Page 50: SUBCLINICAL HYPOTHYROID

HOW TO OPTIMIZE HOW TO OPTIMIZE THYROID ACTIVITY AND TREATMENTTHYROID ACTIVITY AND TREATMENT

WHAT TO DO WHAT TO AVOID

DIET 1500-2500 CAL/DAYORGANIC PALEOLITHIC FOODSIRON RICH FOODS

LOW CALORIE, LOW FAT DIETSSKIPPING MEALSINDUSTRIALIZED FOODSALCOHOL, VINEGAR CAFFEINEEXCESS ANIMAL PROTEINFIBER RICH CEREALS

SLEEP SLEEP SUFFICIENTLY 6-9 HRS/NIGHT

SLEEP DEPRIVATION

STRESS SOME STRESS MANAGEMENTTECHNIQUE

PROLONGED STRESSEXCESSIVE PHYSICAL ACTIVITY

HERTOGHE, T; The Hormone Handbook. International Medical BooksSurrey, UK, 2006, p87.

Page 51: SUBCLINICAL HYPOTHYROID

OTC THYROID AGENTSOTC THYROID AGENTSAGENT CONTENTS

HOMEOPATHIC THYROID STIMULATOR

THYROID 5C, NATIVE GOLD 8X, BLACK CURRANT BUDS 1DH, BLOODTWIG DOGBERRY BUDS 1 DH, SWEET ALMOND BUDS 1DH, ETHANOL, GLYCERIN, WATER

OTC THYROID TISSUE NEW ZEALAND SHEEP THYROID TISSUE, RICE POWDER, DI-CALCIUM PHOSPHATE, GELATIN

OTC THYROID TISSUE PLUS CO-FACTORS

NEW ZEALAND BOVINE THYROID, L-TYROSINE, ANTERIOR PITUITARY, L-ASPARTIC ACID, IRIS VERSICOLOR, KELP

Page 52: SUBCLINICAL HYPOTHYROID

HOMEO AND RMRHOMEO AND RMR

3030

202517761716.67

0

500

1000

1500

2000

2500

3000

3500

NO MEDS HOMEO 50 HOMEO 100 HOMEO 150

RMR

n=5 n=2 n=1n=5

Had to consume too many doses per day to maintain effect

Page 53: SUBCLINICAL HYPOTHYROID

OTC THYROID AND RMROTC THYROID AND RMR

23052210

1825

0

500

1000

1500

2000

2500

NO MEDS 300 MG 600 MG

RMR

n=3 n=5n=4

Had to consume too many doses to maintain effect

Page 54: SUBCLINICAL HYPOTHYROID

TISSUE AND COFACTORSTISSUE AND COFACTORS AND RMR AND RMR

1797.14

1925

16101618

1755

14501500155016001650170017501800185019001950

NO MEDS 2/DAY 3/DAY 4/DAY 6/DAY

RMR

n=4 n=7 n=3 n=6 n=1

Page 55: SUBCLINICAL HYPOTHYROID

RX THYROID PREPARATIONSRX THYROID PREPARATIONSAGENT EQUIVALENT

DOSE½ LIFE ADDITIVES

CYTOMEL 25 MCG 1.4 DAYS CALCIUM SULFITE, GELATIN, STARCH, STEARIC ACID, SUCROSE, TALC

SYNTHROID 0.1 MG 6-7 DAYS ACACIA, SUGAR, CORN STARCH, LACTOSE, MAGNESIUM STEARATE, POVIDONE, TALC

DESSICATED38 mcg T49 mcg T3

1 GRAIN 60 MG

3-7 DAYS CALCIUM STEARATE, DEXTROSE, MICROCRYSTALLINE CELLULOSE, SODIUM STARCH GLYCOLATE, OPODY WHITE

Page 56: SUBCLINICAL HYPOTHYROID

SYMPTOM SCORE SYMPTOM SCORE WORST TO BESTWORST TO BEST

Page 57: SUBCLINICAL HYPOTHYROID

RMR Response to MedicationRMR Response to Medication

0

500

1000

1500

2000

2500

3000

25 mcg / 100 mcg/60 mg

50 mcg/ 200mcg/120 mg

75 mcg/300mcg/180 mg

100 mcg/400 mcg/240 mg

Cytomel

Synthroid

Levoxyl

Armour

Naturethroid

Tissue andCofactorsOTC

Page 58: SUBCLINICAL HYPOTHYROID

RMRRMR

1875

1980

2055.74

2019

1750

1800

1850

1900

1950

2000

2050

2100

NO MEDS AT TARGET 2nd Cohort HYPER

RMR

Page 59: SUBCLINICAL HYPOTHYROID

PREFIRE NORMALPREFIRE NORMAL

69.86

90.58

111.3

132.02152.74

0

20

40

60

80

100

120

140

160

2STVD 1STVD MEAN 1STVD 2STVD

PREFIRE

1STVD= 20.72N = 281Normal 70-153

Page 60: SUBCLINICAL HYPOTHYROID

FIRE NORMALFIRE NORMAL

152.04178.84

205.64232.44

259.24

0

50

100

150

200

250

300

2STVD 1STVD MEAN 1STVD 2STVD

FIRE

1 STVD = 26.80N = 281NORMAL 152-259

Page 61: SUBCLINICAL HYPOTHYROID

FIRE-PREFIRE NORMALFIRE-PREFIRE NORMAL1 STVD = 21.24N = 281NORMAL 52-137

Page 62: SUBCLINICAL HYPOTHYROID

REFLEX PARAMETERSREFLEX PARAMETERS263.26

108.84

154.41147.83

118.05

29.6

111.3

205.64

94.26

181.64

127.1

60.93

0

50

100

150

200

250

300

NO MEDS AT TARGET 2nd Cohort HYPER

FIREPREFIREFIRE-PREFIRE

n=281 n=101 n=14n=281

Page 63: SUBCLINICAL HYPOTHYROID

CHANGE IN BBTCHANGE IN BBT22ndnd Cohort Cohort

96.54

96.79

96.4

96.45

96.5

96.55

96.6

96.65

96.7

96.75

96.8

BBT

NO MEDNORMAL

Page 64: SUBCLINICAL HYPOTHYROID

CHANGE IN WEIGHTCHANGE IN WEIGHT22ndnd Cohort Cohort

171.62

168.68

167167.5

168168.5

169169.5

170170.5

171171.5

172

POUNDS

NO MEDNORMAL

Page 65: SUBCLINICAL HYPOTHYROID

CHANGE IN BMICHANGE IN BMI22ndnd Cohort Cohort

27.3

26.58

26.2

26.4

26.6

26.8

27

27.2

27.4

BMI

NO MEDNORMAL

Page 66: SUBCLINICAL HYPOTHYROID

HYPERTHYROID SIGNSHYPERTHYROID SIGNS

PALPITATIONS 6:815 0.7% TACHYCARDIA 4:815 0.4% SHAKEY/HYPER 2:815 0.2% HAIR LOSS 1:815 0.1% HYPERTENSION 1:815 0.1% TOTAL 14:815 1.7%

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SONORA QUEST NORMALSSONORA QUEST NORMALSTEST LOW END

NORMALHIGH END NORMAL

TSH 0.45 4.5

T3U 23.4 42.7

T4 4.5 12.5

T7 1.2 4.3

FREE T3 1.8 5.4

FREE T4 0.8 1.9

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TSHTSH2.29

0.69

0.01

0.87

0.195

0

0.5

1

1.5

2

2.5

NO MEDS DESS TARGET 2nd Cohort HYPER

TSH

< 66 msecs 52-137 msecs

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AT TARGETAT TARGET (FIRE-PREFIRE<66)(FIRE-PREFIRE<66)

30.92

3.032.72.7

7.53

1.655.772.92

7.86

32.54

0

5

10

15

20

25

30

35

T3U T4 T7 FREE T3 FREE T4

NO MEDSTREATED

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AT TARGETAT TARGET(RMR CHANGE >(RMR CHANGE > 355)355)

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DESSICATED THYROID AND SERUM DESSICATED THYROID AND SERUM THYROID HORMONESTHYROID HORMONES

30.79

33.39

7.77 8.3

2.37 2.66 3.3

6.85

1.46

8.3

0

5

10

15

20

25

30

35

T3U T4 T7 FREE T3 FREE T4

WORSTBEST

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CHANGE IN SERUM HORMONESCHANGE IN SERUM HORMONES22ndnd Cohort Cohort

STAYED IN NORMAL RANGE

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HASHIMOTO’S AND RMRHASHIMOTO’S AND RMR

0

500

1000

1500

2000

2500

3000

START MED DX MED CHANGE BEST

PATIENT 1PATIENT 2PATIENT 3PATIENT 4PATIENT 5PATIENT 6MEAN

30 DAYS AFTER

ANTIBODIES STILL HIGH

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REFLEXES AND HASHIMOTO’SREFLEXES AND HASHIMOTO’S

294.75

174.5

229198.8 195.67

120.8117.33

120.25

137.2

108.297.1772.4

0

50

100

150

200

250

300

350

START MED DX MEDCHANGE

BEST

FIREPREFIREFIRE-PREFIRE

30 DAYS AFTER

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HASHIMOTO’S AND TSHHASHIMOTO’S AND TSH

6.58

3.84

2.86

0.030

1

2

3

4

5

6

7

STARTMEDS

DX CHANGEMED

BEST

TSH

30 DAYS AFTER

ANTIBODIES STILL HIGH

ANTIBODIES NOT RECOGNIZING (BINDING) NEW MED

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THYROID EFFECTS ON THYROID EFFECTS ON SERUM LIPIDSSERUM LIPIDS

N=30

SIMILAR TO A STATIN DRUG

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ADAPTING THYROID DOSE ADAPTING THYROID DOSE TO ENVIRONMENTTO ENVIRONMENT

DOSE INCREASE DOSE(5-20% MORE)

LOWER DOSE(5-20% LESS)

CONDITIONS INSUFFICIENT EFFECTSWINTERIN THE MOUNTAINSEXERCISING A LOTHIGH PROTEIN DIETLOW VEGGIE/FRUIT DIETLOW CALORIE DIETBETA BLOCKERSORAL ESTROGENSLEEP DEPRIVATIONSITUATIONS REQUIRING MENTAL ALERTNESS

EXCESSIVE EFFECTSSUMMERAT THE BEACHEXCESSIVE STRESSLOW PROTEIN DIETHIGH VEGGIE/FRUIT DIETCAFFEINATED DRINKSUNTREATED CORTISOL DEFICIENCYANDROGENS IN WOMENGROWTH HORMONE TREATMENTINSULIN TREATMENT

HERTOGHE, T; The Hormone Handbook. International Medical BooksSurrey, UK, 2006, p89.

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COST OF THYROID MEDSCOST OF THYROID MEDSPHARMACYPHARMACY30 day supply30 day supply

ARMOURARMOUR120 mg120 mg

SYNTHROIDSYNTHROID200 mcg200 mcg

CYTOMELCYTOMEL50 mcg50 mcg

WALGREENSWALGREENS $13.79$13.79 $28.19$28.19 $46.49$46.49

OSCOOSCO $21.69$21.69 $39.00$39.00 $75.00$75.00

K-MARTK-MART $15.97$15.97 $29.69$29.69 $48.97$48.97

COSTCOCOSTCO $10.19$10.19 $21.17$21.17 $41.89$41.89

AVERAGEAVERAGE $15.41$15.41 $29.51$29.51 $53.09$53.09Many on synthetic thyroid require both T3 and T4

Combination Therapy $82.60 for 30 day supply

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THYROID MYTHSTHYROID MYTHS DOES SUBCLINCAL HYPOTHYROID NEED TO BE

TREATED ?– HEALTH RISK IS HUGE IF UNTREATED

IS TSH THE BEST CLINICAL MARKER ?– INSENSITIVE NEAR NORMAL

GETS TOO SMALL BEFORE FULL CLINICAL EFFECT – RECEPTOR ACTIVITY DOESN’T REFLECT METABOLIC DEMAND

IS IODINE GOOD FOR THYROID FUNCTION ?– DECREASES THYROID FUNCTION IF NOT DEFICIENT

ARE SYNTHETIC THYROID MEDS MORE PRECISE AND MORE SCIENTIFIC THAN NATURAL ?– NATURAL THYROID IS BIOIDENTICAL, U.S.P. AND HAS > EFFECT– HALF-LIFE IS LONG IN MOST THYROID MEDS– MOST PEOPLE END UP ON 2 SYNTHETIC MEDS

IF SYNTHROID ALONE CAN’T CONVERT T4 TO T3 IF CYTOMEL ALONE T4 GOES TO ZERO