2018 Oregon Dental Conference Course Handout - Betsy Reynolds, RDH Course 9154: "The Mighty Thyroid: Linking Thyroid Function to Oral and Systemic ...

2018 Oregon Dental
        Conference®
        Course Handout

            Betsy Reynolds, RDH

 Course 9154: “The Mighty Thyroid: Linking
Thyroid Function to Oral and Systemic Health”
               Friday, April 6
                9 am - 12 pm

The Mighty Thyroid
                                                 Presented by:
                                            Betsy Reynolds, RDH, MS

Presenter Disclosures for Betsy Reynolds, RDH, MS
Acts as a Key Opinion Leader for Philips/Discus
     • In that capacity, she receives educational grant funding for presentation development
     • She is not an employee of either company and has no vested interest in sales of any product
         manufactured or distributed by Philips/Discus
Additionally, she has received funding from GC American for her 2015 presentation at the ADA Annual Session
Ms. Reynolds has received financial reimbursement from Parkell for authoring CE articles available at:
www.parkell.dentalaegis.com and financial support to assist with presentation expenditures
Following the presentation, course participants will be able to:
     • Understand the role the thyroid gland plays in health and disease.
     • Formulate dietary recommendations for patients receiving treatment for thyroid disease.
     • Modify in-office procedures to accommodate thyroid medication interactions.
     • Recognize oral and systemic signs and symptoms of thyroid malfunction.
     • Devise appropriate home care recommendations for patients with thyroid dysfunction
Agenda:
    • Introduction
    • Systemic Disorders of the Thyroid
    • Hyperthyroidism
    • Hypothyroidism
    • Thyroid Cancer
    • Oral Manifestations of Thyroid Disease
    • Treatment Recommendations
    • Headliners
The American Thyroid Association (ATA) is the world’s leading professional association of medical specialists
dedicated to education and research to improve thyroid disease prevention, diagnosis and treatment; improving
thyroid patient care; and educating the public about thyroid health and diseases

Prevalence and Impact of Thyroid Disease
    •   An estimated 20 million Americans have some form of thyroid disease and it has been suggested that
        more than 12% of the U.S. population will develop a thyroid condition during their lifetime
    •   Up to 60% of those with thyroid disease are unaware of their condition
    •   Women are five to eight times more likely than men to have thyroid problems—one woman in eight will
        develop a thyroid disorder during her lifetime
    •   Undiagnosed thyroid disease may put patients at risk for certain serious conditions such as cardiovascular
        diseases, osteoporosis and infertility
    •   Pregnant women with undiagnosed or inadequately treated hypothyroidism have an increased risk of
        miscarriage, preterm delivery, and severe developmental problems in their children

Research Advancements in Thyroid Disease
Research funded by the American Thyroid Association over the past 40+ years has accomplished:
    • Mandatory screening of newborns for congenital hypothyroidism and early treatment that has prevented
        mental retardation
    • Cost-effective methods to detect thyroid cancer
    • Groundbreaking work in brain development and thyroid hormone function
    • Promising Graves’ disease genetic research that may lead to improved prognosis and new preventive
        treatments

•    An experimental drug that may prove useful for treatment and prevention of eye problems associated
         with Graves’ disease

Meet the Thyroid!
The thyroid gland is located in the front of the neck attached to the lower part of the larynx and to the upper part
of the trachea
The thyroid has two sides called lobes that lie on either side of the trachea—the lobes are usually connected by a
strip of thyroid tissue known as an isthmus (however, in some cases, there are two separate thyroid lobes without
an isthmus)
Through hormonal activity, the thyroid regulates metabolic functions such as:
     • Breathing
     • Heart rate
     • Central and peripheral nervous systems
     • Body weight
     • Muscle strength
     • Menstrual cycles
     • Body temperature
     • Cholesterol levels
     • Much more!
As an endocrine gland, the thyroid uses dietary iodine to produce hormones such as:
     • Triiodothyronine (‘T3’)
     • Thyroxine (‘T4’)
The process by which the thyroid uses iodine is actually quite complicated and certain steps are still unclear—
essentially, iodine is converted to its free elemental form (‘iodide’) and then enters the thyroid gland through a
special transport mechanism
Iodide then undergoes a process called oxidation and is incorporated into intermediate hormones called MIT
(Monoiodotyrosine, which contains 1 iodide) and DIT (Diiodotyrosine, which contains 2 iodides)—these
compounds then combine to form the active hormones, tri-iodothyronine (T3) and thyroxine (T4)
These hormones are then stored in the thyroid gland and released into the blood stream
Key: Without iodine, the thyroid cannot make hormones vital to health
Two glands in the brain—the pituitary and hypothalamus—play important roles in maintaining thyroid hormone
balance
When thyroid hormones are low, the hypothalamus produces Thyroid Releasing Hormone (‘TRH’) that signals the
pituitary gland to release Thyroid Stimulating Hormone (‘TSH’)
The increased levels of TSH ‘stimulate’ the thyroid to produce more thyroid hormone to bring blood hormone
levels back to normal
The three glands and the hormones they produce make up the ‘Hypothalmic-Pituitary-Thyroid Axis’

T3 and T4
Although the thyroid gland produces more T4 (80%) compared with T3 (20%), T3 is 300% more active than T4—
additionally, much of the T4 is converted into the more active T3 inside the cells of the body
When the Thyroid Malfunctions:
Hyperthyroidism (‘Thyrotoxicosis’)
Hyperthyroidism is a condition in which the thyroid gland is overactive and makes excessive amounts of thyroid
hormone
In simple terms, all the metabolic processes are ‘speeded up’—for example, the pulse rate is rapid (over 100) and
occasionally irregular (atrial fibrillation), bowel function is increased (diarrhea), and the sweat glands work
excessively
The nervous system is also stimulated so that the patient becomes irritable and anxious
Despite increased appetite, the patient usually loses weight because food intake cannot keep up with the
increased breakdown of body proteins

Cardiac Symptoms of Hyperthyroidism:
    • Tachycardia
    • Changes in heart rate and force of cardiac contraction
    • Systolic heart murmur
    • Hypertension

Other symptoms of Hyperthyroidism include:
   • Heat intolerance
   • Trouble sleeping
   • Hand tremors/Finger clubbing
   • Goiter (Side views are beneficial!)
Causes for Hyperthyroidism:
Toxic nodular or multinodular goiter—lumps or nodules in the thyroid gland that cause the thyroid to produce
excessive amounts of thyroid hormones
    • Toxic nodular or multinodular goiter is the result of focal and/or diffuse hyperplasia of thyroid follicular
         cells
    • The prevalence of toxic nodular goiter increases with age and in the presence of iodine deficiency
    • In addition, inflammation of the thyroid gland—called thyroiditis—may result from a viral, bacterial or
         immune reaction which may temporarily cause symptoms of hyperthyroidism

De Quervain's Thyroiditis (‘DQT’)
De Quervain's thyroiditis (also called ‘subacute or granulomatous thyroiditis’) was first described in 1904 as a
painful and rapid swelling of the thyroid gland
In cases of DQT, the thyroid gland discharges excess thyroid hormone into the blood resulting in a hyperthyroid
state—however, the thyroid quits taking up iodine (radioactive iodine uptake is very low), and the hyperthyroidism
generally resolves over the next several weeks
Signs and Symptoms of DQT:
     • Patients frequently become ill with fever and prefer to be in bed
     • Thyroid antibodies are not present in the blood, but the sedimentation rate (which measures
         inflammation) is very high
Although this type of thyroiditis resembles an infection within the thyroid gland, no infectious agent has ever been
identified making antibiotic therapy ineffective
Treatment is usually bed rest and aspirin to reduce inflammation
Occasionally cortisone (steroids, which reduce inflammation) and thyroid hormone (to ‘rest’ the thyroid gland)
may be used in prolonged cases
Nearly all patients recover with the thyroid gland returns to normal after several weeks or months
A few patients will become hypothyroid once the inflammation settles down and therefore will need to stay on
thyroid hormone replacement indefinitely
Recurrences are uncommon

Medications containing iodine (such as amiodarone) may cause the thyroid gland to overproduce thyroid
hormones
Amiodarone is a very effective anti-arrhythmic drug—and it causes thyroid dysfunction in about 15%–28% of
patients after 2–3 years of treatment
It is also an iodine-rich compound with some structural similarity to thyroxine (T4)
Amiodarone contains approximately 37% iodine by weight—each 200-mg tablet is estimated to contain about 75
mg of organic iodide (8-17% of which is released as free iodide)
Standard maintenance therapy with 200 mg amiodarone can provide more than 100 times the daily iodine
requirement
Amiodarone and its metabolites may have a direct cytotoxic effect on the thyroid follicular cells
Patients considering amiodarone therapy should have a full thyroid work-up prior to starting the medication
regime

Instruct patients about the adverse effects of amiodarone therapy—because the development of thyrotoxicosis is
sudden and explosive, instruct patients to watch for symptoms and to seek treatment promptly

Hamburger Thyrotoxicosis
Community-wide outbreaks of ‘hamburger thyrotoxicosis’ resulting from inadvertent consumption of beef
contaminated with bovine thyroid gland have been reported
Case Report: Source: Parmar MS, Sturge C. Recurrent hamburger thyrotoxicosis. CMAJ: Canadian Medical
Association Journal. 2003;169(5):415-417. Accessed 12 May 2017 at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC183292/
A 61-year-old woman with a history of recurrent episodes of transient thyrotoxicosis presented with:
     • 3-week history of weight loss of ~9 pounds
     • Palpitations
     • Increased sweating
     • Mild tachycardia (112 beats/minute)
     • Fine tremor of the hands
While she had no thyroid enlargement, a clinical diagnosis of hyperthyroidism was confirmed by elevated free
thyroxine (T4) and suppressed thyroid-stimulating hormone (TSH)
Her symptoms resolved spontaneously and her free T4 returned to normal within 8 weeks
Further questioning into the patient's dietary history revealed that she lived on a farm with her husband—every
couple of years they slaughtered a cow from their herd to use as their main source of meat
Inquiries to the couple's local butcher revealed that he was unaware of the prohibition against ‘gullet trimming’—a
procedure whereby muscles from the bovine larynx are harvested—and had inadvertently been contaminating
edible meat with thyroid tissue
The butcher used meat from the neck of the patient's cows to make patties, which were usually consumed by the
patient within a couple of months of butchering—her husband, who was not affected by any thyroid problems, did
not consume these patties, preferring other cuts of meat
The patties could not be tested, as the patient had finished the current batch a month before consumption of
contaminated beef was suspected as the cause of her thyroid problems—however, ‘the temporal association of
episodes of transient hyperthyroidism with availability of meat from a slaughtered cow over the previous 11 years
is highly supportive of hamburger thyrotoxicosis’

Some women may develop hyperthyroidism during pregnancy or in the first year after giving birth
During pregnancy, the hormone HCG (‘human chorionic gonadotropin’) is produced—it has mild thyroid
stimulating effects and, as a result, can cause some symptoms of hyperthyroidism
In situations of multiple pregnancies (twins, triplets) HCG levels are even higher, and symptoms can be more
pronounced
HCG levels peak at ~10 weeks—temporary subclinical (no apparent symptoms) hyperthyroidism occurs in 10%-20%
of normal pregnant women during this period and these women typically do not require treatment
The most common cause of hyperthyroidism is the autoimmune disorder Graves’ disease—Graves' disease (GD) is
caused by autoimmune stimulation of the TSH receptors leading to hyperthyroidism
In mothers with Graves’ disease, levels of anti-thyrotropin receptor antibodies predict the risk for fetal and
neonatal thyroid dysfunction--Source: Banigé M et al: Fetal and neonatal thyroid function in relation to maternal
Graves' disease; Best Practice & Research Clinical Endocrinology & Metabolism , Vol (18) 2; p. 289 – 302. Accessed
on 13 May 2017 at: https://secure.jbs.elsevierhealth.com/action/showCitFormats?pii=S1521-
690X%2804%2900019-3&doi=10.1016%2Fj.beem.2004.03.009&code=ybeem-site
KEY: The binding of IgG to the thyrotropin receptors leads to the production of T3 and T4 as it mimics TSH-
thyrotropin binding—as IgG is not part of the negative feedback cycle that regulates the levels of circulating T3 and
T4, individuals with Graves' disease often possess high levels of T3 and T4 while having low levels of TSH
‘When managing a patient with Graves’ disease at the beginning of pregnancy, one of the main issues is prediction
of fetal and neonatal dysthyroidism. [Anti-thyrotropin receptor antibodies] levels in the mother are one of the
main predictors because their action can directly activate the fetal or neonatal thyroid gland or indirectly induce
fetal hypothyroidism because relative overtreatment of the mother induces hypothyroidism.’--Source: Maïa

Banigé, MD; Department of Neonatology, Obstetrics and Gynecology; University Hospitals Paris Nord Val de Seine;
study author
‘We clearly show in a large number of cases that there are precise TRAb cutoffs that can be used to establish the
best perinatal follow-up and that fine-tuning of the mother’s thyroid status and ultrasound monitoring of the fetal
thyroid should be used to avoid or predict fetal or neonatal dysthyroidism.’--Source: Researchers’ statement

About 35% of individuals also develop Grave’s ophthalmopathy which is an inflammatory disease of the orbital
tissues—in these cases, the immune system attacks the muscle and tissue behind the eye resulting in a buildup of
adipocytes and fibroblasts resulting in bulging eyes and vision complications
Smoking significantly worsens the outcome of Graves’ ophthalmopathy
Grave’s Disease is associated with neutropenia in one in seven patients at diagnosis—neutrophil counts increase
with treatment with ATD and are related to reduction in thyroid hormone concentrations
Oral Manifestations of Hyperthyroidism
    •   Increased susceptibility to caries
    •   Increased risk of periodontal diseases
    •   Enlargement of extraglandular thyroid tissue (posterior tongue)****
    •   Mandibular and/or maxillary osteoporosis
    •   Accelerated dental eruption
    •   Burning Mouth Syndrome
Osteoporosis and Hyperthyroidism:
Osteoporosis and increased fracture associated with thyroid malfunction is a hotly debated topic with no real
consensus—although there appears to be a stronger link between increased thyroid hormone output and negative
effects on bone metabolism
      • A Great Resource:
          Tuchendler, D and Marek B: The Influence of Thyroid Dysfunction on Bone Metabolism. Thyroid Research
          7 (2014): 12. PMC. Web. 13 May 2017
‘Thyroid hormones are necessary to normal development and function of human skeleton. This is evidently visible
in conditions of hyper- and hypothyroidism. Although it is still unclear if bone changes observed in [a] state of
thyrotoxicosis are related to lack of TSH or to excess of thyroid hormones or both of them.’
‘Overt hyperthyroidism leads to decreased BMD and increased fracture risk. Subclinical hyperthyroidism also
causes a small reduction in BMD and increased risk of fracture but only in men and postmenopausal women.’
Researchers at the University of Manchester School of Dentistry in England created a way of identifying patients
with osteoporosis that uses a software-based approach to detecting osteoporosis through routine dental
radiographic examination designed to measure the thickness of the mandible
The research team drew on ‘active shape modeling’ technology developed by the Division of Imaging Sciences of
the University of Manchester to automatically detect mandibular cortex widths of less than 3 millimeters—a key
indicator of osteoporosis—during the radiographic process
 ‘At the start of our study we tested 652 women for osteoporosis using the current 'gold standard,' and highly
expensive, DXA test. This identified 140 sufferers. Our automated X-ray test immediately flagged-up over half of
these. The patients concerned may not otherwise have been tested for osteoporosis, and in a real-life situation
would immediately be referred for conclusive DXA testing. As well as being virtually no extra work for the dentist,
the diagnosis does not depend on patients being aware that they are at risk of [developing] the disease…Just by
introducing a simple tool and getting health care professionals working together, around two in five sufferers
undertaking routine dental X-rays could be identified. The test might even encourage older women to visit the
dentist more regularly.’--Researcher's statement

Treatment of Hyperthyroidism
    •   Antithyroid medications (primarily methimazole; propylthiouracil is now used only for women in the first
        trimester of pregnancy)—these medications interfere with the production of thyroid hormones
    •   Radioactive iodine therapy to damage the cells that make thyroid hormones
    •   Surgical removal of part of or the entire thyroid gland

Treatment of hyperthyroidism secondary to Grave’s Disease aims to reduce serum thyroid hormone
concentrations and often antithyroid drugs (‘ATDs’) are used initially
KEY: Grave’s disease normally responds well to treatment—however hypothryroidism is commonly
observed

Many people are unaware that in the first half of the 20th Century, fluoride was used medically as an anti-thyroid
drug—administered to slow thyroid function in patients with hyperthyroidism
Fluoride was found to be extremely effective at suppressing thyroid function at very low doses—2-5 mg per day
over a period of months
Headliners: Are Fluoride Levels in Drinking Water Associated with Hypothyroidism Prevalence in England? A
Large Observational Study of GP Practice Data and Fluoride Levels in Drinking Water; Stephen Peckham et al;
Centre for Health Services Studies, University of Kent (Canterbury); results appearing in J Epidemiol Community
Health; published online first 24 February 2015; as reported by Becky McCall for Medscape; posted 04 Mar 2015;
accessed on 11 Mar 2016 at: http://www.medscape.com/viewarticle/840873
Higher levels of fluoride in drinking water appear to be associated with an increased risk for hypothyroidism in a
new study from England—raising concerns about the validity of community fluoridation of water as a safe public-
health measure
In particular, when a comparison was drawn between a completely fluoridated area (0.7 mg/L or more) and a non-
fluoridated area (0.3 mg/L or less), nearly TWICE the risk for hypothyroidism was detected in the fluoridated area!
 ‘I think the results clearly demonstrate an increased risk of hypothyroidism associated with areas of [high] water
fluoridation. [The study also]…raises questions about the safety of community fluoridation.’
‘The findings are meaningful and plausible and deserve to be taken seriously. [T]hese results should prompt a
rethinking of the whole practice of adding fluoride to drinking water in all countries.’
 ‘[T]he large size of the study population minimized bias and the researchers accounted for the major known
predictors of thyroid function—including age, sex, iodine intake, and perchlorate exposure…The prior
recommendation of a fluoridation range from 0.7 to 1.2 mg/L is still the operative one, with most US states
targeting a fluoride level of about 1 mg/L—the same as in the UK. If a similar study were to be conducted in the US,
I would expect to see similar results.’
Levels of fluoridation in the United Kingdom are comparable to those in the United States—in 2011, there was a
proposed recommendation to decrease fluoride levels in drinking water to 0.7 mg/L in the United States but the
recommendation of 0.7 mg/L is still only a proposal and very few US states or municipalities have made any
changes
Researchers estimate that people today who live in communities with fluoridated water supplies have a range of
exposure of 1.6 to 6.6 mg per day
Another Fluoride Tidbit:
      • Fluorine and iodine (both members of the halogen group of atoms) have an antagonistic relationship—in
           excess, fluoride can interfere with iodine uptake and prevent iodine from functioning properly

Hypothyroidism
Occurs when the thyroid gland does not make enough thyroid hormones (T3 and T4) to meet the body’s needs
Over 10 million Americans have hypothyroidism—~2 out of 100 individuals—and many do not know they have it!
Women are more likely to have it than men and the chances for developing hypothyroidism increases with age—
over 10% of Caucasian women over 60 years of age in the United States and Canada have an under-functioning
thyroid gland
The signs and symptoms associated with hypothyroidism occur because there is a deficiency of thyroid hormone
secretion and all metabolic processes in the body slow down—resulting in poor appetite, intolerance to cold, dry
skin, brittle hair, fatigue, constipation, muscle weakness, poor memory retention and hoarseness
Examination may reveal dry, scaly skin with a thickening of surface and underlying tissues (‘myxedema’), very slow
reflexes, and decreased heart rate

Problems may arise when outside factors act upon the thyroid metabolism cycle which can lead to disruptions in
TSH levels, decreased production of T4, incomplete conversion of T4 to T3 or imbalance in the ratio of T3 to
reverse T3***
Typically, when T4 loses an atom of iodine—a process known as ‘monodeiodination’ or ‘T4 to T3 conversion’—it
becomes T3
In some cases, the body conserves energy by converting the T4 instead into Reverse T3 (‘RT3’)—an inactive form of
T3 that is incapable of delivering oxygen and energy to the cells
If there is a preferential conversion of T4 to reverse T3, the reverse T3 can act as an antagonist to T3 at the
receptor level—factors that may lead to a preferential conversion to reverse T3 include high cortisol levels,
glucocorticoids, stress, excess estrogen and nutritional deficiencies such as selenium, iodine, zinc and iron
Considered a ‘stress hormone’, cortisol levels increase during periods of chronic stress—causing a decrease in TSH
secretion (which lowers thyroid hormone production) and inhibiting the conversion of T4 to active T3 while
increasing the conversion of T4 to reverse T3
Factors that increase TRH secretion include the following:
     • Cold temperatures
     • Pregnancy
     • Circadian Rhythms***
Factors that decrease TRH secretion include the following:
     • T3/T4 hormones (negative feedback)
     • Stress***
Headliners: The Impact of Sleep Deprivation on Hormones and Metabolism; Source: Eve Van Cauter, PhD et al;
Medscape Neurology. 2005;7(1); accessed on 12 May 2017 at: http://www.medscape.org/viewarticle/502825
The release of hormones by the pituitary is markedly influenced by sleep
As seen in the HPT Axis discussed earlier, the pituitary gland is greatly affected by substances made by the
hypothalamus (and vice versa)
Another example of this glandular relationship is the Hypothalmic-Pituitary-Adrenal Axis (‘HPA Axis’)
Researchers discovered that partial sleep loss affected circulating levels of pituitary-dependent hormones which
lead to an increase in early evening levels of the stress hormone cortisol produced in the adrenal glands
Normally, cortisol concentrations are rapidly decreasing to attain minimal levels shortly before habitual bedtime—
the rate of decrease of cortisol concentrations in the early evening was approximately 6-fold slower in subjects
who had undergone 6 days of sleep restriction than in subjects who were fully rested
After 6 days of 4-hour sleep time, the normal nocturnal thyroid-stimulating hormone (TSH) rise was strikingly
decreased and the overall mean TSH levels were reduced by more than 30%
Additionally, free thyroxine index (‘FT4I’) was higher in the sleep-restricted study participants than in the fully
rested cohort—strengthening the negative feedback mechanism to the thyroid gland

Excess Estrogen and Thyroid Function
Excess estrogen increases levels of thyroid binding globulin (TBG)—the proteins that thyroid hormone is attached
to as it is transported through the body
When thyroid hormone is bound to TBG, it is inactive—it must be cleaved from TBG before it can activate cellular
receptors
When TBG levels are high, the percentage of free thyroid hormones drops
The most common causes of elevated TBG secondary to excess estrogen are birth control pills and hormone
replacement therapy

Considerations of Selenium in Thyroid Health
In patients with Hashimoto's disease, selenium supplementation has been shown to decrease anti-thyroid
antibody levels and improves the ultrasound structure of the thyroid gland
The National Institutes of Health lists selenium supplements as possibly effective for autoimmune thyroiditis
(Hashimoto’s thyroiditis) but the agency deems the supplements possibly unsafe when taken in high doses or long-
term—low-dose, long-term use has been shown to increase the risk of developing diabetes and likely may interact
with medications including immunosuppressants, anticoagulants and antiplatelet drugs, statins and blood thinners

‘The idea that everyone should be taking selenium supplements in the off-chance they could help is not warranted
and potentially dangerous. People should focus on getting selenium from their diets, which isn’t difficult in places
like the U.S. [and Canada].’--Jason Baker, M.D.; assistant professor of clinical medicine; Weill Cornell Medical
College (New York)

Iodine and Thyroid Health
Headliners: What Causes Thyroid Disease?; Alan Christianson; naturapathic medical doctor; posted 22 Jun 2015;
accessed 9 Mar 2016 at: http://www.huffingtonpost.com/alan-christianson/what-causes-thyroid-
disea_b_7557870.html
The thyroid is the only part of the body that needs iodine—this is unusual because every other nutrient we know
of is used for many body processes with a large variety of reactions
Another unusual thing about iodine uptake and the thyroid is that an iodine transport mechanism is needed to get
the nutrient inside gland—all of the other nutrients the body uses are found in adequate amounts in the
bloodstream but the bloodstream cannot carry adequate iodine for the thyroid
For that reason, the thyroid has a pump that pulls iodine inside of the gland at concentrations up to 100 times
what is found in the blood—this pump can be part of the problem in thyroid disease because it can pull toxins
inside the thyroid along with the iodine
Ironically, the best-documented toxins to trigger thyroid disease include iodine itself—other thyroid toxins (called
‘endocrine disruptors’) include perchlorate, lead, mercury and over 200 other environmental chemicals

Fire Retardants (PBDEs)
PBDEs (‘polybrominated diethyl ethers’) disrupt thyroid function by blocking the uptake of iodine—eventually
taking its place in the thyroid (mimicking and disrupting thyroid hormones in the process)
PBDEs have been linked to lower IQ and are proven to negatively affect neural and physical development in
children and developing infants

Perchlorate
Found in rocket fuel, explosives, fireworks, and fertilizers, this common environmental chemical noticeably
disrupts thyroid function
Similarly to PBDEs, perchlorate replaces iodine in the thyroid and leads to decreased thyroid activity
Water contains the highest concentrations of perchlorate—using a high-quality water filter may also help filter out
perchlorate

Organophosphate Pesticides
Consuming vegetables and fruits that have pesticide residue is one of the most common ways endocrine disruptors
enter the thyroid
Organophosphate pesticides have been shown to cause infertility in men, slow brain development in children, and
have even been shown to affect thyroid function
Always choose organic when purchasing food to avoid these pesticides

Phthalates
Phthalates are added to plastics to aid durability and flexibility; yet, their negative health effects have been
constantly reported in various studies all across the world
Research has confirmed that phthalates inhibit sperm cell development
These chemicals have also been linked to obesity, diabetes, and thyroid conditions
Phthalates can easily leach into water, and people drinking from water bottles are the most susceptible to chronic
exposure
Always store foods and liquids in glass whenever possible

Perfluorinated Chemicals (PFCs)

It has been estimated that 99% of Americans have PFC accumulation in their bodies
PFCs have the power to accumulate in the body and are extremely difficult to get rid of once they are stored
PFCs are commonly used to make non-stick pans—during cooking, some of these chemicals escape into food
Avoiding non-stick cookware is extremely important
PFCs disrupt hormone function and have been tied to infertility, ineffective sperm, heart disease, thyroid disease,
high cholesterol, and low birth-weight in babies
Research has confirmed PFCs (especially PFOA and PFHxS) negatively affect thyroid hormone levels
According to a 2017 report, some 16.5 MILLION Americans in 33 states may be drinking water containing unsafe
levels of organic compounds known as PFAs—which has also been linked to high cholesterol, obesity and cancer--
As reported in TIME; 30 JAN 2017
Headliners: Researchers: Potentially dangerous chemicals found in fast-food wrappers; Study results published
in Environmental Science & Technology Letters; 1 FEB 2017; As reported by Michael Hawthorne; Chicago
Tribune; results appearing in the Idaho Statesman; 2 FEB 2017
For over 30 years, fast-food companies have relied on the chemical industry to keep grease and oil from soaking
through burger wrappers, French fry cartons, and pizza boxes
Researchers began to realize that those compounds—PFCs—were causing cancer, liver damage, reproductive
trouble and hormonal imbalances during development
It turned out that food wrappers were a MAJOR source of exposure—under oath, a former DuPont chemist
described how customers ingested the chemicals every time they ate a French fry
McDonald’s, Burger King and other chains pledged to stop using PFCs and manufacturers began to phase them
out—in 2016, the FDA followed up with a ban on three PFCs used in packaging
In a study released in 2017, a THIRD of samples collected from McDonald’s, Burger King, Starbuck’s and other
restaurants contained FLUORINE—a key building block in PFCs

Back to Iodine
Before the 1920s, iodine deficiency was common in the Great Lakes, Appalachian, and Northwestern U.S. regions
and in most of Canada—since the introduction of iodized salt, the ‘goiter belt’ has been virtually eliminated
However, many other parts of the world do not have enough iodine available through their diet and iodine
deficiency continues to be an important public health problem globally—approximately 40% of the world’s
population remains at risk for iodine deficiency
KEY: Both over- and under-production of thyroid hormone are associated with goiter!
     • In hyperthyroidism, the goiter is the result of inflammation of the gland
     • In hypothyroidism, the goiter develops as the thyroid attempts to make more thyroid hormone in the
         absence of sufficient dietary iodine
Headliners: The Silent Epidemic of Iodine Deficiency; Nancy Piccone; appearing online at Lifeextension.com;
posted October 2011; accessed 11 Mar 2016 at: http://www.lifeextension.com/magazine/2011/10/the-silent-
epidemic-of-iodine-deficiency/Page-01
In the developed world, iodine deficiency has increased more than fourfold over the past 40 years—nearly 74% of
normal, ‘healthy’ adults may no longer consume enough iodine
The health benefits of reducing salt intake have been well established—millions of Americans have slashed their
use of salt to protect themselves against high blood pressure and cardiovascular disease AND have cut iodine
intake in the process

Hypothyroidism
Hashimoto’s Thyroditis
In the case of any autoimmune disease, the main feature is the production of antibodies that attack the healthy
tissue of the body
KEY:
     • Patients first experience symptoms of hyperthyroidism (sudden weight loss, rapid heartbeat, anxiety, high
          blood pressure and hot flashes)—however, as levels of hormone clear from the blood and drop, patients
          experience hypothyroid symptoms like fatigue, depression, weight gain, constipation and mood swings

•   This pattern repeats until thyroid hormones becomes depleted and patients are subsequently diagnosed
        with a low thyroid state
Systemic Manifestations of Hypothyroidism
    • Cold intolerance
    • Constipation
    • Forgetfulness and personality changes***
    • Modest weight gain (mainly due to fluid retention and decreased metabolism)
    • Paresthesia of the hands (carpel tunnel) and feet (caused by deposition of proteinaceous ground
        substance in the ligaments around the wrist and ankle)
    • Women may experience irregular or absent menstrual cycles
    • Dull facial expression
    • Hoarse voice
    • Slow speech
    • Facial puffiness and periorbital swelling (due to infiltration with the mucopolysaccharides hyaluronic acid
        and chondroitin sulfate)
    • Drooping eyelids
    • Hair is sparse, coarse, and dry
    • Skin is coarse, dry, scaly, and thick
    • Hypothermia
    • Bradycardia (slow heart rate)
    • Facial rash

Headliners: Are You Living Life with Thyroid Brain Fog?; October 24, 2014 by Dana Trentini; posted on 24 Oct
2014; written by Dr. Hugh Melnick (mythyroidmd.com); accessed 4 Mar 2016 at:
http://hypothyroidmom.com/are-you-living-life-with-thyroid-brain-fog/
accessed 3/4/16
Poorly managed hypothyroidism can have a powerful effect on the brain
Increased depression and anxiety—hypothyroidism has been shown to increase depression seven-fold!—have long
been associated with thyroid disorders--Source: Larisch R et al: Depression and anxiety in different thyroid function
states. Horm Metab. Res. 2004 Sep;36(9):650-3. Accessed on 11 Mar 2016 at:
http://alt.support.thyroid.narkive.com/aA94BsmU/it-s-not-all-in-our-heads-hypo-increases-depression-7-fold
Critical Mood Deterioration (‘CMD’)
These three words are how medical experts and research analysts describe the mentally foggy state that many
hypothyroid patients find themselves in—in fact, current studies indicate that an underactive thyroid can take a
significant toll on mental health because EVERY system slows (including neurological functions)
Symptoms of CMD include:
     • Inability to concentrate
     • Detachment from personal relationships and activities
     • Low self-esteem
     • Depression
     • Inability to connect details
     • Short-term memory problems
     • Slowed mental reactions
     • Confusion
Unfortunately, the neurological symptoms that about 5% of all hypothyroidism patients suffer from are largely
underestimated or outright ignored by a lot of practicing medical professionals

Case Report (Source: Dudhia SB, Dudhia BB. Undetected hypothyroidism: A rare dental diagnosis. J Oral
Maxillofac Pathol 2014;18:315-9)
‘Obtaining an understanding of thyroid dysfunction is of significant importance to the dentist for two reasons.
First, the dentist may be the first to suspect a serious thyroid disorder and aid in early diagnosis. If a suspicion of

thyroid disease arises for an undiagnosed patient, all elective dental treatment should be put on hold until a
complete medical evaluation is performed. Once the hypothyroid patient is under good medical care, no special
problems are presented in terms of dental management, except for dealing with the malocclusion and enlarged
tongue if present. Our patient had come with chief complaint of malaligned teeth, but suspecting hypothyroidism,
we first referred her to the endocrinologist and once the thyroid disease was under control, we planned our dental
treatment.’--The research team

Treatment of Hashimoto’s:
Levothyroxine (also known as Synthroid, Eltroxin, and some other trade names) is first line conventional medical
therapy for hypothyroidism
Ideally, levothyroxine provides synthetic T4 (thyroxine) which is subsequently converted to T3 by tissues
throughout the body—supplementing only T4 depends on conversion to have effect at the tissue level
This treatment also is designed to provide feedback to the pituitary gland which produces TSH—bringing down
elevated TSH found in hypothyroidism
Generally speaking, thhe correct dose of thyroxine is determined by normal TSH (0.3-3.5milliU/L)***, a normal
Total T3 (1.2-3.4 nmol/L) and a T4 level in the upper half of normal or just above (normal range 50-165 nmol/L)
KEY: The correct dose of T4 can ‘normalize’ TSH levels but may not resolve symptoms of hypothyroidism or
resolve the autoimmune process present in Hashimoto’s hypothyroid
Patients often complain that even though they are in treatment for their thyroid condition, they do not feel better
physically or mentally
According to Pamela Wartian Smith, MD, MPH, the standard test for low thyroid might not provide a clear
understanding of thyroid function—a ‘normal’ test result that is in the lower range of acceptable TSH levels may be
too low for some people!
Typically, hypothyroidism is diagnosed with a simple blood test for TSH (if thyroxine is LOW, the body will produce
higher levels of TSH to compensate)—therefore, a TSH reading of ≥5.0 mlU/L (milli-international units per liter) is
significantly elevated to confirm a diagnosis of hypothyroidism
If a person remains symptomatic even when TSH levels are within the ‘normal’ range, the problem could be with
the laboratory used to analyze the blood draw (many laboratories use different reference ranges)
Mainstream medicine generally relies on a normal TSH range from 0.5 mlU/L to 5.0 mlU/L—other doctors will only
diagnose hypothyroidism once TSH is above 10.0!

For these reasons, it is extremely important to demand a COMPLETE thyroid panel when seeing a physician
According to www.endocrineweb:
https://www.endocrineweb.com/conditions/thyroid/thyroid-function-tests
Serum thyroxine                     T4              4.6-12 ug/dl
Free thyroxine fraction             FT4F            0.03-0.005%
Free Thyroxine                      FT4             0.7-1.9 ng/dl
Thyroid hormone binding ratio       THBR            0.9-1.1
Free Thyroxine index                FT4I            4-11
Serum Triiodothyronine              T3              80-180 ng/dl
Free Triiodothyronine l             FT3             230-619 pg/d
Free T3 Index                       FT3I            80-180
Radioactive iodine uptake           RAIU            10-30%
Serum thyrotropin                   TSH             0.5-6 uU/ml***
Thyroxine-binding globulin          TBG             12-20 ug/dl T4 +1.8 ugm
TRH stimulation test Peak           TSH             9-30 uIU/ml at 20-30 min
Serum thyroglobulin l               Tg              0-30 ng/m
Thyroid microsomal antibody         TMAb            Varies with method
Thyroglobulin antibody titer        TgAb            Varies with method
Reverse T3                           rT3            10-24 ng/dL***

•   As hyperthyroidism is associated with fracture risk, does exogenous levothyroxine use increase the risk
        for fractures?
        Excessive intake of thyroid supplements resulting in subclinical hyperthyroidism may occur in as many as
        20% of patients (particularly the elderly)!
    •   Patients who begin taking levothyroxine in middle age may need lower doses with advancing age—and
        overtreatment is common despite requirements for regular thyroid-stimulating hormone (TSH)
        monitoring

Something to ponder:
Use of levothyroxine is increasing—in the United States, the number of prescriptions for levothyroxine increased
from 97 million in 2007 to 120 million in 2014 making levothyroxine the most prescribed drug in the USA--Source:
Rodriguez-Gutierrez, Rene et al: Levothyroxine overuse: time for an about face?; appearing in The Lancet Diabetes
& Endocrinology; Vol 5 (4): p.246 - 248 ; accessed 13 May 2017 at:
https://secure.jbs.elsevierhealth.com/action/showCitFormats?pii=S2213-8587%2816%2930276-
5&doi=10.1016%2FS2213-8587%2816%2930276-5&code=lancet-site

Recommendations:
TSH levels should be obtained at least annually in patients taking levothyroxine
Levothyroxine should not be taken concomitantly with multivalent cations (ie, iron and calcium) or food
Patients should be instructed on how to take levothyroxine properly
     • Levothyroxine should be taken at a consistent time to avoid fluctuations in TSH levels
     • Some research suggests bedtime administration of levothyroxine may be more effective than morning
         administration
Headliners: Effects of Evening vs Morning Levothyroxine Intake: A Randomized Double-Blind Crossover Trial;
Bolk N, et al; A. Arch Intern Med. 13 Dec 2010; 170(22):1996-2003; study results accessed on 10 Mar 2016 at:
http://www.thenddc.com/are-you-prescribing-the-wrong-thyroid-medication/
Patients are nearly always instructed to take levothyroxine in the morning, but Dutch researchers are suggesting
that perhaps a bedtime dose would be a better option
 ‘Levothyroxine taken at bedtime significantly improved thyroid hormone levels. Quality-of-life variables and
plasma lipid levels showed no significant changes with bedtime vs morning intake. Clinicians should consider
prescribing levothyroxine intake at bedtime.’--Statement of investigators
For those patients taking levothyroxine, considering a change in timing of medication with appropriate follow-up
testing may be worth it—discussion with the treating physician is ALWAYS recommended before making any
changes in medication protocol
KEY: Standard prescription hormones (like Synthroid) only contain T4—if symptoms of hypothyroidism persist,
medications containing T4 and T3 (generally in a 4:1 ration) may be prescribed

Desiccated Thyroid
Desiccated thyroid at one point was the ONLY medication option for underactive thyroid and has been around the
longest
Because it is made from the whole gland, desiccated thyroid is considered a more complete product that provides
supplementation of thyroid hormones closest to what would be produced naturally—many patients choose this
medication after starting with levothyroxine because they prefer a natural product and experience better results in
symptom reduction
Because desiccated thyroid is NOT synthetic and is derived from a natural source that will vary from batch to
batch, it is very important to use a reputable brand that is standardized and formulated carefully—in the United
States, there are many products with desiccated thyroid in non-standardized amounts and pose a major health risk
Known simply as Thyroid (made by Erfa) in Canada and under several brands available in the United States,
desicated thyroid is the powdered thyroid gland of pigs—it provides T4 and T3 as well as additional hormones
produced by the thyroid gland (T2, T1, calcitonin)

In 2014, patients who were taking (and loving!) Erfa’s Thyroid began reporting a major return of their hypothyroid
symptoms—according to the Medical Director for Efra Canada, Dr. Henri Knafo, the company changed the facility
from which the tablets were made but not the ingredients
A major effort to change Thyroid back to its original formulation has not worked thus far—users of the ‘new’ drug
are reporting more fatigue and facial rashes

Why does Hashimoto’s occur?
Trigger Theories
Triggers like poor diet, stress, toxins and illness can create negative changes in the microbiome—friendly bacteria
that normally support health become suppressed while opportunistic and pathogenic bacteria take center stage
This can lead to a whole host of health conditions including autoimmunity
Microbe triggers include the bacteria Yersinia Enterocolitica—which has surface peptides that mimic receptors on
the thyroid
     • The receptors are so similar that when the immune system mounts a response to yersinian, it also attacks
          thyroid tissue
     Headliners: Organization Finds Yersinia enterocolitica in Most Pork Samples; As reported by Greg Cima for
     The American Veterinary Medical Foundation; posted on 31 Dec 2012; accessed on 10 Mar 16 at:
     https://www.avma.org/News/JAVMANews/Pages/130115y.aspx
     • A product testing organization found Yersinia enterocolitica in 69% of pork samples tested—the test
          results from Consumer Reports indicated the organization tested for the presence of certain bacteria in
          about 200 samples from pork chops and ground pork bought in six U.S. cities—the article also noted that
          121 of 132 Yersinia isolates tested for drug resistance were resistant to at least one antimicrobial
     • About 98,000 people in the U.S. were sickened (generally diarrhea and abdominal pain) by Y.
          enterocolitica annually from 2000-2008—the bacteria are most often spread to humans through
          contaminated food (particularly undercooked or raw pork)
     • Yersinia enterocolitica cross the epithelial barrier in the ileal portion of the small intestine—to survive,
          these bacteria resist phagocytosis by macrophages and downregulate inflammation
     • As a result, bacteria resist host immune defenses in subepithelial tissues which allows them to invade and
          infect distant tissues--Source: War and peace at mucosal surfaces by Philippe J. Sansonetti; appearing in
          Nature Reviews Immunology. 4, 953-964 (December 2004)
     • Once yersinia has disseminated throughout the body, the immune system mounts an antibody-mediated
          attack that affects BOTH the microbe and thyroid cells
Headliners: Virologic and Immunologic Evidence Supporting an Association Between HHV-6 and Hashimoto's
thyroiditis; E. Caselli, M. C. Zatelli, R. Rizzo, et al. PLOS Pathogens, vol. 8, no. 10, Article ID 100295, 2012;
accessed on 8 Mar 16 at http://www.hindawi.com/journals/tswj/2013/867389/
     • A 2012 study linking Human Herpes Virus 6A (‘HHV-6A’) to Hashimoto’s thyroiditis (‘HT’) found that HHV-
          6A was detected significantly more frequently among thyroid fine needle aspirates from HT individuals
          than controls (82% versus 10%)
     • The presence of HHV-6A infection was found localized in thyrocytes (rather than in lymphocytes)
          infiltrating the lesion
     • Additionally, the study demonstrated that thyroid cells infected with both HHV-6A and HHV-6B became
          susceptible to Natural Killer Cell-mediated killing—providing evidence of a potential mechanism for HHV-
          6A/B-induced autoimmunity
     • A 2015 study led by Rizzo and Caselli from the University of Ferrara also analyzed fine needle thyroid
          aspirates and found HHV-6 in 100% of the tests of HT sufferers (compared to only 25% in control)
     • They also demonstrated that an HHV-6 infection correlated with higher levels of a particular type of NK
          cell associated with a potent release of cytokines—leading to speculation that these NK cells might play
          an important role in disease activity and viral infection

Viruses (such as HTLV-1, enterovirus, rubella, mumps virus, HSV, EBV and parvovirus) are linked with Hashimoto's
thyroiditis—these tiny microbes promote inflammation, provoke overstimulation of the immune system and may
create the same type of molecular mimicry seen with yersinia
Research is still working on finding the exact mechanisms that trigger the self-immune attack in the presence of
these viruses

Wolff-Chaikoff Effect
The Wolff-Chaikoff Effect (‘WCE’) refers to an acute adaptive response to high doses of iodine—the increased
intracellular iodide blocks the organic-binding and coupling reactions in the thyroid (functionally turning off the
thyroid in the process)
It is often used to prepare the thyroid gland for surgery
The WCE is an effective means of rejecting the large quantities of iodide in order to prevent the thyroid from
synthesizing excess quantities of thyroid hormones
The acute Wolff-Chaikoff effect generally lasts for a few days and then the normal synthesis of thyroxine (T4) and
triiodothyronine (T3) returns
In some patients—especially those with Hashimoto’s and previously treated Graves' disease—the escape from the
inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues
The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal—
but patients who develop transient iodine-induced hypothyroidism must be followed long-term because many will
develop permanent primary hypothyroidism

For adults who are not lactating or pregnant, the US Institute of Medicine, and jointly by the WHO, United Nations
Children’s Fund (UNICEF) and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD),
recommend a daily iodine intake of 150 μg and state a tolerable upper level of 1,100 μg per day
Sources of iodine exposure and potential excess:
Diet
     • Kelp (per g): 16–8,165 μg
     • Bread (per slice): 2.2–587.4 μg
     • Milk (per 8 oz): 88–168 μg
     • Fish fillet (per g, dry weight): 0.73 μg
     • Iodized salt: Variable
Other sources
     • Vitamins (prenatal, labelled content per daily serving): 75–200 μg
     • Amiodarone (per 200 mg): 75,000 μg
     • Iodinated contrast (free iodine content, per CT scan): 13,500 μg
     • Topical iodine (povidone iodine): variable, usually 1–5%
     • Expectorants, mouthwashes, vaginal douches: variable
     • Saturated solution of potassium iodide (per drop): 50,000 μg
KEY: Hydrogen peroxide is created in the thyroid to help convert iodine to its usable form—this can be
inflammatory without adequate selenium levels to protect tissue by neutralizing free radicals
     • Excessive iodine intake on its own can fuel autoimmunity by causing even more hydrogen peroxide to be
         made—while deficiency can lead to goiter and low thyroid function, too much can make autoimmunity
         worse
     • When selenium is taken in from the diet it is used to synthesize proteins
     • There are 3 classes of selenoproteins that the body makes—one of which is iodothyronine deiodinases
         (DDIs) which are involved with converting T4 into the active T3 form
     • Selenium deficiency will increase cellular damage and set off autoimmunity—explaining why the thyroid is
         so susceptible to the development of Hashimoto's in a selenium deficient dietary state

Gluten Trigger
Many believe that there is a clear link between gluten consumption and Hashimoto's Thyroiditis—according to
study investigations, the structure of gliadin (a component of gluten) is very similar to thyroid cells

The more gluten that is consumed, the more the immune system responds by making antibodies to the thyroid
Headliners: Two of a Kind—Research Connects Celiac and Thyroid Diseases and Suggests a Gluten-Free Diet
Benefits Both; Cheryl Harris, MPH, RD and Gary Kaplan, DO; appearing in Today’s Dietitian; Vol. 12 No. 11 P. 52;
11/2010; as reported by Breana Noble; News Max; posted 08 Mar 2016; accessed at:
http://www.newsmax.com/FastFeatures/celiac-disease-Hashimotos-thyroiditis-link/2016/03/08/id/718160/
on 3/10/16
Research demonstrates that the autoimmune disorder Hashimoto’s thyroiditis and Celiac Disease are linked—once
diagnosed with one autoimmune disease, many people are at risk of developing another
Today’s Dietician reported that, in one research project, half of the patients with Celiac illness also had
Hashimoto’s
According to Beyond Celiac, patients with the gluten-related disorder are four times more likely to have
Hashimoto’s than the average population
The Celiac Support Association reported that Celiac Disease causes difficulty with absorption of thyroid hormones
Many patients with Celiac Disease are on a gluten-free diet—the diet not only lessens symptoms of Celiac illness, it
also enhances the absorption of medications for Hashimoto’s disease (Source: National Center for Biotechnological
Information)
Another study showed that serum anti-tissue transglutaminase antibodies are found in patients with Celiac
Disease—these antibodies bind to the thyroid which purportedly leads to autoimmune hypothyroiditis
Even with the link between the two illnesses, most patients are not cross-screened when diagnosed with either
one—it is clear that people are better off if they are tested for both diseases--(Source: Beyond Celiac)

Oral Manifestations of Hypothyroidism
    •    Salivary gland enlargement
    •    Compromised periodontal health***
    •    Macroglossia***
    •    Glossitis
    •    Dysgeusia
    •    Delayed eruption
    •    Enamel hypoplasia (especially in deciduous dentition)
    •    Anterior open bite
    •    Micrognathia
    •    Thick lips
    •    Mouth breathing
    •    Delayed wound healing***
    •    Thickening of the tongue and lips occurs due to an increase in accumulation of subcutaneous
         mucopolysaccharides (such as glycosaminoglycans)—these substances cannot be degraded in a
         hypothyroid state
Case Report (Source: Kothiwale S, Panjwani V. Impact of thyroid hormone dysfunction on periodontal disease. J
Sci Soc 2016; 43:34-7. Accessed on 11 Mar 2016 at: http://www.jscisociety.com/article.asp?issn=0974-
5009;year=2016;volume=43;issue=1;spage=34;epage=37;aulast=Kothiwale)

Inflammation and Thyroid Function
Studies have shown that the stress inflammatory cytokines (specifically IL-1β, IL-6 and TNF-α) down-regulate the
HPT axis and reduce levels of thyroid stimulating hormone (TSH)
    • It has also been demonstrated that one single injection of tumor necrosis factor alpha (TNF-α) reduced
         serum TSH, T3, free T4, free T3 and hypothalamic TRH for 5 days
    • TNF-α was also found to decrease the conversion of T4 to T3, reduce thyroid hormone uptake, and
         decrease the sensitivity of the thyroid to TSH
    • In order for thyroid hormone circulating in blood to have a physiological effect, it must first activate
         receptors on cells—inflammatory cytokines have been shown to suppress thyroid receptor site sensitivity
Thyroid Dysfunction and Cardiovascular Health

Thyroid dysfunction creates unfavorable disturbances in lipid profiles—elevating low-density lipoprotein (LDL) and
total cholesterol levels and raising the risk of atherosclerosis
Hypothyroidism also weakens the heart muscle and decreases contractile strength—arrhythmias can occur during
exercise
Restoring normal thyroid function helps reverse multiple cardiovascular risk factors (especially adverse lipid
profiles)—yet, mainstream medicine traditionally relies on thyroid hormone therapy for hypothyroidism which
may increase cardiac metabolic rate***
Adrenal glands secrete noradrenaline (‘norepinephrine’) to compensate for a lack of thyroid hormone—and
noradrenaline raises the heart rate
Unfortunately, it’s hard to secrete just a little norepinephrine, so the heart rate becomes elevated, blood pressure
rises, and anxiety increases
Often, medications like beta blockers are prescribed for hypertension and benzodiazepines for anxiety, when what
is needed is thyroid hormone—lab results will show a ‘normal’ TSH level but low Free T3 and Free T4 levels in
conjunction with a low body temperature confirm the hypothyroid state
Key: Controlling oral inflammation is extremely beneficial!

Dental Alerts!
     • Benzodiazepines, barbiturates, and narcotic analgesics may cause respiratory and cardiac depression in
         patients with hypothyroidism
     • Thyroxine (T4) replacement drugs can be synergistic with adrenergic agents (such as epinephrine used in
         anesthetic agents)
Headliners: Beware of Biotin; Eric Seaborg; Endocrine News; Jan 2016
Many physicians are encountering an increasing number of confounding thyroid hormone lab results caused by
patients taking large doses of biotin
The problem is that almost all immunoassays today contain biotin because they rely on the biotin–streptavidin
attraction to either anchor the assay’s antibodies to a capture surface or capture them once they have reacted
with a patient sample--Stefan K. Grebe, MD, PhD; professor, laboratory medicine & pathology; co-director, the
endocrine laboratory at the Mayo Clinic in Rochester, MN
In the case of competitive immunoassays—usually used for low molecular weight targets (such as T4, T3, and
cortisol)—biotin interference causes a falsely high or low result
‘I saw somebody just yesterday who has had an extensive workup for hyperthyroidism. A lot of her tests look like
she has Graves’, but she is taking massive doses of biotin. She probably doesn’t have any thyroid problem. We
could be treating people for Graves’ disease who don’t have it, and that’s really scary.’--Carol Greenlee, MD;
endocrinologist; Grand Junction, Colorado
‘When your lab results don’t make sense in terms of the clinical picture, or in terms of the constellation of lab
results you have received, you should always think first of an assay interference—one of which is biotin—before
you think of really exotic reasons for this to have happened, such as TSH-secreting pituitary tumors.’--Stefan K.
Grebe, MD, PhD; professor, laboratory medicine & pathology; co-director, endocrine laboratory; Mayo Clinic
(Rochester, MN)
‘We have huge signs in my office that ask people if they are taking biotin—in each exam room, over the
phlebotomy chair, and at the front desk. We had all these nice pictures on our walls, but the biotin thing alarmed
us so much that we don’t care about our decorations in our office anymore.’--Carol Greenlee, MD; endocrinologist;
Grand Junction, Colorado
When treating thyroid patients in the dental setting, be sure and ask about biotin supplementation!

Other Treatment Recommendations:
If a suspicion of thyroid disease arises for an undiagnosed patient, ALL elective dental and dental hygiene
treatment should be put on hold!
Avoid BPA-containing composite material
      • Bisphenol A is a known endocrine disruptor and should be avoided in endocrine disorders such as thyroid
          disfunction
      Speaking of BPA: