Tag: thyroid

Take Care of Your Thyroid – Part Two – Hyperthyroidism

So what exactly is hyperthyroidism?

Your thyroid gland produces a hormone (thyroxin) that sensitives all your cells to the metabolism stimulating effects of adrenal hormones. You can think of thyroid hormone as your body’s metabolic cruise control system. It sets the speed of your metabolism, from how warm you are to how fast your heart beats. While adrenalin comes and goes in spurts, thyroid hormone sets the long-term tempo. Normally, your thyroid gland produces just the right amount of hormone. Hyperthyroidism is an over-production of thyroid hormone, causing an increase in temperature, heart rate, muscle contraction and nerve firing. Too much thyroid hormone therefor causes rapid, irregular pulse rate, low grade fever, muscle trembling, anxiety or panic, irritability and fits of rage. Imagine drinking a whole pot of espresso. It’s not fun. Furthermore, it puts a stress on your heart.  Hyperthyroidism is classified into several types: 

Grave’s disease, 

Hyperfunctioning thyroid nodules (Toxic Thyroid Adenoma and Toxic Multinodular Goiter) and 

Thyroiditis (Hashimoto’s, post-partum and subacute or DeQuervain’s). 

All of these conditions are forms of thyroid autoimmune disease, meaning that your immune system has attacked your own thyroid.  Taken together, thyroid autoimmune diseases affect 7-8% of the population, totaling up to 24 million people in the United States, up to 10% of women and 3% of men.  In other words, hyperthyroidism is a relatively common condition, particularly in women. I also suspect it is under diagnosed for reasons you will read later.

Grave’s disease

At 70 to 80% of all cases of hyperthyroidism, Grave’s disease is the most common form of the disease.  It occurs most frequently in women over the age of 20, occurring in about 2% of this demographic.  

Grave’s disease is an autoimmune disorder.  More than 85% of all autoimmune patients are female.  As part of a broader trend, the incidence of autoimmune disease in general is estimated to be between 14.7 and 23.5% of the population and that incidence is rising.   This increasing incidence is very likely to be due to environmental toxins.

What are the symptoms of Grave’s disease?

Fever, heat intolerance, nervousness, anxiety, insomnia, fits of rage, sweating, tremor, heart palpitations, rapid heart rate and profound fatigue.  In women, menses are scant and infrequent.

Objective signs include fever and an elevated resting heart rate.  I have measured a heart rate of over 120 beats per minute in a patient who was resting in bed.  This went on for a few weeks accompanied by a fever of 99 to 100 degrees.  Even to stand up is exhausting when the body is working that hard to raise metabolism.  As opposed to fever caused by infection where the patient wants to get under the covers and stay warm, in Grave’s disease, the patient has heat intolerance and throws off the sheets.  Sweating occurs to dissipate heat.  In some cases, the patient may also exhibit protruding eyes (exophthalmos).  Swelling of the thyroid gland (goiter) is common in Graves disease. The lack of these signs does not rule out thyroid disease.

Hyper-functioning thyroid nodules (Also known as Toxic Thyroid Adenoma and Toxic Multinodular Goiter)

There are several kinds of thyroid nodules.  They differentiated by whether or not they are actively producing hormones and also by their composition.  Some nodules are mere fluid filled cysts.  Others are filled with a colloid.  The nodules that produce symptoms are doing so because they are producing extra thyroid hormones.  These hyper-functioning thyroid nodules produce symptoms of hyperthyroidism as discussed above.

How are nodules detected?  In a physical exam, the doctor stands behind you and feels the thyroid with his or her fingertips.  The thyroid gland is wrapped around the trachea (windpipe), in the hollow just above the sternum. In a normal person, the thyroid is barely detectable and feels equal when comparing right and left sides.  A nodular thyroid feels lumpy or asymmetrical.  Nodules are generally non-tender, the exception being de Quervain’s thyroiditis. 

Rule out thyroid cancer

While the incidence of thyroid cancer is low, the consequence of failing to detect it early is high.  Only about 5% of palpable thyroid nodules are cancerous.  The warning sign in palpation is that the lump feels hard and attached to deeper tissues.   Your doctor will order other tests if a lump feels suspicious.

Hashimoto’s thyroiditis

Hashimoto’s is a chronic, sub-acute autoimmune destruction of the thyroid gland.  

Hashimoto’s is harder to diagnose because symptoms of Hashimoto’s thyroiditis are symptoms of low thyroid function, namely fatigue, weight gain, low temperature/intolerance to cold, dry skin and hair, frequent heavy menstrual periods, hoarseness and lack of mental clarity. Many doctors do not check for the autoimmune component and just treat it as hypothyroidism.

Goiter is the usual clinical finding in Hashimoto’s, with the thyroid commonly though not always, being 2-3 times it’s normal size.  

Post-partum Thyroiditis

The stresses of pregnancy, childbirth, nursing and early childcare can induce thyroiditis in susceptible women.  Typically, an episode of hyperthyroidism occurs 2-6 months post-partum and resolves without treatment within a year.  About a quarter of these women develop hypothyroidism four or more years later.

Regarding pregnancy, sub-clinical hypothyroidism does not reduce rates of conception but does increase the rate of spontaneous abortion.

Sub-Acute or DeQuervain’s thyroiditis

The etiology of de Quervain’s is thought to be a viral infection.  Being an acute inflammatory condition, the thyroid nodules are tender to palpation.  The thyroid is generally asymmetrically enlarged and firm.  

Symptoms of de Quervain’s are hyperthyroid symptoms while the infection is raging, followed by symptoms of hypothyroidism when the autoimmune damage is done.   Fever can range from 100 to 101 degrees F.  Symptoms may include neck, jaw, throat and ear pain.  It is often confused with upper respiratory or dental infection in the early stages and in fact is often a sequel to an upper respiratory infection.  There may be pain with swallowing or turning the head.   Patients with de Quervain’s are more likely to be profoundly fatigued and confined to bed than those with other forms of thyroid disease.

De Quervain’s is self-limiting, generally resolving within a few months, though chronic hypothyroidism (Hashimoto’s) is a common sequel.  

Lab testing in the acute stage shows elevated T4 and T3 with decreased TSH and elevated ESR (Erythrocyte Sedimentation Rate is a general measure of inflammation).

Differential Diagnosis

If you experience recent onset of extreme fatigue, malaise, heart palpitations, insomnia, emotional instability and tremors, you should ask your doctor to test you for hyperthyroidism. While waiting to see your doctor, start taking and recording your temperature and your pulse rate. A thermometer and pulse oximeter are both readily available at your local drug store. Measure yourself and write down the date and time of your measurements in a notebook or by other means.  Hyperthyroidism causes rapid heart rate and mild fever. Keeping a log of your temperature and pulse will help track the severity of your disease and the progress of your treatment. 

Unless you recently gave birth or are recovering from an infection, you likely have Grave’s disease. Your doctor will palpate your thyroid to check for swelling and also order blood tests to make a differential diagnosis. Most doctors will only order a TSH (Thyroid Stimulating Hormone) to determine whether or not you have hyperthyroidism. They do not typically order tests that quantify the autoimmune component. This is because the treatment for hyperthyroidism is to suppress thyroid hormone production with a bromide based drug or radioactive Iodine, not to try and modify the immune response.  A TSH below 0.3 is indicative of hyperthyroidism. I have listed other tests below that can be helpful in determining what is happening with the immune system and make a more informed differential diagnosis. I order these in addition to TSH, plus T4, T3 and reverse T3 (see prior article on hypothyroidism).

Test name Reference range Indication if high
Anti microsomal antibodies < 35 Units/ml Auto immune thyroiditis
Anti-thyroglobulin antibodies > 2 IU/ml Thyroid cancer or Hashimoto’s
Thyroid peroxidase antibody > 2 IU/ml Hashimoto’s or Grave’s
TSH receptor antibody <10% Grave’s

If you have hyperthyroid signs and symptoms following an acute infection, you would expect the diagnosis to be de Quervain’s hyperthyroidism.  If the onset followed the birth of a child, expect post-partum thyroiditis to be the diagnosis.  Neither de Quervain’s, nor post-partum thyroiditis are known for producing palpable swelling of the thyroid gland.  In lab testing, de Quervain’s patients can also expect an elevated ESR.  In both cases, elevated T3 and T4 with decreased TSH can be expected.

Hashimoto’s is more difficult to diagnose because it develops slowly.  It is an autoimmune thyroiditis but results in more destruction of tissue and therefore the clinical presentation is hypothyroidism.  The patient is cold, tired, has dry skin and thinning hair with a loss of the lateral third of the eyebrows (see article on hypothyroidism).  In her or his case, the thyroid gland is likely to be palpably enlarged and nodular.  Lab tests include elevated anti-microsomal and antithyroglobulin antibodies with decreased peroxidase antibodies.  Because of the possibility of thyroid cancer, I always refer out to her or his primary care physician or a specialist for evaluation in patient’s with thyroid nodules.

Etiology

So how does a patient get autoimmune thyroiditis?  The usual risk factors are genetics, prolonged high stress, female gender, environmental toxins, infections and low Selenium.  Let’s take these one at a time.

Genetics

There is a genetic predisposition to Grave’s disease that can be determined through HLA testing (The association is between HLA B8 and DW3 in Caucasians and DW35 in persons of Japanese descent), however it appears to be triggered by infection, stress and/or environmental toxins. Hashimoto’s also has a genetic pre-disposition.  In Caucasians, the HLA-B8, DR3 haplotype is associated with atrophic autoimmune thyroiditis.  HLA-DR5 is associated with goitrous autoimmune thyroiditis.  There is a high prevalence of autoimmune thyroiditis in Down’s syndrome, Turner’s syndrome and familial Alzheimer’s  further suggesting a genetic susceptibility.

High stress/ Low adrenal function

Stress provokes an increase in metabolic rate so that the person has the energy to deal with the crisis.  To raise metabolism, our bodies produce thyroid hormone, which sensitizes cells to adrenal medullary hormones, epinephrine and norepinephrine.  These are the hormones that increase metabolic rate.  The adrenal cortex produces hormones that balance water, salt, blood sugar, reduce inflammation, etc.  They are cooling, nourishing hormones.  High stress and insufficient adrenal cortical hormones to help the body cope with that stress may allow the development of autoimmune thyroiditis. 

Female Gender

Women are over three times more likely to have autoimmune thyroid disease than men.  The stress of childbirth is also a cause of autoimmune thyroiditis.  Post-partum thyroiditis is an example of the effect of physical stress leading to this condition and is of course, a form of the disease that is limited to women.  

Environmental toxins

The common lab tests for Grave’s and Hashimoto’s disease are antiperoxidase antibodies and anti thyroglobulin antibodies.  Several studies have demonstrated an association between exposure to PCB’s (polychlorinated biphenyls), dioxins, BPA (bisphenol A), perchlorate, DDE, hexachloroenzene and other toxins with elevated levels of these antibodies. 

How big a problem is this?  According to the National Health and Nutrition Examination Survey III, 13% of the total U.S. population is positive for both of these antibodies.  Thirteen percent is over thirty-nine million people!  That’s thirty-nine million Americans, whose immune systems are gunning for their thyroids.  Not all of those people have overt thyroid disease but individuals with both antibodies were 23 times more likely to be clinically hypothyroid and 12 times more likely to have sub-clinical hypothyroidism.  Individuals with both antibodies and a TSH over 2.5 were forty times more likely than the general population to have clinical hypothyroidism.  Remember, a TSH of 2.5 is ideal. In other words, your immune system could be attacking your thyroid and your lab test for thyroid disease could still be normal.

Infections

The last straw (in a patient already burdened with stress and toxins) can be an acute infection.  This would be diagnosed as de Quervain’s hypothyroidism but as you can imagine, the stresses that lead to de Quervain’s are likely to have been present for some time. 

Low Selenium

A little known nutritional factor in autoimmune thyroid disease is Selenium deficiency.  Selenium is a trace mineral.  To understand why Selenium is important, you must first understand that the thyroid gland converts Iodide to Iodine and then attaches Iodine to Tyrosine to make the hormone thyroxine (T4) using hydrogen peroxide, a potent oxidant at both steps.  If you have ever put hydrogen peroxide on a cut, you know that it fizzes as it tears cells apart.  That’s what makes it an effective antibacterial.  To protect your healthy cells, the thyroid produces glutathione peroxidase, a Selenium dependent enzyme.  Glutathione peroxidase neutralizes hydrogen peroxide.  If you are deficient in Selenium, you cannot produce adequate glutathione peroxidase and the resulting excess hydrogen peroxide damages your cells.  In response to this damage, the immune system begins to regard the thyroid gland as a source of trouble and starts coding antibodies against the thyroid.  If you recall, one of those enzymes discussed above is antithyroiperoxidase or anti-TPO.  Is this making sense?

Selenium is so important that the thyroid gland has higher concentrations of Selenium than the liver.  Furthermore, deficiency of Selenium is associated with cancer of the thyroid.  Exposure to chemicals that disrupt the thyroid’s ability to make glutathione peroxidase such as DDT, increase the risk of thyroid cancer.  Prolonged stimulation by high levels of TSH increases cellular differentiation in the thyroid and increases the risk of neoplasia.  High TSH is often a response to low levels of Iodine (see below) and high levels of exposure to toxic chemicals.  Add high TSH to prolonged exposure to thyroid disruptor chemicals and you have a recipe for thyroid cancer.  The rate of thyroid cancer in the United States has more than doubled over the last 30 years.

Clinically, if a hyperthyroid patient takes Iodine without first ensuring adequate levels of Selenium, symptoms are likely to worsen.  Of course, Selenium can be given as a nutritional supplement but the therapeutic range is very small.  The RDA is 400 mcg’s per day and toxicity can occur with as little as 1000 mcg’s per day.  Blood, urine or hair analysis can be performed to determine if the patient has adequate selenium.  The lab I use to test levels of minerals and heavy metals is Doctors Data in Chicago.  

A more traditional East Asian method of supplementing Selenium is to use Huang Chi or Radix Astragalus as this herb contains a concentration of Selenium.  This herb is used in many tonic formulas, notably Ginseng and Astragalus Formula or Bu Zhong Yi Chi Tang.  This is often the best formula for the adrenal deficient patient who is pre-clinical for a thyroid disorder or the patient with Hashimoto’s thyroiditis.  Furthermore, Astragalus Membranous is not only known to raise serum Selenium levels, it also boosts immunity to viral infection by raising levels cytokine and T cell immunity.  By helping to protect the body against infection, it reduces the risk of de Quervain’s thyroiditis.  

Acupuncture and Chinese Medicine

According to the oldest Chinese medicine text, “A superior physician prevents disease.  An inferior physician treats disease”.  Of course, patients don’t usually come in until they are sick but whenever possible, in our office we focus on prevention.  In the pre-clinical stage, we often see patients who are anxious and run down.  They are not yet sick but their lifestyle is spreading their energy too thin.  To these patients, I sometimes relay an old Chinese saying, “If we don’t change direction, we will end up where we are headed”.  Using acupuncture and tonic herbs to relax and strengthen the patient may get their attention so they will be more open to following our advice.  A program of Tai Chi, Chi Gung, yoga or other relaxation techniques and breathing exercises can really help.  We counsel patients to set priorities, accept limits and let go of trying to be and do everything.

Acupuncture can modulate immune response and reduce inflammation in the acute stage of the disease.  In the post-acute hypothyroid stage (Hashimoto’s), acupuncture and tonic herbs can help to modify the immune response and raise metabolism.  Nutritional therapy is also very helpful.

L-Carnitine

During the acute stage of hyperthyroidism, the amino acid L-Carnitine can be used to prevent or minimize the symptoms and physiologic changes associated with elevated levels of T3 and T4.  The dosage required is 2 – 4 grams per day of oral L-Carnitine, given in a divided dose.   

L – Carnitine is a normal amino acid found most abundantly in meats.  The supplemental form is made by bacteria and is easily absorbed and utilized as it is in a free, single amino acid form as opposed to complexes with other amino acids as it is normally found in food.  The mechanism of action for L-Carnitine is that it blocks the uptake of T3 and T4 at the cell nucleus.  Thyroid hormone works by causing transcription of DNA in the cell nucleus that increases receptor sites for catacholamines in the cell membrane.  Without access to the nucleus, T3 and T4 cannot raise metabolism and cause hyperthyroidism.  

Iodine

Since T3 and T4 are made from Iodine, it would be natural to assume that taking Iodine would worsen hyperthyroidism because the body would be able to make more of the hormones.  This is true in the acute stage, particularly if there is a lack of Selenium.  But in the post-acute stage, taking Iodine can actually decrease the levels of antithyroglobulin antibodies and antiperoxidase antibodies found in Hashimoto’s disease.

What to do?

First of all, make an appointment with your doctor. In this office, we are not medical doctors, let alone endocrinologists. We do not prescribe drugs. We offer nutritional support, lifestyle recommendations and supportive care. While it is true that we have helped many patients with thyroid disorders improve their health and it is also true that we provide treatment for aspects of thyroid disease often ignored by medical doctors, there are some cautions to bear in mind. First of all, if your heart rate is above 100 at rest, you may need to take medications to reduce the amount of thyroid hormone produced and reduce its effects on your heart. Secondly, if you have nodules on your thyroid gland, those should be checked for cancer.

The next thing to do is start measure and recording your resting pulse rate and temperature. Make a chart with these headings: Date, Time, Pulse Rate, Temperature, Symptoms. You are the only person who is with you all the time. We doctors are not. By taking an active role in your health, you will notice what helps you and what hurts you. There may be foods that make you better or worse, sleep patterns, stressors, etc. Be an expert in what makes you feel good.

Last, strive to maintain a relaxed, happy mood. Fear and anxiety hurt you. Anger hurts you. These emotional states trigger a flood of hormones that arouse your immune system and cause more destruction. A friend once said, “You can’t afford the luxury of a negative thought.” Sure your spouse may deserve a good tongue lashing but the person who will suffer is you. I have one patient who put her Grave’s disease in remission largely by walking away from everything stressful in life. She won’t even read the news or watch a suspenseful movie. It’s not worth it to her. She is happy gardening, cooking and reading, so that’s where she puts her focus. Does life still bring crisis that must be managed? Of course. We all have major life events that require us to get into high gear. We just don’t have to be in that heightened state all the time. It may be a habit. We may have built our roles and personalities around unsustainable demands.  Many of us are attracted to high stress activities, whether it is completing a big project at work, skiing down a steep hill or engaging in emotional dramas. Adrenaline makes us feel more alive. It may not seem possible to disengage from these high stress activities – that we “have to” do (fill in the blank), but many of them are optional. If you can turn a diagnosis of hyperthyroidism into a change towards a happier, less stressful life, the suffering will at least have meaning and possibly be worthwhile. Let the crisis be an opportunity to create a healthier, happier life.

Wishing you the best of health,

David Wells, D.C., L.Ac., MS (Nutrition).

 

 

 

References:

 Neufeld M, Blizzard RM.  Polyglandular autoimmune diseases. In: Pinchera A, Doniach D, Fenzi GF, eds. Symposium on Autoimmune Aspects of Endocrine Disorders. New York, NY: Academic Press’ 1980:357-365.

 Dayan CM, Daniels GH. Chronic autoimmune thyroiditis. N Engl J Med 1996;335:99-107.

 Progress in Autoimmune Diseases Research, NIH Autoimmune Diseases Coordinating Committee, Report to Congress, March, 2005

 Progress in Autoimmune Diseases Research, NIH Autoimmune Diseases Coordinating Committee, Report to Congress, March, 2005

 SEER Fact Sheet Thyroid, NIH 2009, www.cancer.gov

 Othman S, Phillips DIW, Parkes AB, et al. A long-term follow-up of postpartum thyroiditis. Clin Endocrinol (Oxf) 1990;32:559-564. [Medline]

 Pratt D, Novotny M, Kaberlein G, Dudkiewicz A, Gleicher N. Antithyroid antibodies and the association with non-organ specific antibodies in recurrent pregnancy loss. Am J Obstet Gynecol 1993;168:837-841. [Medline]

 Merck Manual, 2010

 Neufeld M, MacLaren N, Blizzard, R.  Autoimmune Polyglandular Syndromes. Pediatric Annals 9:4. 1980. p 48.

 Dayan CM, Daniels GH. Chronic autoimmune thyroiditis. N Engl J Med 1996;335:99-107.

 Shnell LM, Gallo MV, Ravenscroft J, DeCaprio AP. Persistent organic pollutants and anti-thyroid peroxidase levels in Akwesane Mohawk youg adults. Environ Res 2009;109:86092.

 Tsuji H, Sato K, Shimono J, et al. Thyroid function in patients with Yusho; 28year follow-up study. Fukuoka Igaku Zasshi 1997;88:231-235. 

 Spencer CA, Hollowells JG, Kazaosyan M, Braverman I.E. National Health and Nutrition Examination Survey III thyroid-stimulating hormone (TSH)-thyroperoxidase antibody relationships demonstrate that TSH upper reference limits may be skewed by occult thyroid dysfunction. J Clin Endocrinol Metab 2007;92:4236-4240.

 Surks MI, Hollowell JG. Age-specific distribution of serum thyrotropin and antithyroid antibodies in the U.S. population: implications for the prevalence of subclinical hypothyroidism. J Clin Endocrinol Metab 2007:92:4575-4582.

 Aaseth, J., Frey, H., Glaattre, E., Norheim, G., Ringstad, J. and Thomassen, Y. Selenium Concentrations in the human thyroid gland. Biol. Trace Element Res. 1990:24, 147-152

 Santini F, Vitti P, Ceccarini G, Mammoli C, Rosellini V, Pelosini C, Marsili A, Tonacchera M, Agretti P, Santoni T, Chiovato L, Pinchera A. Endocrinol Invest. 2003 Oct;26(10):950-5.

 Hard GC. Environ Health Perspect. 1998 Aug;106(8):427-36.

 Chen AY, Jemel A, Ward EM. Increasing incidence of differentiated thyroid cancer in the United States, 1988-2005. Cancer. 2009;18:784-791.

 Dong Xiang-yu, Ni Qian, Shen Yang. Effect of Astragalus Injection on levels of blood selenium and immunity function in children with viral myocarditis Chinese Journal of Integrative Medicine. Vol 10, No 1, 2004:29-32.

 Benvenga S, Amato A, Calvani M, et al. Effects of carnitine on thyroid hormone action. Ann N Y Acad Sci. 2004 Nov;1033:158-67.

 Benvenga S, Lakshmanan M, Trimarchi F. Carnitine is a naturally occurring inhibitor of thyroid hormone nuclear uptake. Thyroid. 2000 Dec;10(12):1043-50.

 Benvenga S, Ruggeri RM, Russo A, et al. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial. J Clin Endocrinol Metab. 2001 Aug;86(8):3579-94.

 Rink T, Schroth HJ, Holle LH, et al. Effect of iodine and thyroid hormones in the induction and therapy of Hashimoto’s thyroiditis. Nuklearmedizin. 1999;38(5):144-9.

Scenic waterfall in Japanese garden

Take Care of Your Thyroid – Part 1 – Hypothyroidism

Marsha is tired all the time. She wakes up with a dull headache and needs coffee before she can be civil with her husband and kids. Her skin is dry despite practically soaking in lotion. Her hair is getting thinner and more brittle. She has gained a lot of weight and feels cold much of the time, so much so that she wears socks to bed.

Janet also feels tired but in her case, she feels wired and tired. Her pulse is fast and her skin is moist. She feels anxious and irritable. She has a hard time sleeping. What do these two women have in common? They both have thyroid problems.

Of course, men can have thyroid problems too. It’s just a lot more common in women. According to the American Thyroid Association, “Women are five to eight times more likely than men to have thyroid problems.” They go on to say, “One woman in eight will develop a thyroid disorder during her lifetime.”i

The following article will help you understand how your thyroid works, what the lab tests mean and what you can do to improve your thyroid function. I have included enough detail to make you an expert. I suggest you read the whole article, skimming any sections that seem too technical. Take what information you need and can use. You can always come back to this article to answer any questions that may arise.

Please note – I am not an endocrinologist or even a medical doctor.  Use this article as a resource while working with your physician.

Where is my thyroid?

The thyroid gland is located just above the sternum. It is a butterfly shaped gland, wrapped around the trachea. Inside the thyroid are the parathyroid glands. The thyroid is part of the “fight or flight” nerve and hormone system. Thyroid hormones increase energy, speed and body heat. The parathyroids are part of the “rest and digest” system. Parthyroid hormone helps the body to nourish and repair itself, primarily by directing calcium back to the bones when it is not needed elsewhere. The function of the parathyroids has to be replaced in the case of thyroidectomy (removal of the thyroid) because the parathyroids are embedded in the thyroid gland.

What is thyroid hormone made of?

The thyroid gland produces thyroid hormones, primarily T4, though also smaller amounts of T3 and T2 respectively. T4 is made of an amino acid called Tyrosine plus four molecules of the mineral Iodine (Hence the name, T4). T4 is the transport form of the hormone. T3 is Tyrosine plus three Iodine molecules and T2 has two molecules of Iodine. T3 is the active form of the hormone.

One of the causes of hypothyroidism is insufficient Iodine in the diet. Many parts of the world don’t have sufficient Iodine in the soil, so the foods grown in that soil or the animals that depend on that food are deficient in Iodine. People eating those grains, vegetables and animals therefor don’t get enough Iodine. A severe form of mental retardation called Cretinism was common before Iodine was added to salt. Subclinical Iodine deficiency is still common.

The amino acid Tyrosine is a normal component of the diet and should not need to be supplemented, though there are some people with insufficient enzymatic ability to split Tyrosine molecules off from the rest of the protein in their food and thus do have a need for Tyrosine supplementation. These people are the exception and can be identified by testing serum amino acids. Clues that helped me to find Tyrosine deficiency in a few patients were the failure to produce endorphin in response to acupuncture, general lack of zest for life and extreme sensitivity to air pollution. The poor response to acupuncture and lack of joy is because Tyrosine is also needed to make endorphin, dopamine and norepinephrine – hormones that cause pain relief, reward and excitement. The exagerated response to air pollution (extreme fatigue) is because certain pollutants block the conversion of Phenylaline (another amino acid) into Tyrosine, resulting in low levels of the substrate needed to make endorphin, dopamine and norepinephrine as well as thyroxine.

What does thyroid hormone do?

In brief, thyroid hormone raises the metabolic rate of the cells, that is, the rate at which cells burn fat and oxygen to make energy. Thyroid hormone does this by making the cell sensitive to adrenal hormones. Adrenal hormones in turn, speed the metabolic rate.

You might wonder why thyroid hormone is needed since adrenal hormones actually control the burn rate of fat and oxygen. The answer is that adrenal hormones come and go in little spurts that would make your energy level rise and fall like someone driving a car by pumping the gas pedal up and down. Thyroid hormone smoothes and regulates the overall rate of metabolism. If there is not enough thyroid hormone, the “gas” doesn’t reach the “engine”. You can think of thyroid hormone as the “cruise control”, setting the overall rate of energy production.

In general, men have larger adrenal glands and more muscle mass than women and thus can tolerate a lower functioning thyroid and not have symptoms.

How does thyroid hormone get where it needs to go?

Most of the hormone produced by the thyroid gland is in the form of T4 (In fact, fourteen times more T4 than T3). T4 is a very stable form of the hormone, but because T3 is the active form of the hormone, T4 must be converted to T3 in the tissues.

Ninety-nine point five (99.5) percent of the T4 and T3 are bound to proteins called thyroid-binding globulin (TBG), transthyretin (TTR) and albumen. Of these, TBG binds 75% of the thyroid hormone, TTR 20% and 5% is bound to albumin. These are very stable molecules that serve as a reservoir of thyroid hormone outside the thyroid gland itself. If there were no pool of circulating protein-bound thyroid hormones, depletion of the hormones could occur within hours of the thyroid ceasing production. As it is, the thyroid could stop making hormone for 24 hours and amount in the blood would only decrease by 10% and 40% for T4 and T3 respectively. This allows thyroid production to fluctuate without affecting available levels of the hormones. Another advantage to being bound to large protein molecules is that there is less loss of the hormone in the urine than there would otherwise be.

The different carrier proteins also direct the delivery of thyroid hormone to particular parts of the body. Most notably, transthyretin (TTR) delivers thyroid hormone across the blood-brain barrier to the brain and nervous system, and across the placenta to the fetus.

As noted earlier, there is a small amount (0.5%) of unbound T4 and T3 in the bloodstream. The T4 and T3 must become free of the transport protein in order to enter the cells of the target tissues. In lab tests, the free T4 and T3 fractions can be measured separately from total T4 or total T3.

Once at the cell membrane, T4 and T3 must cross the cell membrane with the help of cellular thyroid hormone transporters and then bind to the nuclear thyroid receptors in the nucleus of the cell. Thyroid disruptors like PCB’s, BPA, dioxin and flame-retardants can block crossing the cell membrane.,

Conversion of T4 to T3.

Once inside the cell, T4 must be converted to T3. This occurs with the help of enzymes called deiodinases. There are three types of deiodinase, designated as Type I, II and II Regardless of which type is involved, for deiodination to result in metabolically active T3, one molecule of iodine must be removed from the outer ring of the T4. Removal of an iodine molecule from the inner ring produces an inactive form of T3 called “reverse T3” or rT3. Types I and II produce metabolically active T3. Type III produces rT3. Type III is used to reduce excess levels of T3 in the brain and in the placenta and fetus. Excess T3 could stimulate abnormal cellular differentiation, particularly in the fetus.

Type I deiodinase is produced in the liver, kidney, thyroid, pituitary and heart but primarily in the liver. The liver is thought to be the main source of peripheral T3 production and also the main location for clearance of plasma reverse T3. Type I is the most dependent on adequate selenium levels of the three types.

Type II is produced in the central nervous system, pituitary, skeletal muscle, cardiac muscle and brown adipose tissue. Both Types I and II are blocked by the presence of mercury, arsenic, cadmium, lead, PCB’s, FD&C red dye #3, the pesticide methoxychlor and a UV agent used in sunscreens called octylmethoxycinnamate. Blocking the action of Type I or II deiodinase results in less T3 and thus lowered metabolism.

How does thyroid hormone raise energy level?

T3 increases transcription of beta-adrenergic receptors and decreases transcription of alpha-adrenergic receptors on the cell membrane. Beta-adrenergic receptors bind with circulating catacholamines such as norepinephrine (adrenal hormone), stimulating glycolysis and glycogenolysis (the burning of glucose and glycogen to make energy). In contrast, when catacholamines bind with alpha-adrenergic hormones, metabolism is reduced. Thyroid hormone is also an insulin antagonist. It stimulates lipid turnover, free fatty acid release and cholesterol synthesis. In short, T3 encourages converting both fat and glycogen into energy.

Additionally, thyroid hormone maintains calcium mobilization and is necessary for the contractility of mysosin filaments in the muscles. It is necessary for central nervous system, skeletal and sexual maturation and is also required for protein synthesis and the formation of apoenzymes.

From this it is easy to understand how lack of thyroid hormone activity causes poor muscle and ligament development, low energy, cold body temperature, inability to think clearly, accumulation of fat, etc. Beyond the obvious, energy is required to power every metabolic process. Low energy equals reduced health in every respect.

How is the production of thyroid hormone regulated?

The short answer is that the pituitary produces a hormone called thyroid-stimulating hormone or TSH, which in turn stimulates the thyroid to produce more thyroid hormones. The production of TSH is in turn regulated by hypothalamus. The hypothalamus makes thyroid-releasing hormone (TRH). TRH causes the pituitary to produce TSH.

The hypothalamus is in turn influenced by the weather (prolonged cold causes increases in TRH production), the amount of circulating iodine in the blood, fasting (lowers metabolism to conserve energy) and other factors. Think of the hypothalamus as a little lab in your head, constantly measuring blood chemistry and other information and deciding what hormones are needed. The hypothalamus sends this information to the pituitary. In turn, the pituitary issues the orders to the glands to make appropriate amounts of hormones needed to deal with current environmental conditions.

With such a beautifully balanced system, what can possibly go wrong?

Hmm, let me count the ways…

Excluding pathology such as tumors of the pituitary, genetic abnormalities, infectious disease, etc., the most common conditions of the thyroid are hypothyroidism and hyperthyroidism. Let’s start with hypothyroidism.

Hypothyroidism

Hypothyroid means low-functioning thyroid. Remember, a low functioning thyroid results in low energy production. Hypothyroidism can be caused by

  1. Inadequate stimulation by the pituitary.
  2. Inadequate production of T4 by the thyroid gland (Primary hypothyroidism).
  3. Inadequate conversion of T4 to T3 in the tissues (Peripheral thyroid resistance).
  4. Auto-immune destruction of the thyroid gland or its hormones (covered in a following section).

Let’s take these one at a time.

Inadequate stimulation by the pituitary.

The pituitary produces thyroid-stimulating hormone (TSH). The normal range for TSH in the blood is .4 – 4.5 mlU/L. Symptoms of hypothyroidism in patients whose blood levels of TSH are under .4 indicate under-production of TSH by the pituitary. Blood levels of TSH over 4.5 in persons with symptoms of hypothyroidism indicate that the patient’s thyroid gland is not responding to the TSH.

It should be noted that the current lab standard of up to 4.5 mU/L may be missing many people who are clinically hypothyroid. The National Academy of Clinical Endocrinology recommended in 2002 that the target TSH level for thyroxine replacement should be between 0.3 and 3.0 mU/L. Adopting this new guideline would bring the number of people with abnormal thyroid function to as much as 20 percent of all adults, up from 4.6 percent under the current guidelines. In guidelines published by the National Academy of Clinical Biochemistry the report states, “In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 because 95 percent of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mU/L”.

What does TSH do?

TSH stimulates a plasma membrane transport system called NIS that allows sodium to be pumped out of the cell and iodine pumped in to the cell. This allows the cell to concentrate iodine 20 to 40 times more than the level found in the plasma. A number of thyroid disruptors, chiefly perchlorate, thiocyanate, bromate and nitrate, compete with iodine for binding to the NIS protein. This competition results in less iodine getting into the follicular thyroid cell and thus less production of thyroid hormones.

Inadequate production of T4 by the thyroid gland.

To produce thyroid hormones, the thyroid gland must have adequate supplies of iodine, protein (chiefly Tyrosine) and several co-factors, including selenium, zinc, Vitamins C, A, E, B12 and alpha-lipoic acid (also known as ALA or Thioctic Acid). The most common limiting factor is Iodine.

Iodine

For over fifty years, iodine deficiency has been known to be the primary cause of hypothyroidism. While most people believe that iodized salt has solved the problem of iodine deficiency in this country, many researchers do not believe this to be the case. For one thing, only about half the population uses iodized salt. For another, many people are on low-salt diets. More importantly, iodization of salt assumes the standard need for iodine to be 150 micrograms per dilution for adults. Compare this to the average ingestion of 13.8 mg Iodine consumed in Japan. Best case, the average American is getting 1 percent of the Iodine as the average Japanese person.

Bromine

A further problem with Iodine is that we are no longer getting Iodine in all our baked goods. Up until the 1980’s, Iodine was added to flour to strengthen the dough and allow for greater rise. So for example, in the 1960’s a slice of bread contained 150 micrograms of Iodine. Since the 1980’s, Iodine has largley been replaced with Bromine. The National Health and Nutrition Survey (NHANES) found that Iodine levels have declined 50% in the United States during the period from 1971 to 2000. Worse, Bromine binds to the same receptor sites as Iodine but Bromine is a carcinogen. Since the breasts, ovaries and prostate (in addition to the thyroid gland) concentrate Iodine or Bromine, this may be at least partially responsible for the increased rates of cancer in these organs since the 1980’s. Fortunately, England and Canada ban the use of Bromate in flour and California lists it as a carcinogen. For this reason, many bakers and millers (such as King Arthur Flour) only use iodated flour.ii

Halogens

Bromine is one of a group of similar chemicals. Iodine, Bromine, Fluorine and Chlorine are collectively known as halogens (Latin for “Salt formers”). These molecules share characteristics that make them able to interact with the same receptor sites in the body. What this means is that in place of Iodine, one of these other molecules can bind to that spot, preventing Iodine from doing it’s job.

Bromine (also bromate or bromide) is not only found in breadstuffs, it is in flame-retardants and thus is found in most furniture fabrics, carpeting, etc. It is used as a fumigant on crops and also a disinfectant in swimming pools. It can also be found in sodas and many prescription items.

Fluoride is added to the water supply and to toothpaste. In addition to interfering with thyroid hormone function, fluoride is implicated in causing rickets, hip fractures, bone cancer and death. Sodium fluoride is used as rat poison.

Chlorine is a widely used disinfectant (also added to our water supply), is in many cleaning products (such as Cloroxtm) and is found in many pesticides and other environmental pollutants. These pollutants are ubiquitous. One study of 5,994 Texans found that 99.5% of those tested had significant levels of organochlorine pesticide (DDE) residues in their blood. An Environmental Working Group study tested cord blood from 10 infants born in US hospitals in 2004. A total of 287 toxic compounds were found, including 147 PCB’s (polychlorinated biphenyls) and 212 chlorinated pesticides. These toxins bio-accumulate in the fat stores of the body, becoming increasingly concentrated with age.

Thiocyanates

Thiocyanate inhibits Iodine uptake into the thyroid by interfering with the NIS. The half-life of thiocyanate is around six days. Brassica family vegetables (broccoli cauliflower) contain thiocyanate. Thiocyanate is reduced by cooking and only about half of it is absorbed in the GI tract. Cigarettes on the other hand are a greater source of thiocyanate. The breast milk of smokers has been found to have four times more thiocyanate than that of non-smokers and half as much Iodine. The take-home message is to avoid smoking and second-hand smoke, and to cook brassica family vegetables.

Nitrates

Nitrates are found in many good foods such as lettuce, beans, squash, beets and carrots. Nitrites are added as a preservative to prepared meats and fish, and nitrate runoff from agriculture is in the water supply. Nitrates also interfere with Iodine uptake by the thyroid but their half-life is about five hours. Cooking also reduces the nitrate content of vegetables. Using a water filter and cooking vegetables can reduce nitrate load. Consuming additional Iodine can counter the effects of thiocyanates and nitrates.

Inadequate conversion of T4 to T3 in the tissues.

As discussed earlier, conversion of T4 to T3 requires a selenium-dependent enzyme called I 5’ deiodinase (Type I). Deficiency of selenium can result in a lack of this enzyme and as a result, a lack of T3 despite normal circulating levels of T4. Besides selenium deficiency, many other substances can block the activity of I 5’ deiodinase, including cigarette smoke, pesticides, plastics, heavy metals and even some foods.

Of the factors listed above, the most important blockers are the heavy metals, mercury, cadmium and arsenic). This is because these heavy metals bind with the enzyme I 5’ deiodinase and prevent it from removing one iodine from the appropriate ring of the Tyrosine-Iodine complex (T4). While healthy foods like tofu and broccoli weakly bind with the enzyme, heavy metals form very tight bonds that are slow to release. The half time of mercury excretion from the body is over two years. That means if you are exposed to mercury today, in two years, half of it will still be in your body. In four years, one quarter of that mercury will still be in your body!

After iodine deficiency, the most important nutrient deficiency is selenium. This is because the enzyme I 5’ deoiodinase is made from selenium. Deficiency can cause a “14-fold decrease” in T4 to T3 conversion.iii Though Selenium deficiency must be severe to cause a deficiency of I 5’ deiodinase,iv insufficient Selenium increases risk of auto-immune thyroiditis because Selenium is needed to make the protective anti-oxidant enzyme glutathione peroxidase.

The next most important group of thyroid disrupters is plastics and pesticides such as DDE, BPA, Dioxin, bromates, etc. These also have a very long life. For example, DDE, a breakdown product of DDT (which was banned in 1972) has been found in samples of breast milk around the world, sometimes at levels exceeding what would be allowed on the market in a commercial milk product. These toxins accumulate in fat stores and concentrate up the food chain, ultimately in animal products that we consume.

There is some evidence that elevated levels of the stress hormone cortisol and also of insulin can inhibit the conversion of T4 to T3.v

Auto-immune destruction of the thyroid gland or its hormones.

Hypothyroidism is frequently the result of auto-immune destruction of the thyroid gland or it’s products. The auto-immune diseases of the thyroid are Grave’s disease and Hashimoto’s thyroiditis. The lab tests to detect and monitor these conditions are anti-thyroglobin antibodies and antimicrosomal antibodies.

What are the symptoms of hypothyroidism?

Since thyroid hormone is necessary to make energy, the primary symptoms are fatigue and cold. However, thyroid hormones have many other direct effects and also affect activity of other hormones.

I created a symptom survey to use with my patients. The way I use this survey is to total the answers in the “Yes” column. A total score over 10 is suggestive of hypothyroidism. Count the number of “Yes” answers. A number greater than 10 suggests further investigation is warranted.

I am tired much of the time Yes No
I often have headaches in the morning that wear off during the day Yes No
My skin is dry Yes No
My hair is thin Yes No
I feel stiff and achy in the morning Yes No
I waer socks to bed to keep my feet warm Yes No
I use moisturizing lotion on my arms, legs or body Yes No
I have difficulty losing weight or avoiding weight gain Yes No
I tend towards constipation (less than one bowel movement a day) Yes No
My fingernails are brittle Yes No
I am not very interested in sex Yes No
My hair seems thin and breaks easily Yes No
I feel depressed Yes No
I have difficulty thinking quickly Yes No
My reaction time seems slow Yes No
Moderate exercise makes me short of breath Yes No
I feel achy and stiff unless I exercise or take a hot shower or bath Yes No
My skin feels puffy or swollen Yes No
I feel best with more than 8 hours of sleep per night Yes No
I feel heart palpitations or have been told I have mitral vale prolapse Yes No
I have to urinate frequently (more than 6 times per day) Yes No
I have difficulty remembering things Yes No
The outer third of my eyebrows has thinned or disappeared Yes No
My pulse rate is below 65 even though I don’t exercise extensively Yes No
I feel sleepy during the day Yes No
I need coffee, cola or tea to think clearly in the morning Yes No
My feet and ankles appear puffy or swollen Yes No
My knees lock when I stand (rather than being slightly flexed) Yes No
I feel light-headed if I stand up too quickly Yes No
I am double jointed (such as bend my thumb back towards my wrist or do the splits) Yes No
(Men only) I have difficulty achieving or maintaining an erection Yes No
(Women only) I have very painful menstrual cramps Yes No

Beyond symptoms, how do we test for it?

Blood work

The most commonly used test is Thyroid Stimulating Hormone or TSH. This test measures the amount of TSH produced by your pituitary gland because presumably, the pituitary knows how much thyroid hormone you need. Doctors use this test to determine the correct dose of thyroid hormone to prescribe. If the TSH is high, this means that your pituitary is trying to raise your thyroid hormone production. If it is low, this means the pituitary is trying to reduce the amount of thyroid hormone production. As noted above, the ideal range of TSH is around .4 to 3.0 (not the upper limit of 4.5 recommended by most labs). In fact, for women wishing to become pregnant, a TSH greater than 2.5 is associated with implantation failure and early pregnancy loss.vi,vii

Most medical doctors begin by ordering a TSH. If that is normal, they generally look no further because the indication for prescribing replacement hormone is a high TSH. If the TSH is high (indicating that the pituitary thinks that thyroid hormone levels are low), then the doctor will likely order a T4 test next.

A more comprehensive panel may include; Free T4, Free T3, Thyroid Binding Globulin (TBG) and reverse T3 ( rT3). This gives a much fuller picture of where the dysfunction exists. Remember, T4 is the transport form of the hormone while T3 is the active form. While they are each bound to globulin (protein) they are not metabolically available. That’s why testing Free T4 and Free T3 gives a picture of the levels of hormone actually interacting with cells. Even this picture can be misleading because some of the T3 may be the inactive, reverse T3 (rT3) form because the deiodinase enzyme was disrupted by exposure to heavy metals, plastics or other pollutants. If rT3 is elevated, hair Mercury levels (Doctors Data) and serum GSH are additional tests that may be employed.

If auto-immune thyroid disease is suspected, these additional tests may be ordered;

Anti-Thyroperoxidase (TPO) Antibodies, TSH receptor antibodies (TRAb) and antithyrogobulin antibodies (Tg). particularly if the patient has hypothyroid symptoms despite normal TSH, Free T4 and T3 tests.

Physical exam

  • The single most distinguishing sign of advanced hypothyroidism is thinning or loss of the lateral third of the eyebrows. This can advance to the point that only the medial third of the eyebrow remains.
  • Thinning of head hair, both in terms of the number of hairs and the thickness of each individual hair is another strong indication.
  • Dry skin is most readily seen on the calves and forearms, though frequently, the earliest indicator is dry, cracked heels.
  • Obesity is another possible indicator, particularly if accompanied by fluid swelling in the feet and legs.
  • Ligamentous laxity is another sign. You can test the tone of the ligaments by asking the patient to bend their thumb backwards or touch their palms to the floor.
  • When testing reflexes, you may note slow reflexes in hypothyroid individuals.
  • Low blood pressure is another sign. This can be felt in the pulse but can be quantified with a blood pressure cuff. A further test is to take blood pressure lying down, then standing. In a normal person, the blood pressure will not fall when rising from a lying to standing position and may in fact rise 5 mm Hg. In someone with adrenal fatigue/hypothyroidism/poor sympathetic tone (or a number of other medical conditions) the blood pressure will drop when rising to a standing position. A systolic drop of 20 points or a diastolic drop of 10 points is defined as orthostatic hypotension.viii (A drop of 20 points may indicate Cushing’s Syndrome (excessive cortisol production). Additional signs associated with Cushings Syndrome include a round or “moon” face, fat deposited above the collarbone and in the upper back “dowager’s hump”, dark pigmentation in the creases of the hands, purple stretch marks, obesity in the trunk but muscle loss in the arms and legs).ix
  • Heart palpitations. More than two “skipped beats” per minute is abnormal and may be due to hypothyroidism.
  • Multiple areas of point tenderness. Hypothyroidism is essentially the same as chronic fatigue syndrome and fibromyalgia.x

Basal Temperature

By far the most important test of all is to take your temperature every morning when you wake up and write down the number. Do this every morning for at least a week.

Normal temperature is 98.6 degrees. The range of normal is a full degree plus or minus 98.6. If the your temperature is consistently below 97.6, a hypo-metabolic condition is present. After a few days or weeks of intervention, this test can be repeated to get an indication of whether or not the treatment is working.

This test is cheap, effective and empowers you to track your progress. The importance of this test is that, regardless of blood test results to the contrary, if the temperature is low, the metabolism is low. An analogy I use is that, “You can measure the gas or oil in your car but if the engine is cold, it isn’t running”. If the temperature is low and you don’t feel good, keep looking until you find the problem.

(In the 1970’s, the basal temperature test was popularized by Broda Barnes MD, whose books, “Hypothyroidism – the Unsuspected Illness” and “The Riddle of Heart Attacks Solved” posited that as much as 40% of the US population was suffering from hypothyroidism and that cardiovascular disease, including high cholesterol is a result of hypothyroidism.)

Differential nutritional diagnosis

To treat the hypothyroidism nutritionally, we need to understand thyroid hormone deficiency from a biochemical point of view. That understanding allows us to diagnose and intervene in a more holistic way. The main nutritional interventions are to screen for and treat iodine deficiency and/or halogen excess, to screen for and treat problems with conversion of T4 to T3, chiefly heavy metal intoxication, and to screen for and treat organochlorine toxicity. We should also determine if the hypothyroidism is due to auto-immune thyroid disease such as Grave’s or Hashimoto’s.

Iodine deficiency/Halogen excess

Iodine deficiency can be screened using hair or whole blood trace-mineral analysis. These are also useful tests to screen for selenium and zinc deficiency as well as toxic amounts of mercury, arsenic, cadmium and lead. A more specific test for Iodine deficiency and halogen excess is the Urine Halides test. In this test (available through Doctor’s Data in Chicago), patients take 50 mg of Iodine by mouth, then collect their urine for 24 hours and send a sample to the lab. This test assumes that if the patient has all the Iodine needed, he or she will excrete 90% of the ingested Iodine in the urine. Greater percentages of iodine retained by the body suggest greater levels of Iodine deficiency.

T4 to T3 conversion

If T4 is not being converted to T3 by Type I or II deiodinases, Type III deiodinase will convert T4 to reverse T3 (rT3). A blood test for rT3 can be ordered from many labs.

Remember, converting T4 to T3 requires a selenium-dependent enzyme (Type II or II deiodinase). Tissue samples (hair or blood) can be examined by atomic absorption mass spectrometry to determine levels of normal nutrients such as selenium and also toxic elements such as mercury. These tests are also performed by Doctor’s Data. You can order test kits by calling 800-323-2784.

GSH

An indirect way to measure the level of organochlorine burden (from pesticides, plastics, flame retardants, etc.) is to measure GSH (Glutathione). GSH is the most abundant and most important intracellular antioxidant. GSH is involved in the detoxification of heavy metals, toxic halides and organochlorines. A low level of GSH implicates a high body burden of these toxins and predicts a difficult detoxification process. Doctor’s Data offers a blood test to accurately assess GSH levels. If levels are found to be low, supplementation with whey protein, alpha lipoic acid, curcumin, magnesium and N-Acetyl Cysteine (NAC) have been found to effectively increase GSH levels.

Supplementation and detoxification

In addition to drinking more water, consuming more fiber, getting aerobic exercise and taking the GSH supporting nutrients listed above, there are other nutritional interventions that may help protect and repair your thyroid funciton.

Iodine

If Iodine levels are sub-optimal and other halides are high, the best treatment is to supplement with Iodine, either as tablets or as Lugol’s Solution. Lugol’s is potassium iodide in water. It was first compounded in 1829 and has been used as an antibiotic and disinfectant ever since. One drop of 5% Lugol’s Solution contains about 6.25 mg of Iodine. It is available over the counter in Canada and Mexico or online. Tablets equivalent to two drops of Lugol’s Solution are available under the trade name Iodoraltm. Dr David Brownstein MD uses between one and four tablets of Iodoral with his patients, dosed according to results of the Urine Halides test. I never use more than one per day.

Many people consume seaweeds (nori, kelp, hijiki, wakame) to get Iodine. These are available in Japanese restaurants, grocery stores and as powdered supplements. Seaweeds are a source of Iodine and other nutrients, including compounds that aid in detoxification. Unfortunately, they also contain Bromine. For that reason, I don’t recommend them as a treatment or preventative for hypothyroidism.

Unrefined salt such as sea salt is also helpful in eliminating toxic halides. Salt is mostly Sodium Chloride. The chloride portion can displace other toxic Chlorine compounds in the body. Sea salt contains all 72 minerals found in the sea and in your bloodstream in roughly the same proportions as are found in your blood. Traditional Asian foods that utilize sea salt are Miso and Tamari. These foods are made by combining beans, grains and sea salt in a jar and allowing them to ferment. The fermentation process forms complexes of the salts with the proteins of the beans and grains. Excess salt can cause high blood pressure, so again, I don’t think salt is as good as taking Iodine. With both salt and seaweeds, use them to taste, not as a medicine.

Heavy metal detox

Similar to the way halides like Bromine bind to receptors meant for Iodine, the heavy metals, Mercury, Arsenic and Cadmium bind to receptors meant for Selenium and Zinc. Raising levels of Selenium and Zinc helps to displace heavy metals. GSH precursors like whey protein and alpha lipoic acid can allow metal detoxification with minimal side effects.

Supportive strategies include increasing dietary fiber, exercise, drinking water and sweating. Increasing dietary fiber traps toxins excreted by the liver through the bile. Exercise mobilizes fats, increasing turnover and release of stored toxins. Water dilutes toxins, facilitating elimination through the kidneys and skin. Sweating is a great way to eliminate toxins. Many holistic practitioners use far infrared saunas and other means to increase sweating.

Caffeine and Caffeine Substitutes.

As noted earlier, caffeine acts in a manner similar to thyroid hormone. Many undiagnosed hypometabolic people depend on coffee to wake up and do their work. In a perfect world, they might instead get 8 hours of sleep or reduce their stress, though I understand that is very unlikely to happen. I suggest that we think of coffee as a drug to palliate the effects of high stress and not enough sleep. Like all drugs, coffee has it’s side effects. Many people rely on coffee, caffeinated soft drinks, etc. to get through their day. If you need caffeine, I recommend green tea or chocolate instead of coffee or colas. Also, for people with intact thyroid glands that are just not performing up to par, the less we rely on taking thyroid hormone substitutes like caffeine, the less we are asking our thyroid glands to do on their own. Your thyroid will produce less thyroxine if you are drinking coffee or colas. This is not to say that anyone should quit drinking coffee suddenly. I am only suggesting that we take the lowest effective dose to maintain healthy function and that we choose the stimulant with the least side effects.

Green Tea

Other strategies include using chlorophyll and foods that contain chlorophyll to increase excretion of fat-soluble toxins in the feces. Additionally, polyphenols in white and green tea have been shown to increase the excretion of fecal fat, carrying those toxins out of the body. Green tea has a long history of safe use in Asian cuisine and medicine. In addition to helping to excrete toxins, the caffeine in tea acts like T3. This is because caffeine increases the circulating levels of the catacholamines epinephrine and norepinephrine and increases their intracellular effects. The intracellular effect occurs because caffeine inhibits the intracellular enzyme (phosphodiesterase) that inactivates cAMP (cyclic adenosine monophosphate). Less inhibition means less breakdown of cAMP. The resulting increase in cAMP prolongs the effects of catacholamines.

This means tea can be a helpful transition to a healthy metabolic state. You can use green tea to help you feel better while working to improve your thyroid function. However, any form of caffeine, including chocolate, can lose its beneficial functions when used regularly because the body adapts and becomes dependent. For that reason, I suggest only using caffeine as needed.

Green tea raises metabolic rate in an amount greater than can be attributed to its caffeine content. This may be due to the epigallocatechin gallate found in green tea. That compound plus theoflavins in green tea are thought to be responsible for reported anti-cancer effects.

Green or white tea is a far better source of caffeine than coffee for a variety of reasons. For one, the caffeine in tea is bound in a double molecule that has to disassociate before it can interact with your body. This makes the caffeine in green tea hit your system in a time-released manner compared to coffee. Coffee is not bound as a double molecule. Furthermore, coffee has a number of additional compounds that cause other health problems, everything from bladder irritation to irregular heartbeats.

Chocolate

Chocolate is in my opinion, even better. While the caffeine in coffee reaches peak levels in 30-60 and has a half-life of 2.5 to 5 hours, the half life of theobromine (the caffeine like substance in chocolate) reaches peak levels in 2-3 hours and has a half life of 7-12 hours. This is in part because it is fat-soluble rather than water soluble like coffee. Chocolate is also about a tenth as potent as coffee.

Additionally, very dark chocolate has many health benefits. A Canadian study of 44,500 people found that those who ate one serving of chocolate per week were 22% less likely to have a stroke than people who ate none.xi Even eating up to 100 grams of chocolate per day is linked to a lower risk of heart disease and stroke.xii Also, consuming chocolate also improves athletic performance in cyclists, probably due to the flavenoids in chocolate that enhance the release of nitric oxide in the blood vessels.xiii Nitric oxide dilates blood vessels and reduces oxidative damage in the blood vessels.

Prevention

Avoiding tobacco smoke, using a water filter for all drinking and cooking water, using only organic fruits, vegetables and grains wherever possible, using iodinated bakery products can help prevent ingestion of thyroid disruptors. Goitrogenic foods should be eaten with moderation. These include soy, flax, kale, canola oil, and raw cruciferous vegetables such as broccoli, bok choy, cauliflower, cabbage, brussels sprouts, mustard greens and others. The cruciferous vegetables are healthy foods but should be eaten cooked rather than raw. Ground flax seed can be very effective in lowering your serum choleterol and reducing the risk of hormone dependent cancers, but I wouldn’t recommend more than 1 TBS per day. There is no reason to consume Canola oil other than it is added to so many prepared foods and is thus very hard to avoid. Additional measures include avoiding toxic chemicals like cleaning products and pesticides and using a sauna or exercise to increase sweating.

Acupuncture and Chinese herbs

Acupuncture is known to normalize neurotransmitters, cytokines, hormones and thus most bodily functions.xiv Traditional Chinese methods of point selection customized according to patient syndrome are the best guide in this regard. Moxa (a hot coal of Artemesia Vulgaris) is traditionally applied near REN4-6, ST36, SP6 and on the back at UB23 and GV4, with additional points added based on syndrome differentiation.

Many tonic formulas raise metabolic activity. In traditional Chinese medicine, symptoms and signs are the basis for prescribing, not lab tests. My favorite formula for hypometabolism (thyroid and/or adrenal insufficiency) is Ginseng and Astragalus (Bu Zhong Yi Chi Tang). It was traditionally used for weakness and fatigue after an illness.xv One of it’s indications is faintness upon rising from a recumbant or sitting position (blood pressure drop). The Astragalus in this formula also provides a lot of Selenium. Glutathione Peroxidase is a Selenium dependent enzyme that protects the thyroid gland from oxidative damage, reducing the risk of auto-immune thyroid disease. The whole formula is as follows:

Huang Qi (Radix Astragali)

Zhi Gan Cao (Radix and Rhizoma Glycyrrhizae Prep)

Bai Zhu (Rhizoma Atractylodis Macro)

Ren Shen (Radix and Rhizoma Ginseng)

Dang Gui (Radix Angelica Sinensis)

Chen Pi (Pericarpium Citri Reticulatae)

Sheng Ma (Rhizoma Cimicifugae)

Chai Hu (Radix Buplerui)

Shen Jiang (Rhizoma Zingiberis Recens)

Da Zhao (Fructus Jujubae)

The licorice (Glycyrrhizae) in this formula slows the breakdown of cortisol, delaying the onset of fatigue.

From a Chinese medicine perspective, thyroid hormone insufficiency is functionally equivalent to Chi Xu (energy deficiency) and Yang Xu (heat deficiency) with further diferentiation possible according to affected organ systems, i.e., Spleen Qi Xu would include digestive symptoms such as bloating, loose stools, hemorroids, poor appetite/craving for sweets in addition to the other symptoms associated with hypothyroidism.

Summary

The best way to get started is to take the symptom survey above and if your score suggests a problem, start measuring your basal temperature. If your temperature is consistently below 97.6, schedule a meeting with your doctor and bring the results of your basal temperature and symptom survey. You can then discuss whether lab testing would be appropriate.

In terms of labs, a TSH is helpful, but a panel including TSH, T4, T3, rT3, would give a fuller picture. If rT3 is elevated, consider the Hair Mineral Analysis (includes heavy metals) and Urine Iodine tests, both from Doctor’s Data. Adding GSH to the blood testing would quantify the ability of the body to deal with toxic load. Auto antibody tests could be added if auto-immune thyroid disease is suspected.

Nutritional treatment strategies including hair sample testing for deficiency of Iodine, Selenium, and Zinc, as well s testing for excess of the heavy metals Mercury, Arsenic and Cadmium. Iodine sufficiency can be tested more reliably with a provoked urine test. If mineral deficiencies are noted, supplementation can then be taken with re-testing six to twelve months later.

If heavy metals were found or if GSH blood levels were found to be low, detoxification with water, fiber, supplementation with whey protein, alpha lipoic acid, curcumin, magnesium and N-Acetyl Cysteine (NAC) may be helpful.

In all cases, mild aerobic exercise is recommended, starting slow and building up gradually. If you feel exhausted the day after exercise, you did too much. Cut your exercise level to the point that you feel better the next day, but by all means, don’t stop exercising.

Small amounts of coffee, tea or chocolate may be needed to get you through your day while your thyroid is getting stronger, but the ultimate goal is to minimize dependency. Chinese herbs may also provide a bridge to wellness, but again should not be used long term.

Getting 8 hours of sleep will cure many people of mild hypothyroidism.

If you are reasonably healthy and want to raise your metabolic rate, exposure to cold can be helpful. Like exercise, this has to be started slow and increased slowly.

Continue measuring your temperature and pulse rate to evaluate your progress. The goal is to get your temperature to 98.6 when you awake in the morning, without raising your pulse rate above 72 bmp. You will be able to track the effects of any changes you make in your daily routine, sleep, exercise, caffeine, supplements, etc. My goal in writing this article is to empower you to do the things you can do and assist your doctor in helping you to recover.

Best,

David Wells, D.C., L.Ac. MS (Nutrition).

 

 

 

 

 

ihttps://www.thyroid.org/media-main/press-room/

iihttps://www.kingarthurflour.com/professional/bromate.html

iiihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1148561/

ivhttps://www.ncbi.nlm.nih.gov/pubmed/10875250

vhttps://www.ncbi.nlm.nih.gov/pubmed/2838733

vi Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and postpartum.

Stagnaro-Green A, Abalovich M, Alexander E, Azizi F, Mestman J, Negro R, Nixon A, Pearce EN, Soldin OP, Sullivan S, Wiersinga W, American Thyroid Association Taskforce on Thyroid Disease During Pregnancy and P ostpartum.

Thyroid. 2011 Oct; 21(10):1081-125.

vii Subclinical hypothyroidism and pregnancy outcomes.

Casey BM, Dashe JS, Wells CE, McIntire DD, Byrd W, Leveno KJ, Cunningham FG

Obstet Gynecol. 2005 Feb; 105(2):239-45.

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