Hypothyroidism Type 2
by Jerry Tennant, , MD, MD(H), PScD
I am grateful to Dr. Starr for beginning my education in the treatment of hypothyroidism and for asking me to write this chapter on an alternative way to diagnose and treat hypothyroidism that will be more acceptable to most medical boards than the methods developed by Dr. Broda Barnes and Dr. Starr himself.
Hypothyroidism is one of the most important issues causing failing health. Thyroid hormone is one of the primary controls of the voltage in every cell in the body and thus affects every cell’s function (the other one is fulvic acid).
Despite its central role in health, hypothyroidism is one of the conditions most poorly understood and thus also most poorly managed in the U.S. There are many reasons for this: lack of education of physicians, interference of politics, poor understanding of the issues by medical boards, financial concerns of the pharmaceutical industry, interference by the FDA, etc.
Hypothyroidism Type 2
Dr. Starr has developed a sophisticated system for correction that has helped thousands of patients recover their health. However, his system tends to ignore blood tests and instead uses muscle testing and basal body temperature for diagnosis and treatment of hypothyroidism. He has and can achieve success utilizing this system primarily because he practices in Arizona under his MD(H) license. Only Arizona and Nevada have Integrative/Homeopathic medical boards that are independent from the MD medical boards and allow their licensed physicians to prescribe prescription medications such as thyroid hormone. In the other states, the MD/DO medical boards sanction doctors or remove their license to practice medicine if they attempt to treat hypothyroidism according to Dr. Starr’s system. Therefore, it is necessary to have an alternative system that works and still is acceptable to MD/DO medical boards.
Every physician and every patient should understand that there is no perfect system to diagnose and treat hypothyroidism. Each system, whether supported by or condemned by medical boards, has its successes and failures.
Diagnosis of Hypothyroidism
Symptoms and Physical Signs
In the beginning, physicians used primarily symptoms and physical findings to diagnose and treat hypothyroidism. These are still very useful but rarely used by today’s physicians to diagnose and treat hypothyroidism. Since thyroid hormone affects every cell in the body, every symptom you can name can be caused by or influenced by thyroid hormone deficiency. However, about 80% of the following symptoms are almost always present in hypothyroidism:
1. Problems with weight (very easy to gain or extremely hard to lose, despite sensible food intake and exercise).
2. Problems with body temperature (feeling chilly when others don’t).
3. Cold feet and/or hands.
4. Needing to wear socks to bed.
5. Having to dress in layers during the day.
6. Decreased sweating.
7. Slow to heat up with exercise.
8. Problems with rate of body processes (decreased reaction time).
9. Slowed reflexes.
10. Sluggish bowel/constipation.
11. Sluggish liver / high cholesterol (an elevated cholesterol was considered diagnostic of hypothyroidism for many years until drug companies found they could make more money selling statin drugs instead of thyroid hormones).
12. Problems with energy (severe fatigue or utterly exhausted by end of day or times during day when energy drops out completely, feeling like the plug is pulled on your energy).
13. Problems with mood (depression or negative thinking or less than full improvement taking antidepressants).
14. Problems with skin (adult acne,eczema, very dry skin, puffiness/bags around the eyes).
15. Problems with hair (very dry like straw, brittle, easily breaking, easily falling out, loss of outer eyebrows).
16. Problems with nails (brittle, thin, cracked, peeling).
17. Problems with throat or neck (hoarseness for no reason, difficulty swallowing, easily choking, thick tongue, frequently bitten, intolerance to clothing/jewelry snug around neck).
18. Exercise does not feel good, muscle mass/strength does not improve with exercise.
It is significant to remember that studies have shown success in treating chronic depression and bipolar disorder with thyroid hormone (T3) in cases that have failed with all other therapies.
Basal Body Temperature
Perhaps the next item to be widely used in the diagnosis and treatment of hypothyroidism was basal body temperature. One of the strongest proponents of this was Broda Barnes, MD. His studies suggested that hypothyroidism was present if the first morning temperature was below 97.8 °F. He found that normal basal temperature was between 97.8 and 98.2 °F.
There are several problems with using body temperature. First it is not easy to accurately measure the temperature of a living organism as compared to a room or outdoors. The temperature of living organisms is constantly changing and is often different from the right to the left side of the body. The literature contains many studies comparing the temperature of various orifices in the body with a thermometer in the pulmonary artery (core body temperature). Each study found something different. These differences confirm the difficulty in getting reliable temperature readings no matter whether you use the ear, mouth, forehead, axilla, or rectum to measure it. This variability can confound the use of body temperature as a guide to diagnose and treat hypothyroidism.
Another problem with using basal temperature as a guide is that thyroid isn’t the only thing that affects body temperature. Temperature is controlled by the temperature center in the hypothalamus of the brain. Our body temperature is controlled not only by thyroid hormone but also by adrenalin, a hormone made by the adrenal medulla (inner part of the adrenals). It is also affected by skin receptors, eating, exercise, clothing/covers, touching others, etc.
Adrenalin is made from the amino acid tyrosine, vitamin C, and vitamin B6. The body’s source for amino acids like tyrosine is controlled by stomach acid. Normally when you eat proteins, stomach acid breaks them into amino acids including tyrosine. If you don’t have adequate stomach acid, you have lost your source of tyrosine and you will be deficient in adrenalin. Thus, the hypothalamic temperature regulation will malfunction even with enough thyroid hormone if you don’t have stomach acid. Making stomach acid requires iodine, zinc, vitamin B1 and salt.
Another problem I found with trying to use Drs. Barnes and Starr’s methods as a guide for thyroid was that in a large number of patients, I could not get their temperature to rise to normal no matter how much thyroid hormone I gave them. I was unaware of the role of adrenalin at the time and only later discovered the fact that anti-thyroid antibodies would destroy the desiccated thyroid I was using.
Lack of Stomach Acid and Thyroid Antibodies
The body does not become allergic to amino acids—only to proteins. Behind our chest bone (sternum) is the thymus gland. It contains the database of all the proteins that are you. When white blood cells are made, they pass through the thymus and the database is downloaded into them. They then patrol the blood stream. When they meet a protein, they check to see if it is in the database. If so, they know it is a protein you made and is “you”. If the protein isn’t in the database, the white cell assumes the protein is a virus or bacteria and calls in the immune troops to make antibodies to destroy the protein.
Under normal conditions, the body takes the proteins that you consume and breaks these down into amino acids which provide the building blocks your body needs to produce its own proteins. However, if you don’t have stomach acid you cannot break proteins into amino acids. Instead, you absorb the proteins you consume. These proteins are not recognized in the database. This results in you making antibodies and becoming allergic to everything you normally eat.
Desiccated thyroid (Armour, NatureThroid, Westthroid) is made by dehydrating pig thyroid glands. The glands contain not only thyroid hormones but the proteins of the thyroid gland itself. If you take desiccated thyroid and you don’t have enough stomach acid to break the proteins into amino acids, you will make antibodies against those proteins. Thus, your antibodies will inactivate the product and it won’t work well for you.
Iodine and Thyroid Disease
Iodine is necessary to make thyroid hormone. However, it has many other important functions. Every cell in the body that secretes something (almost all cells) need iodine as the “truck” that moves the secretion from inside to outside the cell.
Many physicians believe that there is enough iodine in table salt to fulfill the needs of the body. However, this appears not to be correct. Studies by Abraham and others suggest that most adults need about 12-25 mg per day. The amount in table salt is about 1/1,000th of what the body needs.
Some physicians do not use iodine in patients with autoimmune Hashimoto’s disease. I respectfully disagree. If you do not allow patients with Hashimoto’s disease to consume iodine, you have sentenced all of the other tissues in the body to malfunction. In addition, without iodine, one cannot make stomach acid. Without stomach acid, you become allergic to everything you normally eat including the protein portion of grains called gluten. Gluten antibodies cross-react with the thyroid and damage it. Thus no iodine —> no stomach acid —> gluten antibodies —> further damage to the thyroid gland.
In contrast, Dr. David Brownstein has suggested that Hashimoto’s disease is actually due to lack of iodine.
Hydrogen peroxide is a byproduct of oxidative phosphorylation. It is this production of hydrogen peroxide that is so critical to the oxidation process of iodine. Hydrogen peroxide and TPO help to oxidize iodide to form iodine. If there is a deficiency in iodine, which is common when ingesting the RDA for iodine, there will not be enough substrate (i.e., iodine) to produce iodinated lipids. —The lack of d-iodolactone and other iodinated lipids results in a loss of the ‘brake’ in the pathway to oxidize iodide. This may result in temporary production of too much hydrogen peroxide. This excess hydrogen peroxide can damage the enzyme TPO.
The body’s response to TPO damage is to produce anti-bodies against TPO or anti-TPO antibodies. A diagnosis of Hashimoto’s disease requires the presence of anti-TPO antibodies. As the damage worsens, surrounding proteins can also be damaged such as thyroglobulin. Damaged thyroglobulin will result in the body producing antibodies against thyroglobulin—anti-thyroglobulin antibodies.
I personally give all my patients iodine and encourage them to take it the rest of their lives. I have not regretted doing so. If one should get a detox episode, it is easily reversed with large doses of oral sea salt to overcome the effects of released bromide.
Anatomically, Hashimoto’s disease and fluoride poisoning are indistinguishable one from each other. Iodine helps detoxify the body from fluoride.
Muscle testing is a technique where one’s muscle strength is used to get information. There are three basic forms of it. One is to test the electronic polarity of the body. If you press your right palm to your right forehead, you will be strong when someone presses down on your outstretched left arm or tests the strength of a circle made with the thumb and ring finger of your left hand. Now if you press the same palm to the right back of your scalp, you will now be weak because you have pressed the plus polarity of your right palm to the plus polarity of the back of the right skull. Notice that no questions were asked. One is just placing the plus polarity of your right palm to minus polarity of your right forehead or to the plus polarity of your right posterior scalp.
The next system is similar in that no questions are asked but rather a substance is placed into your magnetic field to see if it strengthens or weakens you. Test with an arm or circle of fingers and see that the patient is strong. Then place a substance in their field. For example, place a tablet of vitamin C against the breast bone. Testing now will likely show strength. Now place an alcohol sponge (with isopropyl alcohol = rubbing alcohol) against the breast bone and testing will show weakness indicating the body doesn’t want the alcohol. In this way you can test most any substance.
The third method asks questions. It is assumed that the body or the universe knows all the answers. In this method, the one doing the testing asks a question either out loud or silently and then tests for strength. The question must be asked in such a way that the answer is either yes or no. For example, one might ask, “The proper dose of hormone needed is greater than 65 mg.” If you get a weak (“no” response), the next question might be, “The proper dose of hormone needed is greater than 15 mg.” By continuing this process, you can identify the proper dose.
The latter system of asking questions is most likely to give false information. First the doctor/therapist/questioner must personally be in balance. Otherwise false answers will occur. Next, the person being questioned must be in balance or testing is also impossible. Of course, most medical boards would not support the use of this method.
Dental Infections and Thyroid Function
The thyroid gland gets its voltage to function via the spleen/stomach acupuncture system. If there is a dental infection in the upper molars, the voltage in this system is diminished and affects the thyroid. In addition, dental infections put out severe toxins called thioethers and gliotoxins. If you have a root canal or an infected crown or infection under a filling in the upper molars, these toxins will follow the acupuncture meridian (fascia) to the thyroid and damage it.
The thyroid gland is controlled by the parasympathetic system. If you have the Bowling Ball Syndrome, you will be stuck in sympathetic-on/parasympathetic-off. This should be corrected with the Tennant BioModulator to restore parasympathetic function. See the chapter on the Bowling Ball Syndrome in my Healing is Voltage book.
Medical boards outside of Arizona and Nevada will almost certainly require that the physician prescribing thyroid hormone would have blood tests supporting the need for thyroid hormone and the dose given. Unfortunately, there are many problems with the blood tests.
The pituitary gland produces the hormone TSH (thyroid stimulating hormone) when the temperature center in the hypothalamus produces TRH (thyroid releasing hormone). TSH causes the thyroid gland to release mostly T4 (levothyroxine) and some T3 (triiodothyronine).
Most physicians have been taught that as you increase T4 in the blood, it suppresses the pituitary’s ability to make TSH. That is not entirely correct.
“Local control of cellular thyroid levels is mediated through three different deiodinase enzymes present in different tissues in the body:
1. Type I deiodinase (D1) increases cellular thyroid activity by converting inactive thyroxine (T4) to the active triiodothyronine (T3) at the cellular level.
2. Type II deiodinase (D2) increase cellular thyroid activity by converting inactive thyroxine (T4) to the active triiodothyronine (T3) in the pituitary.
3. Type III deiodinase (D3) reduces cellular thyroid activity by converting T4 to the anti-thyroid reverse T3 (reverse T3).
Because it is the activity of these deiodinases and transport of T4 and T3 into the cell that determines tissue and cellular thyroid levels and not serum thyroid levels, serum thyroid hormone levels may not necessarily predict tissue thyroid levels under a variety of physiologic conditions. D1 (cellular) but not D2 (pituitary) is suppressed and down-regulated (decreasing T4 to T3 conversion at the cellular level) in response to:
1. Physiologic and emotional stress.11-22
4. Weight gain.
5. Leptin resistance 47-91
6. Insulin resistance.
9. Inflammation from autoimmune disease
10. Systemic illness.11,100,102-115
11. Chronic fatigue syndrome.
13. Chronic pain.116-120
14. Exposure to toxins and plastics.126-134
The stressors listed above cause D1 to down-regulate and decrease conversion of T4 to T3 at the cellular level. However, these stressors have the opposite effect on D2 and the conversion of T4 to T3 in the pituitary. While these stressors decrease tissue levels of active T3, they cause D2 to increase the level of T4 to T3 conversion in the pituitary, reducing TSH levels at the same time that tissue levels of T3 are falling.
The importance of this is the realization that each region that influences thyroid hormone function operates with different enzymes and thus functions almost independently of the other systems in the thyroid mechanism! Thus, you cannot assume the rest of the system is functioning normally even though you have evidence that one portion of the system is working. For example, you cannot assume that the thyroid function at the cellular level is normal just because the TSH test is normal.
“Pituitary T3 levels are determined by D2 activity, which is 1000 times more efficient at converting T4 to T3 than the D1 enzyme present in the rest of the body1,7,10,46,145-146 and is much less sensitive to suppression by toxins and medications.147 In the pituitary, 80-90% of T4 is converted to T34,148,149 while only about 30-50% of T4 in the peripheral tissue is converted to active T3.149,150 This is due to the inefficiency of D1 and the presence of D3 in all tissues of the body except the pituitary that competes with D1 and converts T4 to reverse T3.”7
Note that since only about 30-50% of T4 is converted to T3 at the cellular level, treating patients with only T4 (levothyroxine) to correct the TSH level leaves one not knowing the status of thyroid function at the cellular level. However, this is the “standard-of-practice” for many physicians and the agencies that regulate them.
If one gives a patient only T3, the patient often feels much better but the TSH levels will go very high. Since the controllers of TSH are pituitary levels of T3, thermoregulation in the hypothalamus with release or decrease in TRH (Thyroid Regulating Hormone), and increased levels of blood T4, one must explain why increased levels of blood T3 does not suppress TSH production. Possible explanations are that increased blood T3 does not cause an increase in pituitary T3 (not likely) or that blood levels of T4 but not T3 suppress TRH. I have not found studies that answer this question. The working hypothesis that blood levels of T4 control the release of hypothalamic TRH and indirectly TSH is useful in clinical practice.
The TSH test was developed in the late 1960s and put into practice in 1971. Only 29 patients were used to develop the “normals”, and normal was said to be 1-10. Twenty-nine patients is an inadequate sample and is not statistically significant. Over time, the values for “normal” have been changed. However, this is a big problem. Almost all labs report a normal TSH as 0.4-4.6.
The following is quoted from the LabCorp website:
Spurious increase from antibovine TSH antibodies by double-antibody technique has been reported. TSH may be affected by glucocorticoids, dopamine, and by severe illness, and these remain limitations even for the new, sensitive TSH assays. TSH suppression in hypothyroidism with severe illness has been reported with TSH increase with recovery. Normal TSH levels in the presence of hypothyroidism have been reported with head injury.
Iopanoic acid, ipodate, and an anti-arrhythmic drug, amiodarone, cause changes in thyroid test results including increases in T4, free T4, and TSH and decreases of T3. TSH is not elevated in secondary hypothyroidism.
Probably no single test, even the sensitive immunoassays, can be expected to adequately reflect thyroid status under all circumstances. Among possible problems are the recovery phase of non-thyroidal illness, states of resistance to thyroid hormone, thyrotropin-producing tumors, thyroid status in acute psychiatric illness, early in thyrotoxicosis and in subacute thyroiditis.
In patients who are receiving replacement therapy, the dose should be adjusted so serum TSH values range from 0.3-3.0 μIU/mL. An exception is thyroid hormone replacement treatment after thyroidectomy for differentiated thyroid cancer, in which case, a mildly to moderately suppressed TSH level is generally desirable. It is reasonable to consider serum TSH measurement for pregnant women or women planning to become pregnant with a family history of thyroid disease, prior thyroid dysfunction, symptoms or physical findings suggestive of hypo- or hyperthyroidism, an abnormal thyroid gland on examination, type 1 diabetes mellitus, or a personal history of autoimmune disorder. Suggested upper limit for the TSH reference range for pregnant women and preconception is: first trimester -<2.5 μIU/mL, and 3.0 μIU/mL in the second and third trimesters.
It is of interest that this information never appears on lab reports. Lab reports list normal as 0.4-4.6. So if the result is between 3.0 and 4.6, the doctor will tell you that your thyroid is normal despite the information on the lab’s website that this is abnormal. I asked the LabCorp medical director why the reports say 0.4-4.6 is normal when the literature on their website says 0.3-3.0 is normal. He didn’t have an answer. This leads to the majority of physicians under-diagnosing and under-correcting most hypothyroid patients!
January 2003 American Academy of Clinical Endocrinology press release:
“Until November 2002, doctors had relied on a normal TSH level ranging from 0.5 to 5.0 to diagnose and treat patients with a thyroid disorder who tested outside the boundaries of that range. Now AACE encourages doctors to consider treatment for patients who test outside the boundaries of a narrower margin based on a target TSH level of 0.3 to 3.0. AACE believes the new range will result in proper diagnosis for millions of Americans who suffer from a mild thyroid disorder, but have gone untreated until now.”
“National Academy of Clinical Biochemistry: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease: Published Guidelines” (US, 2002).
. . . given the high prevalence of mild (subclinical) hypothyroidism in the general population, it is likely that the current upper limit of the population reference range is skewed by the inclusion of persons with occult thyroid dysfunction....
. . . In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L because >95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/L....
A serum TSH result between 0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard L-T4 replacement dose for primary hypothyroidism.
Thus we can see that the lab results for TSH that most doctors rely upon to diagnose and treat hypothyroidism uses lab “normals” that are over ten years out of date. In addition, most doctors are unaware that TSH is managed locally in the pituitary by a different enzyme system than at the cellular level. Although TSH is far from a perfect test, it is a useful guide if the proper normals of 0.3-2.0 are used. Remember it is not valid in pregnancy, after chemotherapy, in debilitated patients, when certain drugs like amiodarone are taken, when stored iron levels (ferritin) are below 70, etc.
Remember that T3 is the active form of thyroid hormone so T4 must be converted to T3. This conversion requires iodine, selenium, zinc, iron, cortisol, progesterone, glutathione, and hydrogen peroxide (made from vitamin C). If one of these is missing or if the stressors mentioned above are present or if one is taking steroids, T4 is converted by the enzyme D3 into a fake hormone called Reverse T3 (RT3). RT3 has the ability to fit into the T3 receptor but will not work. It is like a key that fits into the lock but can’t turn the tumbler. It blocks real T3 from the receptor. Thus the more RT3 you have, the more hypothyroid you are.
Many cases of depression or bipolar disorder have a normal or low free-T3 (FT3) but an increase in RT3. The depression or bipolar disorder can often be corrected by decreasing the RT3 and/or increasing the T3.
One can often decrease the RT3 levels by supplementing the nutrients listed above. If increased RT3 levels are present, you must increase the amount of T3 given. Treating with only T4 doesn’t work.
What one really needs to know is the amount of T3 available to cells and the amount of RT3 that keeps T3 from accessing cell receptor sites. Thus the most critical tests to use for analysis of thyroid status in a patient are FT3 and RT3. First you want the FT3 as high as you can get it without the patient having symptoms of hyperthyroidism. Generally you want to have it between 3.0 and 4.0 because most patients feel good at this level and don’t have hyperthyroid symptoms. Most labs list up to 4.5 as normal.
The next thing you want to do is look at the FT3/RT3 ratio. You want it to be >20. That means you have more than 20 molecules of FT3 for every molecule of RT3 and thus there won’t be an overwhelming number of RT3 molecules blocking the function of T3.
Calculating the FT3/RT3 ratio seems complicated at first because FT3 and RT3 are usually reported by the labs in different quantities. For example one might be reported in micrograms per deciliter and the other in picograms per deciliter. To get the ratio, you must convert them so they are in the same measurement.
The easiest way to calculate the ratio is to be sure that the FT3 number has one more zero than the RT3. So if the FT3 is 3.8 and the RT3 is 321, you must add zeroes to the FT3 to be one more zero than 321 or 3800. Thus we added three zeroes to 3.8. Now we can divide 3800/321 and get 11.8. Since this number is less than 20, we see that even though we have what would seem to be plenty of FT3 (between 3.0 and 4.0), it still isn’t enough to overcome so much RT3 and thus we must give even more T3. Otherwise the patient will continue to be hypothyroid and suffer the symptoms of hypothyroidism. Of course we will focus on the things causing an excess of RT3 including vitamin and mineral deficiencies, lack of stomach acid, dental infections, scars, and toxins to lower the RT3 levels. You can find more information about these things in my book, Healing is Voltage.
Hypothyroidism is a dilemma for American citizens. The majority of our physicians are not trained to understand how the hypothalamic TRH, the pituitary TSH, the thyroid gland T4/T3, the cellular T3, and the blocking RT3 all function almost independently because of their different enzymes D1, D2, D3 function independently. Various illnesses and medications can make the TSH test move to normal while simultaneously decreasing cellular T3 by up to 80%. My office staff and I struggle daily when I order FT3 and RT3 on my patients. They take the lab request slip to their doctors instead of the lab and their doctors change my orders and get lab tests that ignore the FT3 and RT3. The patients then expect me to manage their thyroid function when the most important tests are missing. This just emphasizes the fact that most physicians are not being trained to understand how the thyroid system works.
Thus the patient is left in a dilemma. Their family doctor is usually following outdated lab normals, total reliance on TSH and Total T4 blood levels to guide them, and insisting that prescribing only T4 in the form of levothyroxine (Synthroid) is the only proper form of thyroid treatment. This is called “Standard-of-Care” medicine and doctors that do anything different must be prepared to defend themselves to their colleagues.
The medical literature is quite clear that this is outdated and inappropriate care. However, it is the care that is usually available. The patient is left to try to find a physician that understands how hypothyroidism really works and how to correct it using appropriate levels of T4 and T3 to correct levels of FT3 and RT3 so that the system is functioning at the cellular level where it matters.
So what is a physician to do who wants to help his/her patients and still have the laboratory evidence to support what they do? I suggest the following:
1. Have the history that supports the diagnosis. I use a questionnaire that allows me to score the amount of symptoms.
2. Document the physical signs of hypothyroidism.
3. Get the following labs: TSH, FT4, FT3, RT3.
4. Use desiccated thyroid as it is the only source of T2 (T3 controls cell membranes and T2 controls mitochondria).
5. Give enough hormone to get the TSH below 2.0. People usually feel better if you get it below 1.0.
6. Give enough T3 to get the FT3 levels between 3.0 and 4.0.
7. Check the FT3/RT3 ratio. If it is below 20, increase the amount of T3 you are giving and be sure they are taking adequate amounts of iodine, selenium, zinc, iron (ferritin >70), cortisol, progesterone, glutathione (must have stomach acid to make it), and vitamin C to make hydrogen peroxide to reduce the RT3 levels.
8. Check the ferritin level and correct it if it is less than 70.
9. Give iodine as Lugol’s solution or dehydrated Lugol’s solution (Lugol’s Plus)
Conversion for Different Forms of Thyroid Hormone
Most physicians are trained in the use of synthetic T4 (levothyroxine) but not in the use of other forms of thyroid hormone. There is some confusion about how to convert from one form to another.
It is generally considered true that T3 is about four times as effective as T4. Therefore, pharmacology textbooks say that 100 micrograms of T4 is the equivalent of 25 micrograms of T3. Perhaps this is because the enzyme D1 converts about 25-50% of T4 to T3 since T4 is not effective at the cell membrane at all.
The package insert for desiccated thyroid says that one grain (about 65 mg) of desiccated thyroid contains 38 micrograms of T4 and 9 micrograms of T3.
The problem is that if you take a patient that is on one grain (60-65 mg) of desiccated thyroid and give them 38 ug of T4 and 9 ug of T3, their TSH will always go up significantly and they will feel tired. The same is true if you take a person on 100 ug of Synthroid (levothyroxine) and put them on 38 ug of T4 and 9 ug of T3. Thus in practice, this conversion doesn’t work.
If you assume it is true that T3 is four times as effective as T4, then the 9 ug of T3 said to be in one grain of desiccated thyroid would be equal to 4 x 9 = 36 ug of T4. Add 36 to the 38 ug of T4 said to be in one grain and you get 38 + 36 = 74 ug of T4. In spite of this, the pharmacology books say one grain of desiccated thyroid is the same as 100 ug of T4. Thus the package insert for desiccated thyroid and the pharmacology books say different things.
In actual day-to-day clinical practice of following the TSH, FT4 and FT3 labs and how patients feel, the one grain = 100 ug instead of 74 ug is closer to correct.
This conversion chart is based upon the belief that one grain of desiccated thyroid is equal in effectiveness to 100 ug of T4 and that T3 is four times as effective as T4. The T4 equivalency column is the sum of T4 plus T3 x 4 columns.
Observe that the 38/9 formula listed in the package insert in desiccated thyroid is equivalent to 45 mg and not 60 mg of desiccated thyroid.
Levothyroxine (T4) comes in a limited number of dose forms but often at dosages that are close to what you need. However, T3 (Cytomel) comes only in 5, 25, and 50 ug sizes. Thus if you need say 20 ug, you will have to have the patient take four of the 5 ug tablets. The cost of 5 ug is the same as the cost of 25 ug at many pharmacies. As of this writing, each 30 tablets of 5 ug is $23. So if the patient needs to take four of these each day, the monthly cost for the T3 is $82.00. Then you must also add in the cost of the T4 which may be as low as $4.00 for a monthly total of $86.00. You can get the same thing compounded at most compounding pharmacies for between $20-30. Thus, compounding is much less expensive than using standard pills at the least expensive pharmacies.
Desiccated Thyroid in the Elderly
I often get letters from some committee saying that I am prescribing inappropriately for elderly patient by giving desiccated thyroid instead of synthetic T4 (levothyroxine). They give the following references to support their position.
J Am Geriatr Soc. 2015 Nov;63(11):2227-46. doi: 10.1111/jgs.13702. Epub 2015 Oct 8.
American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults.
By the American Geriatrics Society 2015 Beers Criteria Update Expert Panel.
The 2015 American Geriatrics Society (AGS) Beers Criteria are presented. Like the 2012 AGS Beers Criteria, they include lists of potentially inappropriate medications to be avoided in older adults. New to the criteria are lists of select drugs that should be avoided or have their dose adjusted based on the individual's kidney function and select drug-drug interactions documented to be associated with harms in older adults. The specific aim was to have a 13-member interdisciplinary panel of experts in geriatric care and pharmacotherapy update the 2012 AGS Beers Criteria using a modified Delphi method to systematically review and grade the evidence and reach a consensus on each existing and new criterion. The process followed an evidence-based approach using Institute of Medicine standards. The 2015 AGS Beers Criteria are applicable to all older adults with the exclusion of those in palliative and hospice care. Careful application of the criteria by health professionals, consumers, payors, and health systems should lead to closer monitoring of drug use in older adults.
© 2015, Copyright the Authors Journal compilation © 2015, The American Geriatrics Society.
Thyroid. 2014 Dec;24(12):1670-751. doi: 10.1089/thy.2014.0028.
Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement.
A number of recent advances in our understanding of thyroid physiology may shed light on why some patients feel unwell while taking levothyroxine monotherapy. The purpose of this task force was to review the goals of levothyroxine therapy, the optimal prescription of conventional levothyroxine therapy, the sources of dissatisfaction with levothyroxine therapy, the evidence on treatment alternatives, and the relevant knowledge gaps. We wished to determine whether there are sufficient new data generated by well-designed studies to provide reason to pursue such therapies and change the current standard of care. This document is intended to inform clinical decision-making on thyroid hormone replacement therapy; it is not a replacement for individualized clinical judgment.
Task force members identified 24 questions relevant to the treatment of hypothyroidism. The clinical literature relating to each question was then reviewed. Clinical reviews were supplemented, when relevant, with related mechanistic and bench research literature reviews, performed by our team of translational scientists. Ethics reviews were provided, when relevant, by a bioethicist. The responses to questions were formatted, when possible, in the form of a formal clinical recommendation statement. When responses were not suitable for a formal clinical recommendation, a summary response statement without a formal clinical recommendation was developed. For clinical recommendations, the supporting evidence was appraised, and the strength of each clinical recommendation was assessed, using the American College of Physicians system. The final document was organized so that each topic is introduced with a question, followed by a formal clinical recommendation. Stakeholder input was received at a national meeting, with some subsequent refinement of the clinical questions addressed in the document. Consensus was achieved for all recommendations by the task force.
We reviewed the following therapeutic categories: (i) levothyroxine therapy, (ii) non-levothyroxine-based thyroid hormone therapies, and (iii) use of thyroid hormone analogs. The second category included thyroid extracts, synthetic combination therapy, triiodothyronine therapy, and compounded thyroid hormones.
We concluded that levothyroxine should remain the standard of care for treating hypothyroidism. We found no consistently strong evidence for the superiority of alternative preparations (e.g., levothyroxine-liothyronine combination therapy, or thyroid extract therapy, or others) over monotherapy with levothyroxine, in improving health outcomes. Some examples of future research needs include the development of superior biomarkers of euthyroidism to supplement thyrotropin measurements, mechanistic research on serum triiodothyronine levels (including effects of age and disease status, relationship with tissue concentrations, as well as potential therapeutic targeting), and long-term outcome clinical trials testing combination therapy or thyroid extracts (including subgroup effects). Additional research is also needed to develop thyroid hormone analogs with a favorable benefit to risk profile.
Note that this study does NOT say that desiccated thyroid is contraindicated in the elderly. It simply states the opinion that levothyroxine is as good as other methods of therapy even though it is more expensive.
Update on Medication Quality Measures in
Medicare Part D Plan Star Ratings-2016
Understanding the CMS Quality Evaluation System
There are multiple components to CMS’ evaluation of medication-related quality across Medicare Parts C and D. CMS creates plan ratings that indicate the quality of Medicare plans on a scale of 1 to 5 stars with 5 stars being the highest rating. The overall star rating is determined through numerous performance measures across several domains of performance. Each measure is awarded a star rating and the individual measure stars are then aggregated at the domain and summary level. Only a small number of plans receive a 5-star summary rating from CMS, with most plans receiving 3 to 4 stars.
Medicare Advantage plans that include drug benefits (MA-PDs) are rated on performance measures for Parts C and D. For Part C, a subset of the HEDIS measure set from NCQA is used for evaluation. Medicare Part D stars are applicable to MA-PDs and stand-alone PDPs. The stars are assigned based on performance measures across four domains. The four Part D domains are:
1. Drug Plan Customer Service
2. Member Complaints, Problems Getting Services, and Choosing to Leave the Plan
3. Member Experience with Drug Plan
4. Drug Pricing & Patient Safety
There are 15 individual measures of quality in the 2016 Part D ratings based on 2014 prescription drug claims). Medication safety and adherence measures are in the domain of Drug Pricing & Patient Safety. Five PQA measures are included in this domain for the 2016 Star Ratings. These include three of PQA’s medication adherence measures in the following therapeutic categories: HMG-CoA inhibitors (statins), Renin Angiotensin System Antagonists, and Oral Diabetes Medications. Two measures of medications safety or MTM are also included, High risk medications in the elderly and Comprehensive Medication Review (CMR) Completion Rate. The CMR Completion Rate measure is new for 2016. Each measure is assigned a weighting factor. Outcomes and Intermediate outcomes are weighted higher. The PQA measures in the plan ratings and their respective weighting are described on the following page.
In addition to the plan ratings, CMS also uses the “Display Measures” to provide further evaluation of Part D plans. The Display Measures are not included in the plan ratings, but are used to facilitate quality improvement by the plans. The Display Measures include three PQA-supported measures of medication safety (drug-drug interactions; excessive doses of oral diabetes medications; Statin Use in Persons with Diabetes). An additional measure, HIV antiretroviral medication adherence, is reported to plans in their Safety Reports. CMS maintains a “Patient Safety website” that provides the benchmarks and scores to the plans across both the Display Measure and Plan Ratings Measures.
Who Manages the Star Ratings System?
CMS manages the star ratings system and uses contractor support for this effort. For example, CMS contracts with Acumen, LLC for the analyses of Medicare data to generate the rates for the medication measures. PQA maintains the PQA-supported performance measures and updates the technical specifications and drug-code lists for the measures every six months. PQA also shares new measures that are endorsed by PQA with CMS and provides some technical guidance on the use of the measures within the plan ratings. CMS tests updates to the PQA-supported measure specifications and drug-code lists and implements these as they deem appropriate.
A Look at the PQA-supported Medication Measures Included in the Part D Plan Ratings
High-risk medications in the elderly (HRM). This NQF-endorsed measure was adapted from the HEDIS measure known as Drugs to be Avoided in the Elderly (DAE). The HRM/DAE measures identify the percentage of older adults (>65yo) who receive a medication that is considered to put the patient at high-risk for an adverse drug-related event. The list of medications in this measure was derived from the Beers’ List that was originally developed in the 1990s, but updated in 2002. The American Geriatrics Society (AGS) provided updated recommendations for the Beer’s List in 2012 and again in 2015. NCQA and PQA considered the AGS recommendations when updating their performance measures in 2012 and plan a measure update in 2016.
Proportion of Days Covered (PDC). PDC is the PQA-recommended methodology for estimation of medication adherence for patients using chronic medications. This metric is also endorsed by the National Quality Forum (NQF). The metric identifies the percentage of patients taking medications in a particular drug class that have high adherence (PDC > 80% for the individual). There are three rates reported in the Star Ratings. One for blood pressure medications (renin angiotensin system antagonists [RASA]); one for statin medications, and one for diabetes medications (not including insulin).
Medication Therapy Management (MTM) Program Completion Rate for Comprehensive Medication Review (CMR) (new for 2016). CMS added this measure to the Star Rating after reporting it to plans as a display measure for several years. The measure calculates the percentage of beneficiaries who met eligibility criteria for the MTM program and who received a CMR with a written summary in the CMS standardized format. Currently this measure is assigned a weight of “1” since it is a new process measure.
Julie Kuhle, BS Pharm
Vice President, Measure Operations
Pharmacy Quality Alliance
Note that this does NOT state that desiccated thyroid is harmful for the elderly either!
Writing this chapter has not been easy. Most of the readers are not MD’s or DO’s or other physicians that can write prescriptions. Thus I have attempted to write in a way that lay people can understand why their doctors are telling them that their thyroid function is normal when it is not. However, it is necessary for me to write in a way that explains to those physicians that do read this chapter how they might better serve their patients and the facts published in standard, peer-reviewed journals that tell us there is a better way to help our patients. Remember that I was trained the same way they were and only by reading my journal articles at night did I come to realize I could do better. I am sharing my experiences so that it is easier for my colleagues to find this information than to have to follow the road I had to travel to find it. My hope is that my efforts will make it easier for physicians to help their patients and that those suffering will find good health.
Jerry Tennant, MD, MD(H), PScD
Brownstein D. Iodine: Why You Need It, Why You Can’t Live Without It. 3rd. ed. Medical Alternatives Press; 2008.
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