1) TREATMENT – introduction

  • The new TSH reference standards
  • When start the treatment?
  • Subclinical hypothyroidism
  • Progression to overt clinical hypothyroidism
  • Upper limit of normal TSH in subclinical hypothyroidism
  • Management of subclinical hypothyroidism
  • Special case: women anticipating pregnancy and pregnant women


  • Treatment guidelines
  • Levothyroxine
  • Hypothyroidism is caused by an autoimmune disease
  • What means TSH-suppressive dosages of thyroid hormone?
  • Hormone replacement therapy: no risk of osteoporosis

3) OPTIMIZATION MEDICATION: slow-released compounded T3

  • Advantage of T3 therapy
  • T3 adjunctive treatment of depression
  • T3 therapy, fibromyalgia and chronic fatigue syndrome
  • T3 therapy, leptin resistance and overweight
  • T3 therapy and Wilson's Temperature Syndrome (WTS)


  • Hashitoxicosis and goiter
  • Treatment of postpartum thyroiditis
  • Treatment in the elderly
  • Adrenal fatigue and hypothyroidism
  • Hypothyroidism/infertility/pregnancy/breastfeeding
  • Treatment of central hypothyroidism


TREATMENT – introduction

New TSH reference range
The classic treatment of thyroid deficiency is far from satisfying number of patients. It does not take into account parameters ignored by most doctors or which have no involvement in the management of these patients. But before considering treating, one such parameter, and not least, is a matter of diagnosis. Who has a hypothyroid condition or not?

The big myth that persists regarding thyroid diagnosis is that an elevated TSH level is always required before a diagnosis of hypothyroidism can be made. The key point is to know what rate of TSH is considered elevated and, therefore, the rate at which to treat or not.
Since 1973, according to a consensus among specialists in the thyroid, the traditional reference range of TSH is 0.5 to 5.0 mIU/L. Result higher than 5.0 indicates hypothyroidism, whereas result below 0.5 shows hyperthyroidism. Thus, the upper limit 5.0 was crucial deciding treatment.
In 2002, the TSH normal range has been modified. The AACE (American Association of Clinical Endocrinologists), upsetting tradition, proposed standards TSH between 0.3 and 3.0 mIU/L, as opposed to the previous range of 0.5 to 5.0 mIU/L. TSH level higher than 3.0, should be indicative of hypothyroidism, whereas a reading that is below 0.3 should indicate hyperthyroidism. Due to the narrow reference range, there is a better chance of early diagnosing and treating people with thyroid disorders. Thus, these new standards help to explain the various symptoms remained unexplained, and that patients are experiencing. AACE suggests that physicians consider thyroid treatment in patients whose TSH is tested outside the target reference range of 3.0 mIU/L (patients now diagnosed with hypothyroidism), even if the rates of free T3 and T4 hormones are within their standard ranges.
AACE believed that the use of a new range would result in proper diagnosis for millions of Americans who suffer from a mild thyroid disorder, but have gone untreated until now. AACE estimates that the new guidelines actually double the number of people who have abnormal thyroid function, bringing in USA the total to as many as 27 million, up from 13 million thought to have the condition under the old guidelines. AACE made the decision to narrow the range because of data suggesting many people may have low-level thyroid problems that could be improved with treatment, and a narrow TSH range will give doctors reason to more carefully consider those patients.

This recommendation is controversial. Most general practitioners and endocrinologists are still using the old standards, leaving unfortunately millions of people undiagnosed and suffering from debilitating symptoms. They still consider individuals with a TSH between 3.0 and 5.0 mIU/L completely healthy, or that the alleged symptoms have nothing to do with the thyroid. However, at TSH levels as high as 3.0 to 5.0 many hypothyroid sufferers don't feel well.
After exclusion of persons with goiter, anti-thyroid antibodies, and personal or family history of thyroid disease, it was determined that the mean serum TSH is 1.5 mIU/L. Many patients with TSH's of greater than 1.5 (not 5.0) have classic symptoms and signs of hypothyroidism.
Data from the twenty-year follow-up Whickham Survey studies (one of the largest studies of thyroid problems), published in 1995, demonstrated that individuals with a serum TSH exceeding 2.0mIU/L at their primary evaluation had an increased odds ratio of developing hypothyroidism over the next 20 years, especially if thyroid antibodies were elevated (Click Here).
According to a recent Whickam Survey follow-up study, it is likely, in future, that the upper limit of the serum TSH reference range will be reduced to 2.5 mIU/L.
Dr. Stephen Langer, coauthor with Dr. James Scheer of Solved: The Riddle of Illness, on thyroid diseases, says: "Even a small deficiency of thyroid hormones can cause a number and an incredible variety of symptoms that carry out a real sabotage on our physical, emotional and mental health".

The pituitary gland also does not always react to a lack of thyroid hormones T4 and T3 by increased TSH production. This is the case in secondary hypothyroidism (5-10% of cases) due to hypothalamic or pituitary disorder. The blood levels of T4 and T3 are low and the TSH level is low as well (and thus the direct cause of the thyroid failure), although, in this circumstance, TSH can be in the standard, posing a real diagnostic problem if TSH only is measured.

However, TSH test alone cannot help in giving a clear picture of the thyroid gland function. Doctors should run a full thyroid blood panel (TSH, free T4, free T3, and antibodies for evidence of autoimmune disease), and investigate fully the patient's medical history, symptoms, family history and thorough physical exam. Certain medicines can interfere with the thyroid hormonal tests, which is why you should tell your doctor about all the drugs you are using. Additionally, measurement serum cholesterol and testing for anemia should be done. I always ask as well for basal body temperature.

When start the treatment?
Doctors distinguish subclinical hypothyroidism and (overt) clinical hypothyroidism. This distinction is especially biological order. If, in the terminology, the symptoms are typically more pronounced in clinical hypothyroidism, the two clinical forms may have the same signs and symptoms. That is why, to my opinion, the distinction doesn't make much sense. Decision of treating should be based on the clinical context and, as we will see, on the presence or absence of high antibodies levels, and not rely on TSH elevation. Both forms may have "normal" TSH levels. As subclinical hypothyroidism is the form most commonly encountered in medical practice, I will fully detail it.

Subclinical hypothyroidism
The term subclinical hypothyroidism, also called mild thyroid failure, is used to define that grade of primary hypothyroidism in which there is a mildly elevated TSH concentration in the presence of serum free T4 and T3 levels within normal reference range. This condition occurs in 3% to 8% of the general population. Like (overt) clinical hypothyroidism, it is more common in women than men, and its prevalence increases with age. After the sixth decade of life, the prevalence in men approaches that of women, with a combined prevalence of 10%. The routine screening of TSH has revealed an increased number of patients with abnormal thyroid function, yet not necessarily symptomatic. But several studies have shown that some patients with subclinical hypothyroidism actually have clinical manifestations of thyroid failure. Thus, the term "subclinical" is not quite accurate, but no better term has been proposed. This has leaded to several debates between specialists regarding the diagnosis and management of those patients.

Subclinical hypothyroidism is caused by the same disorders as those that cause (overt) clinical hypothyroidism, and the most common cause of elevated TSH is of immune nature, namely Hashimoto's autoimmune thyroiditis (with increase in thyroid antibodies). The most important implication of subclinical hypothyroidism is its high likelihood of progression to clinical hypothyroidism.

Progression to overt hypothyroidism
Subclinical hypothyroidism is most commonly an early stage of hypothyroidism. Several studies have shown that subclinical hypothyroidism may progress to clinical (overt) hypothyroidism in approximately 2-5% cases annually. That means that up to 50 % of subclinical hypothyroidism patients will develop an overt hypothyroidism within a decade (only 4 % will have their TSH normalized). That means that a certain percentage of patients maintain a status quo of their subclinical hypothyroidism condition. In elderly persons with high levels of antibodies, the risk of progression may be closer to 20 % per year.

What is the upper limit of normal TSH level in subclinical hypothyroidism?
In other word, what is a mild elevated TSH level? As we said above, lowering the upper limit of normal for the serum TSH level from 5.0 to 3.0 or even 2.5 mIU/L has been proposed, but such proposals have been met with some critiques (Click Here). The strongest argument in favor of lowering the upper limit of normal for the serum TSH level is a high detection of elevated thyroid antibodies in people with TSH between 3.0 and 5.0 mIU/L, and thus the higher potential for progression to overt clinical hypothyroidism. The presence of anti-thyroid antibodies is indeed a factor that influences the progression to overt hypothyroidism, as well as the amplitude and duration of TSH elevation. Anti-thyroid antibodies can be detected in 80% of patients with subclinical hypothyroidism, and 80% of patients with subclinical hypothyroidism have a serum TSH of less than 10 mIU/L.
Consideration of these possible outcomes affects the decision about whether to treat or to simply monitor patients without treatment. But if the goal of treatment is to prevent progression to clinical hypothyroidism, the expectation of these patients is to be rid of their present symptoms, as subtle as they are, that plague their lives of everyday.

Management of subclinical hypothyroidism
Diagnosis of subclinical hypothyroidism (TSH >3 mIU/L and normal levels of T4 and T3) with negative findings on anti-thyroid antibody, and with no evidence of low thyroid symptoms should be confirmed with routine screening tests at one month and repeated every six months, having exclude non-thyroid illness and drug interference. No treatment will be offered. Measuring antibodies will be performed once a year.

If in the medical community the clinical importance of subclinical hypothyroidism, the benefit of therapy for mild elevation of TSH and the exact upper limit of normal for the serum TSH level remain subjects of debate (which I do not participate), general guidelines have been offered. There is reasonable evidence and consensus on the need to treat subclinical hypothyroidism in the presence of risk factors for thyroid failure, such as:

Family history of thyroid disease
Personal history of thyroid disease
Presence of anti-thyroid antibodies
Presence of another autoimmune disease
Radiation treatment to head, neck or chest
Medications: lithium, amiodarone, iodine
Old age
Female infertility associated with subclinical hypothyroidism
High total or LDL cholesterol levels to prevent a heart disease

Thus, greater magnitude of TSH > 3.0 mIU/L and duration of this TSH elevation and higher titers of anti-thyroid antibodies increase the probability that the condition will progress to overt hypothyroidism and, therefore, increase the potential benefit of hormone replacement therapy.
Management of the symptoms and restoring well-being come first. Studies have shown that dry skin, cold intolerance, easy fatigability, constipation, muscle cramps or other common symptoms of hypothyroidism were significantly more common in the patients with raised TSH levels > 3 mIU/L, and that these symptoms may benefit from treatment with thyroid hormone. This has been confirmed in my medical practice. Because patients with subclinical hypothyroidism (sometimes with only a few clinical signs, or just a persistent and debilitating fatigue) may have mild abnormalities of serum lipoproteins, those patients with persistent TSH elevation > 3 mIU/L should be offered hormone therapy to try to lower their total serum cholesterol and LDL cholesterol levels before considering lipid-lowering therapy.

Do not believe that in the medical community the decision to treat (overt) clinical hypothyroidism (elevated TSH with low thyroid hormone) is consensual. Here as well it remains controversial in terms of elevation of TSH levels, and whether to treat clinical hypothyroidism with TSH levels below 10 mIU/L is still subject of debates. Some doctors will even tell you that there is no hypothyroidism as TSH is not greater than 10 mIU/L, or that TSH less than 10 mIU/L should not be treated. Such doctors are to flee at once.

In summary, my opinion is that with a TSH> 3 mIU/L, whether the rate of thyroid hormone is low (clinical hypothyroidism) or normal (subclinical hypothyroidism), and symptoms suggestive of a failure of the thyroid, hormone replacement therapy is needed, and especially in the presence of elevated thyroid antibodies (and whatever, in this case, the degree of hypothyroidism). The hypothyroid patient does not bother biological considerations or subtleties in therapeutic decision.
More precisely, whatever the levels of TSH, all patients with any degree of hypothyroidism (overt clinical or subclinical hypothyroidism) due to autoimmune Hashimoto's thyroiditis (presence of anti-thyroid antibodies) should be treated with thyroid hormone replacement. That sums up the majority of cases. Treatment should be for life, the patient remaining hypothyroid when he or she ceases the use of thyroid hormone. Once the patient has begun taking the treatment, antibody levels should usually decrease. But in autoimmune Hashimoto's thyroiditis, taking hormone replacement is not enough, I will discuss shortly.

Suspicion on clinical evidence of hypothyroidism could be delayed in the elderly because symptoms such as fatigue, constipation and other early manifestations of thyroid insufficiency can be attributed to aging itself. The high prevalence in the elderly of a thyroid failure and the difficulty of establishing an early clinical diagnosis suggest that regular routine screening for hypothyroidism is useful in this age group, but some authors, which I belong to, argue for selective therapy.

Special case of women anticipating pregnancy and pregnant women
Even mild or subclinical hypothyroidism is known to adversely affect fertility. Research has shown that women with thyroid disease are at more risk than previously thought of infertility, of miscarriage, or of having infants who have birth defects, including abnormalities of the heart, kidney or brain, and other defects such as cleft lip and cleft palate. (Click Here)
A study published in 2002 reported on Argentine researchers [Source: Abalovich M, and al. "Overt and subclinical hypothyroidism complicating pregnancy," Thyroid. 2002 Jan], found that when treatment with hormone replacement was not sufficient (meaning that the women had persistently elevated TSH levels), the outcome of pregnancy was spontaneous abortion (miscarriage) in 60% of the overt clinical hypothyroid patients and in 71.4% of subclinical hypothyroid patients. Twenty percent of overt hypothyroid patients and 7.2% of the subclinical hypothyroid had premature delivery. When hormonal treatment was sufficient and adequate, 100% of overt hypothyroid patients and 90.5% of subclinical hypothyroid patients carried the pregnancies to term, with no miscarriages. Miscarriages, premature and term deliveries in patients who were euthyroid (normal thyroid function) on hormone replacement therapy at the time of conception were respectively 4%, 11.1% and 84.9%.

During pregnancy, there is a substantially increased need of thyroid hormones and a substantial risk that previously unnoticed subclinical or latent hypothyroidism will progress to overt hypothyroidism.
Interestingly, another important finding of the researchers was that among patients taking hormone therapy for hypothyroidism prior to conceiving, almost 70% had to increase their dose during pregnancy.
Overall, the researchers concluded that the success of a pregnancy doesn't depend on whether the hypothyroidism was overt or subclinical, but primarily on receiving adequate treatment.

There is consensus on the need to treat subclinical hypothyroidism of any magnitude in pregnant women and women who are contemplating pregnancy, to decrease the risk of pregnancy complications and impaired development in utero of the offspring. And the risks are even higher in presence of elevated anti-thyroid antibodies.
According to endocrinologists, a woman with evidence of thyroid disease symptoms, however small they may be, without elevation of anti-thyroid antibodies, but even more in the presence of elevated antibodies (signing autoimmune Hashimoto's thyroiditis), will find it hard to get and/or maintain a pregnancy if her TSH level is higher than 2 mIU/L, optimally between 1 and 2.

Dr. Elizabeth Vleit, founder of the women's medical center "Her Place", at All Saint's Hospital in Fort Worth, Texas, and author of Screaming to be Heard: Hormonal Connections Women Suspect… and Doctors Ignore, writes: "All the symptomatic patients along with significantly elevated thyroid antibodies and normal TSH, have to be treated with thyroid hormone in order to feel normal… A woman may experience the symptoms of thyroiditis months to years before TSH goes up".


Levothyroxine, the thyroid hormone replacement, whose trade names are Eltroxine, Euthyrox, Levoxyl or Synthroid, is the preferred treatment for the majority of doctors. It is used for the management of primary hypothyroidism and secondary/central hypothyroidism.

Guidelines treatment
In primary hypothyroidism, treatment is monitored with the well-being of the patient, suppression of symptoms, and restoration of thyroid function with a TSH within reference range. Ideal target for TSH level should be, approximately, of 1.0 – 1.5 mIU/L. TSH levels below 0.3 mIU/L, or even lower, without signs of hyperthyroidism are quite good, and do not mean that the posology has to be reduced. Most physicians only rely on TSH level to determine their patients' "proper" dose of thyroid replacement. Free T4 and T3 should be always measured. Unless free T4 and free T3 values are factored into the clinical picture, the true cellular delivery of thyroid medication is not known. Ideal target for T4 and T3 levels should be within the upper third of their ranges.
For most patients, the initial dose of levothyroxine is 50 mg per day and then increased or lowered after the first blood test after 6 to 8 weeks, not before, according to clinical and laboratory response to treatment. The weekly dose is often calculated by the physician and is used to better adjust and allocate the dosage. Treatment should be initiated at a lower daily dose in elderly patients, patients with coronary artery disease and in patients with long-standing severe hypothyroidism.

In patients with central hypothyroidism (low TSH), treatment is tailored according to free T4 and T3 levels which should be maintained in the upper half of the normal range. Monitoring of TSH has no interest here. Other pituitary hormones should be evaluated in patients with central hypothyroidism.

In patients with persistently symptoms and/or elevated TSH despite an apparently adequate dose of levothyroxine, poor compliance, malabsorption and the presence of drug interactions should be checked, and a search for adrenal insufficiency (adrenal fatigue). But other therapeutic options should be offered. They will be detailed later.

Levothyroxine is a synthetic form of the thyroid hormone thyroxine (T4). Synthetic T4 is identical to that produced in the human thyroid gland. The fact that levothyroxine T4-only (as monotherapy) remains the current standard for management of hypothyroidism is based on a widely held assumption that the body, according to its needs, will convert T4 to the biological active form T3. Based on this assumption, most general practitioners and endocrinologists believe that the normalization of TSH with a T4-only preparation demonstrates adequate tissue levels of thyroid hormone. If some hypothyroid patients will do fine on it, many others will have only partial or temporary relief of their symptoms.
Many published studies show that a significant percentage of patients taking T4-only hormone continues to suffer from various thyroid symptoms, some very serious, despite the normalization of TSH levels. That means the condition is not being optimally managed. The doctors have no alternative but to prescribe, among other drugs, antidepressants, tonics, or counseling psychotherapy.

When closely examined, the manner in which patients with hypothyroid symptoms are conventionally treated correlates poorly with the underlying physiology. Many published reports show that the TSH level does not correlate with various tests of tissue metabolism, and, consequently, that TSH level is a poor indicator of thyroid function.

The symptoms of low thyroid, which are numerous and variably expressed, can be related to any organ or system in the body, and partly depends on the person's genes. Each organ tissue controls locally its own thyroid metabolism. For example, the brain has one mechanism for controlling the amount of thyroid hormone available to the brain but it is different from other tissues such as the liver. There are many mechanisms by which each tissue controls the amount of thyroid hormone which gets into its cells. One mechanism involves the deiodination of thyroid hormones. There is an enzyme in the cell which deiodinates T4 and makes the active T3 (taking off one iodine from thyroxine T4). These enzymes are called deiodinases. Every tissue has different types of deiodinases. To just give you one example: if you starve animals and study the deiodinases in the brain and liver, you find that the activity of the brain deiodinases go up by 10 times while at the same time the liver deiodinases activity goes down - not up. This mechanism is obviously meant to preserve the functioning of the brain under starvation conditions and not metabolize too much thyroid hormone in the liver. Therefore the control of thyroid metabolism is in every individual tissue. The problem with this is: if a tissue needs more thyroid hormone (such as the brain with depression), there is no way for the brain to signal the thyroid that it needs more sent up to it. The thyroid merrily goes on putting out the same amount of thyroid hormone. So the patient can have symptoms related to low thyroid hormone in the brain (for example) but the thyroid doesn't do anything about it. The pituitary gland not being at all aware of such a special request from the brain, the TSH level remains where it is. But if you give thyroid hormones in an adequate dose, the brain symptoms will disappear. Meanwhile the other tissues and organs adapt to the increased circulating hormones that you have used to fix the brain with. The adaptation of the tissues to different levels of circulating hormones has been shown in the literature.

Now let's see what does the pituitary gland. The pituitary cells, which have TSH in them, are the most sensitive cells in the body towards circulating thyroid hormone levels. The TSH production in the pituitary gland which is stimulated by local active hormone T3 production (in the pituitary gland itself), does not necessarily reflect peripheral conversion from T4 to T3 in other tissues. Studies have shown that normalization of plasma TSH and T4 with T4-only preparations (levothyroxine) procures adequate tissue levels of T3 to only a few tissues, including the pituitary gland (therefore normal TSH), but almost all other tissues are deficient. That explains why TSH levels can normalize when symptoms reflect improper conversion of T4 outside of the pituitary gland. This explains why TSH level is a poor indicator of thyroid function and, therefore, the normalization of TSH does not indicate an optimal therapeutic dose of levothyroxine. So, when those general practitioners and endocrinologists treat hypothyroidism by following the TSH and seeking to make it normal, the pituitary cells are happy, but it will lead to what their patients remain inadequately treated.

Making tissue metabolism normal should be the goal of all treatment with hypothyroid patients. Studies have also demonstrated that it is almost impossible to achieve normal tissue levels of T3 by giving T4-only preparations unless supra-physiological levels of T4-only are given (indicating doses in excess of those normally produced by the body, which are TSH-suppressive doses). I will discuss later. The authors conclude: "The current replacement therapy of hypothyroidism should no longer be considered adequate… It is no surprise that the majority of patients on T4-only preparations will continue to suffer from symptoms of hypothyroidism despite they have been told that their TSH levels were normal".

Symptoms remaining are the key to treatment. In most cases, patients may be helped by a more appropriate thyroid hormone dosage or form. But we do not succeed to get rid of all the symptoms, or prevent the progression of the disease, if is ignored a critical parameter, which I will describe now.

Hypothyroidism is caused by an autoimmune disease
One of the biggest challenges facing those with hypothyroidism is that the standard of care for thyroid disorders is hopelessly inadequate. Patients with thyroid disorders and the practitioners who treat them believe that a single substance, levothyroxine, a synthetic thyroid hormone (Elthroxine, Euthyrox, Synthroid) will magically reverse the course of the disease. It's should be just a question of proper dosage. Unfortunately, in the vast majority of cases this approach is not effective. Patients may get relief for a short period of time, but inevitable symptoms return or the disease progresses. What is the problem? The problem is that hypothyroidism is caused by an autoimmune disease.

Studies show that 90% of people with hypothyroidism are producing antibodies to thyroid tissue. This causes the immune system to attack and destroy the thyroid, which over time causes a decline in thyroid hormone production. This autoimmune form of hypothyroidism, called Hashimoto's disease, is the most common autoimmune disorder, affecting between 7-8% of the US population (including subclinical and overt hypothyroidism). While not all people with Hashimoto’s have hypothyroid symptoms, thyroid antibodies have been found to be a marker for future thyroid disease.

Most doctors know hypothyroidism is an autoimmune disease. But most patients don't. The reason doctors don't tell their patients is simple: it doesn't affect their treatment plan. Most of them don't even look for antibodies. It is true that the underlying cause of immune system disorder is unknown, and therefore cannot be treated. But doctors mistakenly believe that conventional and non-conventional medicine has no immune-stimulating treatments that fight against autoimmune diseases. This does not belong, moreover, to their therapeutic arsenal. They only know of immunosuppressive therapies. In the case of Hashimoto's disease, side effects from the use of immunosuppressive drugs are more harmful than the potential benefits.

What patients with Hashimoto's disease need to understand (which includes the vast majority of patients with hypothyroidism), as well as their doctors, is that they do not have a problem with their thyroid gland, they have a problem with their immune system attacking the thyroid. This is crucial to understand, because when the immune system is out of control, it's not only the thyroid that will be affected.
Hashimoto's patients often manifest a poly-endocrine autoimmune pathology. This means that in addition to have antibodies to thyroid tissue, it's not uncommon for them to have antibodies to other tissues or enzymes, to mention celiac disease and type 1 diabetes.

The standard of care for a Hashimoto's patients is to simply wait until the immune system has destroyed enough thyroid tissue to classify them as hypothyroid, and then consider the appropriate time to give them thyroid hormone replacement, according to clinical and laboratory criteria for each doctor. Some common symptoms associated with their condition will often require additional drugs, such as depression, insomnia, insulin resistance, constipation, distal paresthesias (tingling in the extremities), or diffuse pain.
The treatment isn't going to work very well – or for very long. Hashimoto's disease can't be treated successfully with hormone replacement therapy without addressing the autoimmune component.

Let me take a closer look at why thyroid hormone treatment doesn't work, or stops working overtime. In Hashimoto's autoimmune thyroiditis the body attacks itself. The body's immune responses to this self-attack by the immune system causes prolonged inflammation and subsequent tissue destruction. And inflammation has a profound effect on all aspects of thyroid metabolism and physiology: inflammation causes hypothalamus-pituitary-thyroid axis disruption, decreased thyroid receptors function, and decreased conversion of T4 to T3 (Click Here).

Most synthetic hormone medications on the market are levothyroxine T4 preparations (Eltroxine, Euthyrox, Synthroid). They only increase the levels of thyroid hormones (usually T4, and possibly T3) in the blood. No matter how much we give a T4 medication to someone with inflammation, it's not going to restore a suppressed hypothalamus-pituitary-thyroid axis, improve receptor function, or increase conversion of T4 to T3. The only way to do that is to address the problem at its root by regulating the immune system by an immune-stimulating treatment, and thus decrease inflammation. Then, giving supra-physiological dose of T4 preparation may do the job or may not be necessary. More often, in my experience, giving immune stimulating treatment will help reducing the usual dose of T4 medication.

Of course, the levothyroxine (T4) is necessary, but it is one piece of the puzzle. And patients who don't convert, or not enough, T4 to T3 will do better on adding T3 medication (I'll talk about later) to their T4 medication, or on bio-identical medication containing both natural T4 and T3 (in a 4.22:1 ratio). Most people who don't do well with T4-only medication have problems converting T4 to T3. If T4 synthetic hormone is the standard treatment in mainstream medicine, the two other treatment protocols just mentioned have greater effectiveness to my opinion:

  • Both synthetic T4 and time-released T3 administered simultaneously in combination;
  • Desiccated thyroid extract, an animal-based thyroid extract. It is also a combination therapy, containing natural forms of T4 and T3 (ratio 4.22:1). It also contains calcitonin, T1 and T2, which are not present in synthetic hormone medications.

In addition, certain minerals, other pieces of the puzzle, are required to activate the enzyme 5' - deiodinase necessary to convert T4 to T3. Selenium and zinc play a crucial role in the conversion process, and many hypothyroid individuals are deficient in one of them or in both (Click Here).

As I have mentioned previously, routine thyroid testing should include thyroid antibodies, even in absence of evident low thyroid symptoms. It must be systematic after 50 years old or after menopause. These autoantibodies, characteristic of Hashimoto's thyroiditis, can exist in the body for many years before causing damage to the thyroid or altering the levels of thyroid hormones, and drastic change in sexual hormones in pre-menopause and menopause can trigger for an increased immune system activity. Autoantibodies are not inactive in the body. Anyway, elevation of thyroid antibodies tells the thyroid is in progress of thyroid failure, yet with no signs of clinical failure or TSH elevation. Conventional or non-conventional immune-modulating or stimulating treatments should be right away given to try to prevent, as much as possible, the onset of the disease. Such treatments exist. I prescribe them in my clinic; they will not be given in this presentation.

What means TSH-suppressive dosages of thyroid hormone?
When doctors who treat their patients with T4-only preparations are content to maintain a blood level of TSH in the normal reference values (TSH up to 5.0 mIU/L in the upper unmodified standard limit), it is common to have persisting symptoms, some light, others debilitating. Those patients are told that their remaining symptoms have nothing to do with their thyroid, thus all kind of symptomatic treatments are being prescribed. The rigid adherence to bring TSH to the so-called "normal range" does not show whether a patient has enough circulating T3 to maintain normal metabolism in cells.
We saw earlier that the ideal target for TSH should be, approximately, of 1.0 to 1.5 mIU/L.
A given person may need higher or lower dosage of thyroid hormone T4 in order to feel well and to function optimally. This proper dose, which allows a complete elimination of symptoms, may end up with a TSH lab very low below range (TSH < 0.5 or TSH < 0.3 in the new range), and not one hint of hyperthyroidism. That is what we call TSH-suppressive dosages of thyroid hormone.

Most physicians, including endocrinologists, believe that a slumped TSH, for example at 0.1 or 0.01 mIU/L, is an indication that the dose of thyroid hormone should be reduced (except with thyroid cancer). "These are doctors that think that ink spots on a piece of paper tell the truth more than symptoms… Don't let doctors hold you hostage to lab results! [Source: The Thyroid Madness, mistakes patients make – or their doctors make for them!]
One study showed that 80% of the time, a dose of levothyroxine that produced a suppressive effect of TSH does not cause a hyperthyroid state, or, in other words, that the TSH-suppressive dose of levothyroxine was no indication within 80% of the time that the patient was overdosed in hormone replacement.

Dr. Lowe has found that TSH-suppressive dosages of levothyroxine can also reduce a patients' risk for disease. Lower dosages of levothyroxine have been found to be associated with progression of coronary atherosclerosis, and higher dosages (including TSH-suppressive dosages) associated with a halting of the progression. In his studies, Dr. Lowe has extensively tested patients and determined that there is nothing harmful to patients in having their TSH suppressed by these dosages of thyroid hormone. Dr. Lowe believes the hypothyroid patient has two options: "She can submit to using a replacement dosage of thyroid hormone and remain symptomatic, thus risking premature death from cardiovascular disease, or she can find a physician who will completely ignore her TSH level and find a dosage of thyroid hormone that produces normal tissue metabolism".

Thyroid replacement therapy: No risk of osteoporosis
Hypothyroidism itself is not considered a risk factor for osteoporosis. Only hyperthyroidism (excess thyroid hormone in the blood) affects bone density. But too much thyroid hormone replacement given to hypothyroid patients can have similar effects to naturally occurring hyperthyroidism. (Click Here)

A study released in June, 2000, at the World Congress on Osteoporosis in Chicago, Illinois, presented by Dr. Martin Stenstrom of the University of Gothenburg in Sweden, found that taking levothyroxine does not increase the risk of osteoporosis, but must be carefully monitored to ensure levels do not become too high (study on more than 750 women, over an 18 months period).

An October, 1998 study reported on in the Journal of gynecological Endocrinology found that levothyroxine TSH-suppressive therapy, if carefully carried out and monitored, has no significant effect on bone mass (Gyneco Endocrinal 1998 Oct;12(5)333-7, "Bone mineral density in premenopausal women receiving levothyroxine suppressive therapy.")


OPTIMIZING MEDICATION: slow-release compounded T3

Unsatisfactory health condition in number of hypothyroid patients, even well balanced with levothyroxine (T4) in term of serum TSH levels (TSH within reference norm), is due mostly to an insufficient availability of T3 in one or several peripheral tissues.
Functional hypothyroidism occurs when T4 metabolism produces an excess of reverse-T3 in relation to T3 free (T4 normally produces T3 and reverse-T3 in equal quantity). Reverse-T3 which has no biological activity, ties up to thyroid receptors, acting as an antagonist to T3 at the receptor levels. As well, when reverse-T3 reaches high levels, it further inhibits, especially in the liver, the 5'- deiodinase enzyme, needed for T4 conversion to T3 (thus, reverse-T3 creates a retro-inhibition on T3 free production). Consequently, no thyroid metabolism is stimulated, or not enough by the remaining active T3. Reverse-T3 must be displaced and replaced by the proper biological active T3 if metabolism is to normalize. In most cases, however, this is made almost impossible by a T4-only therapy, since, as a result of what has been said, much of this exogenous T4 (which contains only T4 - at the risk of repeating myself) will have its conversion to T3 itself hampered. Thus, with a T4-only therapy, the body will not have a sufficient source of replacement of T3 against excessive reverse-T3 in the circulation and in the cellular receptors (free T3 is not originally from the thyroid gland, but the result of the conversion of T4) - unless you give a supra-physiological dose of T4-only, as we have seen. It is the reverse-T3 that contributes largely to create all the symptoms of hypothyroidism.

In an article published in the International Journal of Pharmaceutical compounding, Vol.9 No. 4 July/August 2005, Martin Milner, ND, Center for Natural Medicine, Inc. Portland, Oregon, writes: "In absence of adequate biologically active T3, symptoms of hypothyroidism remain, despite an adequate level of T4 in the serum and a normal TSH level. Since most of the conversion of T4 into T3 happens in the cells, serum levels of free T3 and reverse-T3 may be normal even when T3 and reverse-T3 levels are not in balance. It is as though the cells are starving for biological active T3 in the midst of plenty. Unfortunately the "plenty" is plenty of T4 and reverse-T3 rather than the essential biologically active T3… Many patients continue to suffer with hypothyroid symptoms even though they are taking T4 medication [Euthyrox or Synthroid]. Their blood levels of TSH and T4 are normal, yet symptoms persist".

Dr. Lowe writes: "I have found that many hypothyroid patients also have cellular resistance to thyroid hormone. Most of these patients don't benefit much from T4 alone, but some of them do from desiccate thyroid (T4/T3 combination), presumably because of the relative high T3 content. Some we have to switch to synthetic T3 because they don't benefit from desiccate thyroid. We've stopped altogether giving patients T4 alone."

It was recognized that some hypothyroid patients do not get a good resolution of their symptoms or condition of well-being with a monotherapy levothyroxine (T4-only) and prefer a combined T4/T3 therapy or T3-only monotherapy. The dosage of the hormones in T4/T3 preparations respects their physiological ratio. Some doctors opt for adding to Euthyrox or Synthroid a slow-release compounded T3 with escalating doses until the symptoms disappear completely.

In my daily practice, with years of experience in the field, and brought to treat together fibromyalgia and hypothyroidism frequently associated, I widely use combination therapies (T4/T3), monotherapy slow-release compounded T3-only or adding it to Euthyrox or to Synthroid.

Advantage of the T3 therapy
The slow-release compounded T3 contains a sustained-release agent (HPMC) which allows its prolonged liberation during the day. This mode of action releases each time a dose of T3 which has a short duration of action, with a peak that occurs after 1 to 2 hours. This repeated immediate biological availability for the cellular metabolism provides its interest. The half-life of T3 oral medication is 0.75 days (whether it is immediate or slow-release), while the half-life of T4 medication is 6.7 days (which allows, sometimes, to be given only 6 or 5 days a week) (Click Here).

T3 adjunctive treatment of depression
Many anti-depressant treatments of depression have been found to work better with the addition of thyroid hormone T3. This benefit for depression treatment is true even when the patient has no thyroid deficiency.
An article published in Am J Psychiatry 158, 1617-1622, October 2001, American Psychiatric Association, concluded on the efficacy of T3 in accelerating clinical response to tricyclic antidepressants in patients with non-refractory depression. Furthermore, indicating that women may be more likely than men to benefit from this intervention.
This concerns as well women suffering from fibromyalgia, which are often given antidepressants, especially tricyclic (amitriptyline: Elatrolet, Elatrol), as first-line treatment, and even more those with hypothyroidism frequently associated to fibromyalgia. In these cases, added T3 therapy may be of a great help.

In addition, psychiatric studies have shown that treating hypothyroidism with T3 in addition to conventional T4 can markedly improve mental function and reduce depression in hypothyroid patients.

T3 therapy, Fibromyalgia and Chronic Fatigue Syndrome
Signs and symptoms of fibromyalgia resemble those of hypothyroidism although most fibromyalgic patients have normal thyroid function tests results (euthyroidism).
A study has shown effectiveness and safety of T3 therapy for euthyroid fibromyalgia: a double-blind placebo-controlled response-driven crossover study [John C. Lowe, MA, DC, Richard L. Garrison, MD, Alan J. Reichmann, MD, Jackie Yellin, BA, Mervianna Thompson, RN, MSN, APN, Daniel Kaufman, MD: Clinical Bulletin of Myofascial Therapy, 2(2/3):31-58, 1997]. Results suggest that euthyroid fibromyalgia is a clinical phenotype of partial peripheral resistance to thyroid hormone.

As I have already demonstrated, fibromyalgia (as well as chronic fatigue syndrome) is an auto-immune disease. Fibromyalgia alone or associated with auto-immune hypothyroidism (which is often the case) will greatly benefit from an immune-modulating or stimulating therapy, together with T3 long-acting medication. The same efficiency protocol will be given for chronic fatigue syndrome alone or associated with auto-immune hypothyroidism (Click Here).

T3 therapy, resistance to leptin, and obesity
Evidence was made a large number of overweight patients or obese have a metabolic problem rather than a problem of willpower or lifestyle. Treatment resistance to leptin is focused on treating the elevated leptin. Because there is poor T4-to-T3 conversion, and increase conversion to reverse T3 (antagonist to T3 active hormone), time-released T3 is the optimal treatment. It is true that giving thyroid hormone to lose weight is not appropriate, but that's not what we are doing, here we are correcting a hormonal deficiency. The higher the reverse T3, the lower is the metabolism, and many such individuals have a metabolism that is 20 to 40% lower than expected for their body mass index. The higher the reverse T3, the more ineffective T4-only preparations will be. Until the metabolic abnormalities are addressed, diet and exercise will certainly fail to achieve long-term success. Most patients have been on numerous diets, including a low-carbohydrate diet, and lifestyle changes may have result in initial weight loss, but temporary; patients are prone to regaining weight unless the reverse T3 issue is addressed.

A French team (Stephanie Decherf, Barbara Demeneix et al Laboratory Evolutions of Endocrine Regulations – Musée d'histoire naturellle and CNRS) showed that thyroid hormone T3 represses the expression of a key gene whose mutations are one of the causes of obesity in humans.

T3 therapy and Wilson's Temperature Syndrome (WTS)
The term "Wilson’s syndrome" was coined in 1990 by E. Denis Wilson, a US physician. Not to be confused with Wilson's disease, a medically recognized condition caused by a defect in copper metabolism. Wilson’s (temperature) syndrome, also called Wilson’s thyroid syndrome or WTS, is a medicine concept which is not recognized as a medical condition by mainstream medicine. Its supporters describe Wilson's syndrome as a mix of various common and non-specific symptoms which they attribute to low body temperature and impaired conversion of T4 to T3, despite normal thyroid function tests. The Wilson's protocol (WT3) involves the use of supra-physiological cycling dosing of sustained release T3 (long-acting T3) in order to reset low basal body temperature. The treatment has created a controversy, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels (without bothering to measure them also), the WT3 therapy can be used to regulate metabolism despite normal thyroid hormone levels. The sustained release T3 (SR-T3) prescription is based exclusively on low body temperature and presentation of symptoms.

The syndrome's manifestations include fatigue (persistent or relapsing fatigue), anxiety, irritability, depression, headaches, insomnia, muscle aches, decreased memory and concentration, low sex drive, unhealthy nails, easy weight gain, overall lack of well-being, and many other symptoms such as hair loss, fluid retention, pre-menstrual syndrome. Wilson wrote that the syndrome can manifest itself as "virtually every symptom known to man". These symptoms resemble those of conventionally recognized hypothyroidism and of fibromyalgia (FMS) and chronic fatigue syndrome (CFS), except that WTS requires low body temperature as diagnostic of WTS.

Although WTS does not require the strict definition of fatigue lasting for more than 3 months (which defines the CFS), it still appears that in most cases WTS is indistinguishable from CFS, except that WTS includes patients who have mild fatigue and it does not require other symptoms to be present at the same time. CFS includes sometimes fever as one potential temporary symptom, while WTS requires low body temperature. It is known that hypothyroidism includes cold intolerance, and CFS patients often self-report low range average body temperatures, although not always noted clinically.

Body temperature is controlled by an elaborate thermoregulatory system that modulates heat production and heat loss so that the core temperature is maintained within a narrow range. The thermoregulatory center of the brain is located in the pre-optic region of the anterior hypothalamus. Due to daily circadian variations, normal body temperature fluctuates from a lowest of 36.1˚C (97˚F) between 2:00 and 6:00 a.m. and a highest on 37.8˚C (100˚F) between 5:00 and 7:00 p.m.

Since many factors can affect the thermoregulatory control, many patients who have low body temperature do not suffer from WTS. Low body temperature in itself is not diagnostic of WTS, without a minimum of one accompanying symptom. However, low body temperature appears in the WTS as a biological marker that consistently and predictably improves under treatment during the progression of the disease state to the recovery of health.

The use of medication for T3 patients with euthyroid hypo-metabolic state (low metabolism state with normal thyroid function) has been described in the early 1950s. The euthyroid hypo-metabolism has been described as a set of very similar to CFS symptoms and includes fatigue, lethargy, irritability, cognitive impairment, headache and musculoskeletal pain in the absence of any known underlying cause and normal TSH. Studies by Kurland (not me), Sonkin, Title and Morton reported the effectiveness of synthetic hormone therapy T3 (liothyronine sodium) to eliminate hypo-metabolic symptoms.

Wilson says that low body temperature hypothyroid symptoms in the presence of normal thyroid function tests are not due to hypothyroidism, although the hypothesis of impaire conversion of T4 to T3 has been issued. To distinguish this condition from hypothyroidism, he named it Wilson's temperature syndrome. He states that it is especially brought on by stress, and can persist after the stress has passed. He says that the main diagnostic sign is an oral body temperature that averages below 98.6 °F (37.0 °C), and that the diagnosis is confirmed if the patient responds to a few months treatment with SR-T3. He says that certain herbs can also help support normal body temperatures.
Current medical literature is identifying euthyroid patients who exhibit hypothyroid symptoms as thyroid resistance (resistance to thyroid hormone). Not only is it possible that the conversion thyroid problem (T4 to T3) might occur, but there is evidence that thyroid resistance might well be a secondary response to the initial trigger causing CFS. Thyroid resistance shares many of the same symptoms as CFS, including, among others, headaches, anxiety, fatigue, and recurring sore throats.

Chronic Fatigue Syndrome (CFS) shares many features with fibromyalgia syndrome (FMS). The predominance of pain or fatigue is the primary means of distinguishing between these two syndromes. Studies found that supra-physiological doses of T3 produced significant improvement in all measured FMS parameters, including measurement of tender point sensitivity, Visual Analog Scale measurement of symptom intensity.

Immune system defect is now known to be involved in certain amount of CFS and FMS patients. The etiological cause is still not known. However, it is hypothesized that it might be due to decreased thyroid function. Thyroid resistance has been associated with increased infections, such as chronic sore throats.
Stress stimulates the hypothalamic-pituitary-adrenal axis which leads to increased levels of cortisol. Increased levels of cortisol inhibit thyroid function, and low thyroid function has shown to affect cortisol levels.

In conclusion, CFS/WTS might have a variety of causal factors that compromise immune system such as stress or other insults that come from virus, bacteria (I have already discussed in this presentation), toxics, or other triggering agents that upset the body's normal functioning. After the initial insult to the body, CFS/WTS symptoms remain, perhaps due to thyroid hormone resistance or peripheral thyroid hormone conversion problems.
Regardless of the mechanism, WT3 therapy seems to restore metabolism to the vast majority of patients. Body temperature is used in determining dosage and cycle length. I will not detail the protocol. Once symptoms improve or resolve, patients are able to wean off SR-T3 therapy, temperature been normalized. According to studies, patients often report no return of symptoms after the treatment has been discontinued. Some patients do relapse, but a very short cycle of SR-T3 will bring them back to normal. Patients whose oral temperatures are not successfully raised to or near 37˚C (98.6˚F) seem to retain less benefit from treatment.
It is known that high doses of exogenous T3, as it is the case in the Wilson's protocol (i.e. supra-physiological doses of T3), suppress T4 levels due to negative feedback inhibition of TSH. It is speculated that T4 suppression is an important effect of the Wilson's protocol that is essential to its effectiveness.
Based on clinical observations, many patients are completely freed of fatigue, depression, muscles aches and other complaints related to WTS.

Adverse reactions to liothyronine sodium (SR-T3) are generally due to therapeutic over-dosage, and thus are characterized by typical symptoms of hyperthyroidism (e.g., tachycardia, irritability, nervousness, and increased bowel motility). In rare instances, allergic skin reactions have been observed in patients taking liothyronine sodium.

If I took the time to detail Wilson's syndrome, it is not because it is unknown to most doctors and patients, but because of useful information on euthyroid hypo-metabolism despite symptoms of hypothyroidism, on thyroid hormone resistance, and their relationships with fibromyalgia and chronic fatigue syndrome. It also recalls, in many ways, all that has been said all along this presentation. It also confirms the effectiveness of treatment with extended-release T3, which does not deserve to be demonstrated.
But the American Thyroid Association stated in 2005 that "a thorough review of the medical literature has found no scientific evidence supporting the existence of Wilson's Syndrome". The statement added that many of the symptoms described by Wilson are nonspecific and rather typical of depression, anxiety, and psychological and social stress. It also notes that a similar set of symptoms occurs in the alternative diagnoses of neurasthenia, chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, chronic Epstein-Barr virus syndrome, and chronic candidiasis. Finally, the Association notes that supplementation with such high doses of SR-T3 prescribed in the Wilson's protocol is particularly difficult and problematic.
The Mayo Clinic website similarly warns that Wilson's syndrome is not an accepted medical diagnosis, and advises patients against this therapy associated with the "syndrome". But doctors formed to the protocol express its effectiveness, and hundreds of practitioners are using it of over the world (I am not among them).



Hashitoxicosis, other thyroiditis, and goiter
If a patient with Hashimoto's thyroiditis has a temporary phase of Hashitoxicosis (hyperthyroidism condition), a beta-blocker medication may be given to decrease palpitations and reduce shakes and tremors. As symptoms improve, the medication is tapered off since the thyrotoxic phase is transient. Anti-thyroid medications are not used for the thyrotoxic phase since the thyroid is not overactive (this hyperthyroidism is due to leaking hormones stocked in the inflamed thyroid gland), by some doctors do give anti-thyroid medications, such as Carbimazole, alone or together with a beta-blocker.

Patients with chronic lymphocytic Hashimoto's thyroiditis may present a goiter. Although a feeling of tightness in the neck is common, thyroid pain and tenderness are rare and suggest an alternative diagnosis of subacute granulomatous thyroiditis (painful De Quervain's thyroiditis), other forms of thyroiditis, or even malignancy, this latter especially if associated with rapid or asymmetric growth of goiter or cervical lymphadenopathy. Patients with subacute thyroiditis may respond dramatically to a short course of corticosteroids, whereas those with painful Hashimoto's thyroiditis may have only temporary or no benefit at all. Some patients with painful Hashimoto's respond to Levothyroxine and aspirin, whereas others may require surgical intervention for unremitting pain.

How is postpartum thyroiditis treated?
Treatment depends on the phase of thyroiditis and degree of symptoms that the patients exhibit. Women presenting with thyrotoxicosis (the hyperthyroid phase) is treated like it has just been mentioned.
The hypothyroid phase is often treated with thyroid hormone replacement. If the hypothyroidism is mild, and the patient has few, if any, symptoms, no therapy may be necessary. If thyroid hormone therapy is begun, treatment should be continued for approximately 6-12 months and then tapered to see if thyroid hormone is required permanently. It is always important to try do discontinue thyroid hormone after postpartum thyroiditis, since 80% of patients will remain normal thyroid function. However, normal TSH with tested positive thyroid antibodies means that the thyroid is in process of failing at any time. Some doctors, in such cases, call for a light treatment even if the patient is asymptomatic; they are right.

Treating the elderly and patients with heart disease
Thyroid dysfunction is common in elderly patients, with most having subclinical hypothyroidism. Elderly patients, particularly people with heart conditions, should start with very low doses of thyroid replacement, and be closely monitored.

Adrenal fatigue and hypothyroidism
Adrenal insufficiency, if present, needs to be rectified prior to initiating thyroid hormone replacement. Thyroid replacement in the setting of adrenal insufficiency may precipitate adrenal crisis. Drug of choice for the treatment of adrenal insufficiency are hydrocortisone, cortisone, and prednisolone.
Adrenal fatigue and estrogen dominance are very similar in their symptom presentation and share a lot in common. Most women who have one tend to have the other to some degree. Fixing adrenal function and estrogen dominance go hand-in-hand and it is therefore difficult to fix one while ignoring the other.

I have already mentioned that, according to endocrinologists, a woman with overt or subclinical hypothyroidism will find it hard to conceive at higher TSH's than 1 or 2 mIU/L.
Women who have hypothyroidism before becoming pregnant may need to increase their dose of levothyroxine during pregnancy.
Women who are first diagnosed with overt or subclinical hypothyroidism during pregnancy should be treated immediately, with quick acceleration to therapeutic levels. There are no risks to the developing baby when the pregnant woman takes appropriate doses of thyroid hormones. The pregnant woman with hypothyroidism should be monitored regularly and doses adjusted as necessary.
At any time, before conceiving or during pregnancy an immune stimulating therapy should be given in presence of anti-thyroid antibodies. It may treat infertility or help getting pregnant, it will help maintain pregnancy. The therapy is safe for the mother and the baby, and is well tolerate.

Levothyroxine (T4) or prolonged action T3 preparations taken during breastfeeding have no adverse effects on the infant. So, if such treatments are necessary to the mother, there is no reason to discontinue breastfeeding.

Treatment of central hypothyroidism
The management of central hypothyroidism is complicated by the fact that the TSH cannot be used to monitor therapeutic response to levothyroxine therapy. Only a free T4 level helps to adjust the replacement dose. As in primary hypothyroidism, when appropriately treated, management of central hypothyroidism can result in prompt resolution of symptoms.
Patients who have hypothyroidism caused by a pituitary tumor may need surgery. However, surgery may not cure the hypothyroidism. Patients still may need thyroid replacement.

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