The Thyroid Gland

The Thyroid gland is one of the largest endocrine glands. The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage (which forms the laryngeal prominence, or ‘Adam’s Apple’) and at approximately the same level as the cricoid cartilage.

The butterfly shaped thyroid gland is composed mainly of spherical sacs called follicles, the walls of which produce two important hormones, Triiodothyronine (T3) and Thyroxine (T4), collectively known as thyroid hormones (TH). T3 and T4 are synthesized from both iodine and tyrosine.

Almost every cell in the body has receptors for TH and it has widespread effects. The thyroid gland is unusual among endocrine glands as it can store large quantities of hormones, maintaining about 100 days’ supply of TH. The thyroid gland also produces calcitonin from para-follicle cells located between the follicles. An important effect of this hormone is to inhibit the loss of calcium from bones into the blood. It is most important in childhood, when skeletal growth is rapid.

Thyrotropin-releasing hormone (TRH) from the hypothalamus and the thyroid stimulating hormone (TSH) from the pituitary stimulates the production and release of thyroid hormone. Blood levels of thyroid hormone feed back to the pituitary and hypothalamus to stimulate or inhibit activity. Malfunctions of the hypothalamus and pituitary feedback loop can inhibit proper thyroid hormone production.

The thyroid gland controls how quickly the body uses energy, makes proteins, and controls how sensitive the body should be to other hormones.

Thyroid hormones are involved in the following processes in the body:

Basic metabolic rate (BMR)

    TH increases BMR by stimulating the conversion of fuels (glucose and fats) to energy in cells. When BMR increases metabolism of carbohydrates fats and proteins increases

Temperature regulation

    TH stimulates cells to produce and use more energy which results in more heat being given off raising body temperature.

Carbohydrate and fat metabolism

    TH promotes the use of gluclose and fats for energy, and enhances cholesterol turnover, thus reducing cholesterol

Growth and development

    TH acts with growth hormone and insulin to promote normal development of the nervous system in fetuses and infants, and normal growth and maturity of the skeleton

Reproduction

    TH is necessary for normal development of the male reproductive system. TH also promotes normal female reproductive ability and lactation.

Heart function

    TH increases heart rate and force of contractions of the heart muscle, and enhances sensitivity of cardiovascular system to signals from the sympathetic nervous system.

Aging affects both the production of the body’s hormones and the way in which target organs respond to them. Output and responses to thyroid hormones which control the body’s metabolism may decline with age alongside a loss of muscle tissue, which uses more energy than fat areas. This means that metabolic rate decreases with age so the body burns fewer calories. Unless this is counteracted by exercise to increase muscle, older people can develop a susceptibility to rise in body fat levels.

The function of the thyroid gland is to take iodine, found in many foods, and convert it into T4 and T3. Thyroid cells are the only cells in the body which can absorb iodine. These cells combine iodine and the amino acid tyrosine to make T3 and T4. T3 and T4 are then released into the blood stream and are transported throughout the body where they control metabolism (conversion of oxygen and calories to energy). Every cell in the body depends upon thyroid hormones for regulation of their metabolism. The normal thyroid gland produces about 80% T4 and about 20% T3, however, T3 possesses about four times the hormone “strength” as T4.

While iodine is important for thyroid function, too much iodine could be harmful to thyroid function. A minimum of 60 micrograms of elemental iodine per day is required to make thyroid hormone. Humans have the ability to conserve the iodine within their bodies if there is a deficiency of iodine consumed in foods.

The thyroid gland is under the control of the pituitary gland. When the level of thyroid hormones (T3 & T4) drops too low, the pituitary gland produces Thyroid Stimulating Hormone (TSH) which stimulates the thyroid gland to produce more hormones. Under the influence of TSH, the thyroid will manufacture and secrete T3 and T4 thereby raising their blood levels. The pituitary senses this and responds by decreasing its TSH production.


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Hypothyroidism

Hypothyroidism is when the thyroid gland does not produce enough thyroid hormones. Hypothyroidism can affect women, men, teenagers, children and infants. Hypothyroidism is also hereditary. An estimated 2 million people worldwide have a thyroid condition. This estimate may be low due to be misdiagnosis and incorrect testing done by the mainstream medical community.

Causes of Hypothyroidism

Hashimoto’s thyroiditis is the most common cause of hypothyroidism. Hashi’s is an autoimmune disorder that occurs when your immune system produces antibodies that attack your own tissues.

In third world countries iodine deficiency is the number one cause of hypothyroidism.

Exposure to radiation from dental and medical x-rays.

Radiation therapy used to treat cancers of the head and neck can affect your thyroid gland.

Treatment for hyperthyroidism. People who produce too much thyroid hormone (hyperthyroidism) are often treated with radioactive iodine (RAI) or anti-thyroid medications to reduce and normalize their thyroid function. However, in some cases, treatment of hyperthyroidism can result in permanent hypothyroidism. RAI can also affect other organ and gland in the body. Please see the section on hyperthyroidism.

Surgical removal of all or a large portion of your thyroid gland can diminish or halt hormone production. In that case, you’ll need to take thyroid hormone for life. Any kind of thyroid surgery is not recommended unless it is the last resort.

A number of medications can contribute to hypothyroidism.

      Amiodarone, a heart drug
      Antithyroid drugs like propylthiouricil and methimazole
      Lithium, for psychiatric treatment
      Propranolol, a beta blocker
      Phenytoin and Carbarnazepine – to treat epilepsy
      Some antidepressants
      Interferons and interleukins – to treat hepatitis, MS and other conditions
      Chemotherapy – sunitinib (Sutent), imatinib (Gleevec)

Other medical conditions – Hemochromatosis, scleroderma and amyloidosis.

Congenital disease – Approximately 1 in 3,000 babies in the United States is born with a defective thyroid gland or no thyroid gland at all. In most cases, the thyroid gland didn’t develop normally for unknown reasons, but some children have an inherited form of the disorder. Often, infants with congenital hypothyroidism appear normal at birth. Most states now require newborn thyroid screening.

Hypopituitarism

Pregnancy – Some women develop hypothyroidism during or after pregnancy (postpartum hypothyroidism), often because they produce antibodies to their own thyroid gland. See the section on pregnancy.

A number of foods can contribute to hypothyroidism. These foods are called goitrogens because they can trigger the enlargement of the thyroid (a goiter) as well as hypothyroidism. They block the conversion of T4 hormone to T3, the active form of thyroid hormone. This is not a complete list.

      Almond seeds
      Brussels sprouts
      Cabbage
      Cauliflower
      Corn
      Kale
      Turnips
      Soy
      Broccoli
      Rutabaga
      Mustard greens
      Spinach
      Peaches
      Pears
      Strawberries
      Radishes
      Millet
      African cassava

Symptoms

      Depression
      Cold hands
      Weight gain
      Cold feet
      Feeling cold all over
      No stamina
      Constipation
      Planter Fasciitis
      Thinning eyebrows especially on the outside
      Dry hair
      Aching joints
      Dry skin and/or cracking skin
      Losing hair on head and body
      High blood pressure
      Low blood pressure
      High cholesterol
      Diabetes Type 1 and Type 2
      PMS
      Fatigue
      Osteoporosis
      Sleep apnea
      Air hunger
      Foggy thinking
      Carpal tunnel
      Ringing in the ears
      Forgetfulness
      Low body temperature
      Fluid retention
      Broken and/or peeling fingernails
      Acne Varicose veins
      Tightness in your throat
      Swelling of the throat
      Dysphasia
      Suicidal thoughts
      No sex drive
      No menstrual cycle
      Infertility
      Irregular menstrual cycles
      Lack of motivation
      Moodiness
      Lactose intolerance
      Acid reflux
      Puffy face
      Sluggishness
      Pale skin
      Goiter

Testing

The basic tests that should be run to determine hypothyroidism are:

  • TSH – to check for possible pituitary issues (low iron will also suppress TSH even with low thyroid levels as will low cortisol)
  • Free T4 (FT4) – the stored thyroid hormone
  • Free T3 (FT3) – the active thyroid hormone
  • TPO anti-bodies (thyroid peroxidase) – to check for Hashimoto’s TgAb (thyroglobulin antibodies)

You will also need to get a complete iron panel with ferritin. See the section on iron.

Just because your lab results are in range does not mean that they are okay and that you do not have hypothyroidism.

TSH is a pituitary hormone and not a good indicator of thyroid function. The TSH test was manufactured by Abbott labs, the makers of Synthroid.

The TSH is inversely correlated with pituitary T3 levels. With physiologic stress, depression insulin resistance, diabetes, aging, dieting, inflammation and numerous other conditions this may increase pituitary T3 levels. Pituitary T3 levels are often associated with diminished cellular and tissue T3 levels and increased reverse T3 levels. The pituitary is both anatomically and physiologically unique, reacting differently to inflammation and physiologic stress than every other tissue in the body. The conditions above stimulate local mechanisms to increase pituitary T3 levels (reducing TSH levels) while reducing T3 levels in the rest of the body. Thus, with physiologic or emotional stress, depression or inflammation, the pituitary T3 levels do not correlate with T3 levels in the rest of the body. Thus TSH is not a reliable or sensitive marker of an individual’s true thyroid status.

TSH when taking desiccated thyroid or T3 only will be suppressed.

Your FT4 results should be no higher than half the range. A higher FT4 would indicate an RT3 (reserves T3) issue or a hyper swing if you have Hashimotos’s. A very low FT4 result would indicate a cortisol issue. This would be true whether or not you are taking desiccated thyroid. Your FT3 results should be at the top of the range. A higher FT3 would indicate a Hashimoto’s swing or T3 pooling. T3 pooling is when the T3 pools in serum and does not get into the cells. This happens when you have a cortisol issues or iron issue or both. This could be either high or low cortisol or iron. When taking desiccated thyroid your FT3 should be at the top of the range or a little over. When taking T3 only your FT3 should be over range.

If you have TPO anti-bodies then you have Hashimoto’s. If you’re antibodies are low, then they are probably not attacking your thyroid, but it is important to know that you have the antibodies and to treat accordingly.

If you find that you have TPO antibodies, then you should also test for food sensitivities and celiac disease.

Treatment

The best medication on the market for treating hypothyroidism is desiccated thyroid. This would include Armour, Nature-throid, ERFA, Thyroid-S. Desiccated thyroid contains all the hormones that your own thyroid would produce. These hormones are T4, T3, T2, T1 and calcitonin.

Desiccated thyroid is started at one grain, and increased by ½ grain every 7 to 10 days, based on symptoms. Once you have reached three grains, you want to hold your dose they are for 4 to 6 weeks to allow the T4 to building your system. After 4 to 6 weeks new thyroid labs should be done.

Cytomel is the brand name for T-3. T-3 only is used when one has a RT3 issues. Please see the section on RT-3.

Myxedema psychosis, more colloquially known as myxedema madness, is a relatively uncommon consequence of hypothyroidism, such as in Hashimoto’s thyroiditis or in patients who have had the thyroids surgically removed and are not taking Desiccated Thyroid Hormones.

A chronically under-active thyroid can lead to slowly progressive dementia, delirium, and in extreme cases to hallucinations, coma, or psychosis, particularly in the elderly.

Thyroid hormone replacement therapy with desiccated thyroid in these patients usually reverses the psychotic symptoms, but may not help with cognitive deficits caused by changes in metabolic activity in the central nervous system.

The “myxedema” part of the name simply refers to the non-pitting edema common to hypothyroidism.

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Hashimotos Thyroiditis

Overview

Hashimoto’s thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease, which means that the body’s immune system attacks it own healthy cells and tissues. This leads to inflammation, which leads to an underactive thyroid gland or hypothyroidism.

The immune system makes antibodies that attack cells in the thyroid and interfere with their ability to produce thyroid hormone. Large numbers of white blood cells called lymphocytes accumulate in the thyroid. Lymphocytes make the antibodies that drive the autoimmune process.

Physiologically, antibodies against thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Hashimotos’s was the first disease to be recognized as an autoimmune disease. It was discovered by a Japanese specialist Hakaru Hashimoto.

Symptoms

  • Mania
  • Sensitivity to heat and cold
  • Paresthesia
  • Panic attacks
  • Tachycardia
  • Reactive Hypoglycemia

Also see sections on Hypothyroidism and Hyperthyroidism

Testing

The basic test that should be run to determine hypothyroidism are:

  • TSH – to check for possible pituitary issues (Low iron will also suppress TSH even with low thyroid levels as will low cortisol)
  • Free T4 (FT4) – the stored thyroid hormone
  • Free T3 (FT3) – the active thyroid hormone
  • TPO anti-bodies (thyroid peroxidase) – to check for Hashimoto’s
  • TgAb (thyroglobulin antibodies)

Also needed is a complete iron panel with ferritin. See the section on iron.

Just because your labs results are in range does not mean that they are okay and that you do not have hypothyroidism.

Treatment

Desiccated thyroid is probably the best treatment for Hashimoto’s, unless reverse T3 has risen too high due to hyper swings. Then synthetic T3 only may be the better choice. You may have to raise your desiccated thyroid faster than someone who has central hypothyroidism. The purpose of raising desiccated thyroid faster is to stop the attack on your thyroid. Increasing thyroid hormones will help rebuild your immune system and stop the attack.

The hyper/hypo swings associated with Hashimoto’s can be difficult and in some cases a person will just have to ride these out until they have taken enough desiccated thyroid to suppress TSH and stop the attack.

A person can have both Hashimoto’s and Graves’ disease.

Myxedema psychosis, more colloquially known as myxedema madness, is a relatively uncommon consequence of hypothyroidism, such as in Hashimoto’s thyroiditis or in patients who have had the thyroids surgically removed and are not taking Desiccated Thyroid Hormones.

A chronically under-active thyroid can lead to slowly progressive dementia, delirium, and in extreme cases to hallucinations, coma, or psychosis, particularly in the elderly.

Thyroid hormone replacement therapy with desiccated thyroid in these patients usually reverses the psychotic symptoms, but may not help with cognitive deficits caused by changes in metabolic activity in the central nervous system.

The “myxedema” part of the name simply refers to the non-pitting edema common to hypothyroidism.


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T3 Pooling

What is Thyroid pooling? This is when the thyroid hormone T-3 collects or pools in the blood and does not get into the cells.

How does T3 Pool? The cause of T-3 pooling can be any one of the following or a combination of the following:

  • High cortisol
  • Low cortisol
  • High iron
  • Low iron
  • Medications
    • beta blockers
    • Amiodarone
    • Iodinated contrast media
    • Lithium

How do I stop my T-3 from pooling? By addressing or taking care of the reason for the pooling. You will also have to decrease your thyroid medication. This is done to avoid a thyroid dump.


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Thyroid Dump

What is a thyroid dump? This is when the T-3 that has been pooling is released into your cells.

What does a thyroid dump feel like? The symptoms will vary from person to person.

  • A feeling of speediness
  • High heart rate
  • Anxiety
  • Heart palpitations
  • Insomnia
  • Nervousness
  • trembling hands
  • manic

These symptoms can be either mild or extreme.

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Hyperthyroidism

Overview

Hyperthyroidism is when your thyroid makes too much T4 and T3. This is also know as overactive thyroid.

Causes

  • Getting too much iodine
  • Graves’ disease (accounts for most cases of hyperthyroidism)
  • Inflammation (thyroiditis) of the thyroid due to viral infections or other causes
  • Noncancerous growths of the thyroid gland or pituitary gland
  • Taking large amounts of thyroid hormone
  • Tumors of the testes or ovaries

Symptoms

  • Difficulty concentrating
  • Fatigue
  • Frequent bowel movements
  • Goiter (visibly enlarged thyroid gland) or thyroid nodules
  • Heat intolerance
  • Increased appetite
  • Increased sweating
  • Irregular menstrual periods in women
  • Nervousness
  • Restlessness
  • Weight loss (rarely, weight gain)

Other symptoms that can occur with this disease:

  • Breast development in men
  • Clammy skin
  • Diarrhea
  • Hair loss
  • Hand tremor
  • Weakness
  • High blood pressure
  • Itching – overall
  • Lack of menstrual periods in women
  • Nausea and vomiting
  • Pounding, rapid, or irregular pulse
  • Protruding eyes (exophthalmos)
  • Rapid, forceful, or irregular heartbeat (palpitations)
  • Skin blushing or flushing
  • Sleeping difficulty

Testing

  • TSH – to check for possible pituitary issues (low iron will also suppress TSH even with low thyroid levels as will low cortisol)
  • Free T4 (FT4) – the stored thyroid hormone
  • Free T3 (FT3) – the active thyroid hormone
  • TPO anti-bodies (thyroid peroxidase) – to check for Hashimoto’s
  • TSI (thyroid stimulating immunoglobulin) to check for Graves’

Treatment

How the condition is treated depends on the cause and the severity of symptoms. Hyperthyroidism is usually treated with one or more of the following:

  • Antithyroid medications
  • Radioactive iodine (which destroys the thyroid and stops the excess production of hormones) See the section on RAI.
  • Surgery to remove the thyroid. See section on thyroidectomy.

If the thyroid must be removed with surgery or destroyed with radiation, you must take thyroid hormone replacement pills for the rest of your life.

Beta-blockers are used to treat some of the symptoms, including rapid heart rate, sweating, and anxiety until the hyperthyroidism can be controlled. Beta blocker interfere with the conversion of T4 to T3.

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Graves’

Overview

Graves’ disease is an autoimmune disorder that leads to over activity of the thyroid gland (hyperthyroidism).

Graves’ ophthalmopathy

About half the people with Graves’ disease show some signs and symptoms of a condition known as Graves’ ophthalmopathy. In Graves’ ophthalmopathy, inflammation and other immune system events affect muscles and other tissues around the eyes. The resulting signs and symptoms may include:

  • Bulging eyes
  • Excess tearing
  • Dry, irritated eyes
  • Gritty sensation in the eyes
  • Pressure or pain in the eyes
  • Puffy eyelids
  • Reddened or inflamed eyes
  • Light sensitivity
  • Double vision
  • Limited eye movements, resulting in a fixed stare
  • Blurred or reduced vision (rare)
  • Ulcers on the cornea (rare)

Graves’ dermopathy

An uncommon manifestation of Graves’ disease, called Graves’ dermopathy, is the reddening and thickening of the skin, most often on your shins or the top of your feet.

Causes

Graves’ disease is the most common cause of hyperthyroidism. It is caused by an abnormal immune system response that causes the thyroid gland to produce too much thyroid hormones. Graves’ disease is most common in women over age 20. However, the disorder may occur at any age and may affect men as well.
Symptoms

  • Anxiety
  • Breast enlargement in men (possible)
  • Difficulty concentrating o Double vision
  • Eyeballs that stick out (exophthalmos)
  • Eye irritation and tearing
  • Fatigue
  • Frequent bowel movements
  • Goiter (possible)
  • Heat intolerance
  • Increased appetite
  • Increased sweating
  • Insomnia
  • Menstrual irregularities in women
  • Muscle weakness
  • Nervousness
  • Rapid or irregular heartbeat (palpitations or arrhythmia)
  • Restlessness and difficulty sleeping
  • Shortness of breath with exertion
  • Tremor
  • Weight loss (rarely, weight gain)

Testing

  • TSH – to check for possible pituitary issues
  • Free T4 (FT4) – the stored thyroid hormone
  • Free T3 (FT3) – the active thyroid hormone
  • TPO anti-bodies (thyroid peroxidase) – to check for Hashimoto’s
  • TSI (thyroid stimulating immunoglobulin) to check for Graves’

Treatment

The purpose of treatment is to control the overactivity of the thyroid gland.

Beta-blockers don’t inhibit the production of thyroid hormones, but they do block the effect of hormones on the body. They may provide fairly rapid relief of irregular heartbeats, tremors, anxiety or irritability, heat intolerance, sweating, diarrhea and muscle weakness.

Beta blockers include:

  • Propranolol (Inderal)
  • Atenolol (Tenormin)
  • Metoprolol
  • Nadolol (Corgard)

Beta blockers aren’t often prescribed for people with asthma, because the drug may trigger attacks. The drug may also complicate management of diabetes. Abruptly discontinuing the use of the drug can cause serious heart problems.

Hyperthyroidism is usually treated with one or more of the following:

  • Antithyroid medications
  • Radioactive iodine
  • Surgery

Anti-thyroid medications interfere with the thyroid’s use of iodine to produce hormones. These prescription medications include propylthiouracil and methimazole (Tapazole).

When these two drugs are used alone, a relapse of hyperthyroidism may occur at a later time. Taking the drug for longer than a year, however, may result in better long-term results.

Anti-thyroid drugs may also be used before or after radioiodine therapy as a supplemental treatment.

Side effects of both drugs include rash, joint pain, liver failure or a decrease in disease-fighting white blood cells. Methimazole isn’t used to treat pregnant women because of the slight risk of birth defects. Therefore, propylthiouracil is the preferred anti-thyroid drug for pregnant women.

If you have radiation and surgery, you will need to take replacement thyroid hormones for the rest of your life, because these treatments destroy or remove the gland.

Some of the eye problems related to Graves’ disease usually improve when hyperthyroidism is treated with medications, radiation, or surgery. Radioactive iodine can sometimes make eye problems worse. Eye problems are worse in people who smoke, even after the hyperthyroidism is cured.

Sometimes prednisone (a steroid medication that suppresses the immune system) is needed to reduce eye irritation and swelling.

You may need to tape your eyes closed at night to prevent drying. Sunglasses and eye drops may reduce eye irritation. Rarely, surgery or radiation therapy (different from radioactive iodine) may be needed to return the eyes to their normal position.

Expectations (prognosis)

Graves’ disease often responds well to treatment. However, thyroid surgery or radioactive iodine usually will cause hypothyroidism. Without getting the correct dose of thyroid hormone replacement, hypothyroidism can lead to:

  • Depression
  • Mental and physical sluggishness
  • Weight gain
  • Antithyroid medications can also have serious side effects.

Complications
Complications from surgery, including:

  • Hoarseness from damage to the nerve leading to the voice box
  • Low calcium levels from damage to the parathyroid glands (located near the thyroid gland)
  • Scarring of the neck
  • Eye problems (called Graves’ ophthalmopathy or exophthalmos)
  • Heart-related complications, including:
  • Rapid heart rate
  • Congestive heart failure (especially in the elderly)
  • Atrial fibrillation
  • Thyroid crisis (thyrotoxic storm), a severe worsening of overactive thyroid gland symptoms
  • Increased risk for osteoporosis, if hyperthyroidism is present for a long time
  • Complications related to thyroid hormone replacement
  • If too little hormone is given, fatigue, weight gain, high cholesterol, depression, physical sluggishness, and other symptoms of hypothyroidism can occur
  • If too much hormone is given, symptoms of hyperthyroidism will return


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RT3

Overview

Reverse triiodothyronine (reverse T3, or RT3) is a molecule that is an isomer of triiodothyronine (T3). It is derived from thyroxine (T4) through the action of deiodinase.

RT3, unlike T3, does not stimulate thyroid hormone receptors. However, rT3 binds to these receptors, thereby blocking the action of T3. Reverse T3 (RT3) is what is made when the “wrong” iodine atom is removed from T4; it’s a “mirror image” molecule to T3 and is not bio-active. This in itself is not a problem, the problem is that in excess it fits into the T3 receptors and gets stuck there blocking the action of T3 on the body. This means that your body doesn’t respond properly to T3 leading to hypothyroid symptoms despite a within range TSH and within range T3 and T4 levels in the body. This is what we refer to as “Tissue Resistance to Thyroid Hormone”.

Causes

  • The prolonged use of T4 only thyroid meds – Synthroid, Levoxyl, Levothyroxine, Unithroid, Eltroxin, Levaxin, Norton, Eutrosig, Oroxine and others.
  • Beta Blockers
  • High iron
  • Low iron
  • High cortisol
  • Low cortisol
  • Amiodarone
  • Iodinated contrast media
  • Lithium
  • Under or improper treatment of Hypothyroidism
  • Long Term Illness including viral load
  • Glucose over 140
  • Low Calorie Diet
  • Below 30G daily Carbohydrate Diet

Symptoms

  • Continuing hypothyroid symptoms while on at least 3 grains of desiccated thyroid
  • See the section on hypothyroid symptoms
  • Free T4 labs results above midrange
  • Any time FT4 is higher in range than FT3 in it’s range
  • FT3 that will not rise in spite of increased natural thyroid

Testing

  • TSH – to check for possible pituitary issues (low iron will also suppress TSH even with low thyroid levels as will low cortisol)
  • Free T4 (FT4) – the stored thyroid hormone
  • Free T3 (FT3) – the active thyroid hormone
  • Reverse T3 (RT3) -
  • TPO anti-bodies (thyroid peroxidase) – to check for Hashimoto’s Thyroiditis
  • TgAb (thyroglobulin antibodies)

It is then the ratio of RT3 and FT3 that need to be determined. A ratio below 20 shows an RT3 issue.

You will also need to get a complete iron panel with ferritin. See the section on iron.

Treatment

Treatment for RT3 starts by addressing the reason for the RT3. This could mean altering cortisol, iron or medications.

The treatment for RT3 is Cytomel (T3) in slowly increasing doses until the T3 receptors have been cleared. The starting dose for T3 is usually 12.5 mcg divided into two dose (first thing in the morning and in the early afternoon) additional doses are add in 5 – 7 days so that you will eventually be dosing T3, four times day, 4 hours apart with the last dose at bedtime. Most will need between 75-100mcg of T3.

The body will not tolerate higher doses of T3 without the reason for RT3 being addressed.

Examples of How to Calculate FT3/RT3 and TT3/RT3 Ratios

Which example to use depends on the units of the test used by your lab. I have listed several common sets of units.

Free T3 and RT3

A healthy FT3/RT3 ratio is 20 or greater.

FT3 pmol/LRT3 pmol/L These results need to be changed so that the ratio is correct. Multiple FT3 by 1000 then divide the result by RT3.Ex. FT3 5.4, RT3 567(5.4 × 1000) ÷ 567 = 9.5
FT3 pmol/LRT3 nmol/L These results will give the correct ratio.  Divide FT3 by RT3.Ex. FT3 5.9, RT3 0.385.9 ÷ 0.38 = 15.5
FT3 pg/mLRT3 pg/mL These results need to be changed so that the ratio is correct. Multiple FT3 by 1000 then divide the result by RT3.Ex. FT3 2.6, RT3 258(2.6 × 1000) ÷ 258 = 10
FT3 pg/dLRT3 ng/dL These results will give the correct ratio. Divide FT3 by RT3.Ex. FT3 403, RT3 25, 403 ÷ 25 = 16
FT3 pg/dLRT3 pg/mL These results need to be changed so that the ratio is correct. Multiple FT3 by 10 then divide the result by RT3.Ex. FT3 397, RT3 474(397 × 10) ÷ 474 = 8.3
FT3pg/mL
RT3 ng/dL
These results need to be changed so that the ratio is correct. Multiple FT3 by 100 then divide the result by RT3.Ex. FT3 2.9, RT3 23(2.9 × 100) ÷ 23 = 12.6
FT3 pmol/L
RT3 ng/dL
These results need to be changed so that the ratio is correct. Divide FT3 by 0.0154 then divide the result by RT3.Ex. FT3 4.5, RT3 30.3(4.5 ÷ 0.0154) ÷ 30.3 = 9.6

Total T3 and Reverse T3

The ratio should be greater than 10 for T3/RT3.

T3 ng/dLRT3 pg/mL These results need to be changed so that the ratio is correct. Multiple T3 by 10 then divide T3 byRT3.Ex. T3 123, RT3 295(123 × 10) ÷ 295 = 4.2


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Thyroidectomy

What doctors do not tell you about thyroidectomy is that once they remove your thyroid you now have a life threaten condition. You will need to wear a medical alert bracket. You cannot live without thyroid hormones!!!!!

There are very few reasons to have a thyroidectomy and this should only be done as a very last resort.

These conditions are NOT a reason to have your thyroid removed

  • Goiter
  • Thyroid nodules
  • Hashimoto’s
  • Any kind of Hypothyroidism

Thyroidectomy may only be necessary in thyroid cancer and Graves’, but again only after all other treatment options have been tried.

Surgery-related complications, including:

  • Scarring of the neck
  • Hoarseness due to nerve damage to the voice box
  • Low calcium level due to damage to the parathyroid glands (located near or in the thyroid gland)

Myxedema psychosis, more colloquially known as myxedema madness, is a relatively uncommon consequence of hypothyroidism, such as in Hashimoto’s thyroiditis or in patients who have had the thyroids surgically removed and are not taking Desiccated Thyroid Hormones.

A chronically under-active thyroid can lead to slowly progressive dementia, delirium, and in extreme cases to hallucinations, coma, or psychosis, particularly in the elderly.

Thyroid hormone replacement therapy with desiccated thyroid in these patients usually reverses the psychotic symptoms, but may not help with cognitive deficits caused by changes in metabolic activity in the CNS.

The “myxedema” part of the name simply refers to the non-pitting edema common to hypothyroidism.

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RAI-RadioactiveIodine

Iodine-131 (131I), also called radioiodine (though many other radioactive isotopes of this element are known), is an important radioisotope of iodine. It has a radioactive decay half-life of about eight days. Its uses are mostly medical and pharmaceutical. It also plays a major role as a radioactive isotope present in nuclear fission products, and was a significant contributor to the health hazards from open-air atomic bomb testing in the 1950s, and from the Chernobyl disaster, as well as being a large fraction of the contamination hazard in the first weeks in the Japanese nuclear crisis. This is because I-131 is a major uranium, plutonium fission product, comprising nearly 3% of the total products of fission (by weight). I-131 is also a major fission product of uranium-233, produced from thorium.

Due to its mode of beta decay, iodine-131 is notable for causing mutation and death in cells that it penetrates, and other cells up to several millimeters away. For this reason, high doses of the isotope are sometimes less dangerous than low doses, since they tend to kill thyroid tissues that would otherwise become cancerous as a result of the radiation. For example, children treated with moderate dose of I-131 for thyroid adenomas had a detectable increase in thyroid cancer, but children treated with a much higher dose did not. Likewise, most studies of very-high-dose I-131 for treatment of Graves disease have failed to find any increase in thyroid cancer, even though there is linear increase in thyroid cancer risk with I-131 absorption at moderate doses. Thus, iodine-131 is increasingly less employed in small doses in medical use (especially in children), but increasingly is used only in large and maximal treatment doses, as a way of killing targeted tissues. This is known as “therapeutic use.

Iodine-131 can be “seen” by nuclear medicine imaging techniques whenever it is given for therapeutic use, since about 10% of its energy and radiation dose is via gamma radiation. However, since the other 90% of radiation (beta radiation) causes tissue damage without contributing to any ability to see or “image” the isotope, other less-damaging radioisotopes of iodine are preferred in situations when only nuclear imaging is required. The isotope I-131 is still occasionally used for purely diagnostic (i.e., imaging) work, due to its low expense compared to other iodine radioisotopes. Very small medical imaging doses of I-131 have not shown any increase in thyroid cancer. The low-cost availability of I-131, in turn, is due to the relative ease of creating I-131 by neutron bombardment of natural tellurium in a nuclear reactor, then separating I-131 out by various simple methods (i.e., heating to drive off the volatile iodine). By contrast, other iodine radioisotopes are usually created by far more expensive techniques, starting with reactor radiation of expensive capsules of pressurized xenon gas. Much smaller incidental doses of iodine-131 than are used in medical therapeutic uses, are thought to be the major cause of increased thyroid cancers after accidental nuclear contamination.These cancers happen from residual tissue radiation damage caused by the I-131, and usually appear years after exposure, long after the I-131 has decayed.

RAI will affect not only thyroid tissue, but any tissue in the body that used Iodine.

Precautions

Some precautions are necessary because of the small amount of radiation that emanates from the neck where the RAI is stored for a few days after treatment.

  • Avoid prolonged contact with others, especially children and pregnant women.
  • In general, a distance of one arm’s length should be maintained between the person treated and others who spend more than two hours next to the patient in any 24 hour period. This applies especially to children and pregnant women. While brief contact with a person after treatment is acceptable, sleeping together, watching television, going to movies, long care or plane trips should be avoided for approximately 11 days after the treatment.
  • Sharing food and utensils, including glasses, bottles, cans of soda, water, beer, etc., should also be avoided. Dishes and eating utensils should be rinsed before being put with those of the rest of the family. Paper plates and plastic utensils should only be used if they are immediately disposed of outside the home. Cooking is fine, as long as the utensil used to taste the food while cooking is not re-used before rinsing.
  • Drink lots of liquids, void often, and flush twice.
  • The treated person should drinks lots of liquids, especially water, to help remove the RAI from the system, flush the toilet twice after using it, and be sure to thoroughly clean up any spilled urine. Laundry need not be washed separately unless the treated person has sweated heavily, or soiled his or her clothing in some way.
  • No pregnancy or breast-feeding. Iodine is concentrated and excreted in breast milk.
  • Pregnant women should not be treated with RAI, and pregnancy should be avoided for six months following treatment.

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