Hypothyroidism
Clinically serious low thyroid function will exhibit oral temperature as low as 93°F on rising from sleep, with symptoms of sluggishness and mild depression.
Causal Factors [B]
The two most common causes of hypothyroidism are chronic lymphocytic thyroiditis (Hashimoto’s disease), an autoimmune form of thyroid condition, and iatrogenic causes due to radioactive iodine.
Autoimmune Disease [C]
Autoimmune disorders, such as chronic lymphocytic thyroiditis, are the most common cause of thyroid problems in the United States. Also known as Hashimoto’s disease, chronic lymphocytic thyroiditis commonly begins between the ages of 30 and 50. It affects women more often than men (8:1), and often causes a goiter. Approximately 20% of patients have symptoms of hypothyroidism when first diagnosed, while for the majority hypothyroid, symptoms will follow the goiter. Other forms of autoimmune disease may exist concomitantly with Hashimoto’s thyroiditis, such as Addison’s disease, rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, and pernicious anemia.
Iatrogenic [C]
Treatments for hyperthyroidism, such as thyroidectomy, Iodine 131 therapy, and antithyroid drugs, are common causes of hypothyroidism. Other prescribed agents that may block thyroid hormone synthesis include lithium carbonate, oral hypoglycemic agents, 6-mercaptopurine, P-aminosalicylic acid (PAS), amiodarone (antiarrhythmic, antianginal), tricyclic antidepressants, and interferon. Drugs associated with altered peripheral conversion of T4 to T3 include dexamethasone (corticosteroid), propylthiouracil, lopanic acid (radiographic contrast agent), amiodarone, and propanolol (beta blocker).9
Secondary Hypothyroidism [C]
Pituitary disease can be caused by tumors, surgery, radiation therapy, or Sheehan’s syndrome. Each of these causes a decrease in pituitary gland size and functioning. When the pituitary gland gets smaller as the result of tumors, surgery, or radiation, it cannot produce enough thyroid-stimulating hormone (TSH). Sheehan’s syndrome occurs when there is necrosis (cell death) of the pituitary gland typically related to childbirth in women.
Tertiary Hypothyroidism [C]
Just as the pituitary gland releases TSH to tell the thyroid gland to produce thyroid hormone, there is a hormone released from the hypothalamus, an area in the brain that tells the pituitary gland to release parathyroid hormone. Although it is rare, there is sometimes a problem with the hypothalamus, in which thyrotropin-releasing hormone is not released. This can be caused by radiation to the brain, trauma to the head, or other conditions that affect the hypothalamus.
Peripheral Hypothyroidism [C]
Decreased conversion of T4 to T3, excess reverse T3, or thyroid hormone resistance can result in a peripheral hypothyroidism, in which the thyroid gland is functioning normally but the cells experience a lack of active thyroid hormone.
Other Pathologies [C]
Certain diseases that affect the connective tissues in the body (for example, sarcoidosis, amyloidosis, and scleroderma) can affect the thyroid gland as well. When these diseases reach the thyroid gland, they add tissue (typically connective tissue) that is different from thyroid gland tissue, which ends up taking the place of the thyroid gland tissue. The connective tissue that replaces the thyroid gland tissue does not have the ability to produce thyroid hormone.
Congenital Disease [C]
Although it is rare, approximately 1 in 5,000 babies are born with a malfunctioning thyroid gland or no thyroid gland at all.
Postpartum Thyroiditis [C]
Fluctuating thyroid function after childbirth is common (5% to 10% of patients in some studies) and was first described in the 1970s. Thyroid inflammation may occur several months after childbirth, resulting in the development of clinical hyperthyroidism. In some patients, the hyperthyroid phase will be associated with significant damage to the thyroid as a consequence of the inflammation, and hence the hyperthyroid phase will be followed by the development of hypothyroidism.
Organophosphate Pesticides [C]
Organophosphate pesticide levels correlate with endocrine pathologies. Organophosphate pesticides have shown to decrease TSH levels, free T4, and free T3. They also increased adrenocorticotropic hormone and cortisol levels. Hexachlorobenzene (HCB), a commonly used pesticide, is highly lipophilic and accumulates in fat tissue. In a study performed at the Environmental and Respiratory Unit in Spain, it was found there was a negative association between serum HCB concentrations and total T4 levels (a decrease of .32 microg/dl per each unit, 1 ng/ml). These results suggest there is an effect on thyroid function. It could also be a contributing factor to peripheral metabolism of thyroid hormones. The importance of eating organic foods cannot be overemphasized for endocrine health.10
Toxic Metal Exposure [C]
Exposure to toxic metals, such as cadmium, mercury, and lead, can result in altered thyroid hormone metabolism. Researchers have concluded that heavy metal toxicity damages antioxidant enzyme systems that protect cell membranes from lipid peroxidation. Increased lipid peroxidation in the presence of heavy metals can affect thyroid gland function and peripheral conversion of thyroid hormones.11
Stress [C]
Low thyroid function often is triggered after trauma or grief and may act as a coping mechanism for a stressful situation. In critical illnesses and stressful situations, drugs and chemicals can alter the functions of neurotransmitters, which consequently affect pituitary hormone secretion. Even changes in serum cortisol within normal range can cause significant alterations in thyroid hormone levels.12
Nutrition [C]
Fasting or deficiency of vitamins (riboflavin, niacin A, E), minerals (Se, I, Fe, Zn, K), or amino acids (cysteine, tyrosine) can lead to hypothyroidism.13 Conversely, excess consumption of certain foods, known as goitrogens, can induce hypothyroidism. These include brassicas (cabbage, kale, brussel sprouts, mustard, cauliflower), rutabagas, peanuts, turnips, peaches, pears, spinach, and soy.14
Lifestyle [C]
Aerobic exercise, full spectrum light, and stress management all seem to support proper thyroid function and peripheral conversion. Conversely, stress, sleep deprivation, and excess alcohol intake appeared to impair thyroid hormone function.15
Signs and Symptoms [B]
Subclinical hypothyroidism refers to patients who exhibit typical hypothyroid symptoms of cold intolerance and fatigue. They have normal levels of thyroxine, while slightly elevated TSH levels. Patients can also have normal thyroid tests and exhibit hypothyroid symptoms; this is identified as Wilson’s Temperature Syndrome.
Common signs of moderate to severe hypothyroidism include hypertension, bradycardia, coarse hair, periorbital swelling, yellow skin due to elevated beta carotene, delayed relaxation of deep tendon reflexes and surprisingly carpal tunnel syndrome. Physical exam will reveal an enlarged, normal or small, but firm consistency of the thyroid. However although less common there can also be variety of other concomitant symptoms such as megacolon, cardiomegaly, and congestive heart failure. There is one documented case in which a heart transplant was not needed after simply taking thyroid hormone replacement alone.
Post-partum hypothyroidism occurs transiently after pregnancy, accounting for 5% to 10% of patients, while 20% of women over age 50 years have subclinical hypothyroidism indicated by normal levels of T3, and T4, and mild elevated TSH. Subclinical hypothyroid needs to be treated not only for symptomatic relief but also due to its close association with hypercholesterolemia and cardiac abnormalities.
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F/S
Hypothyroid Symptoms
- Fatigue
- Cold intolerance
- Depression
- Weight gain
- Weakness
- Joint aches
- Constipation
- Dry skin
- Hair loss
- Menstrual irregularities
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Testing [C]
There is only one diagnostic test needed in screening for primary thyroid disease, TSH levels. TSH is the single most sensitive indicator of thyroid function in the non-stressed state. Thyroid antibodies, an indicator of autoimmune thyroid disease, help to predict clinical hypothyroidism. However, currently there is no lab test for peripheral function of thyroid hormones, except symptoms and low body temperature. Many patients who have Wilson’s Temperature Syndrome will exhibit adrenal insufficiency and low blood pressure commonly found in chronic fatigue syndrome and fibromyalgia syndrome.
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F/S
Deficiencies Leading to Hypothyroidism
by Impairing T3 to T4 Conversion
- Trace Minerals: selenium, iodine, iron, zinc
- Vitamins: vitamin A, B2, E
- Amino Acids : cysteine, tyrosine
- Energy Compounds: glucose ATP, NAD, NADH-O2
- Nutrition fasting, starvation, anorexia, protein calorie malnutrition, lack of hydrocarbons, lack of fats (severe deficiency)
- Hormones: GH, TSH, insulin, FSH, melatonin, prolactin
- Environmental pesticides
Excesses Leading to Hypothyroidism
- Trace Minerals cadmium, lithium, copper (impair T3-T4 conversion)
- Nutrition high soy diets (impair T3-T4 conversion)16, 17
- Hormones estrogen dominance18, stress hormones: catecholamines, ACTH, cortisol,vasopressin, angiotensin II, glucagon, rT3
- Medications beta-blockers, propyl-thiouracil PTU, theophylline,
- clomipramine, amiodarone, chemotherapeutic agents,
- Phenytoin, röntgen contrast products19
- Toxins alcohol, digestive toxins: cholera, botulinum, candida, cyanide, thiocyanate20
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Conventional Medical Treatment [SH]
Often Armour thyroid (desiccated bovine thyroid tissue) or Synthroid is prescribed. However, the use of a holistic approach, with an understanding of the effects of the peripheral metabolism of thyroid hormones, may reduce or eliminate the need for drugs.
Naturopathic Medical Treatment and Prevention [SH]
Botanical Medicine [C]
Ashwagandha (Withania somnifera): Studies have been conducted to investigate the effects of ashwagandha on thyroid and liver function. Mice given high doses (1.4g/kg) of the root extract showed significant increases in serum levels of T3 and T4. Furthermore, the extract was shown to reduce hepatic lipid peroxidation significantly while increasing the activity of superoxide dismutase and catalase. These results indicate that ashwagandha stimulates both thyroid and hepatic antioxidant activity.21-23
Kelp: Seaweed therapy (kelp) at 5 g per day seems to help relieve many of the symptoms of iodine remineralization and strengthens the thyroid gland. Clinically, we have seen it to be useful but not curative for most patients, although one other colleague reported excellent results. TSH may respond after 2 to 4 months with 5g per day. It is also helpful in patients with thyroidectomies and as an adjunctive treatment with thyroid hormone replacement. It contains weak hormone activity with the compound di iodotyrosine.24
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Selected Clinical Studies and Literature Reviews
For a study of thyroid dysfunction and the use of seaweed therapy, see Ryan Drum, “Thyroid Function and Dysfunction,” in Selected Clinical Studies and Literature Reviews, pp. xx – xx.
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Clinical Nutrition [C]
Tyrosine: This amino acid attaches to iodine atoms to form active thyroid hormones. Low plasma tyrosine levels have been associated with hypothyroidism, low blood pressure, low body temperature, and restless leg syndrome.
Iodine: Anywhere between 150 mg to 50 mg daily can be prescribed. Hypothyroid symptoms can often decrease quickly with simply the use of this element.25
Selenium: Selenium is used for the formation of selenocysteine. This trace mineral has been shown to have strong effects on peripheral thyroid function because it is the cofactor for hepatic 5’-deiodinase. Selenium has been found to influence metabolism of thyroid hormones positively. In a randomized clinical trial of 24 critically ill patients, parenteral supplementation of 500 mcg of sodium selenite b.i.f. for week 1, then 500 mcg daily for two weeks, and 100 mcg for week three, free T3 levels were restored. Selenium supplementation also has been shown to decrease thyroid peroxidase levels in Hashimoto’s disease.26,27
Triiodothyronine (SR-T3): One specific thyroid hormone, sustained release triiodothyronine (SR-T3), has gained popularity in the complementary and alternative medical community in the treatment of fatigue, with a protocol (WT3) pioneered by Dr Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6°F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson’s Temperature Syndrome (WTS).
Although there have been clinical studies historically using T3 in patients who are euthyroid based on normal TSH values, the use of T3 in clinical practice, specifically the WT3 protocol, has gained significant popularity in the alternative medicine community. This treatment has created a controversy in the conventional medical community, however, 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, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms.
Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression, and cognitive dysfunction.28 Low body temperature, depression, and chronic fatigue indicate a hypometabolic state not unlike that of hypothyroidism.29-30 WT3 therapy may well re-establish normal functions.
