If you suffer from fatigue, excessive moodiness, depression or other common complaints you could have a thyroid issue. The thyroid gland affects almost every aspect of health. It is the most common physical cause of depression. It controls your metabolic rate and can cause hair loss, skin changes, and weight gain.
Both low thyroid (hypothyroidism) and high thyroid (hyperthyroidism) are SYMPTOMS of underlying inflammation. Your thyroid “disease” may be a natural reaction, your body’s attempt to adapt and heal from infections (bacterial, viral, fungal or parasitic), a reaction to foreign proteins (allergies, environmental chemicals, food additives) or a “runaway” reaction to your own antibodies from fighting these invaders.
Note: Subclinical hypothyroid and even clinical hypothyroidism often will test as “normal.” Use of thyroid treatments and adjustment of dosage should always be based on how you feel, rather than a test level.
Hyperthyroidism is an autoimmune issue which must be closely monitored. If you experience unexplained weight loss, a rapid heartbeat, unusual sweating, swelling at the base of your neck or other symptoms associated with hyperthyroidism, see your doctor.
What can I do?
Western Medicine
Western physicians typically prescribe levothyroxine (T4, Synthroid®) as the only treatment. Many people have a poor response and do much better with a mixture of T4 and T3 (triiodothyronine, Cytomel), although you may need to “push” your physician. An alternative is to use natural desiccated thyroid (Armour® and others). Note: Do not take desiccated thyroid if your thyroid antibodies are elevated. These hormones are available by prescription, or through IAS (International Anti-aging Systems) of Great Britain. They can legally mail you up to 2 months of levothyroxine or desiccated thyoid, and have an excellent track record of safety and reliability.
Western Naturopathy
The Western Naturopathic approach to thyroid imbalance is to reduce hidden factors that affect the thyroid and stimulate metabolism. This means finding the underlying problems that are contributory, which can be as simple as iodine deficiency, and as complex as liver and digestive problems, autoimmune issues or liver problems.
Traditional Chinese Medicine
In Traditional Chinese Medicine, both hyperthyroidism and hypothyroidism are considered to be a Yin/Yang imbalance. In Chinese terms, when Yin is deficient it cannot control the Yang energy from escaping outward and upward, and this “reckless” movement of Yang brings about the characteristic symptoms of hyperthyroidism. When Yang is deficient, it simply cannot produce the vital energy necessary to keep the body functioning well, and symptoms of hypothyroidism result.
Three patterns of Yin Deficiency are differentiated for hyperthyroidism: Kidney Yin Deficiency with Excess Heat; Heart/Liver Yin Deficiency; and Heart/Kidney Yin Deficiency.
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Research
Acetyl-L-carnitine (ALC): ALC has been shown to be helpful with hyperthyroidism (J Clin Endocrinol Metab. 2001 Aug;86(8):3579-94), angina (Drugs Exp Clin Res 1991;17:225-35), congestive heart failure (Int J Clin Pharmacol Ther Toxicol 1988;26:217-20), heart attack (Postgrad Med J 1996;72:45-50; J Am Coll Cardiol 1995;26:380-7), kidney disease (J Am Soc Nephrol 2002;13:708-14), age related fatigue (Drugs Aging 2003;20:761-7), and sperm motility associated with infertility (Fertil Steril. 2004 Jun;81(6):1578-84). ADHD (Drugs Aging 2003;20:761-7). One study found that carnitine helps inattentive type ADHD but no hyperactive type (J Child Adolesc Psychopharmacol. 2007 Dec;17(6):791-802).
“L-carnitine is effective in both reversing and preventing symptoms of hyperthyroidism and has a beneficial effect on bone mineralization. Because hyperthyroidism depletes the body deposits of carnitine and since carnitine has no toxicity, teratogenicity, contraindications and interactions with drugs, carnitine can be of clinical use.” (J Clin Endocrinol Metab. 2001 Aug;86(8):3579-94). L-Carnitine, used with magnesium, reduces frequency and intensity of migraine headaches (Biol Trace Elem Res. 2012 Dec;150(1-3):42-8).
Bovine desiccated thyroid: Many people state that they have been helped with bovine thyroid, although reliable research is not available. Bovine thyroid is not strongly bio-active, although it may improve symptoms.
Glutathione: Glutathione plays important roles in antioxidant defense, nutrient metabolism, and regulation of cellular events (including gene expression, DNA and protein synthesis, cell proliferation and apoptosis, signal transduction, cytokine production and immune response, and protein glutathionylation). Glutathione deficiency contributes to oxidative stress, which plays a key role in aging and the pathogenesis of many diseases (including kwashiorkor, seizure, Alzheimer’s disease, Parkinson’s disease, liver disease, cystic fibrosis, sickle cell anemia, HIV, AIDS, cancer, heart attack, stroke, and diabetes). (J Nutr. 2004 Mar;134(3):489-92.)
Glutathione deficiency is associated with aging, age-related macular degeneration (Free Radic Biol Med 1998;24:699-704), diabetes (Metabolism 1998;47:993-7), lung and gastrointestinal disease (Ital J Gastroenterol Hepatol 1999;31:401-7), pre-eclampsia (Am J Obstet Gynecol 1993;169:1456-61; Obstet Gynecol 1998;92:1012-5), Parkinson’s disease and other neurodegenerative disorders (Ann Pharmacother 1995;29:1263-73; J Neural Transm 1997;104:661-77;Free Radic Biol Med 1999;27:515-20), and poor prognosis in AIDS (FASEB J 1997;11:1077-89; Proc Natl Acad Sci USA 1997;94:1967-72.
Guggul: Guggul is an extract of the gum resin of the Commiphora mukul tree, which is native to India. It thyroid-stimulating activity. It seems to increase T3 synthesis by increasing conversion of T4 to T3. Several rate studies show effectiveness, although reliable human research is not available. Anc Sci Life v.2(1); Jul-Sep 1982; Curr Ther Res 1999;60:220-7; Planta Med. 1988 Aug;54(4):271-7.
Iodine: Sufficient iodine is necessary form thyroid hormone synthesis. It is generally recognized as the most commonly preventable cause of goiter and primary hypothyroidism. Altern Med Rev. 2008 Jun;13(2):116-27. Iodine is often added to table salt, although the rising popularity of specialty salts (which are not iodized) and general decrease in salt intake may put many at risk of deficiency. Interestingly, “therapeutic” doses of iodine inhibit hormone biosynthesis and is sometimes recommended for hyperthyroidism. This use requires close medical supervision.
L-carnitine for Hyperthyroidism: Taking 2-4 grams per day of L-carnitine seems to significantly improve symptoms associated with hyperthyroidism such as palpitations, nervousness, and asthenia. It also seems to reduce elevated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), and ferritin elicited by thyroid hormone “L-carnitine is effective in both reversing and preventing symptoms of hyperthyroidism and has a beneficial effect on bone mineralization. Because hyperthyroidism depletes the body deposits of carnitine and since carnitine has no toxicity, teratogenicity, contraindications and interactions with drugs, carnitine can be of clinical use.” J Clin Endocrinol Metab. 2001 Aug;86(8):3579-94.
Selenium: Plays a role in thyroid function and your immune system needs selenium to work properly. You may have low levels of selenium if you smoke, drink alcohol, take birth control pills or have a condition that prevents your body from absorbing enough selenium such as Crohn’s disease or ulcerative colitis. (USDA).
Selenium 200 mcg/day has been shown to reduce inflammation with autoimmune thyroiditis (Hashimoto’s) J Clin Endocrinol Metab. 2002 Apr;87(4):1687-91.(1) Selenium has been shown to improve conversion of T4 to T3 Clin Sci (Lond). 1995 Dec;89(6):637-42.
Trimethylglycine (TMG): TMG supports methylation and provides glycine. Published research shows three specific benefits of enhancing methylation: (1) Methylation lowers dangerous homocysteine levels, thus lowering the risk of heart disease and stroke. (2) TMG converts homocysteine into methionine and, in the process, produces S-adenosylmethionine (SAMe). (3) SAMe has potent anti-aging effects, and has been shown to alleviate depression, remylenate nerve cells, improve Alzheimer’s and Parkinson’s disease patients, and protect against alcohol-induced liver injury. (lef.org, Am J Med Genet B Neuropsychiatr Genet. 2014 May 7). TMG has been shown to protect the pancreas from alcohol-mediated oxidative stress (Int J Vitam Nutr Res. 2009 Mar;79(2):79-86). DMG (the first metabolite of TMG) enhances both humoral and cell-mediated immune responses in humans (J Infect Dis. 1981 Jan;143(1):101-5). TMG significantly lowers cholesterol and low density lipoproteins (Eksp Klin Farmakol. 2012;75(1):16-8).
*Statements contained herein have not been evaluated by the Food and Drug Administration. The CHS Protocol and our products are not intended to diagnose, treat and cure or prevent disease. Information provided by CHS is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. Any information given is only intended as a sharing of knowledge and information from scientific world literature. You are encouraged to make your own health care decisions based upon your own research of the subject and in partnership with a qualified health care professional.
Thyroid dysregulation is common, with some studies reporting rates as high as 21% of women and 16% of men. Many more people suffer from “functional” hypothyroidism which goes undetected or untreated.
Both low thyroid (hypothyroidism) and high thyroid (hyperthyroidism) are SYMPTOMS of underlying inflammation. Your thyroid “disease” may be a natural reaction, your body’s attempt to adapt and heal from infections (bacterial, viral, fungal or parasitic), a reaction to foreign proteins (allergies, environmental chemicals, food additives) or a “runaway” reaction to your own antibodies from fighting these invaders.
What are the symptoms of thyroid dysfunction?
Energy: Your thyroid controls your energy level. You may fatigue easily, lose interest in trying new things or even in following your normal routine. You also might feel overly energetic for a time, although this often leads to feeling burned out.
Mood: You may feel sad and withdrawn; this feeling is often misdiagnosed as depression. Your physician or psychiatrist may diagnose you with depression and put you on antidepressants (without even testing your thyroid!) Anxiousness and nervousness are symptomatic of hyperthyroidism and sometimes occur with hypothyroid. Panic attacks are not unusual. Taking psychiatric drugs such as antidepressants, tranquilizers and antipsychotics (such as Abilify®) DO NOT fix the problem!
Weight issues: There is a complex relationship between thyroid and weight. You may experience weight loss or gain. You may have loss of appetite, and foods may taste differently, or you may feel constantly hungry.
Sleep: You may experience difficulty falling asleep or staying asleep. You may have such low energy that you sleep too much or need to nap during the day. You may be prescribed sleeping pills such as Ambien®. These DO NOT fix thyroid issues.
Brain Fog: Thyroid dysfunction affects your ability to think clearly (brain fog). It can impair your concentration and make you feel forgetful. Older persons may be misdiagnosed as having “impaired cognitive function” or even dementia and be given dementia drugs such as Aricept®. These chemicals will not help.
Sex hormones: Male and female sex hormones interact with thyroid and other hormones and thyroid dysfunction may cause or be caused by low testosterone, estrogen and progesterone and adrenal hormone imbalance. The result may be decreased libido sex drive), erectile dysfunction, uterine fibroids, and menstrual issues including cramps, irregular periods and heavy bleeding. If you have been diagnosed with fibroids be sure to discuss the thyroid connection with your gynecologist. If they seem hesitant or dismissive this could reflect poor or inadequate training.
Hair, skin and nail changes: Low thyroid function may cause hair to be thin, fine or brittle. Thinning and loss of hair on the outer 1/3 of eyebrows is considered diagnostic. Skin may be thin, pale, fragile, dry, and take on an ivory or yellowish cast. Hand, face and eyelids may become puffy. You may bruise more easily, and nails may become thick and brittle. Your palms and soles may get thick and dry. Hyperthyroidism may cause hair to become coarse, dry and brittle, or to fall out.
Hyperthyroidism may cause your hair to be fine and straight and unable to curl, or even fall out . Skin can become itchy or scaly, or may feel warm and excessively moist or oily. Puffiness around the eyes is common and in advanced cases eyes may appear to bulge. You may have softening of the nails.
Aches and pains: With either high or low thyroid you may have a tightness or lump in the throat. You may have aches and pains in the joints, hands and feet. Muscle weakness is common, as are muscle cramps. Your eyes may be sensitive to light. Your immune system may become compromised or hyper sensitized, and you may have more frequent infections. You may be diagnosed with goiter, an autoimmune disease or sex hormone imbalance. Hyperthyoid may cause constipation, and hypothyroid may cause loose stools. You may notice your heart racing. The thyroid hormones are so interlinked with all body systems that almost any symptom could be related.
Disorders of the Thyroid
PRIMARY HYPOTHYROIDISM
Primary hypothyroidism is the most common form of hypothyroidism. Primary hypothyroidism is caused by factors affecting the thyroid gland itself such as thyroid dysgenesis, environmental damage to the thyroid, inherited metabolic defects and environmental factors such as medications which affect thyroxin synthesis. Primary hypothyroidism generally results in low serum levels of T4 and high serum levels of TSH. The most common cause of primary hypothyroidism in adults in developed countries is autoimmune thyroiditis (Hashimoto’s thyroiditis). Hashimoto’s thyroiditis results when the body forms antibodies against thyroglobulin and the TSH receptors in the thyroid gland. This results in a decreased stimulation of T4/T3 production.
CENTRAL HYPOTHYROIDISM
Central hypothyroidism results from insufficient stimulation of the thyroid gland by the thyroid-stimulating hormone (TSH). Central hypothyroidism can result from abnormalities that interfere with the pituitary release of TSH or factors that affect the regulation of TSH by thyroptin releasing hormone (TRH). Central hypothyroidism generally results in low serum levels of T4 and normal to low serum levels of TSH.
PERIPHERAL HYPOTHYROIDISM
Peripheral hypothyroidism is extremely rare and results when the body is unable to respond to thyroxin. The most common cause is thyroid hormone resistance, a rare, autosomal dominant disorder that results from mutations in the thyroid hormone receptor (Trbeta).
CONGENITAL HYPOTHYROIDISM
Infants born with hypothyroidism are said to be affected with congenital hypothyroidism. In addition to the typical manifestations of hypothyroidism, congenital hypothyroidism, if untreated, can cause stunted growth, apathy, distended abdomen, swollen tongue and mental retardation.
HYPERTHYROIDISM
Hyperthyroidism results from an excess amount of T4 and T3 in the blood stream. In the presence of clinical symptoms the diagnosis of hyperthyroidism can be confirmed when serum measurements indicate increased T4 and/or decreased TSH levels. Hyperthyroidism can be treated through medications such as thionamides, which inhibit the synthesis of T4 and T3, and beta blockers which block the action of thyroid hormones on peripheral cells. Patients who cannot be treated through medications are treated through radioiodine destruction of the thyroid or surgical removal of the thyroid. Surgical removal of the thyroid and sometimes radioiodine treatment can leave the patient permanently hypothyroid.
GRAVES’ DISEASE
Graves’ disease, the most common cause of hyperthyroidism, is an autoimmune disease resulting from the formation of antibodies against thyroglobulin and the TSH receptors in the thyroid gland. The only difference between Hashimoto’s thyroiditis and Graves’ disease is that Graves disease results when these antibodies stimulate thyroid hormone synthesis rather than inhibiting it. Graves’ disease results in increased synthesis of T4 and T3, and can result in exophthalmos, thyroid enlargement and goiter, and vitiligo. People with Graves’ disease may pass on a genetic predisposition and a slightly increased chance of developing Graves’ disease to their offspring.
The endocrine system is one of the body’s main systems for communicating, controlling and coordinating the body’s work. It works with the nervous system, reproductive system, kidneys, gut, liver, pancreas and fat to help maintain and control body energy levels, reproduction, growth and development, internal balance of body systems, called homeostasis, and responses to surroundings, stress and injury.
The endocrine system accomplishes these tasks via a network of glands and organs that produce, store, and secrete certain types of hormones. Hormones are special chemicals that move into body fluid after they are made by one cell or a group of cells. Different types of hormones cause different effects on other cells or tissues of the body.
Thyrotropin-releasing hormone (TRH)
The process of hormone synthesis begins in a part of the brain called the hypothalamus. The hypothalamus releases thyrotropin-releasing hormone (TRH) in response to signal molecules from organs throughout the body. Factors controlling TRH release have not been well studied, although we know that it is strongly influenced by hunger, fasting, and stress. Current knowledge indicates it is inhibited by serotonin, and probably GABA, somatostatin, and corticotropin-releasing factor. Dopamine appears to increase release of both TRH and somatostatin. Glycine deficiency may inhibit GABA release which may in turn increase TRH. Hence, glycine deficiency may increase TSH release (controlled by TRH) and its balance point. This possibly causes the thyroid to be less reactive to low T4 and T3.
The nutritional requirements to support healthy TRH production are poorly understood. High quality protein intake is vital. Formation and release of neurotransmitters involved in regulation indicates a need for adequate glycine, tyrosine, methionine and Vitamin B12.
At one time a thyrotropin releasing hormone test was used for the detection of primary hypothyroidism or hyperthyroidism. With development of the more sensitive TSH test it has fallen out of favor.
Thyroid-stimulating hormone (TSH)
The TRH travels through the venous plexus located in the pituitary stalk to the pituitary gland, also in the brain. In response, the pituitary gland then releases thyroid-stimulating hormone (TSH) into the blood. TSH is released in proportion to TRH levels and as part of a feedback loop in response to low T3. ncreased TSH triggers the thyroid to produce increased thyroglobulin.
TSH is a glycosylated protein. Numerous mutations in the TSH receptor gene have been identified and associated with specific thyroid diseases. Resistance to TSH is a syndrome due to reduced responsiveness of the thyroid gland to biologically active TSH. Inactivating mutations of the TSH receptor may cause primary hypothyroidism due to TSH unresponsiveness.
The nutritional requirements to support healthy TSH function are poorly understood. As with TRH, high quality protein intake is vital. A TSH lab will indicate an imbalance in thyroid hormone levels which many physicians use as a guide to hormone dosage. Significant problems exist with this method, due to the influence of TRH regulator effects, autoimmune effects (which many consider renders TSH interpretation useless), by T4-T3 conversion abnormalities (discussed below) and technical issues surrounding interpretation of values. Autoimmune Thyroid conditions may cause wide swings in measured TSH and severely limit the usefulness of tested TSH levels in guiding treatment.
Many health professionals (most notably alternative practitioners) have abandoned the TSH test and rely on to temperature analysis to demonstrate thyroid function. This is a noninvasive, reliable test that can highlight the need for thyroid support. Sometimes a glass-bulb thermometer is used under the arm. At other times, physicians monitor the readings via the traditional sublingual method. Consistent readings below 97.6 are suggestive of an under active thyroid gland and require more investigation. (Other conditions can also lower body temperature, such as stress, certain medications and certain types of infections).
Thyroglobulin
The next step in the process is production of thyroglobulin, a protein produced and used within the thyroid gland, although some thyroglobulin may exist in blood. This may be an artifact of production or it could fill some undetermined role. Elevated thyroglobulin serum levels may also be found in patients with endemic and multinodular goiter, Grave’s disease, congenital TBG deficiency, benign adenomas and acute thyroiditis.
Thyroglobulin is produced by the thyroid epithelial cells, called thyrocytes, which form spherical follicles. It is a polypeptide made up of neutral and amino sugars. Chemical composition of thyroglobulin varies somewhat from species to species. Nutritional requirements to support appropriate thyroglobulin production are poorly understood.
Thyroglobulin supplementation has been tried as a treatment for hypothyroidism. The drug form, called Proloid, is no longer available. Information is scant on Proloid and a search of the FDA website yields no information. An FDA suit against the manufacturer in 1995 notes stability problems as a reason for discontinuation.
Autoimmune thyroid (Hashimoto’s and Graves’ diseases) are marked by elevated antibodies to thyroglobulin. Many scientists believe patients with autoimmune thyroid should avoid treatment with thyroglobulin containing drugs including desiccated thyroid (such as Armour).
A thyroglobulin test may be ordered when a person has symptoms of hyperthyroidism and/or an enlarged thyroid gland and the doctor suspects that the person may have a thyroid disorder such as Graves’ disease or thyroiditis. It may be ordered at intervals when someone is being treated with anti-thyroid medications (for conditions such as Graves’ disease), to determine the effectiveness of treatment.
A thyroglobulin antibody test is used as part of a thyroid antibody panel to assess for thyroid cancer and Hashimoto’s. Since thyroglobulin antibodies interfere with TSH test results, it is often ordered as part of a thyroid panel.
Thyroid Hormones
Thyroglobulin is converted in the thyroid to T4 and to a lesser extent T3. The thyroid gland also produces T2 (diiodothyronine), T1 (monoiodothyronine) and calcitonin, and it is likely that it releases yet unidentified additional hormones. Substantially more research has been done on nutritional factors affecting thyroglobulin conversion to T4 and T3, although information is still lacking on the other thyroid hormones.
We do know that conversion is highly dependent on adequate stores of iodine and tyrosine (an amino acid produced in the liver from phenylalanine). Conversion appears to also require adequate levels of omega 3 fatty acids, zinc, selenium, and vitamins A, D and E.
There are a growing number of anecdotal reports implicating excessively high Vitamin D3 supplementation with increased TSH and subsequent reduction in release of thyroid hormones. The science is yet to be done on this subject, but calls for caution by those suffering from hypothyroidism. Studies on rats also indicate that docosahexaenoic acid (DHA) supplementation increases TSH levels. Many experts advise having a Vitamin D test at the same time as a thyroid panel.
T4
T4 is a prohormone (a precursor to T3) and does not itself substantially effect the body. It is produced in the thyroid when thyroglobulin is converted in a reaction which requires TSH as a trigger and adequate stores of protein, iodine and tyrosine. About 40 times more T4 is produced than T3. T4, sold as “Synthroid” and others, requires a prescription in the US. As with all hormones, most of the T4 is bound to proteins and is not biologically available. Lab testing for T4 is available but of limited value due to a variety of factors including protein nutritional status. Unbound (Free) T4 is clinically useful in determining correct dosing of thyroid hormones, subject to significant limitations.
T4 to T3 Conversion
The thyroid gland releases very small amounts of biologically active thyroid hormone (triiodothyronine or T3) and larger amounts of an inactive form of thyroid hormone (thyroxine or T4) into the circulation. Most of the biologically active T3 in the circulation and inside cells is created by the removal of one iodine atom from T4 in a reaction catalyzed by selenium-dependent iodothyronine deiodinase enzymes. Three different selenium-dependent iodothyronine deiodinases (types I, II, and III) can both activate and inactivate thyroid hormone by acting on T3, T4, or other thyroid hormone metabolites. Thus, selenium is an essential element for normal development, growth, and metabolism because of its role in the regulation of thyroid hormones.
T3
T3 is the most powerful thyroid hormone, and affects almost every process in the body, including body temperature, growth, and heart rate. T3 is about 4 times more potent that T4. T3 is produced in small quantities directly from thyroglobulin. TSH is inhibited mainly by T3. T3, sold as Cytomel is available by prescription in the US. There are natural and synthetic combinations of T4 and T3 also available.
Many healthcare professionals consider the Free T3 test to be the best assessment for dosing thyroid hormones. The total T3 lab is subject to the same limitations as Total T4 levels.
Reverse T3
About 40% of the T4 released from the thyroid gland is converted into T3, about 40% is converted into Reverse T3 (rT3), and the remaining 20% is metabolized by other pathways. Reverse T3 is not metabolically active, and may block T3 receptor sites. Significant controversy exists over the role of T3 and rT3 balance.
In people with otherwise normal TSH and Free T4, the Free T3 level can drop for numerous reasons, and in many of them, a decrease in Free T3 is accompanied by an increase in Reverse T3. The following are common causes of decreased Free T3: dietary deficiencies of selenium and zinc, low carbohydrate diets, low protein diets, low calorie diets, anorexia, starvation, fasting, chronic and acute illness/Surgery, prolonged cold temperature exposure, sedentary lifestyle, initiation of exercise routine in an out-of-shape person, physical and emotional stress (esp. when it causes an increase in plasma cortisol or epinephrine or causes other adrenocortical activity that lowers thyroidal production of T3 and/or inhibits extra-thyroidal T4 to T3 conversion), certain prescription drugs, heavy chronic alcohol consumption, aging. Excess rT3 may result in continuation of hypothyroid symptoms even with increasing doses of T4 (Synthroid). Some believe an rT3 syndrome called Wilson’s Syndrome can be effectively treated through a program of time-release T3 tablets (which are ordered, with a prescription, from a compounding pharmacy.)
The Reverse T3 test is available individually and as part of the Advanced Thyroid Panel. To order testing click here: 
T2
T2 is a thyroid hormone produced primarily as a byproduct of T3 metabolization. Until recently it was considered an inactive byproduct. Recent research indicates that T2 is an active agent, a “bioactive iodothyronine.” T3 might speed up metabolism and reduce fat storage, and it is touted as a possible weight loss supplement. T2 has been found to have a stimulatory effect on the activity of the enzyme that converts T4 to T3.
As of now there is insufficient research to make a definite conclusion, however supplementation with desiccated thyroid does have the advantage of providing T2 as well. “Very recent evidence leads us to suggest that T2 may be a potentially useful agent for the treatment of diet-dependent overweight (and the consequent hypertriglyceridemia and high cholesterol level) without inducing thyrotoxicosis.” (Immunology, Endocrine & Metabolic Agents, Volume 6, Number 3, pp. 255-265(11)) There is no useful lab test for T2. T2 levels are not typically tested.
T1
T1 is also produced by the thyroid. It’s role in the body has not yet been determined and levels are not typically tested.
Calcitonin
Calcitonin is produced in the thyroid and acts to reduce blood calcium, opposing the effects of PTH. Its importance in humans has not been as well studied (although much is known from animal studies). In animals, it protects against calcium loss from bones during periods of calcium stress (pregnancy, lactation, nutritional deficiency). It prevents postprandial hypercalcemia from absorption of excess dietary calcium; is involved in vitamin D regulation; it is a satiety hormone, inhibiting food intake and appetite. Calcitonin can be used therapeutically for the treatment of hypercalcemia or osteoporosis. subcutaneous injections of calcitonin in patients suffering from mania resulted in significant decreases in irritability, euphoria and hyperactivity and hence calcitonin holds promise for treating bipolar disorder.
Although a calcitonin test is available, insufficient research has been done to establish usefulness. A calcitonin spray, “Miacalcin” is available for treatment of postmenopausal osteoporosis, also as a generic, by prescription only. Desiccated thyroid products do contain calcitonin. Calcitonin levels are not typically tested.
Unsure what to order? Please call us, we can help! Call a CHS healthcare Professional at 714-886-9026 for guidance.
Statements contained herein have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat and cure or prevent disease. Information provided by CHS is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. Any information given is only intended as a sharing of knowledge and information from scientific world literature. You are encouraged to make your own health care decisions based upon your own research of the subject and in partnership with a qualified health care professional.