MY DOCTOR TOLD ME TO STOP MY NATURAL THYROID MEDICATION
At NBH Lifetime Health we often hear the following:
“My TSH was .02 on my last blood test and my Dr. wants me to stop the thyroid supplementation. I am currently taking 2 pills of the thyroid booster. I feel great and do not appear to be having any side effects. What do you suggest I do and is the .02 TSH anything to be concerned about. I do not want to stop taking the Thyroid Booster.”
My TSH has been less than 0.1 since I started Natural Thyroid Supplementation back in 1999. I have lab tests to verify this and I am very healthy at age 65. The conventional “assumption” and training is that if a person’s TSH is “suppressed” then they must be hyperthyroid regardless of the lack of symptoms (bouncing off walls, very skinny, etc.) or circumstances.
TSH is also is typically low if a person has sufficient free T3 and T4 where the body does not have to signal (TSH) for more production. There are many studies on this and they are available in our office anytime (and some are shown below). The “lab results” approach to medicine does not take into account symptoms and seemingly ignores the science.
In defense of the family provider/endrocrinologist, he or she is trained to go by labs and is trained to base his or her diagnosis on lab results. They seldom if ever test the free T3 and seldom go by your results or symptoms. The conventional/pharmaceutical approach is to prescribe a synthetic T4 (snythroid, levoxyl, levothyroxine, etc.). You may be told that if your TSH is suppressed, then you will lose bone and increase your risk of heart disease. However, as you can see below, the science is just the OPPOSITE except in cases of true hyperthyroidism.
The Science of Thyroid
Women with low normal thyroid levels had a 4-fold increase risk of heart disease. This increased risk was equal to the risk of smoking and high cholesterol. Low normal thyroid levels are a strong predictor for heart attacks.” Annals of Internal Medicine 2000; 132: 270-278.
“Low T3 levels are associated with increased heart disease and decreased cardiac function. Replacing T3 increases clinical performance and cardiac output. Adding T3 increases exercise tolerance and quality of life.” CVR & R 2002;23:20-26.
“Low levels of free T3 in patients resulted in increased disability, depression, decreased cognition, and energy and increased mortality.” JAMA Dec. 2004; Vol. 292(2c): 500-504.
“TSH is a good test to diagnose hypothyroidism. However TSH is a poor measure of symptoms of metabolic severity. It is, therefore, the biological effects of thyroid hormone on the peripheral tissue and not the TSH concentration, that reflects the clinical and metabolic effects.” British Medical Journal Feb 2003;Vol. 326:325-326.
There are two types of thyroid hormones, Thyroxine (T4) and Triiodothyronine (T3). T4 is inactive and kept in reserve, T3 is the active hormone. Thyroid hormone initially is produced in the thyroid gland as a storage form of the thyroid called T-4. Once in the body, this circulating T-4 is converted to the active form of T-3 by an enzyme. As we age, the production of T-4 diminishes. In addition, the conversion of T-4 to the active form of T-3 also diminishes, resulting in less stimulation of the cells.
Low thyroid levels results in complaints of fatigue, lack of energy, weight gain and all the other symptoms typical of low thyroid. Tests often show a “normal” thyroid. Patients are treated with synthetic T-4 products and still experience hypothyroid symptoms even though the laboratory test values appear normal. The reason for this is that the treating provider may rely on one thyroid test, TSH or thyroid stimulating hormone. This is an indirect measurement of thyroid function. The new paradigm is to measure the free hormones in our body, which is the Free T-3 in thyroid. The free hormones are the active hormones and are a more accurate indication of the body’s metabolism of the hormone.
About 80% of the thyroid hormones we produce is T4, the inactive thyroid hormone that is typically held in reserve by the body. T3 makes up only 20% of the thyroid hormone, but is about four times more potent than T4 and is the active hormone that the body uses to function. T4 is converted into T3 when thyroid hormone is needed. The problem is that conversion becomes an issue for many reasons including aging, stress, genetics, etc.
The release of the thyroid hormones is controlled by the thyroid stimulating hormone (TSH), which is produced in the pituitary gland. Low circulating levels of thyroid hormone are detected by the hypothalamus which then instructs the pituitary to release TSH. When sufficient amounts are released the hypothalamus communicates with the pituitary to stop or slow down.
Because of this complicated feedback loop, high levels of TSH in the blood often means the pituitary is trying to stimulate production of the thyroid hormone but the thyroid gland is not responding. This condition, known as hypothyroidism, is more common in women and the elderly.
Our Science
“Fibromyalgia is frequently seen in hypothyroidism. There is now evidence to support that fibromyalgia may be due to thyroid hormone resistance (cellular hypo-function).” Medical Hypotheses 2003 Aug;21(2):182-89.
“Combined T4 and T3 therapy resulted in improved symptoms, well-being and weight loss in comparison with straight T4 therapy. A decrease in weight resulted from using higher T3 levels.” J Clin Endocrinol Metab 2005 May;90(5):2666-74.
“Long term high doses of thyroid had no adverse effect in causing osteoporosis or fractures” Cortland Forum July 2001:85-90
“TSH is a good test to diagnose hypothyroidism. However TSH is a poor measure of symptoms of metabolic severity. It is, therefore, the biological effects of thyroid hormone on the peripheral tissue and not the TSH concentration, that reflects the clinical and metabolic effects.” British Medical Journal Feb 2003;Vol. 326:325-326.
“Even exceptionally high doses of thyroid do not cause osteoporosis or fractures.” Normal Metabolic. Research 1995 Nov; 27(11):503-7.
“Even though the TSH is in the normal range, patients continue to have persistent symptoms despite adequate replacement doses. These patients are still symptomatic due to low T3 levels.” BMJ Feb. 2003; Vol 326:295-296.
“Patients that took a combination of T4 and T3 experienced better mood, energy, concentration and memory and improved well-being. Patients on just T4 experienced no change.” New England Journal of Medicine Feb. 1999;340:424-9
“Women with low normal thyroid levels had a 4-fold increase risk of heart disease. This increased risk was equal to the risk of smoking and high cholesterol. Low normal thyroid levels are a strong predictor for heart attacks.” Annals of Internal Medicine 2000; 132: 270-278.
“Low T3 levels are associated with increased heart disease and decreased cardiac function. Replacing T3 increases clinical performance and cardiac output. Adding T3 increases exercise tolerance and quality of life.” CVR & R 2002;23:20-26
“Low levels of free T3 in patients resulted in increased disability, depression, decreased cognition, and energy and increased mortality.” JAMA Dec. 2004; Vol. 292(2c): 500-504.
“Low normal thyroid levels result in increased cholesterol, increased heart disease, fatigue, low energy, depression, and memory loss. Thyroid replacement eliminates thee risks. No study has shown any harm or adverse effect of treatment.” Consultant 2000 Dec: 2397-2399.
“Long term thyroid replacement with high doses has no significant effect in bone density or fractures.” Lancet 1992 Jul 4; 340(8810):9-13.
“Thyroid levels should be raised to the upper normal range for a young person. This results in optimal cognition, memory, cerebral function.” Journal of Gerontology; 1999 Vol. 54:109-115
“Combined thyroid therapy with T4 and high dose T3 resulted in improvement of symptoms and well being, whereas straight T4 did not. Not only did they feel better, but the patients taking both T4 and T3 also lost weight. The straight T4 did not.” Journal of Clinical Endocrine Metabolism 2005 May; 90(5):2666-74
“Over 40 studies prove that thyroid replacement does not lower bone density or cause increase risk of fracture.” Cortland Forum; 2001 July:85-89.
“Decreased T3 levels result in increased cholesterol and heart disease. Treating with T3 improves the lipid profile.” Preventive Cardiol 2001;4:179-182
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