The TSH (Thyroid stimulating hormone) is probably worldwide the most commonly tested marker in the blood when it comes to thyroid disease. Almost every endocrinologist or family doctor swears by the reliability of this hormone when it comes to confirm or rule out thyroid disease.
Usually these doctors only consider this one blood value when it comes to hormonally adjusting a patient with Hashimoto’s thyroiditis or hypothyroidism. This procedure is just as wrong as ignoring other thyroid levels such as fT3, fT4, and related antibodies.
Unfortunately this TSH fairytale has been constantly repeated and passed on for decades in well-known journals and on renowned websites. But the experience of those affected shows, may it be in the HT-MB forum of Dr. Brakebusch, that a hormonal thyroid adjustment according to TSH only, very rarely leads to the desired success.
Often many years are passing by, until the patient notices that an adjustment based only on TSH is not possible, and conflict with their doctor. It is important to know that most Hashimoto patients start to feel more comfortable at a TSH below 1 μIU / ml, and the TSH level does not really say much about whether the body is well supplied with thyroid hormones. But more about that later.
The history of the TSH test
Until the 1960s, the first thyroid tests were based on the measurement of basal metabolic rate, elevated cholesterol and creatine phosphokinase. Patients with elevated blood cholesterol were treated with natural thyroid hormones to lower cholesterol levels. The measurement of the basal metabolic rate was successfully applied in almost every doctor’s practice until the 1940s when it was replaced by the radioactive iodine uptake of the thyroid gland as a test method.
In the late 1960s, the TSH test was introduced and was touted as the method of choice when it came to detecting and treating thyroid disease. Over the next twenty years, the TSH test has evolved, becoming more sensitive and declared as the gold standard in thyroid diagnostics. Each time a new test was developed, it was said to be infallible and reliable, but still today none of these tests has actually been able to detect all cases of hypothyroidism.
Why is an thyroid adjustment based on TSH not possible?
Dr. David Derry MD, Ph. D, a thyroid expert and researcher from British Columbia, explained this question very well in an interview with Mary Shomon. He believes that one possible cause of the inadequacy of the TSH test could be that the pituitary cells, which control the release of TSH, are the most sensitive cells in the body to respond to thyroid hormones.
Which would mean that if you take thyroid hormones adjusted only based on the TSH, you only treat the pituitary gland. The pituitary cells would be happy about the thyroid hormones and regulate the TSH down. As a result, the thyroid would lower hormone production and the rest of the body’s cells, which are less sensitive to thyroid hormones, would fail and not get enough hormones.
In addition, the doctor would continue to lower the thyroid hormone dose with a lowered TSH, which would further worsen the patient’s situation. Due to a TSH-oriented treatment of many physicians, millions of patients thus receive either too little or no prescribed thyroid hormones.
Dr. Derry also stated in the interview that when the TSH test not yet existed, leading clinics around the world have been treated their thyroid patients for about 80 years with hormone doses of between 200 and 400μg. Nowadays, a patient can already be happy if he is prescribed 100μg.
Also, the treatment of thyroid cancer patients looked very different until the 1970s, before the TSH test was introduced: The doctors gave their patients the maximum tolerated dose of thyroid hormones until mildly toxic symptoms appeared. Following this, the dose was minimally reduced until the overdose symptoms, such as tachycardia or sweating, disappeared again.
Dr. Derry also has the opinion that the longer a hormone treatment does not take place, the more difficult it becomes over time to get the symptoms under control.
Limitations in the diagnosis and treatment by pure TSH treatment
Dr. Rowsemitt and dr. Najarian points out that treatment limited to TSH involves several limitations in the diagnosis and treatment of hypothyroidism. On the one hand, the TSH value makes no distinction between secondary and primary hypothyroidism. However, secondary hypofunction is the result of pituitary insufficiency, ultimately leading to low TSH levels.
On the other hand, a TSH deficiency or TSH excess can be caused by a tertiary hypo- or hyperthyroidism. There are disturbances in TRH production in the hypothalamus or problems with signaling in the hypothalamic-pituitary system (Pickardt syndrome).
Apart from that, various drugs and hormones also affect the TSH to a considerable extent. These include, for example, morphine, heparin, glucocorticoids, levothyroxine, catecholamines, somatostatin, octreotide, dolasetron, dopamine and also various nutritional supplements such as biotin. (Source: http://www.thyroidscience.com)
A suppressed TSH value does not pose a problem
Unfortunately, for most physicians, it is still not clear that 95% of the patients, who additional take T3 in the form of thybon, prothyride, novothyral or natural porcine hormones, have a very low or suppressed TSH. In the old leaflet of the thyroid drug Novothyral, earlier there was a note:
“The increase in thyroid hormone concentration under Novothyral leads via a negative feedback mechanism to a suppressed TSH secretion of the pituitary gland.”Source: http://www.pharmazie.com
Also Dr. med. Leveke Brakebusch, a specialist in autoimmune thyroid disease in Konstanz, argues that suppressed TSH is due to T3 ingestion:
“… a latent hyperfunction is a true ongoing overactive function – this is different from taking T3. A decreased TSH is no proof of the existence of hyperfunction. When taking combined preparations, the TSH may be suppressed, eg suppressed, by a short-term increase in T3. Unfortunately, there is no drug that releases T3 delayed. We also see here that a suppressed TSH is by no means to be equated with an overfunction as long as the free values fT3 and fT4 are in the norm. “Source: Dr. med. L. Brakebusch, statement in her Hashimoto forum www.ht-mb.de, accessed on 12.09.06
Does a suppressed TSH increase the risk of osteoporosis?
Often physicians refer to an increased risk of osteoporosis (reduction in bone density) when TSH is suppressed. But this claim is not proven and also one of the leading German osteoporosis experts PD Dr. med. J. Fassbender elaborates on this question:
“In summary, the topic is currently to be assessed in such a way that a significantly increased risk of osteoporosis in TSH-suppressive therapy, but normal peripheral values for fT3 and fT4 is not present, but in peripheral increased values. TSH itself has no direct effect on bone metabolism … “(J. Fassbender, Multimedica Expert Council on Osteoporosis, www.multimedica.de, accessed on 14.03.03)Source: http://schilddruesenguide.de
There are many more on this topic , trusted sources that refute bone resorption due to suppressed TSH.
Anyone who only focuses on TSH treatment for thyroid disease without including the free thyroid levels (fT3 and fT4) and his well-being in the therapy, has little chance of achieving freedom from symptoms and well-being.
Especially with this sensitive topic, it is important to find a competent doctor who puts the patient in the foreground, performs a careful medical history, takes the described symptoms seriously and, above all, considers the free thyroid levels as standard. And if this doctor is then still open for T3 drugs and natural thyroid hormones, you have hit the jackpot and are in good hands.
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