The clinical exams regularly asked are not enough, in case they are “normal”.
Daily, I found myself with the issue of a patient who has been clinically diagnosed hypothyroidism and that brings “normal” clinical exams and therefore is not treated.
Thyroid is a gland that keeps fundamental hormones to our health and survival. The usual clinical exams can be in fact “good” and this does not mean that the patient does not have peripheral hypothyroidism. This happens because of the central level mechanism of regulation, hypophysis is a different mechanism from the peripheral level.
In fact, thyroid keeps mostly a pro-hormone (inactive hormone), the T4. This has then to be converted onto T3, an active hormone. All of the cells in our body have receptors for the thyroid hormones. This only happens also for another hormone, vitamin D.
There are factors that stimulate the production of thyroid hormones, like iron, iodine, tyrosine, zinc, selenium, vitamins E, B2, B3, B6, C & D.
Factors that inhibit this production, like stress, physical or emotional trauma, radiation, and other medications (lithium), fluorine, toxins (pesticides, plastics, mercury, cadmium and lead), the inflammatory and autoimmune diseases like the celiac disease for example, the low calories diets, the infections, which end up being stressful to the body, the hepatic and renal dysfunction, the depression, the obesity, the peripheral resistance to leptin and insulin, the diabetes, the chronic pain, the fibromyalgia and chronic fatigue…
In these situations, the inactive hormone will transform into another hormone that is also not active, but that competes with the active one in areas of connection, making this to not act, which means T4 (thyroxin) will not convert onto T3 (triiodothyronine) but acts in rT3 (reversed T3).
Nevertheless, in theses situations, the deiodinase 2, enzyme that coverts the T4 into T3 to the level of the hypophysis is inhibited.
If deiodinase 2 exists to the level of the hypophysis, it converts T4 into T3, as it is stimulated, the T3 will inhibit the TSH (thyroid’s stimulating hormone) and we’ll have a “normal” TSH. Many times, TSH is only the marker used! However, at peripheral level, for example, in these situations the deiodinase 1, that converts the T4 into T3 is inhibited to peripheral level and the patient has an intracellular hypothyroidism.
Also, the enzyme that converts the T4 into rT3 for example, does not exist on the hypophysis, as in these described situations, the body can be “full” of inactive hormones (rT3), but the hypophysis could have “normal” values as this depends on another regulating mechanism.
I tried to simplify but the system is in fact much more complex in order to comprehend globally what is happening and so that the patient can be treated in a convenient manner.
The alarm is that NORMAL CLINICAL EXAMS (the usually requested for the study of thyroid) DO NOT EXCLUD THE CELLULAR HYPOTHYRIODISM!
Hypothyroidism Clinic (The 8 signs and major symptoms)
- Fatigue, mostly in the morning
- Tendency for depression
- Waking up with swollen face and eyes
- Cold, lack of tolerance (cold hands and feet, cyanosis and chills)
- Muscle cramps (various areas)
- Chronic constipation (sometimes only able to defect every 2 days or more)
- Rheumatic pains, joints stiffness, swelling of joints, muscles….
- Aquiline reflex (extended or absent)
When we think of treatment, we have to think not only about the hormonal medication, but about everything that will interfere with the genesis of the situation. In the first place we have to “take care” of the diet, intestines, sleep, verify the interrelation with other hormones, eliminate the toxins and from that, medicate.
The intestine is an integrative part of our body, as is the monitoring of sugar in blood. The elimination of toxins, nutritive re-education and integrated hormonal modulation, should be verified, as everything within our body is interrelated.
My personal preference goes to the pork dissected hormone, unusual in Portugal and commonly used in the USA and Canada, which I have been making use of for almost 8 years. It is a natural bioidentical hormone, and the brand that I use, is of rigorous laboratory control and persistence of the potency relatively to the existing concentrations of T4 and T3. Alternatively, we also have bioidentical T4 and T3 synthetic.
BENEFITS OF THE T4 + T3
The T4, when given isolated, inhibits the hypothalamo-hypophyseal axis in order to reach efficient doses. Multiple studies, refer greater tolerance but not better efficiency.
The advantages of T4 + T3 are:
- Lowers cholesterol better
- The aquiline tendon reflex is replaced quicker
- Prevents the formation of goitre
- Improvement in more wide symptoms
- We achieve easier the T3 serum level (with T4 we have to give higher doses to reach the same level).
- We achieve with more ease an adequate tissue level than we would with only T4 (studies in mouses)
- The power of T3 is stable, the of T4 varies
- The stability of T3 is also higher than of the T4
- The intestine absorption of T3 when connected to T4 is better than T4 on its own (95% against 35-67%)
- There is inhibition of the conversion of T4 into T3 in numerous situations as we have seen previously and also with ageing and deficit of T3. Therefore, by only giving T4 we not supress the necessary quantity
- It is curious to observe that we need the smallest quantity of T3 for a better conversion of T4 into T3.
This way we supress the minimum quantity of T3 at the same time that we favour the conversion of T4 into T3
- T3 is the most important hormone. Not T4.
- 5 times more T3 than T4 on the tissues
- It is the level of T3 that determines survival and not of T4, in studies of mortality.
The patient should be treated for 2 reasons:
- Because it shows clinical signs and symptoms. Even with normal clinical exams.
- Because it shows a persistently elevated TSH ( >2.5 mUI/L).
After everything said, we know that a normal TSH does not exclude cellular hypothyroidism, therefore the clinic by itself only justifies therapy.
But an elevated TSH is significant, as we have seen by the pathophysiological explanation initially.
Furthermore, if with ageing the TSH elevates and there seems to be a protection of mortality with this elevation, from the 70s ahead I think we should only treat patients that present clinic.