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Hyperthyreoidism and Schizophrenia - a brief biological discussion

Hyperthyreoidism and Schizophrenia - a brief biological discussion

04.10.2013, 13:30 Uhr
Beitrag von wize.life-Nutzer

Schizophrenia and Hyperthyreodism

Today I want to address the thyroid . The first time I encountered a thyroid disorder, represents an hyperfunction in a neighbor. The about in the 50th man in his youth, has already forged prescriptions to get close to estrogens. The fixed idea , he is a wife in a man's body is not his only psychosocial abnormality . So an antipsychotic ( Zyprexa ®) , he was , as he complained of insomnia, prescribed . When I told him about the long term effects of this medication (metabolic syndrome after much to high caloric diet because of blocking the medial preoptic area [MPOA], brain atrophy because of serotonin pathway blockade) , he went off the drug and the insomnia recurred . Now, however, good advice was expensive, even if already the devil-with-the- Beelzebub - expulsion came to an end . Close observation showed me a minimal approach goiter , which gave me, how was shown on curative success, the right track. The gift of Lycopus virginicus (we have then simply made ​​tea, it took nerve to break the poisoning paranoia ; Fintelmann / Weiss („Lehrbuch der Phytotherapie“, Hippokrates, Stuttgart, 10th edition 2002; english version „Herbal Medicine“) recommend the administration of medicinal products , eg Cefavale ® drops , Lycoaktin ® M tablets Thyreogutt ® mono drops / tablets, thyro - loges ® N tablets, to be creeped in up to the specified dose) showed remarkable results after just three days. When I was at the usual time at his apartment door knocking (9 clock in the morning, what I met before therapy was always a patient who complained of his sleepless night) , he just growled at me , he was tired , why I would wake him up so early and he slammed the door in my face . I have never not enjoyed so much before and until today again a closed door !

General Aspects of Endocrionolgy on the example of Thyroidea and β-adrenergic receptor
Even if with the first entry to psychiatry the thyroid hormones T3 and T4 are determined and are in the normal range , this does not mean that no thyroid malfunction subsists. The peculiarity of thyroxine is in deed that it is mainly present in bound form (T4 ), and only when needed as a free hormone (T3 ) is released. What can not be derived from the thyroid laboratory , is the rate of T3 that binds its receptor and is transported to the nucleus, where the receptor -ligand complex exerts its effect . This rate corresponds to the flow of thyroxine from its bound form into the free T3 active form , which also can not be represented in the laboratory.
Let us have a look for a deeper understanding at Hashimoto disease . Among the clinical symptoms , there are all symptoms of epinephrine / norepinephrine overactivity , but the corresponding lab shows normal values ​​! The answer is found in the in Hashimoto overshooting expression of β -adrenergic receptor (see "Basic & Clinical Endocrinology", Greenspan , Gardner, Lange Medical Books / McGraw -Hill ) . Although epinephrine / norepinephrine is increasingly produced, but also increased consumed , so that the blood levels almost unchanged ( possibly reduced with borderline values? ) appears . Especially for the heart this increased receptor expression is confirmed, but in the tibia and the face seems such a malfunction is to be assumed ( myxedema ) .
At this point I can not resist a visit. Greenspan / Gardner / Karam specify , the β -adrenergic receptor mysterious ways sometimes leads to dilatation of the blood vessel , but also to constriction of the blood vessel. This is easily explained. The lack of a second signal from the tissue to the adrenaline / norepinephrine triggerd blood vessel gives constriction , the normal case. If an additional inflammation signal is sent from the tissue, dilatation follows to allow the monocytes immigration. With myxedema this mechanism fails by the following reason : In the blood vessels ( eg in the region of tibia) are pathologically increased in number β -adrenergic receptors, which prevent maturation of monocytes to macrophages . How so? Monocytes also have β -adrenergic receptors , which triggered, initiate the ripening of monocyte to phagocyte. However, the monocytes have to compete for the available (not increased ) epinephrine / norepinephrine with pathologically increased number of receptors of the vessel wall by the laws of thermodynamics. So there is not enough hormone left for monocytes , they can not mature and therefore not emigrate to the tissue. Requested by the inflammatory signal " cleanup " remain unsettled , the cell debris forms a colloid - myxedema !

Evolutionary aspects of Thyroidea
It seems reasonable to penetrate deeper into the evolution of physiology of the thyroid . You really have to say goodby to the thought of more is better and a little does not hurt so much . The thyroid is different.
Evolutionary the thyroid gland arose from the struggle of the body against radioactive iodine . Well there is no natural radioiodine any more today . But it was in ancient times , when life was created . At that time it was essential to release the inevitably ingested strong radiation of iodine as fast as possible . Based on ​​this defense mechanism the endocrine system developed . But conserved is the handling of iodine as a strong poison .
So the organism is set up to deal with almost any large amounts of iodine . It gets in trouble only if the ingested iodine quantum varies . For this it is not configured . This flexibility could not develop because the evolutionary pressure that could lead to such flexibility was not available. Only in very modern times heavy fluctuations of the iodine content in the diet gives a selection pressure.

Peaks of selection pressure to the Thyroidea to tolerate fluctuating iodine uptake in the 20th century
Triggered by the observation that absolute iodine deficiency as in mountainous habitats , leading to iodine deficiency disease , the iodization of table salt was introduced in Germany in the 1970s . Certainly a significant change in the iodine intake of the population. Another example is the iodization of bread at the U.S. West Coast habitats in the 1950s . There, the occasion was the increasing number of cases of thyroid cancer caused by radioactive iodine fallout because of carried out in the Pacific, above-ground nuclear weapons tests.
For the American west coast is an increase in thyroid disorders that have become physically conspicous after the iodization of bread evident.

The problem to measure thyroid hormone turnover
But what about the mental disorders ? State of the art of medicine is to first check the thyroid hormone levels in suspected schizophrenia, to exclude a thyroid disorder as the cause of aggressive behavior and other symptoms of schizophrenia. The problem with this differential diagnosis is, however , an increased thyroid activity leads not necessary to increased hormone levels in the blood. It is probable ( evolutionarily justified , see above) that these raised blood levels can be observed only in the rarest cases !
How should now but to deal with this problem ? Of course, one could perform a diagnostic radioiodine . Here the iodine metabolism is measurable, hence turnover of thyroid hormones (and not just their blood levels ) and therefore half the truth of a hidden hyperthyroidism. But one may not do this . First, there is of course the burden of the body with radiation. On the other hand, the administration of radioiodine for diagnostic purposes is often associated with the complication of a thyroid disorder. The iodine intake is changed drastically with this. Furthermore, this study is very expensive .
I spontaneously do not see how we could kill this problem. Even if it were possible to measure the iodine turnover somehow in general, the problem remains that the thyroid gland responds to large or small iod in diet also with the production of different hormone derivatives . These derivatives are different in their potency of the hormone molecule with respect to the iodine content ( evolutionarily related adaptation to habitats with high and low iodine food ) .

In cases of suspected schizophrenia a physiological thyroid lab is not an exclusion criterion for the differential diagnosis of hyperthyroidism. The native clinical picture without prior neuroleptic gift (!)( circadian rhythm , often shifted) decides. When in doubt (better : in general) a cost-effective test with the above Lycopus virginicus therapy should bring the decision .

What should be done, eventually, to give this proposal a statistic base, is to compare the difference of violent crime rates before and after the iodinization of bread at the U.S. Westcoast.

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