Guest guest Posted July 23, 2004 Report Share Posted July 23, 2004 Gail, You wrote: > > ... However, one thing I still don't know, specifically regarding > Hashimoto's. Do you think it possible that in humans, after a large % > of the thyroid has been destroyed through the autoimmune process, > perhaps the process in people also stops, leaving just enough thyroid > function to keep people alive? ... Hypothyroid symptoms can be pretty severe just from a reduction in T4 levels. The window for the euthyroid state is fairly narrow. A severe reduction, let alone a complete shutdown, leads to coma and death. T3 is essential for metabolism, which in turn is essential for life. An autoimmune attack continues as long as antigens (plasma cell daughters of B cells) are produced from the attacked cell line. When the thyroid has been damaged, viable cells are sequestered inside the attacked layers of the gland, protected from the B cell identification process. The thyroid tissue effectively " circles the wagons " to protect what is left inside. We know other tissues also have limited capabilities for the functions of the thyroid, particularly T4 to T3 conversion. It is not clear whether these are also attacked in Hashimoto's. At any rate, a fraction of the thyroid tissue can survive, and sometimes even recover temporarily, while the indicators of the attack, the antigens themselves, are disappearing from the blood. This can recur in cycles, as the surviving cells still need the blood supply, which carries the mediators of the immune response. When these T and B cells recognize a triggering level of the " enemy, " the attack resumes in force. In between full fledged attacks, there are still " scouts " in the blood, antigens at levels too low for blood tests to detect, still occasionally encountering a thyroid cell. Thus, thyroid function can continue to drop, even without the indicators of a full attack. It is when the gland is only partially destroyed, whether the immune system attack is in " remission " or not, that we are vulnerable to the paradoxical oscillation, when a sudden reduction in T4 ingestion can actually cause the T3 level to rise momentarily before it falls. Chuck Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 23, 2004 Report Share Posted July 23, 2004 Thanks Chuck! I'm taking a copy of this so I can read it on paper, which always helps my understanding. I'm getting a grip on things better now though. Fascinating stuff! Gail > Hypothyroid symptoms can be pretty severe just from a reduction in T4 > levels. The window for the euthyroid state is fairly narrow. A severe > reduction, let alone a complete shutdown, leads to coma and death. T3 is > essential for metabolism, which in turn is essential for life. > > An autoimmune attack continues as long as antigens (plasma cell > daughters of B cells) are produced from the attacked cell line. When the > thyroid has been damaged, viable cells are sequestered inside the > attacked layers of the gland, protected from the B cell identification > process. The thyroid tissue effectively " circles the wagons " to protect > what is left inside. > > We know other tissues also have limited capabilities for the functions > of the thyroid, particularly T4 to T3 conversion. It is not clear > whether these are also attacked in Hashimoto's. > > At any rate, a fraction of the thyroid tissue can survive, and sometimes > even recover temporarily, while the indicators of the attack, the > antigens themselves, are disappearing from the blood. This can recur in > cycles, as the surviving cells still need the blood supply, which > carries the mediators of the immune response. When these T and B cells > recognize a triggering level of the " enemy, " the attack resumes in > force. In between full fledged attacks, there are still " scouts " in the > blood, antigens at levels too low for blood tests to detect, still > occasionally encountering a thyroid cell. Thus, thyroid function can > continue to drop, even without the indicators of a full attack. > > It is when the gland is only partially destroyed, whether the immune > system attack is in " remission " or not, that we are vulnerable to the > paradoxical oscillation, when a sudden reduction in T4 ingestion can > actually cause the T3 level to rise momentarily before it falls. > > Chuck Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 24, 2004 Report Share Posted July 24, 2004 Chuck, What about the hyper swings in Hashi's with unmedicated people? Lots of people (myself included) remember hyper swings from the times we were not medicated for Hashi's. What causes that momentary rise in T3 levels? Jan Chuck B wrote: > > >Hypothyroid symptoms can be pretty severe just from a reduction in T4 >levels. The window for the euthyroid state is fairly narrow. A severe >reduction, let alone a complete shutdown, leads to coma and death. T3 is >essential for metabolism, which in turn is essential for life. > >An autoimmune attack continues as long as antigens (plasma cell >daughters of B cells) are produced from the attacked cell line. When the >thyroid has been damaged, viable cells are sequestered inside the >attacked layers of the gland, protected from the B cell identification >process. The thyroid tissue effectively " circles the wagons " to protect >what is left inside. > >We know other tissues also have limited capabilities for the functions >of the thyroid, particularly T4 to T3 conversion. It is not clear >whether these are also attacked in Hashimoto's. > >At any rate, a fraction of the thyroid tissue can survive, and sometimes >even recover temporarily, while the indicators of the attack, the >antigens themselves, are disappearing from the blood. This can recur in >cycles, as the surviving cells still need the blood supply, which >carries the mediators of the immune response. When these T and B cells >recognize a triggering level of the " enemy, " the attack resumes in >force. In between full fledged attacks, there are still " scouts " in the >blood, antigens at levels too low for blood tests to detect, still >occasionally encountering a thyroid cell. Thus, thyroid function can >continue to drop, even without the indicators of a full attack. > >It is when the gland is only partially destroyed, whether the immune >system attack is in " remission " or not, that we are vulnerable to the >paradoxical oscillation, when a sudden reduction in T4 ingestion can >actually cause the T3 level to rise momentarily before it falls. > >Chuck > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 26, 2004 Report Share Posted July 26, 2004 Jan, You wrote: > > What about the hyper swings in Hashi's with unmedicated people? Lots of > people (myself included) remember hyper swings from the times we were > not medicated for Hashi's. What causes that momentary rise in T3 levels? One more analogy: bad shock absorbers. If the springs in your car are working but the shocks are shot, the suspension acts like what is called an underdamped harmonic oscillator. This is how the pituitary - hypothalamus - thyroid feedback loop behaves all the time. TSH and T4/T3 levels are both like displacement from the equilibrium position. A sudden change in T4 or T3 medication for someone with partial thyroid function is like hitting a bump in the road, causing a repeated up and down motion that slowly goes back to equilibrium. The beginning of Hashimoto's spontaneously changes the spring and shocks back and forth, so it can have the same effect as driving a car with weak shock absorbers over train tracks. When the thyroid fails completely and is replaced by medication, you no longer have an oscillator, so the analogy is limited to at least partial thyroid functioning. Chuck Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 29, 2004 Report Share Posted July 29, 2004 Thanks! I understand it now. Mine used to oscillate into periods of normal activity too, it was really like a pendulum effect after a bump in the road. Jan Chuck B wrote: >Jan, > >You wrote: > > >> >>What about the hyper swings in Hashi's with unmedicated people? Lots of >>people (myself included) remember hyper swings from the times we were >>not medicated for Hashi's. What causes that momentary rise in T3 levels? >> >> > >One more analogy: bad shock absorbers. If the springs in your car are >working but the shocks are shot, the suspension acts like what is called >an underdamped harmonic oscillator. This is how the pituitary - >hypothalamus - thyroid feedback loop behaves all the time. TSH and T4/T3 >levels are both like displacement from the equilibrium position. > >A sudden change in T4 or T3 medication for someone with partial thyroid >function is like hitting a bump in the road, causing a repeated up and >down motion that slowly goes back to equilibrium. The beginning of >Hashimoto's spontaneously changes the spring and shocks back and forth, >so it can have the same effect as driving a car with weak shock >absorbers over train tracks. > >When the thyroid fails completely and is replaced by medication, you no >longer have an oscillator, so the analogy is limited to at least partial >thyroid functioning. > >Chuck > > > > Quote Link to comment Share on other sites More sharing options...
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