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Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 1 to 6 of 6. This is the beginning of the thread.
Posted by Larry Hoover on August 29, 2003, at 7:45:13
I came across this while doing some research. Please be careful how you time your doses of each (if applicable).
Lar
Thyroid. 2001 Oct;11(10):967-71.
The acute effect of calcium carbonate on the intestinal absorption of levothyroxine.Singh N, Weisler SL, Hershman JM.
Department of Endocrinology and Metabolism, Veterans Affairs Greater Los Angeles Healthcare System, California 90073, USA. [email protected]
To determine the acute effect of calcium, we measured levothyroxine absorption after ingestion of thyroxine (T4) with and without simultaneous ingestion of calcium (as calcium carbonate) in seven volunteers without thyroid disease. Serum total T4, total triiodothyronine (T3), free T4, and thyrotropin (TSH) levels were measured after ingestion of 1,000 microg of levothyroxine on two separate visits at 4-week intervals: (1) levothyroxine alone and (2) levothyroxine together with 2.0 g of calcium as calcium carbonate. The amount of absorbed levothyroxine was calculated as the incremental rise in serum T4 level during the first 6 hours multiplied by the volume of distribution for the hormone. When 1,000 microg of levothyroxine alone was given to subjects, the maximum average total T4 absorption was 837 microg (83.7% of the dose ingested) at 120 minutes. When levothyroxine was coadministered with 2.0 g of calcium (as calcium carbonate), the maximum average T4 absorption decreased to 579 microg (57.9% of the dose ingested) at 240 minutes. The total levothyroxine absorption over 6 hours was significantly greater with thyroxine than that with thyroxine and calcium (p = 0.02). The administration of calcium and levothyroxine in these subjects was associated with a significant reduction in the peak increment in serum total T4 (p = 0.02) and free T4 levels (p = 0.03), as well as a significant reduction in the overall increment in serum total T4 (p = 0.003), free T4 (p = 0.002), and total T3 levels (p = 0.01) over four time points (120 minutes, 240 minutes, 360 minutes, 1,440 minutes). In summary, this pharmacokinetic study in seven volunteers indicates that calcium carbonate acutely reduces T4 absorption.
Posted by tealady on August 31, 2003, at 1:32:23
In reply to thyroid replacement and calcium carbonate, posted by Larry Hoover on August 29, 2003, at 7:45:13
Lar, this is well known..all calcium(not just the carbonate form) affects absorption of thyroid meds(T4)...supplements more so than calcium in food..but even say milk, will reduce the amount of T4 reduced. The affect on T3 meds is not so great ..but still there...so T3 meds are OK to take wth food.(as benefits of slower absorption/release outweigh the loss....but not with calcium supplements.
Also iron stops calcium absorption and vice versa..and all need to be spaced about 4 hrs from thyroid meds(at least I would space iron at least 1 hour from thyroid meds, and preferably 2)...or you adjust your thyroid meds. Basically consistency is the answer for most.
On the other hand ..if you feel hyper a nice big dose of calcium and magnesium is just the thing.
It gets real tricky when you are taking thyroid meds, calcium, iron etc a no of times per day..just don't make days with enough hours <g>...so I just time release my thyroid meds and make dosage adjustments..and purposely take with calcium and magnesium at bedtimeBTW you asked once before abut my meds(not real sure if you want to know?)..
I take 3/8Grain Thyroid extract (similar to Armour) + 25mcgT4 ..in a capsule time released for 8 hrs in MethocelE4M 30% of capsule (have a PDF on methocellulose and breakdown times with combos of startches, sugars, cellulose etc if interested) ..with rice filler ground white rice 70%..(own formula)..call this SRT
take 1 SRT in morning , same around 8 hrs later and at bedtime..this one with calc/mag.
Have been trialling SRT3 in afternoon instead of SRT but the hunger pangs hit badly exactly 15 mins after a taking..so now adding in 500mg tryosine with morning dose.
If I wake at around 4.30AM to 5.30am..often,..then morning dose is taken then..so away from brekkie..usually avoid milk with brekkie..except for bit in cup of tea<g>
Meds designed to time release as best as I can get it to normal body slow release..but I KNOW it's impossible. I do take extra if exercise..but I haven't perfected this as yet..so would be nice if adding in the T4 and tryosine could begin to work! I know about the use of T4 as a "storing house" for T3 on demand...My meds are not great but they sure are one heck of a lot better than just taking them not time released.
I have heard (but still no found the research on) that TSH kinda follows the cortisol circadian rhythm by maximizing at night..probably in early hours of morning. I KNOW TSH is higher in morning than in afternoon. I know that TSH stimulates production of T4(and T3)..so I guess this is maximized in the morning, and you would not need as much at night?..really no idea though.So if anyone knows anything about the daily cycle if thyroid hormone in our bodies could they please let me know,or point me to the source, thanks
I know. I'm making it far too complicated for most.Believe me I was "forced" by my body into it.
I had a really bad reaction to T4 meds low dosage, seemed to shut down my metabolism...rare , but I have heard form 2 others it has happened to as well. Some docs think it is because the small T4 amount is enough to stop your own TSH and thyroid hormone production via pit. feedback (D2 instaead of D1), but does not adequately replace your thyroid hormones.
IMO , this is over simplified ..and I did not get TSH and thyroid hormone tests to "prove" what was happening at the time..as I was too hypo to think or move. I do know tht adding in t4 meds (without reducing my 'Armour" actually caused me to go more hypo this year(by symptoms)..but I am perservering as the T4 does smooth things out.The last blood test showed adding in tyrosine oo actually reduced my T4 and raised TSh. I had thought it would raise TSH, as the extra dopamine should do this..but I surprised my T4 dropped as well. I will keep trying
Sorry long winded. I had a bad reactuion last weekend when I tried up "up" the tyrosine , I also took zinc and selenium. I thought I might have gone over to hyper,. I developed what I thought was a too hish T3 headache(a mild centre forehead headache)..bu then it got worse and turned into a mild migraine..typical for me LHS, behind left eye, left sinus involved and upper teeth on that side (6 and 7). Both eyes very glazed and reddish..and fatigue..spent most weekend in bed..always takes 3 days to get over..and until today was still a bit wiped..that was why I had the blood test. I was NOT hyper. My T4 had gone down and my TSH had gone up. Ft3 was actually a little lower too..but acceptable.
So I had not made myself hyper.
Does anyone knopw what ele can give those symptoms..too much noradrenaline? or too much dopamine? ..Anyone else ever had those symptoms?
Jan
Posted by tealady on September 2, 2003, at 22:52:47
In reply to Re: thyroid replacement and calcium carbonate » Larry Hoover, posted by tealady on August 31, 2003, at 1:32:23
Lar,
http://www.dr-bob.org/babble/20030828/msgs/255832.html
I found the Methocel info , if you are interested
http://www.colorcon.com/pharma/mod_rel/methocel/literature/Hydroph_Matrix_Broch.pdfpp 13 of 37 ..graph..click on enlarge to 200% to see it!
All compounding pharmacies I have contacted so far all use METHOCEL E4M..which does look like the current optimal choice for the purpose.
Note thought that with ONLY 25% Methocel, specified percentage of the drug you which to slow release and LACTOSE ..to speed up the release ..you get only about 80% of the drug (THYROID) in 8 1/2 hrs or so...90% in 12 hrs ..and 93% in 14 hrs etc.
Think I've got the drug release rate pretty right as I confirmed with my body temperatures, which are sensitive enough to the thyroid meds to act as a gaugeReally appreciate all your help,
Jan
Posted by Larry Hoover on September 5, 2003, at 7:52:14
In reply to Lar, Re:thyroid replacement , posted by tealady on September 2, 2003, at 22:52:47
> Lar,
> http://www.dr-bob.org/babble/20030828/msgs/255832.htmlFrom that post, I've brought forward some quotes, and I will reply here:
"The last blood test showed adding in tyrosine oo actually reduced my T4 and raised TSh. I had thought it would raise TSH, as the extra dopamine should do this..but I surprised my T4 dropped as well. I will keep trying"
Dopamine should reduce TSH, not raise it. The following document details the relationship comprehensively (see page 4).
http://www.thyroidmanager.org/Chapter4/4-text.htm
You also said:
"I have heard (but still no found the research on) that TSH kinda follows the cortisol circadian rhythm by maximizing at night..probably in early hours of morning. I KNOW TSH is higher in morning than in afternoon. I know that TSH stimulates production of T4(and T3)..so I guess this is maximized in the morning, and you would not need as much at night?..really no idea though.So if anyone knows anything about the daily cycle if thyroid hormone in our bodies could they please let me know,or point me to the source, thanks"
From the above document (page 3):
'TSH secretion in humans is pulsatile 220-223. The pulse frequency is slightly less than 2 hours and the amplitude approximately 0.6 mU/L. The TSH pulse is significantly synchronized with PRL pulse: this phenomenon is independent from TRH and suggests the existence of unidentified underlying pulse generator(s) for both hormones 224. The frequency and amplitude of pulsations increases during the evening reaching a peak at sleep onset, thus accounting for the circadian variation in basal serum TSH levels 225-227. The maximal serum TSH is reached between 21:00 and 02:00 hours and the difference between the afternoon nadir and peak TSH concentrations is 1 to 3 mU/L. Sleep prevents the further rise in TSH as reflected in the presence of increases in TSH to 5-10 mU/ml during sleep deprivation 228,229. The circadian variation of TSH secretion is probably the consequence of a varying dopaminergic tone modulating the pulsatile TSH stimulation by TRH229.1. There is little, if any, significant seasonal change in basal TSH nor are there any gender-related differences in either the amplitude or frequency of the TSH pulses 223. The diurnal rythmicity of serum TSH concentration is maintained in mild hyper- and hypothyroidism, but is abolished in severe short-term primary hypothyroidism, suggesting that the complete lack of negative feedback to the hypothalamus or pituitary or both may override the central influences on TSH secretion.229.2 '
> I found the Methocel info , if you are interested
> http://www.colorcon.com/pharma/mod_rel/methocel/literature/Hydroph_Matrix_Broch.pdf
>
> pp 13 of 37 ..graph..click on enlarge to 200% to see it!Thanks! This is an excellent application for methylcellulose polymers.
> All compounding pharmacies I have contacted so far all use METHOCEL E4M..which does look like the current optimal choice for the purpose.
>
> Note thought that with ONLY 25% Methocel, specified percentage of the drug you which to slow release and LACTOSE ..to speed up the release ..you get only about 80% of the drug (THYROID) in 8 1/2 hrs or so...90% in 12 hrs ..and 93% in 14 hrs etc.It would be virtually impossible to mimic the normal release of T4 with any oral drug regime. You'd have to have an implanted pump to come close. This drug carrier seems to be an excellent way to deliver thyroid hormone.
> Think I've got the drug release rate pretty right as I confirmed with my body temperatures, which are sensitive enough to the thyroid meds to act as a gauge
Way to go, for figuring that out. <grin>
> Really appreciate all your help,
>
> JanI'm glad to help. Let me know if I can help some more.
Lar
Posted by Larry Hoover on September 5, 2003, at 8:30:19
In reply to Lar, Re:thyroid replacement , posted by tealady on September 2, 2003, at 22:52:47
I've been pondering this thyroid issue for a while. There's another line of inquiry to consider.
The deiodinase enzyme (generically) that converts T4 to T3 depends on adequate selenium, as we've discussed. Your lack of response to selenium would pretty much suggest that is dead end. However, there is a still unidentified cofactor for the enzyme that is a sulphur-bearing molecule.
Every time the deiodinase pulls an iodine off T4, it has to be restored to activity by a subsequent reaction with the sulphur molecule. This leads to what is known as ping-pong kinetics. It's like firing and reloading a gun.
The problem right now is that even the state of the art, cutting edge research has not further characterized that sulphur molecule, beyond the fact that it is a sulhydryl (thiol) structure. That's a hydrogen on a sulphur (S-H), analogous to an alcohol group.
So, it may be something to try, to load up on sulphur-containing foods. The obvious amino-acid supplement would be cysteine, or N-acectyl-cysteine (it has a sulfhydryl group). Foods would be egg yolk, onion, garlic (side-effects may be malodorous flatus). There's a conversion pathway in our bodies that requires adequate methionine, so maybe B12/folate/B6, and/or TMG (trimethylglycine, also known as betaine) would ensure that you're processing homocysteine adequately. MSM (methylsulfonylmethane) also takes a little burden off the sulfhydryl processes, so it may contribute.
I'm just brainstorming. Deiodinase is also permanently disable by exposure to a chemical known as PTU. I'll see if I can find out how that is regulated.
Lar
Posted by Larry Hoover on September 5, 2003, at 9:57:57
In reply to Lar, Re:thyroid replacement , posted by tealady on September 2, 2003, at 22:52:47
The link between homocysteine and deiodinase activity is more robust than I suspected. Have you ever been tested for blood homocysteine level?
Homocysteine inhibits dithiothreitol formation, and that stuff may well be the cofactor sulfhydryl molecule that I thought was unidentified.
Lar
This is the end of the thread.
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