Ten days ago I treated myself to yet another round of blood tests.
TSH shot up to 2.88 from 0.11, so definitely 25 mcg is too
little daily T4 supplementation for me. If 50 mcg was too much, then I guess I
need 37.5? I’ll be cutting up pills every night then. Fine.
Magnesium was at the bottom of the acceptable range and
calcium was at the top! That’s got to be bad news, right? Maybe that plays a role in the return of my pain and tiredness?
Estrogen doubled yet again. Progesterone increased as well,
four times the amount I had when I wrote the “Perfect Ten Progesterone” posting, however, it is now only twice as much as my
estrogen, from ten times the amount. So that’s another piece of bad news.
Anti-TPO’s are falling again, 611 from over 700 (so, still a heck
of a lot, they should be below 6!), so moderately good news there, although… I’m
not even sure I should bother checking them anymore.
The CA-125 (an ovarian cancer marker) is higher than last year, 45
instead of <35. I don’t like seeing
it progress, needless to say, the more so as my estrogen is rising as well, steadily,
if you catch my drift…
Total cholesterol at an all time high: 225, with an LDL of 67.
So, still good ratio, but it was 190 five weeks ago… Vacationing in Eastern Europe increases cholesterol, who knew…
For the first time, I did Free T4, Free T3, Total T4, Total T3 and TSH, like so:
The real downer was Total T4, which was under the lower limit! Not by a whole lot, but still! What was that supposed to mean? Lab proof of hypothyroidism? Or was my body adjusting to the lower dose of supplementation? I can't wait to check it again and to talk to someone about this.
For the first time, I did Free T4, Free T3, Total T4, Total T3 and TSH, like so:
The real downer was Total T4, which was under the lower limit! Not by a whole lot, but still! What was that supposed to mean? Lab proof of hypothyroidism? Or was my body adjusting to the lower dose of supplementation? I can't wait to check it again and to talk to someone about this.
Well, on the other hand, I just read today "Levothyroxine And Lung Cancer In Females: The Importance Of Oxidative Stress", by Umberto Cornelli, Gianni Belcaro, Martino Recchia and Annarosa Finco a very credible study suggesting that too much T4 can cause serious issues as well and that one cannot monitor its amounts carefully enough. I see lots of people living with undetectable TSH levels and that cannot be right either. Inducing hyperthyroidism iatrogenically apparently can cause lung cancer in women.
"During the therapy with LT4 even at the steady state condition a peak of the hormone is evident a couple of hours after the administration and may cause a temporary condition of hyperthyroidism and a further increase of oxidative stress.
Oxidative stress is well documented in hypothyroidism [22-24] and is even worsened through treatment with LT4 [1,2]. The difference between the two conditions is that, in case of hypothyroidisms, oxidative stress is due to the reduction of AO [4], whereas, after the LT4 treatment it stems from overproduction of ROS from mitochondria [5,6].
A very simple method that can be used to measure oxidative stress is related to hydroperoxides content in plasma which is considered a very reliable test compared to other common methods since it shows very limited coefficient of variation [25].
An inverse association with fruit and vegetables consumption and lung cancer recently has been documented recently in the EPIC study for 50 to 59 age group, without an effect on specific histological subtypes [26]."So I should start measuring the hydroperoxide levels as well while I fiddle with this dangerous stuff. Also, increase antioxidants intake. I am not so sure about vegetables, finding clean veggies is an ordeal in itself. I will look into supplements.
How to decrease calcium and estrogen and increase
progesterone, magnesium and T4, make CA-125 and Anti-TPOs go away and be
happy?
That’s all I’d like to know.
P.S. on August 17, 2013: Actually, the above sounds outdated. Just an old Peatian "reflex". I no longer believe progesterone is good and estrogen is bad, so I take that back. I will stop caring about the progesterone/estrogen ratio and worry instead about the level of hydroperoxide in my blood. It sounds like a fair trade-off..:)
Plus, the study I mention gave me a nightmare last night. So maybe I should withdraw a bit from worrying about these things altogether, like the doctor said. Just find the time and organize another seaside session...
P.P.S. I just came across a study that supports my decision to stop considering progesterone such a good guy, a study linking it to the emission of hydrogen peroxide: "Progesterone increases skeletal muscle mitochondrial H2O2 emission in nonmenopausal women". Yep. :( And guess what, estrogen is counteracting it, according to the authors. That makes progesterone less than a hypothyroid woman's best friend, because it promotes oxidative stress. Taking this one step further: maybe it was an excess of my natural progesterone which launched the H2O2 destructive festival which may have brought about my Hashimoto's.
P.S. on August 17, 2013: Actually, the above sounds outdated. Just an old Peatian "reflex". I no longer believe progesterone is good and estrogen is bad, so I take that back. I will stop caring about the progesterone/estrogen ratio and worry instead about the level of hydroperoxide in my blood. It sounds like a fair trade-off..:)
Plus, the study I mention gave me a nightmare last night. So maybe I should withdraw a bit from worrying about these things altogether, like the doctor said. Just find the time and organize another seaside session...
P.P.S. I just came across a study that supports my decision to stop considering progesterone such a good guy, a study linking it to the emission of hydrogen peroxide: "Progesterone increases skeletal muscle mitochondrial H2O2 emission in nonmenopausal women". Yep. :( And guess what, estrogen is counteracting it, according to the authors. That makes progesterone less than a hypothyroid woman's best friend, because it promotes oxidative stress. Taking this one step further: maybe it was an excess of my natural progesterone which launched the H2O2 destructive festival which may have brought about my Hashimoto's.
According to Haskell, TSH needs to be low to keep the thyroid from producing any hormones. He believes that the antibodies are to our own thyroid hormones, and prescribes synthetic T4 and T3 (and warns against Armour and other dessicated thyroid replacement). Keep in mind that TSH is produces by the pituitary gland, to tell the thyroid to produce more thyroid hormone. How is a low TSH, then, indicative of hyperthyroid?
ReplyDeleteThe doctor is stupid. Historically cultures would eat the thyroid gland of animals, this was there only source and generally it was done to make sure pregnant women would have heavy babies. Now suddenly natural thyroid is no good, only take synthetic and become a slave to the pharmacy industry.
DeleteIt would be ideal to eat the thyroid gland of animals instead of taking anything, but they make it very hard to get.
First of all, I am not familiar with the minutiae of the Haskell protocol, I have never attempted it myself under his guidance nor have I talked to anyone who has. I am trying a "seat of my pants" version, without T3, to which I have no access and which doesn't really tempt me. I have a hard enough time accepting the extra T4 in my life.
ReplyDeleteBut...
How can we stop the thyroid from producing T4? I imagine the amount of T4 supplementation should be quite important, over 150 mcg... A big quantity. How does one go about supplementing in such amounts? I almost had no TSH in me after 50 mcg of Levothyrox from Merck. It must be a gradual, long process to get there. And then... to reverse that completely? To spring back from the depth of zero personal T4 to plentiful amounts? Again, that should take quite a while. Unfortunately, Dr. Haskell's videos' don't clarify the duration of the entire process.
I must admit, that study warning against too much T4 got my attention. Oxidative stress is what Dr. Haskell points to as well as a possible culprit for the destruction of the gland. And it makes sense, as hyperthyroidism often precedes Hashimoto's, being the initial stage of the disease, the stage where the thyroid gets broken. I don't recall Haskell saying that the antibodies act against our own hormones, they target TPO and TGO, as their names indicate, and those are not thyroid hormones, they are thyroid gland by-products. TPO (thyreoperoxidase) expecially sounds like a really nasty, oxidative element. Oxidative stress => broken thyroid cells => gland debris => need to clean up TPO and TGO, hence, Anti-TPOs and Anti-TGOs. Or that's what I remember from Dr. Haskell's video series.
Now, embarking on excessive artificial T4 supplementation could induce the so called iatrogenic hyperthyroidism, with its own brand of oxidative stress and free radicals attacking the gland itself, shrinking and destroying it further, and causing occasional spikes of hyperthyroidism again, etc, in a vicious circle, until the thyroid is no more and then... it's the lungs' turn? Yikes!
Please tell me I got it all wrong! :)
Are you familiar with that Ray Peat quote where he says that T4 only therapy is great for shrinking the thyroid gland?
ReplyDeleteIt is common knowledge that the thyroid may shrink under T4 protocol. The general interpretation seems to be that it is the loss of function that brings about the shrinkage , in a "use it or lose it" logic.
ReplyDeleteBut after reading the Italian study I mentioned in my blog post, it may very well be the *excess T4* which is causing the oxidative stress under which the thyroid shrinks, in the process I attempted to describe above.
Back to Dr. Haskell, I think he was recommending a TSH around 1, not completely suppressed, while "priming up" the thyroid with all those supplements in order to bring it back "online". That is what I am hoping to achieve as well for now.
When my TSH was below 0.4, I experienced hair loss. If you look on forums -- or places like STTM, many people blame Synthroid/T4 only therapy for that. And Ray Peat also mentioned the hair loss that is brought about by a TSH under 0.4. It may be, in fact, excess T4 that is to blame. Who knows, maybe glandular thyroid supplementation is helping people not get their TSH into the bottom range and preserves some sanity at that level, at least for some.
You were asking me how is a low TSH indicative of hyperthyroid -- the TSH is secreted when T4 levels are low, that is why doctors like to see those two labs and work with them to find the right amount of supplementation. Assuming one doesn't have issues with converting T4 to T3, and I am one of those people, that is a good way to find the ideal amount of supplementation. So I believe I am on the right track without messing with T3 and the rest of the molecules in glandular thyroid.
Ray Peat uses synthetic T4 and T3 himself. Funny how in this case he doesn't go the "natural hormone" route and doesn't claim that synthetic thyroxine is the work of the devil, like he does for progestins...
Ray Peat mentions that too much T4 is not a good idea: "An excess of thyroxine, in a tissue that doesn't convert it rapidly to T3, has an antithyroid action. (See Goumaz, et al, 1987.) This happens in many women who are given thyroxine; as their dose is increased, their symptoms get worse."
I will look for the Goumaz study...
The way I understood it from extensive reading, T3 is something that should be given when the conversion T4-T3 is sluggish. It helps with metabolism rates and symptoms, it is a fast "pick-up". Other than that, I cannot see a use for it? I don't want to raise my temperature and/or my pulse with hormonal supplementation, or at least, not for now. However, I would not mind raising them with diet and lifestyle, if possible.
Ray Peat's recommendation: "Since T3 has a short half life, it should be taken frequently. If the liver isn't producing a noticeable amount of T3, it is usually helpful to take a few micrograms per hour. Since it restores respiration and metabolic efficiency very quickly, it isn't usually necessary to take it every hour or two, but until normal temperature and pulse have been achieved and stabilized, sometimes it's necessary to take it four or more times during the day. T4 acts by being changed to T3, so it tends to accumulate in the body, and on a given dose, usually reaches a steady concentration after about two weeks."
Again, notice the "if" sentence above...:)
"Ray Peat uses synthetic T4 and T3 himself. Funny how in this case he doesn't go the "natural hormone" route and doesn't claim that synthetic thyroxine is the work of the devil, like he does for progestins..."
ReplyDeleteIt's not funny, it's just that the synthetic thyroid has the same chemical composition as the natural thyroid, while progesterone and progestins are different chemically.
"T3 is something that should be given when the conversion T4-T3 is sluggish"
ReplyDeleteRight, and if you are hypothyroid in the first place your conversion would be sluggish.
There are papers showing that T4 to T3 conversion works well among 25 year-old healthy medical students. I'm not aware of any study showing the conversion works well in other groups.
"There are papers", you say? :) Show me the papers! :)))
DeleteOf course you are "not aware of any study showing the conversion works well in other groups", people don't do such studies. It's like saying that you are not aware of studies showing that H2O quenches thirst or O2 is favorable to the breathing process..:)
Of course most people's thyroids on this planet work well and their metabolisms crank up the right amounts of everything! Even my father's thyroid is A-OK and he is 90!
Anyway, I scanned my thyroid labs in the blog post, there, maybe you will believe me when I say that, in my case, the said T4 to T3 conversion is fine. I even find it bewildering: although the T4 reserves are low, the free T3 and free T4 are within limits, so mitochondria are served, and the TSH pedal is being pushed so that more T4 may be on the way. That's how I interpret it, feel free to correct me if you think I am wrong... and thanks for your comments! :)
"Of course most people's thyroids on this planet work well and their metabolisms crank up the right amounts of everything!"
DeleteBroda Barnes, who I think is the best endocrinologist I read, said in the 1970s that 40% of the people were hypothyroid, and the tendency was to increase. So obviously it's not true that most people's thyroid and metabolism work well. At least that's the Ray Peat and Broda Barnes view.
The Ray Peat view is also that if you're not a young healthy 25-year old, your liver is likely not converting T4 to T3 optimally, especially if you were hypothyroid. I just thought you were following Ray Peat's paradigm, but on one of the most important issues, you're doing exactly what he warns against.
"40% of the people were hypothyroid, and the tendency was to increase. So obviously it's not true that most people's thyroid and metabolism work well."
DeleteBut... but...60% IS "most people", even if Barnes' (exaggerated) supposition were correct!
Ray Peat himself is not following what some of his misguided followers call "Ray Peat's paradigm". Peat is always, always taking into consideration each person's circumstances and chances are in my case he would agree that I don't have to take T3 and that my issue is hormone production, not hormone conversion. The gland itself seems to be failing, not the liver or the other tissues responsible for the said conversion.
I found Broda Barnes' views interesting but also extreme, in many instances. I think the STTD people are, again, extreme in their views. This natural thyroid or T4 + T3 trend fails to convince me on many levels.
As to being a Peat follower... the jury is still out on that one. I am a Peat reader and I am following the dietary guidelines without going to extremes (avoiding PUFAs like the plague, cleaning my gut with antibiotics, eating raw carrots daily to get rid of estrogen, taking hormones almost recreationally or obsessing about various pill ingredients.) I think my body should be capable to deal with such minor "ordeals" and overprotection is bad for it in the long run.
Excellent proof that Peat followers are not necessarily promoting Peat's views, but their own perception thereof, you may want to listen to Ray Peat's reaction to the Italian article by listening to the recent "Herb Doctors" show here... Dr. Peat never advocated the use of T3 therapy as a matter of principle and implied that T4 can do the job on its own when conversion is fine. Neither the host, nor the caller that intervened made him say the things you seem to think he thinks (although they both kind of pushed in that direction, so they must have thought the same thing themselves. I tell you, somebody needs to really "stop the natural thyroid madness" already... ;)
DeleteSynthetic T4 is chemically identical to the T4 produced in the body, but synthetic T3 is NOT. All synthetic T3 is "almost" chemically identical to what the human thyroid makes, just as progestins are "almost" chemically identical to progesterone. Where do you draw the line? When does "almost" become carcinogenic?
ReplyDeleteAnyway, one more reason for me to not go the synthetic T3 route... :)
As to progestins vs. progesterone, as many doctors say, they are both guilty until proven innocent. I go with MDs' attitudes on this one and I think Ray Peat has vested interests in maintaining that "natural progesterone" is any better than the progestins studied.
Do you happen to have a link for cytomel not being bioidentical?
DeleteFYI, high Calcium is a marker for hyperparathyroidism. Might want to get PTH and Vit D tested.
Hey Kiran,
DeleteI don't know about "bioidentical", we were discussing "chemical" identification. I picked that up on Wikipedia. Liothyronine sodium aka synthetic T3 aka Cynomel is sodium (S)-2-amino-3-[4-(4-hydroxy-3-iodophenoxy)-3,5-diiodophenyl]propanoate: http://en.wikipedia.org/wiki/Liothyronine. Note that there is a different article on the natural form of the hormone, Triiodothyronine, T3, which is (2S)-2-amino-3- [4-(4-hydroxy-3-iodo-phenoxy)- 3,5-diiodo-phenyl]propanoic acid, see here: http://en.wikipedia.org/wiki/Triiodothyronine.
Thanks a lot for the heads up regarding the hyperparathyroidism, I was reading up on that yesterday..:( My D3 has always been problematic, I never managed to raise it into what is considered the normal range. Looking back on my labs, my PTH has always been within range, in the upper portion, with calcium in the mid-normal area. I need to see what is going on now. I wouldn't be surprised if, like BG variations, this were another effect of T4 supplementation... I hope these are all adjustment issues and my body will soon find its equilibrium.
Meanwhile, more doctor visits... :(
I hope you are doing well!
I think it's all part of the same mess. Excess PTH, high serum calcium and low vit D levels are all bad for ya. :P
DeleteLow vit D can cause raised PTH which increases serum calcium in turn.
Right now, I'm experimenting with increasing vit D to bring down PTH, and it seems to have triggered a whole lot of allergies ...
It did bring my heart rate down though(used to be pretty close to tachycardia), which is good.
Those are the same chemicals at different pHs. A carboxylic acid and it's conjugate base are at equilibrium depending on pH, but the natural and synthetic t3s are identical.
ReplyDelete