Did you know that you can have "normal" CBC labs and STILL have low Ferritin? That is exactly what happened to me. My symptoms were fairly benign at the beginning with my low Ferritin, but due to an abnormally long menstrual flow, I then plummeted with symptoms--my arms tired quickly when I would wash my hair, extreme hair loss, achiness, and depression. And...I was unable to raise my Armour. That's when I discovered my Ferritin to be in the low teens. I got on iron, and managed to raise it to about 58. Got off, and DOWN my Ferritin went. Very strange. I now keep it between 70 - 90.
I didn't say it, but it is my understanding that 3-5 grains is a full replacement dose. I do know a few gals who are on much more, but they seem to have some kind of thyroid hormone resistance.
When you mentioned that a side effect of Synthroid is hair loss--doesnt' surprise me a bit. It's T4 only, and I note that T4-only users have continuing hypo symptoms--and hair loss is one of those. And low Ferritin doesn't help either. When I was on Levothyroxine, my hair kept getting thinner and thinner. I thought it was due to nearing peri-meno, but I was wrong. After I switched to Armour and was allowed to get my free T3 at the top of the range, slowly but surely my hair thickness has come back! I hope that turns out to be true for you! :o)
just curious - but you say antibodies have never been checked? then how do you know you have graves?
the reason for asking is this:...even though your TSH was suppressed...all your symptoms are ones that can be hypo...and were you just on a higher dosage of synthroid that suppressed your TSH? Or are you really Hashi's who just went hyper for a while? i guess i'm wondering if they treated you for hyper (what did they do? RAI?) when you were just still hypo and undertreated on a T4 med. I especially wonder this because of the hair loss. True, TED (thyroid eye disease) is more common to Graves than it is to Hashimoto's...but it can happen with both. sorry for being nosy..but you wouldn't be the first Hashi's person to get RAI for a hyper phase.
A FEW POINTS:
Antibodies aren't necessary to clench to diagnosis of Graves
Pharmacologically 3-5 grains of armour would usually be considered a high dose while 1-3 grains may be normal full replacement based on pharmacodynamic models of thyroid hormone physiology in humans. Studies are still lacking on the exact answer here.
Until we have studies of armour patients followed over years for heart disease (based on TSH levels, etc) I would hesitate in broadcasting statements that Armour does not cause heart problems in the same way endogenous hyperthyroidism does.
Low Ferritin is an early sign of iron deficiency - in LPN's case would check for celiac sprue (anti gliadin & anti endomysial antibodies) and for pernicious anemia (anti-IF and anti-parietal cell antibodies).
In the case of Minnie - I am concerned that 3g of armour may have over-stimulated the heart and aggravated the a-fib - even though dosed 1/2 bid as stated - in that case I would convert to synthroid or levoxyl to see if the a-fib improves (and make sure the TSH is 0.5-2.0).
I believe that people should be cautious in making broad statements about treating thyroid problems - particularly when it comes to TSH and high dose armour -- there are many individual considerations that a clinician should use in making these decisions and such broad statements may be dangerous to an individual who may then try to titrate their own armour dose -- I have personally seen patients in atrial fib and heart failure in such situations.
I used to have a Ferritin as low as yours, and it was miserable--hair loss, depression, achiness, palps, weakness in my arms and legs...plus I was unable to raise my Armour at a certain point without having problems. I finally got wise about it--had it tested. Started on iron--had to take quite a lot--and now I keep my Ferritin between 70 - 90. Made a huge difference, plus I was able to once again raise my Armour and get the full benefit. And by the way, it appears that MANY hypos have low Ferritin, and we're not sure why. I also had to stop seeing Endos--they didn't seem to have ANY knowledge about Armour or it's benefit...or how to dose it. And I KNEW first hand that Armour was working far better for me than Levothyroxine, which I used to be on.
Dr. Mark, it is refreshing to read an Endocrinologist like yourself state that the TSH is not the end-all test, because AACE and so many of your colleagues are rigidly stating that fact ABOVE AND BEYOND the continuing symptoms of patients who are kept in that TSH range. And if a patient on Armour takes enough Armour to rid themselves of symptoms...and has a suppressed TSH...it's the Endocrinologists who are screaming bloody murder and insisting that the patient in now "hyper" and that the patient needs to decrease their Armour, even though there are NO symptoms of hyper and even though decreasing Armour to get the patient back "in range" also causes hypo symptoms to return!
But when you state that you have to rely on studies---those studies are based on patients who are either true hyper, or on patients on T4-only meds, and no studies are addressing those who are on Armour, which changes that feedback loop! So, because of inadequate "studies" (and because of the huge financial power of Abbott labs), patients are being told to decrease or dose according to a TSH and inadequate studies.
When did "studies" and "mainstream thyroidology" become more important than obvious symptoms, or more important than patients who are finally symptom-free, yet are told to decrease their meds so they can fall within an arbitrary range??
It's ludicrous.
But, you also stated that "the individual patient evaluation supercedes any generalized statement that can be made", and that is hopeful. Because there appear to be thousands upon thousands of us..of individuals..whose experiences with Armour and with dosing NOT by the TSH are DISPROVING those "studies" and that "mainstream thyroidology".
The TSH debate continues....it is certainly not the end-all test and we all welcome the day when we have tests that reflect tissue level thyroid activity -- until then, in order to make general treatment recommendations we need to rely on studies that suggest a low tsh may be harmful in certain patients -- body temperature is not dependable to reflect thyroid function. There are certainly other opinions that are well marketed and described -- however, in mainstream thyroidology we depend on studies and expert consensus -- again the individual patient evaluation supercedes any generalized statement that can be made.