Erfa Thyroid dosage based on levothyroxine - Thyroid UK

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Erfa Thyroid dosage based on levothyroxine

Maniacos profile image
Maniacos

Hey guys,

I have huge problems with levothyroxine even with my new dosage (75mcg). You advised me to get bigger dosage (was on 50mcg) but not only it didn't help, it got worse. I plan to beg my doctor to prescribe Erfa Thyroid. What is the dosage equivalent for 75mcg levo? I know I need to start from 30, but later (how long?) 60 maybe?

We don't have those here (animal T4) and our doctors are like "those are bad!", well I think they just don't know them ... She doesn't even want to prescribe T3 ...

Thank you for your time reading this.

Cheers!

11 Replies
shaws profile image
shawsAdministrator

What country are you from?

Unfortunately 'modern-day' doctors rarely know anything about clinical symptoms of hypothyroidism and before blood tests were introduced, we were given a trial of NDT (Erfa etc). Big Pharma is very powerful indeed, with lots of money and have been able to persuade the Endocrinology that an inactive hormone (T4 - levothyroxine) is better than one that contains all of the hormones a healthy thyroid gland would have produced (i.e. NDT).

Usually NDT (Erfa etc) contains T4, T3, T2, T1 and calcitonin. The equivalent of 100mcg of levothyroxine is 1 grain of NDT.

This is a past post which may be helpful:

healthunlocked.com/thyroidu...

You begin on an equivalent dose i.e. 1/2 gr = 50mcg levo (approx). You can increase by 1/4 tablet every two weeks, always keeping a watch on your temp or pulse.If either rises too high drop to previous dose.

Good luck with your new method.

Some of us (myself included) find that levothyroxine doesn't suit because we don't impove at all and even feel worse.

Maniacos profile image
Maniacos in reply to shaws

Thanks! I will try to convince my doctor to prescribe that. I feel horrible from levo but I just found that rT3 is a super sneaky thing.

i.gyazo.com/5176fa097762e9d...

I'm starting to think this is my problem because after the increase to 75mcg levo I feel even worse. Sounds logical. My doctor: "We treated hundreds and never seen your condition" . And this is doctor number 3 ... All are amazed that Levo doesn't work. I just feel super weak and my legs are super stiff. Such an unusual condition ... Thanks again!

shaws profile image
shawsAdministrator in reply to Maniacos

The most who complain about levothyroxine are those that cannot improve on it. Many of our members cannot otherwise they wouldn't be looking for information.

Is your doctor aware that he is giving you an 'inactive' hormone and synthetic (although it might work for many) whereas NDT is made from animals' thyroid glands so more conducive to the human body (I've read). It was the only replacement and used safely since 1892 up until the present day when Big Pharma produced levothyroxine (T4 alone).

Levo should convert to T3 but some people just cannot improve on it. I would also like to know how many extra prescriptions doctors prescribes to patients who aren't improving on levo.

I am also aware that some people have to trial several NDTs.

I wish you a quick recovery.

MaisieGray profile image
MaisieGray in reply to Maniacos

RT3 isn't sneaky at all. It is a metabolite with a distinct purpose; and in the event of high RT3, the aim should be to identify and address what has caused that to be the case, and not simply chase and manipulate numbers as is so often encouraged in some mono-T3 groups in particular. In addition to producing rT3, the type 3 5′-deiodinase enzyme is also responsible for decomposing rT3 into inactive diiodothyronine; and other drugs, for instance beta blockers, can negatively impact the latter, and its elimination from the body - so if RT3 levels are rising and it's at least in part, due to the BBs, increasing T3 is not the solution. Reverse T3 can be elevated in conditions associated with a reduction in the metabolic rate, notably starvation, extreme carbohydrate restriction, chronic heart failure, and the non-thyroidal illness/euthyroid sick syndrome seen in critical illness, the elderly, chronic stress, myocardial infarction, chronic inflammatory states......... In these cases, the rise in rT3 is a consequence, not a cause, of the alterations in intracellular thyroid hormone metabolism directed by the deiodinase enzymes; the relative activities of which are affected by the condition itself. So for instance, if a fire alarm goes off, you don't put your effort into discovering ways of silencing it, or reducing the volume, you investigate where the fire is, and put it out. 🙂

greygoose profile image
greygoose in reply to MaisieGray

Brilliant analogy! :)

Maniacos profile image
Maniacos in reply to MaisieGray

I said sneaky because nobody told me to test it :(

i.gyazo.com/ce9f29cfef5d67b...

I'm with chronic prostatitis for years. I'm guessing this is the reason. But yes, I will investigate further. I barely function for the last 4 months, I need to address that first. I don't even know if I have rT3 problem .. :) Will make some tests on Monday. Thanks.

shaws profile image
shawsAdministrator in reply to Maniacos

I have read several posts about RT3 and there seems to be conflicting info about it but are you aware that T4 (levothyroxine) converts to RT3 and then into T3 (or should do).

I will try and find the link which states this.

Maniacos profile image
Maniacos in reply to shaws

I'm just happy I even found about rT3. It fits so well logically and with my condition. All other theories had some weird logical hole (I just assumed I don't understand enough). We will see. I will keep the forum apprised with the results for sure. Thank you.

shaws profile image
shawsAdministrator in reply to Maniacos

This is an excerpt which might also be helpful:

"However, I personally don't believe that measuring the free T4, free T3, or any other circulating hormone level, is the most effective clinical approach. My belief is based partly on the the studies of Escobar-Morreale and colleagues in Spain.[1][2] Their study results make one thing clear: Circulating free T3 and T4 levels don't allow us to accurately predict the T3 concentration in the cells of most tissues. The evidence suggests that there is simply too much variability between different tissues in the same patient. Moreover, there's too much variability between the tissues of different patients. Even more difficult is accurately predicting the physiological and clinical effects of different circulating free T3 and T4 levels. Again, there's simply too much variability to allow accurate predictions.

Barnes was right when, long ago, he wrote that circulating levels of hormones don't measure what's most important—how the patient's tissues are responding to a dosage of thyroid hormone. Our regimen involves multiple measures of how tissues are responding to a particular dosage, repeated at short intervals in a highly systematic way. Our model of assessment is taken from behavior modification, in which I was trained in the early 1970s. We know from hundreds of trial runs that we can precisely control the metabolic status of most patients only by using these multiple measures of tissue response. We adjust each patient's dosage until these measures tell use we've achieved normal tissue metabolic status—regardless of what the patient's circulating hormone levels are. I concede that you can do some fairly good tweaking by using free T3 and T4 levels. But still, if the patient's tissue responses aren't carefully assessed, the clinician isn't focusing on what's most important—the patient's physiological and clinical responses to treatment.

web.archive.org/web/2010103...

Maniacos profile image
Maniacos in reply to shaws

Thanks!

Some of us do not convert T4 to T3 (the active component) well. Pursue this with an Endo who is knowledgeable. Good luck.

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