Adding on Levothyroxine?

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chmuse said:
Thank you for the resources! I waited eight months to get in with an endocrinologist only for him to tell me to lose weight and that thyroid issues don't cause hair loss.
This gaslighting is inexcusable. I tell everyone who’ll listen to advocate for yourself by learning all that you can, find a good alternative doctor and stay away from end-holes.
 
yelloeyes said:
Okay.. I get now why you laughed.
It wasn't an insult! It would just be a bit early for me!

roxygirl said:
This gaslighting is inexcusable. I tell everyone who’ll listen to advocate for yourself by learning all that you can, find a good alternative doctor and stay away from end-holes.
The problem is the waits to get in! I waited eight months for the last one. I went in armed with plenty of research! But I always appreciate new rabbit holes to dive into. 😊
 
keangkong said:
That generally means your T3 and T4 are below what they ought to be. Although the numbers for your T3 and T4 are normal for many people, your elevated TSH means that your body is saying that it needs more. Doctors rely primarily on TSH in determining whether your body is making enough T3 and T4. I'm speaking generally. Go to an endocrinologist, who will be more knowledgeable than I am on the subject. Taking too much thyroid medicine can quickly cause severe health problems. Don't try adjusting your thyroid levels yourself; doing so is more dangerous than taking grey market tirzepatide if you're too heavy. Wait until January and visit an endocrinologist.
Finding a well educated integrative, functional or a naturopathic ND ( that can prescribe) because Endo’s that depend on the TSH to determine what a “ Free” T4 or “ Free” T3 not a total or an uptake is negligence out of pure ignorance.

In thyroid disease and therapy, even when TSH is normalized, we can still be genuinely hypothyroid if we do not have enough “Free” T3 getting into our thyroid hormone receptors in cells throughout the body.

Most people know there’s two ways we get T3 into our cells’ nuclei:

From circulating Free T3, and

From circulating Free T4 hormone that is converted into T3 at a variable rate.

However, most doctors are not taught about our cells’ and tissues’ high priority for and dependence upon circulating T3, nor are they taught about the largest factor that can reduce T4’s local variable conversion rate to T3, nor are they taught about the direct correspondence between Free T3 levels and T3 nuclear occupancy rate, which determines hypothyroid or euthyroid status both locally and globally in the body.

The body’s dependence on a baseline of healthy circulating T3 is a principle that Antonio Bianco has emphasized in numerous publications.

“ T3 and T4 cannot enter cells by passive diffusion. As they enter the cell, they must be carried on transmembrane thyroid hormone transporters, some of which have a relatively higher preference for T3 and others which have a relatively higher preference for T4.

T3 hormone does not need to be converted . It is already in the active form, ready to bind with receptors. If it is not inactivated to T2 by D3 enzyme expressed in the cell (D3 is not shown in this diagram), a large percentage of T3 entering on transporters can be ushered directly into the nucleus.

Circulating Free T3 fills the bottom layer of the gray sphere of nuclear receptors. Of course, nuclei don’t have “layers,” but TRs are distributed throughout the nucleus. This visually depicts the fact that each tissue depends on a baseline amount of circulating T3.

Deiodinase type 2 (D2) enzyme activity (and in other cells, D1, not shown) converts T4 hormone locally into T3, but at a highly “variable rate” because D2 will be progressively deactivated as T4 rises within reference range. (Analogy: You can imagine that the D2 enzyme is like an office worker who gets overworked and discouraged when too much T4 paperwork gets put on his desk that requires processing.)

T3 converted locally from T4 tops up T3 levels within the nuclear compartment. T4 is the second priority source for T3, a source that enables customization of T3 availability from tissue to tissue, as long as D2 and D1 enzymes can convert T4 locally at a healthy rate. The cell is simply not equipped to make extra T3 supply locally from converted T4 if or when FT3 supply falls short. T4 is nature’s version of “sustained-release T3” except that T3 production is highly variable.

In this particular tissue, a certain percentage of “unoccupied receptors” is necessary for euthyroid status. If too many of the unoccupied receptors are occupied, it will create localized thyrotoxicosis. If too few are occupied, the tissue will be hypothyroid. Therefore, T3 hormone sufficiency is the ultimate determiner of euthyroid status throughout the body.

The T3 bound to receptors will enable genomic signalling. In this cell located in the pituitary thyrotrophs, T3 will perform genetic transcription of TSH mRNA (see the arrow under the gray sphere), which, together with TRH hormone from the hypothalamus, co-regulates the level of TSH hormone secretion. In a different tissue or organ, T3 binding will signal to different genes that enable other essential biological processes to occur.

After binding with TRs for 30 minutes to several hours, each T3 molecule exits the nucleus and returns to the cell’s cytosol (the green area in the model).

The ratio of T3 and T4 hormones floating in the cytosol is then transported out of the cell by the same thyroid hormone transporters that brought T4 and T3 into the cell (exit transport is not shown in the diagram). The rate of hormone influx matches the rate of hormone efflux, much like breathing in and breathing out.

This means that intracellular T3 and T4 ratios and levels directly affect FT3 and FT4 concentrations in blood. There is no “secret compartment” for T3 in the body, no “black hole” that sucks up T3 and never lets it go back into blood. There are only different rates at which each tissue exchanges hormones with blood, and one “global” rate of exchange that is comprised of the net rate of all tissues. The body converts and recycles T3 and T4 hormone among many cells and tissues until they are converted to other thyroid metabolites and/or excreted from the body”
 
chmuse said:
It wasn't an insult! It would just be a bit early for me!

The problem is the waits to get in! I waited eight months for the last one. I went in armed with plenty of research! But I always appreciate new rabbit holes to dive into. 😊
That part is true. It is SO hard to get in with new doctors. It took me 6 months to get my husband into my GP. When I had to switch my son over from his pediatrician it didn't take as long because I asked the doctor directly at my annual.. it was only 3 months 🙄

I need to find a family dermatologist. I am dreading it....
 
Decreasing estrogen levels with menopause also can impair the conversion of T4 to T3 which also contributes to fatigue mood swings weight gain even though the numbers look normal. You need a good endocrinologist and one that will listen to your symptoms
 
I have hypothyroid, I have been prescribed and using Levothyroxine for many years.

My last test results show Elevated TSH, Normal T4, and Low T3.

I did a search and Yes,

GLP1s are in fact inhibiting the T4 to T3 conversion.

Just FYI for anyone else with this condition.

The doc prescribed T3..so we'll see. Interestingly I didnt notice the symptoms since Tirz and Reta keep me feeling great, the random fatigue I attributed to them, and the cold feet to Reta.
 
Samco12 said:
Hi everyone, first time posting here. I’m currently taking CagriSema and I’m down 40lbs so far.

I have access to a basically unlimited supply of 150mcg levothyroxine pills and know it can drastically increase your base metabolic rate.

I’m curious if there is anything seriously wrong with this? I know it can be a bit unhealthy but raising my calories necessary that much would be extremely helpful.
Absolutely, no, don’t do it.

Never ever mess with the homeostasis of the thyroid axis.

Besides that keeping your free hormones high, will do a strain on your heart, you don’t want.

This is not a vitamin pill.
 
keangkong said:
Why should I believe you instead of my endocrinologist?
true, this is the international guidelines.

This is not vitamins, but serious potent medicine, don’t mess with it.
 
Karen Carpenter was taking Levo for weight loss when she died ( other stuff, too). It can cause a heart attack, Graves like symptoms, hair-loss, all kinds of yucky things you don't want to deal with. If your doctor tested you thyroid months ago and you have been losing weight since, then it is pretty unlikely that your levels are still what they were. After I lost 40 pounds, I started getting some scary symptoms, my labs indicated I was hyper-thyroid. After over twenty years of taking thyroid meds, my weight loss cured the condition and I no longer take any thyroid meds.

So my thought is, if you insist on doing this - have your labs checked again, they may not be what they were.

I do find it kind of interesting that people are all over this thread, but a thread about other prescription drugs like HGH, tesamorelin, and so on, and there will be people all over that thread telling you how to dose it and it's okay to use the same needle for three months, just lick it clean before using.

That said, they'll take my Indian bought Tazarotene away from why they pry it from my cold, dead hands, but I guarantee I won't have died of some stupid diet crap that people with eating disorders use to lose weight.
 
roxygirl said:
I know my way around thyroid function and proper testing. The TSH is a pituitary hormone that signals your thyroid to make thyroid hormones. The T4 is an inactive hormone that converts into active thyroid hormone T3. The Free T3 is important because it’s free to enter the cells and is not bound to proteins. The TSH test alone without the actual thyroid tests leave many unwell.

Levothyroxine is T4 is generic for Synthroid. Taking T4 medication will be dependent on converting into T3. This action is not fully looked into by mainstream medicine. I contribute the lack of awareness to add to the obesity problem.

The T3 hormone is needed in all of our organs and when it’s low we experience symptoms in many ways. Low blood pressure, fatigue, low metabolism, low body temperature to name a few. We have more T3 receptors in our heart. There’s a study showing mortality in the ICU having low T3 levels.

I wouldn’t take T4 based on a TSH test. The TSH is such a misleading statistic and leaves many unwell. A TSH can be low or within a range with people still being HYPO. A full panel with “ Free” T4 and T3 is important. Low Free T3 levels is hypo in my experience.

If you did take T4 Levothyroxine coming off of the medication can be problematic. Taking GLP-1 helps inflammation that can help the conversion of T4 into T3.

Autoimmune disorders like Hashimoto are often overlooked too. Testing the TPO and TgAb antibodies are valuable.

roxygirl said:
I know my way around thyroid function and proper testing. The TSH is a pituitary hormone that signals your thyroid to make thyroid hormones. The T4 is an inactive hormone that converts into active thyroid hormone T3. The Free T3 is important because it’s free to enter the cells and is not bound to proteins. The TSH test alone without the actual thyroid tests leave many unwell.

Levothyroxine is T4 is generic for Synthroid. Taking T4 medication will be dependent on converting into T3. This action is not fully looked into by mainstream medicine. I contribute the lack of awareness to add to the obesity problem.

The T3 hormone is needed in all of our organs and when it’s low we experience symptoms in many ways. Low blood pressure, fatigue, low metabolism, low body temperature to name a few. We have more T3 receptors in our heart. There’s a study showing mortality in the ICU having low T3 levels.

I wouldn’t take T4 based on a TSH test. The TSH is such a misleading statistic and leaves many unwell. A TSH can be low or within a range with people still being HYPO. A full panel with “ Free” T4 and T3 is important. Low Free T3 levels is hypo in my experience.

If you did take T4 Levothyroxine coming off of the medication can be problematic. Taking GLP-1 helps inflammation that can help the conversion of T4 into T3.

Autoimmune disorders like Hashimoto are often overlooked too. Testing the TPO and TgAb antibodies are valuable.
I take Armour Thyroid because it also has T3. Most Dr. won’t prescribe Armour Thyroid anymore because they say people don’t need the t3 but I don’t think that is true.

When i first got diagnosed 20 yrs ago, I had a TSH of 4. They said I was normal. I insisted I didn’t feel well and my PC doctor sent me to an Endocrinologist. He tested my total t4, free t4 and t3. My t3 was very low, even though my T 4 was normal.

He put me on Armour Thyroid and said he wanted to try this first. He said normally he would prescribe synthroid but thinks that I may do better on Armour. He was right.

Years later when my insurance changed, my new doctor would only prescribe the synthroid. He said it was a better medicine. After being on it for about 3 months I started no feeling well again, after 6 months he finally prescribed me Armour and it helped me feel well again. It make a big difference for me to have the added t3 as my body does not convert the t4 very efficiently.
 
keangkong said:
Why should I believe you instead of my endocrinologist?
Because they're right. Tsh levels dont tell the whole story, You need at least the TSH + T4+ T3 to know. and then there are the free t4 and t3s etc.

as I mentioned I just found out that my T4 from Levo is not converting adequately to T3.

and GLPs are shown to affect this conversion.
 
desinr-gal said:
Because they're right. Tsh levels dont tell the whole story, You need at least the TSH + T4+ T3 to know. and then there are the free t4 and t3s etc.

as I mentioned I just found out that my T4 from Levo is not converting adequately to T3.

and GLPs are shown to affect this conversion.

My endocrinologist has the lab measure my T3, T4, TSH and a variety of other things. I lack a thyroid glance. As a result, I'm dependent on levothryoxine.
 
keangkong said:
My endocrinologist has the lab measure my T3, T4, TSH and a variety of other things. I lack a thyroid glance. As a result, I'm dependent on levothryoxine.
so why did you make the comment? you were being facetious? Its hard for me to read tone in these posts.
 
Samco12 said:
Hi everyone, first time posting here. I’m currently taking CagriSema and I’m down 40lbs so far.

I have access to a basically unlimited supply of 150mcg levothyroxine pills and know it can drastically increase your base metabolic rate.

I’m curious if there is anything seriously wrong with this? I know it can be a bit unhealthy but raising my calories necessary that much would be extremely helpful.
When people have hypothyroidism, taking synthetic thyroid will help restore their metabolic rate to something more normal. If you don't have hypothyroidism, it likely won't help, or might even hurt, your weight loss effort. The form of thyroid hormone you're talking about is called T4. It's the inactive form. To become the active form, T3, it needs to undergo an enzyme process. But the body can convert T4 into an inactive form as well, called Reverse T3. This actually suppresses your metabolism. So if you feed it a bunch of T4 it doesn't need, it's likely going to convert most of it to reverse T3, which might hurt your efforts.

There is a reason thyroid hormones aren't used for weight loss - it's pretty unpredictable what will happen, and often counterproductive. Even in people who take direct T3, which will raise your metabolic rate, often the body will just cannibalize muscle tissue instead of fat with that excess metabolic rate.
 
Samco12 said:
Hi everyone, first time posting here. I’m currently taking CagriSema and I’m down 40lbs so far.

I have access to a basically unlimited supply of 150mcg levothyroxine pills and know it can drastically increase your base metabolic rate.

I’m curious if there is anything seriously wrong with this? I know it can be a bit unhealthy but raising my calories necessary that much would be extremely helpful.
Look over at MESORX. They have a lot of experience with this as a PED. There are ways to do it with less risk.
 
Apologies for jumping on your thread, but I'm having thyroid issues and finding it difficult to receive treatment.

My blood pressure started dropping about four weeks ago, so I had to stop taking all of my blood pressure medications, and my BP was still 90/55. I also have extreme cold intolerance, extreme difficulty urinating and my sleep is worse than usual. I've been to two walk-ins with those blood pressure readings and received very little feedback. The first walk-in did bloodwork after I insisted, but they only tested my TSH, 5.72. The second walk-in clinic treated me like I was a drug addict and made no attempt to connect the dots.

I have always been subclinical hypothyroid, but only one doctor attempted to treat it. He would not go above 25 mcg, so it was pointless.

I called a third virtual clinic, which prescribed some synthroid, so I thought I was OK for the short term, but they only prescribed 14 pills @25mcg. Even the pharmacist said that was useless and didn't charge me.

I'm not sure what caused the sudden symptoms, as my TSH has been mildly elevated for a long time without these stereotypical symptoms. I did find an old bottle of synthroid from my previous prescription, so I've been taking 50 mcg for a few days and my blood pressure is starting to normalize. I also didn't have the heat set to 80 last night. The urinary symptoms persist, but they may take longer to stabilize.

I know there are a few well known clinics in the US that treat you based on your symptoms and not strictly based on the numbers. Unfortunately, I'm in Canada, so our Endos are a little more rooted in the stone age and it would take months to get a referral.

Any bright ideas regarding the possible cause or solutions?
 
desinr-gal said:
I have hypothyroid, I have been prescribed and using Levothyroxine for many years.

My last test results show Elevated TSH, Normal T4, and Low T3.

I did a search and Yes,

GLP1s are in fact inhibiting the T4 to T3 conversion.

Just FYI for anyone else with this condition.

The doc prescribed T3..so we'll see. Interestingly I didnt notice the symptoms since Tirz and Reta keep me feeling great, the random fatigue I attributed to them, and the cold feet to Reta.
Just to clarify, this isn’t for me but for a close friend, we’re in Italy, she had a thyroidectomy and is on levothyroxine, but her endocrinologist never checks FT3, so I’m trying to understand a bit better.

From what I understood, you didn’t really notice any symptoms and only picked it up from your labs, is that right?

How long had you been on Tirz when you saw those results?

And do you usually include FT3 when you run your labs?

Would really appreciate any insight! 🫶
 
I’m really sorry you’re going through this, that sounds incredibly frustrating, especially not being taken seriously with those symptoms.

A TSH of 5.72 alone doesn’t really tell the full picture, especially with symptoms like low blood pressure, cold intolerance, and what you’re describing overall. It might be worth checking a full thyroid panel (FT3, FT4), not just TSH. In some places FT3 isn’t routinely checked unless specifically requested, so it might be worth asking for a full panel rather than just TSH.

Also, the fact that you’re already noticing improvement after increasing to 50 mcg seems quite meaningful.

I’m not a doctor, but I’d be a bit cautious about adjusting the dose on your own long term, it would really be important to have proper labs and follow-up.

Given how you’re being managed locally, is there any way you could push for a full panel or get access to a private lab just to have clearer data?

Hope you manage to get some proper support soon, that situation sounds really tough.
 
Mara_aa said:
Just to clarify, this isn’t for me but for a close friend, we’re in Italy, she had a thyroidectomy and is on levothyroxine, but her endocrinologist never checks FT3, so I’m trying to understand a bit better.

From what I understood, you didn’t really notice any symptoms and only picked it up from your labs, is that right?

How long had you been on Tirz when you saw those results?

And do you usually include FT3 when you run your labs?

Would really appreciate any insight! 🫶
I didn't really have any symptoms previously, but my TSH has always been elevated. Although I have had times where my blood pressure dropped off a cliff for a short period of time. I assume it was similar to what's happening now.

I did have one really good walk-in doctor a long time ago and he tested everything, including antibodies, but I gather it didn't show anything, as i never got treated. I also had a thyroid ultrasound another time, so it's been on my doctor's radar, but never treated.

I also suffer from Atonic bladder, which i only recently read is tied to hypothyroidism. Unfortunately my urologist never connected the dots. Part of the reason for the worsened urinary symptoms.

I understand the obsession with the numbers, but if I'm experiencing the symptoms of hypothyroidism and synthroid alleviates the symptoms, I really don't care about the numbers? Is it possible that something else is causing the issue, yes, but I have no faith in their ability to diagnose it.

I suffer from a rare form of arthritis, but it took them 30 years to diagnose it, so all the drugs that could have stopped the progression are now useless.
 
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