So T3 & T4 are produced by the thyroid gland. I
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Posted On: 06/30/2024 6:06:42 AM
So T3 & T4 are produced by the thyroid gland.
If the thyroid gland is dysregulated, then you may get lower T3 and T3 or higher T3 and/or T4.
What I was trying to show was that in the 350mg group, the attached pre-poster showed that T3 and T4 were increased. That would suggest that leronlimab somehow caused the thyroid to increase output of both the T3 and T4 hormones.
As you've said, T3 and T4 help burn fat and therefore, may help to eradicate liver steatosis.
Really, I only know of one biochemical stimulatory signal to stimulate the thyroid to produce T3 and T4 and that is TSH. Thyroid Stimulatory Hormone. But, if through the blockage of CCR5, this hormone is somehow increased, then we would have more T3 and T4. As T3 and T4 are consumed by the eradication of fat deposits, temporarily, T3 and T4 levels in the blood serum would decrease, as they went into the eradication of fat, but then TSH would increase to produce more T3 and T4 till homeostasis is achieved.
With less and less fat, there would be less and less need for the same levels of T3 and T4, so over time, as fat deposits decrease, the overall quantity of T3 and T4 produced by the thyroid would decrease, but the same level would be measured in the blood serum because that is where the homeostasis must remain stable. Since there is less fat, less T3 and T4 are necessary to metabolize that fat, but the same amount needs to remain in the blood.
Resmetirom is hardly effective. On average only 9% of patients benefit. But, since that is about 3x better than placebo where only 3% have resolution over same time period, the drug was statistically significant using 900 patients.
I'm thinking leronlimab, by somehow increasing T3 and T4 levels in the 350mg group does a much better job than resmetirom by a better mechanism of action, creating the REAL T3 and REAL T4, and not an artificial copy that lacks iodine that has liver hepatotoxicity attached to it where it is only 9% effective.
Here is a little more on it
If the thyroid gland is dysregulated, then you may get lower T3 and T3 or higher T3 and/or T4.
What I was trying to show was that in the 350mg group, the attached pre-poster showed that T3 and T4 were increased. That would suggest that leronlimab somehow caused the thyroid to increase output of both the T3 and T4 hormones.
As you've said, T3 and T4 help burn fat and therefore, may help to eradicate liver steatosis.
Really, I only know of one biochemical stimulatory signal to stimulate the thyroid to produce T3 and T4 and that is TSH. Thyroid Stimulatory Hormone. But, if through the blockage of CCR5, this hormone is somehow increased, then we would have more T3 and T4. As T3 and T4 are consumed by the eradication of fat deposits, temporarily, T3 and T4 levels in the blood serum would decrease, as they went into the eradication of fat, but then TSH would increase to produce more T3 and T4 till homeostasis is achieved.
With less and less fat, there would be less and less need for the same levels of T3 and T4, so over time, as fat deposits decrease, the overall quantity of T3 and T4 produced by the thyroid would decrease, but the same level would be measured in the blood serum because that is where the homeostasis must remain stable. Since there is less fat, less T3 and T4 are necessary to metabolize that fat, but the same amount needs to remain in the blood.
Resmetirom is hardly effective. On average only 9% of patients benefit. But, since that is about 3x better than placebo where only 3% have resolution over same time period, the drug was statistically significant using 900 patients.
I'm thinking leronlimab, by somehow increasing T3 and T4 levels in the 350mg group does a much better job than resmetirom by a better mechanism of action, creating the REAL T3 and REAL T4, and not an artificial copy that lacks iodine that has liver hepatotoxicity attached to it where it is only 9% effective.
Here is a little more on it
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