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Dr. Mariano, do T4 and T3 cross the blood brain barrier only as free T4 and free T3? Or do all forms of T4 and T3 get across? Some forms easier than others? Since T4 and T3, in whatever form, are all measurements of serum concentrations, can Total T4, Free T4, Total T3, and/or Free T3 (or some combination) be used to infer CSF concentrations?
I believe that this becomes an issue when desiccated thyroid is used as sole replacement therapy. Often this results in normal (or high normal) Free T4, Free T3, and Total T3, but markedly sub-normal Total T4. In this scenario, if CNS hypothyroidism were suspected (and I’m not sure what symptoms would differentiate CNS from peripheral hypothyroidism), would it be desirable, e.g., to achieve a normal Total T4 by decreasing the dose of desiccated thyroid and adding pure T4?
Thanks.@wolverine 1394 wrote:
Dr. Mariano, do T4 and T3 cross the blood brain barrier only as free T4 and free T3? Or do all forms of T4 and T3 get across? Some forms easier than others?
Since T4 and T3, in whatever form, are all measurements of serum concentrations, can Total T4, Free T4, Total T3, and/or Free T3 (or some combination) be used to infer CSF concentrations?
I believe that this becomes an issue when desiccated thyroid is used as sole replacement therapy. Often this results in normal (or high normal) Free T4, Free T3, and Total T3, but markedly sub-normal Total T4. In this scenario, if CNS hypothyroidism were suspected (and I’m not sure what symptoms would differentiate CNS from peripheral hypothyroidism), would it be desirable, e.g., to achieve a normal Total T4 by decreasing the dose of desiccated thyroid and adding pure T4?
Thanks.T3 and T4 are bound to three proteins in the blood:
- Thyroid Binding Globulin (also called Thyroxine-Binding Globulin, TBG)
- Transthyretin
- Albumin
The distribution of thyroid hormones and binding proteins are approximately:
T4: 68% to TBG, 11 % to Transthyretin, 20 % to Albumin
T3: 80 % to TBG, 9 % to Transthyretin, 11 % to AlbuminT4 has a stronger bond to TBG.
T3 has a stronger bond to Transthyretin
Both T3 and T4 have a much weaker bond (approximately 100 to 1000 x less) to Albumin.The thyroid hormones dynamically change between the free state and the bound state. Since the bond to Albumin is weaker, much of what is bound to Albumin may be free at any given moment, but won’t be registered as Free T3 or Free T4. Some portion of T3 and T4 is also free at any given moment but may not be registered as Free T3 or Free T4.
Free T3 and Free T4 give you only a snapshot – one moment in time – of the state. But this state varies from moment to moment.
This is why it is useful to take Total T3 and Total T4 into account to help determine total thyroid function.
This is analogous to Testosterone. Some use “bioavailable” testosterone as a measure of testosterone signaling activity. This would represent testosterone that is free and testosterone that is loosely bound to albumin. However, even tightly bound testosterone to sex-hormone binding globulin (SHBG) has signaling functions via induced conformational changes in the SHBG molecule then binding of testosterone-bound SHBG to SHBG receptors.
—
Thyroid hormone does not directly diffuse into cells.
Thyroid hormone is transported across cell membranes by various transporter molecules. In the brain and in the blood brain barrier (BBB), two known transporter molecules are Thyroid Hormone Transporter Molecule MCT8 and Organic Anion Transporting Polypeptide OATP1C1. MCT8 is also produced in heart, kidney, liver, and skeletal muscle.
There are two blood brain barriers: The Blood Brain Barrier Endothelial cells that line the blood vessels of the brain and are connected to astrocytes of the brain, and the Blood Cerebral Spinal Fluid Barrier Choroid Plexus Epithelial Cells that connect the blood to the Cerebopinal Fluid. The Choroid Plexus filters blood in order to produce Cerebrospinal Fluid.
From blood, T3 and T4 enter the brain via two paths:
1. T3 and T4 are transported into a BBB Endothelium Cell (via OATP). T3 and T4 are then transferred into an attached Astrocyte. In the Astrocyte, Deiodinase D2 coverts T4 to T3. T3 then exits the Astrocyte via MCT8. T3 then enters neurons via MCT8 transporters.
2. T3 and T4 are transported into Blood Cerebral Spinal Fluid Barrier Choroid Plexus Epithelial Cells (via MCT8). They they exit the choroid plexus (via OATP) and enter the Cerebrospinal Fluid (CSF). From the CSF, T3 and T4 are taken up by Tanycytes or Astrocytes. These cells have D2 Diodinase, which convert T4 to T3. Upon exiting these cells, T3 enters neurons.
Notably, neurons have Diodinase D3 enzyme which converts T4 to reverse T3 and T3 to T2.
The presence of thyroid hormone can reduce production of OATP as part of a negative feedback loop control.
—
Within brain cells, there are variations nuclear membrane thyroid transporters. Usually, 90 % of the intracellular T3 is located in the cytosol and 10 % is in the nucleus. In the pituitary gland’s cells, however, 50 % of T3 is in the nucleus.
—
Adding to the complexity of how thyroid hormone works, there is an Intracellular T3 Binding Protein (CTPB) which is produced in high amounts in the brain and heart, though is also widespread in production in the body.
—
Serum measurements of thyroid hormone can’t be used to infer CSF concentrations. Only a spinal tap will be able to tell what the CSF concentrations are.
—
Brain thyroid hormone levels and T3 to T4 ratios are going to be determined at several levels.
For example, the number and types and location of thyroid transporters determines what amount of thyroid hormone gets through.
Variations in the genes for the thyroid transporter molecules will determine how effective they are and how selective they are for T3 or T4 transport – creating a difference between Blood and Brain concentrations of Thyroid hormones.
Variations in Astrocyte and Tanycyte Diodinase D2 production will determine T3 to T4 conversions in the brain, which may be different from the blood.
etc.
—
From my point of view, given the differences that can arise in blood versus brain levels of thyroid hormone and thyroid hormone conversion, it is important to consider in some patients to not only optimize T3 but to also optimize T4 levels.
This is important, for example, in mood disorders. Here, the difference between T3 and T4 treatment becomes apparent.
In major depressive disorder, historically, T3 is a more effective treatment than T4 in reducing depressive symptoms. Spectulating: perhaps T4 to T3 conversion in the brain’s astrocytes and tanycytes is impaired by lack of D2 Diodinase production, among other possible problems in brain thyroid hormone metabolism.
In bipolar disorder, historically, T4 is much more effective than T3 in stabilizing mood. T4 may be used medicinally to reach “hyperthyroid” levels – based on TSH measurements – in psychiatry to stabilize mood in bipolar disorder. Speculating: perhaps, in bipolar disorder, there is a gene mutation in one of the thyroid transport molecules which selectively impairs T3 transport.
If a person is having problems with a T3 treatment or Armour Thyroid Treatment (which is primarily a T3 treatment), then perhaps adding a T4 treatment would be useful. Some patients benefit from combinations of thyroid treatments (e.g. T3 + T4, Armour Thyroid + Levothyroxine) better than single treatments alone.
Thank you, Dr. Mariano, for shedding so much light on what is apparently an extraordinarily complex set of processes.
In dishinguishing between CNS and peripheral hypothyroid symptoms, are you saying that mood disorders would likely be indicative of the former? How about myalgias and low temperatures…CNS or peripheral?
@wolverine 1404 wrote:
Thank you, Dr. Mariano, for shedding so much light on what is apparently an extraordinarily complex set of processes.
In dishinguishing between CNS and peripheral hypothyroid symptoms, are you saying that mood disorders would likely be indicative of the former? How about myalgias and low temperatures…CNS or peripheral?
The original question was about the addition of T4 to an Armour Thyroid Treatment.
And I used major depressive disorder and bipolar disorder as to examples where there is a difference between response to a T4 versus T3 treatment to due differences in brain thyroid hormone signaling and metabolism versus body thyroid hormone signaling and metabolism.
In both major depressive disorder and bipolar disorder, hypothyroidism may occur both in the brain and in the body. For example, nearly every person I see who has bipolar disorder has low thyroid signaling in the body. Thus, many physical signs of hypothyroidism such as low body temperature, dry skin, slow heart rate, slow deep tendon reflexes, etc. can be found in such patients. The late Broda Barnes, M.D. determined this in the 1970s (see his book, Hypothyroidism: The Unsuspected Illness for information).
—
Myalgias may have causes other than low thyroid hormone signaling. For example, the brain (including the blood brain barrier) and the immune system may produce excessive pro-inflammatory cytokines (the signals of the immune system) in an interplay in response to other factors (metabolic-nutritional problems, conditions which raise sympathetic nervous system activity, conditions that increase pro-inflammatory cytokine signaling including other cytokines, etc). This may produce the sensation of muscular pain from abnormal sensory signaling from the peripheral sensory nerves (a neuropathic pain syndrome) or the sensation of muscle pain from central nervous system circuitry (a central pain syndrome).
As an aside: what we call Tension-Type Headaches, from a neurological perspective is actually a hallucination. There is no muscular tension where the pain is located. It is a centrally-generated pain condition. Treatments that work include non-steroidal anti-inflammatory medications. Usually, people don’t call them antipsychotics. But in this case, they are. Tension-type headaches are real in that they are a commonly experienced condition that people can relate to. But technically, they are hallucinations also. They are normal hallucinations, just like dreams are normal hallucinations.
—
Low body temperature may be contributed to by low thyroid hormone in the body. However, it may also be contributed to by metabolic problems.
Thyroid hormone is a signal. The cell that receives will act on it depending on its capacity to act. If there are metabolic-nutritional deficits, then it may not be able to act on the thyroid signal well. Thus symptoms of hypothyroidism may occur.
Examples including iron-deficiency, Vitamin A deficiency, selenium deficiency, mutations of the thyroid hormone transporter molecules, deficiencies in intracellular thyroid binding proteins, mutations in the thyroid hormone receptor, mutations in mitochondrial DNA which impair response to thyroid hormone (hypothyroidism Type 2), etc.
@DrMariano 1405 wrote:
The original question was about the addition of T4 to an Armour Thyroid Treatment.
And I used major depressive disorder and bipolar disorder as to examples where there is a difference between response to a T4 versus T3 treatment to due differences in brain thyroid hormone signaling and metabolism versus body thyroid hormone signaling and metabolism.
In both major depressive disorder and bipolar disorder, hypothyroidism may occur both in the brain and in the body. For example, nearly every person I see who has bipolar disorder has low thyroid signaling in the body. Thus, many physical signs of hypothyroidism such as low body temperature, dry skin, slow heart rate, slow deep tendon reflexes, etc. can be found in such patients. The late Broda Barnes, M.D. determined this in the 1970s (see his book, Hypothyroidism: The Unsuspected Illness for information).
—
Myalgias may have causes other than low thyroid hormone signaling. For example, the brain (including the blood brain barrier) and the immune system may produce excessive pro-inflammatory cytokines (the signals of the immune system) in an interplay in response to other factors (metabolic-nutritional problems, conditions which raise sympathetic nervous system activity, conditions that increase pro-inflammatory cytokine signaling including other cytokines, etc). This may produce the sensation of muscular pain from abnormal sensory signaling from the peripheral sensory nerves (a neuropathic pain syndrome) or the sensation of muscle pain from central nervous system circuitry (a central pain syndrome).
As an aside: what we call Tension-Type Headaches, from a neurological perspective is actually a hallucination. There is no muscular tension where the pain is located. It is a centrally-generated pain condition. Treatments that work include non-steroidal anti-inflammatory medications. Usually, people don’t call them antipsychotics. But in this case, they are. Tension-type headaches are real in that they are a commonly experienced condition that people can relate to. But technically, they are hallucinations also. They are normal hallucinations, just like dreams are normal hallucinations.
—
Low body temperature may be contributed to by low thyroid hormone in the body. However, it may also be contributed to by metabolic problems.
Thyroid hormone is a signal. The cell that receives will act on it depending on its capacity to act. If there are metabolic-nutritional deficits, then it may not be able to act on the thyroid signal well. Thus symptoms of hypothyroidism may occur.
Examples including iron-deficiency, Vitamin A deficiency, selenium deficiency, mutations of the thyroid hormone transporter molecules, deficiencies in intracellular thyroid binding proteins, mutations in the thyroid hormone receptor, mutations in mitochondrial DNA which impair response to thyroid hormone (hypothyroidism Type 2), etc.
Do you think that the presence of axial muscle trigger points and spasticity could be related to brain hypothyroidism? Also, could brain hypothyroidism exacerbate spinal radiculopathy?
@wolverine 1419 wrote:
Do you think that the presence of axial muscle trigger points and spasticity could be related to brain hypothyroidism? Also, could brain hypothyroidism exacerbate spinal radiculopathy?
It would be useful to hypothesize the circuitry involved for these two phenomenon.
TRIGGER POINTS
Myofascial Pain Syndrome – the concept underlying the idea of Trigger Points – is the idea that focal hyperirritability in muscle can cause changes in nervous system function. The cogent question is how?
Trigger points are also though to be caused by microtrauma. Lack of exercise, nutritional deficiencies, insomnia, and repetitive strain are some predisposing factors to the development of microtrauma.
When skeletal muscle is damaged, mononuclear muscle precursors, the satellite cells, are activated to proliferate and form new multinucleated myotubes in the process of muscle regeneration. The injured muscle cells release various signals – including cytokines such as Leukemia Inhibitory Factor (LIF) – that stimulate muscle regeneration.
I am not yet familiar with all of the signals that muscle cells release. I can surmise that some of these are cytokines or eicosanoids which can trigger pain signaling from the sensory nerves monitoring the affected muscle.
Some of these signals may be pro-inflammatory signals that can trigger a local inflammatory response – i.e. active immune system activity. The immune system, in turn, can produce more pro-inflammatory signals to signal distress to the rest of the mind/body.
Hypothyroidism (be it brain or body) can lead to an increase in norepinephrine signaling as a compensatory response to the loss of energy production triggered by thyroid hormone. The elevation in norepinephrine signaling may contribute to insomnia as a risk factor for the development of trigger points. The loss of thyroid hormone signaling may also predispose a person to non-exercise, another risk factor for trigger point development.
Elevated norepinephrine signaling may magnify any incoming nociceptive sensory signal since filtering of the signal is reduced at the thalamus, since norepinephrine is also the stress/distress signal, allowing the pain signal to be processed by the cortex. Thus, pain may be felt more acutely.
Elevated norepinephrine signaling may also trigger the release of pro-inflammatory cytokines from the brain, which then active the immune system. An activated immune system may increase the inflammatory response started at the trigger point. This, in turn, may further increase sensory nerve pain signaling.
Should these pro-inflammatory cytokines shut down adrenal cortex signaling, Hypothalamic-pituitary-adrenal axis dysregulation with low cortisol signaling occurs. This reduces control of the immune system via cortisol. This may exacerbate ongoing inflammatory processes – such as that occurring at the trigger point.
Should elevated norepinephrine signaling lead to a reduction in dopamine signaling, particularly in the nigrostriatal pathways, muscular control may be impaired. This possibly may exacerbate the trigger point by increasing the tendency for dystonia (muscle cramps).
The lack thyroid hormone signaling may impair muscle cell metabolism, e.g. by reducing mitochondrial size. This may impair muscle regeneration and perhaps predispose muscle cells to the development of trigger points.
On the whole, the presence of hypothyroidism may exacerbate the pain caused by focal muscle hyperirritability – i.e. trigger points – at multiple signaling and metabolic levels.
—
SPINAL RADICULOPATHY
In spinal radiculopathy, the nerve roots from the spinal cord are injured by some mechanism such as direct pressure from a herniated disc or degenerative disease. This results in nerve irritability and an inflammatory process.
I wonder what signals the injured nerve releases locally to trigger immune system mediated inflammation, aside from the signal it sends pathologically to the central nervous system.
In any case, hypothyroidism may have similar effects as described in the circuitry for Trigger Points.
—
THYROID HORMONE AND PAIN MANAGEMENT
The above exacerbation of pain syndromes by hypothyroidism is one reason the treatment of hypothyroidism is a useful tool in pain management, as noted by Mark Starr in his book “Hypothyroidism Type 2”.
@DrMariano 1397 wrote:
T3 and T4 are bound to three proteins in the blood:
- Thyroid Binding Globulin (also called Thyroxine-Binding Globulin, TBG)
- Transthyretin
- Albumin
The distribution of thyroid hormones and binding proteins are approximately:
T4: 68% to TBG, 11 % to Transthyretin, 20 % to Albumin
T3: 80 % to TBG, 9 % to Transthyretin, 11 % to AlbuminT4 has a stronger bond to TBG.
T3 has a stronger bond to Transthyretin
Both T3 and T4 have a much weaker bond (approximately 100 to 1000 x less) to Albumin.The thyroid hormones dynamically change between the free state and the bound state. Since the bond to Albumin is weaker, much of what is bound to Albumin may be free at any given moment, but won’t be registered as Free T3 or Free T4. Some portion of T3 and T4 is also free at any given moment but may not be registered as Free T3 or Free T4.
Free T3 and Free T4 give you only a snapshot – one moment in time – of the state. But this state varies from moment to moment.
This is why it is useful to take Total T3 and Total T4 into account to help determine total thyroid function.
This is analogous to Testosterone. Some use “bioavailable” testosterone as a measure of testosterone signaling activity. This would represent testosterone that is free and testosterone that is loosely bound to albumin. However, even tightly bound testosterone to sex-hormone binding globulin (SHBG) has signaling functions via induced conformational changes in the SHBG molecule then binding of testosterone-bound SHBG to SHBG receptors.
—
Thyroid hormone does not directly diffuse into cells.
Thyroid hormone is transported across cell membranes by various transporter molecules. In the brain and in the blood brain barrier (BBB), two known transporter molecules are Thyroid Hormone Transporter Molecule MCT8 and Organic Anion Transporting Polypeptide OATP1C1. MCT8 is also produced in heart, kidney, liver, and skeletal muscle.
There are two blood brain barriers: The Blood Brain Barrier Endothelial cells that line the blood vessels of the brain and are connected to astrocytes of the brain, and the Blood Cerebral Spinal Fluid Barrier Choroid Plexus Epithelial Cells that connect the blood to the Cerebopinal Fluid. The Choroid Plexus filters blood in order to produce Cerebrospinal Fluid.
From blood, T3 and T4 enter the brain via two paths:
1. T3 and T4 are transported into a BBB Endothelium Cell (via OATP). T3 and T4 are then transferred into an attached Astrocyte. In the Astrocyte, Deiodinase D2 coverts T4 to T3. T3 then exits the Astrocyte via MCT8. T3 then enters neurons via MCT8 transporters.
2. T3 and T4 are transported into Blood Cerebral Spinal Fluid Barrier Choroid Plexus Epithelial Cells (via MCT8). They they exit the choroid plexus (via OATP) and enter the Cerebrospinal Fluid (CSF). From the CSF, T3 and T4 are taken up by Tanycytes or Astrocytes. These cells have D2 Diodinase, which convert T4 to T3. Upon exiting these cells, T3 enters neurons.
Notably, neurons have Diodinase D3 enzyme which converts T4 to reverse T3 and T3 to T2.
The presence of thyroid hormone can reduce production of OATP as part of a negative feedback loop control.
—
Within brain cells, there are variations nuclear membrane thyroid transporters. Usually, 90 % of the intracellular T3 is located in the cytosol and 10 % is in the nucleus. In the pituitary gland’s cells, however, 50 % of T3 is in the nucleus.
—
Adding to the complexity of how thyroid hormone works, there is an Intracellular T3 Binding Protein (CTPB) which is produced in high amounts in the brain and heart, though is also widespread in production in the body.
—
Serum measurements of thyroid hormone can’t be used to infer CSF concentrations. Only a spinal tap will be able to tell what the CSF concentrations are.
—
Brain thyroid hormone levels and T3 to T4 ratios are going to be determined at several levels.
For example, the number and types and location of thyroid transporters determines what amount of thyroid hormone gets through.
Variations in the genes for the thyroid transporter molecules will determine how effective they are and how selective they are for T3 or T4 transport – creating a difference between Blood and Brain concentrations of Thyroid hormones.
Variations in Astrocyte and Tanycyte Diodinase D2 production will determine T3 to T4 conversions in the brain, which may be different from the blood.
etc.
—
From my point of view, given the differences that can arise in blood versus brain levels of thyroid hormone and thyroid hormone conversion, it is important to consider in some patients to not only optimize T3 but to also optimize T4 levels.
This is important, for example, in mood disorders. Here, the difference between T3 and T4 treatment becomes apparent.
In major depressive disorder, historically, T3 is a more effective treatment than T4 in reducing depressive symptoms. Spectulating: perhaps T4 to T3 conversion in the brain’s astrocytes and tanycytes is impaired by lack of D2 Diodinase production, among other possible problems in brain thyroid hormone metabolism.
In bipolar disorder, historically, T4 is much more effective than T3 in stabilizing mood. T4 may be used medicinally to reach “hyperthyroid” levels – based on TSH measurements – in psychiatry to stabilize mood in bipolar disorder. Speculating: perhaps, in bipolar disorder, there is a gene mutation in one of the thyroid transport molecules which selectively impairs T3 transport.
If a person is having problems with a T3 treatment or Armour Thyroid Treatment (which is primarily a T3 treatment), then perhaps adding a T4 treatment would be useful. Some patients benefit from combinations of thyroid treatments (e.g. T3 + T4, Armour Thyroid + Levothyroxine) better than single treatments alone.
After reading your comments, Dr. Mariano, it seems that you are saying that even if free serum T4 measurements look consistently good (e.g., 0.8-0.9), that doesn’t necessarily imply that T4 concentrations in the brain will be good. Particularly if total serum T4 runs low (e.g, 4.0). And the best way to encourage good brain levels of T4 is to optimize total serum T4 to at least 8.0. Is that correct? And if so, is it tricky to add levothyroxine to an Armour regimen without raising T3 too high? Thanks.
@wolverine 1469 wrote:
After reading your comments, Dr. Mariano, it seems that you are saying that even if free serum T4 measurements look consistently good (e.g., 0.8-0.9), that doesn’t necessarily imply that T4 concentrations in the brain will be good. Particularly if total serum T4 runs low (e.g, 4.0). And the best way to encourage good brain levels of T4 is to optimize total serum T4 to at least 8.0. Is that correct? And if so, is it tricky to add levothyroxine to an Armour regimen without raising T3 too high? Thanks.
Free T4 of 0.8 to 0.9 is fairly low from a behavioral point of view. My criterion for suboptimal Free T4 is a Free T4 < 1.2
Based on clinical observation, I suspect behavioral hypothyroidism when one of these criteria is met:
- Free T3 < 3.3 (or 330 depending on the units)
- Free T4 < 1.2
- TSH > 2.0
—
There isn’t a way to assess brain levels of thyroid hormones because we don’t have a window into which we can see – outside of a lumbar puncture. For norepinephrine, we can see an approximation of brain levels from a Fractionated Plasma Catecholamine test – so long as the sympathetic nervous system to adrenal medulla circuit is not disconnected (i.e. the serotonin signal at the junction is intact). Diabetes is one example where this circuit is disconnected. But for thyroid hormone, we have no clear direct access.
—
Perhaps one way to do so is actually TSH – since TSH is the brain’s opinion of how much thyroid hormone it needs. Unfortunately, if the brain is not functioning well – as in mental illness or other metabolic-nutritional problem – then TSH may not be produced in sufficient quantities for a given thyroid hormone level. Another confounding variable is that TRH is made by numerous cells outside the hypothalamus – e.g. by the testes, the spine, etc. Thus, TSH may be a response to extra-hypothalamic signaling.
—
At this time, I think the best way to encourage good brain levels of T4 is to optimize Total T4. To an Armour Thyroid treatment, this means adding T4 to Armour Thyroid. It isn’t tricky to do so. If T3 goes too high, reduce the Armour dose. Since the half-life of T3 is much shorter than T4, it is far easier to adjust T3 (which stabilizes after 5 or fewer days) than T4 (which stabilizes after 6 weeks). I would watch for early signs of excessive T3 such as facial skin dryness, chapped lips or palpitations (a sensation of the heart bouncing uncomfortably in the chest).
Dr. M. , this is a very interesting post to me, but it’s hard for my foggy brain to understand most of it. I suffer from what I believe is a myalgia, or fibro pain syndrome. I have knots in muscles behind my neck/shoulders and big ones in my sacral/hip area. I suffer from pain most days and have anxiety about leaving home because of this. I also have 2 bulging discs but I’ve had them for a long time and had some pain from that years ago, but not the type of pain I have now.
I started to have this weird pain syndrome shortly after the removal of an ovary. I have always suffered from sensitivity to cold, cold hands/feet. Around the time of the surgery I also started having emotional issues as well and I was easily stressed. I chocked it up to low sex hormones and took vitamins. Last June I couldn’t take the pain so I started bio estrogen, progesterone and testosterone. After 6 months of not getting rid of these pains I thought I must have some type of thyroid issue. I had a thyroid scan 18 years ago and I was told I had a goiter that went away. I had a sonogram this time and they found complex cysts, nodules and enlargement. My endo wouldn’t treat them, so I found another doctor. I have since been using low doses of Armour and recently my doctor added 10mcg of Cytomel (high reverse T3 of 390). I also take 20mg of hydrocortisone and many supplements.
I’ve noticed some pain is better, but I still get spasms in my low back and I feel like my muscles are always tense even when I’m not. For instance, I’ll be sitting and notice my shoulder is all pulled forward and then I relax it back. When I’m standing I’ll notice my low back and glutes are tight and I have to release them. Very strange. Also, I cannot stand for longer than 5-10 minutes before my lower back goes weak and achy and I need to sit and rest. That is the worst part of all this besides the anxiety.
I feel that the low thyroid is an issue, but even with my levels being good for now I’m still having these pain syndromes.
You mention nutritional deficiencies as a possible problem. My ferritin was 31 several months ago and I read that needs to be higher for thyroid to function. I also had low Vitamin D at 28. Could those deficiencies be the root of my problem? I have been supplementing and getting those numbers up, but the latest levels were: Ferritin 51, Vitamin D, 46.1.
Also I have had several laparoscopic surgeries. Does one lose much blood during these? I also had C-Section 9 years ago. Could those operations plus normal monthly shedding started an iron problem for me?
I can deal with being a little tired, and cold, and the dry skin, and most of the other symptoms, but it’s the muscle pain and anxiety which has me in a depression as well that is very hard to live with.
My latest thyroid levels (none taking before test):
Free T4: 1.15 (0.61-1.76)
Thyroxine: 7.0 (4.5-12.0)
Free T3: 3.6 (2.3-4.2)
Total T3: 185 (85-205)In short, have you found that pain syndromes do get better when iron and D levels and selenium are at optimal levels? Do you think if my thyroid levels above look good, but my ferritin and D are not optimal that this is my pain syndrome problem?
Can laparscopic surgeries cause a lot of blood loss and send one into low iron problems?
Thank you.
@DrMariano 1483 wrote:
Free T4 of 0.8 to 0.9 is fairly low from a behavioral point of view. My criterion for suboptimal Free T4 is a Free T4 < 1.2 Based on clinical observation, I suspect behavioral hypothyroidism when one of these criteria is met:
- Free T3 < 3.3 (or 330 depending on the units)
- Free T4 < 1.2
- TSH > 2.0
—
There isn’t a way to assess brain levels of thyroid hormones because we don’t have a window into which we can see – outside of a lumbar puncture. For norepinephrine, we can see an approximation of brain levels from a Fractionated Plasma Catecholamine test – so long as the sympathetic nervous system to adrenal medulla circuit is not disconnected (i.e. the serotonin signal at the junction is intact). Diabetes is one example where this circuit is disconnected. But for thyroid hormone, we have no clear direct access.
—
Perhaps one way to do so is actually TSH – since TSH is the brain’s opinion of how much thyroid hormone it needs. Unfortunately, if the brain is not functioning well – as in mental illness or other metabolic-nutritional problem – then TSH may not be produced in sufficient quantities for a given thyroid hormone level. Another confounding variable is that TRH is made by numerous cells outside the hypothalamus – e.g. by the testes, the spine, etc. Thus, TSH may be a response to extra-hypothalamic signaling.
—
At this time, I think the best way to encourage good brain levels of T4 is to optimize Total T4. To an Armour Thyroid treatment, this means adding T4 to Armour Thyroid. It isn’t tricky to do so. If T3 goes too high, reduce the Armour dose. Since the half-life of T3 is much shorter than T4, it is far easier to adjust T3 (which stabilizes after 5 or fewer days) than T4 (which stabilizes after 6 weeks). I would watch for early signs of excessive T3 such as facial skin dryness, chapped lips or palpitations (a sensation of the heart bouncing uncomfortably in the chest).
Is it unusual, Dr. Mariano, to have a Total T4 of 4.0 on 3 gr Armour (even before the new formulation)? Particularly when Free T4 (.8-.9), Total T3 (167) Free T3 (445), and Reverse T3 (17) are relatively normal?
Also, if T4 is added to the 3 gr Armour regimen, would you expect to need to decrease the Armour dose?
Thanks.I feel this is a dam good thread I am Hypopituity and feel my Thyroid levels are good at least I feel good. My RT3 is high but this might be from having Heart Bypass sugary. It is said that Armour has changed and now my Caremark drug plain tells me they can’t get Armour any more most people on the web are having the same problems. I am on 4.5 grains of armour and don’t know what to take when I run out. I have about 90 days left of the old form of Armour after this I am out.
Here are my labs from last week.
RT3 38 range 11 to 32 ng/dL.
Aldosterone 6 range upright morning < or = 28 ng/dL.
DHEA-S 130 range 25 to 95 mcg/dL not on supplements.
T3, Total 161 range 97 to 219 ng/dL.
T4, Free 1.0 range .8 to 1.8 ng/dL.
T4 (Thyroxine) Total 8.3 range 4.5 to 12.5 mcg/dL
T3, Free 361 range 230 to 420 pg/dL.
Ferritin 88 range 20 to 380 ng/ml.
Folate Serm. >24 normal > 5.4 ng/mL
Estradiol 21 range 13 to 54 pg/ml
IGF-1 146 range 75 to 228 mg/ml.
None of my Testosterone labs came back was still in process.
Hear are the numbers from 8 weeks ago.
Total T 831 range 250 to 1100 ng/dL.
Free T 173.1 range 46 to 224 pg/mL.
Bio. T 333.4 range 110 to 575 ng/dL.
SHBG 23 range 17 to 54 nmol/L.@pmgamer18 1494 wrote:
I feel this is a dam good thread I am Hypopituity and feel my Thyroid levels are good at least I feel good. My RT3 is high but this might be from having Heart Bypass sugary. It is said that Armour has changed and now my Caremark drug plain tells me they can’t get Armour any more most people on the web are having the same problems. I am on 4.5 grains of armour and don’t know what to take when I run out. I have about 90 days left of the old form of Armour after this I am out.
Here are my labs from last week.
RT3 38 range 11 to 32 ng/dL.
Aldosterone 6 range upright morning < or = 28 ng/dL.
DHEA-S 130 range 25 to 95 mcg/dL not on supplements.
T3, Total 161 range 97 to 219 ng/dL.
T4, Free 1.0 range .8 to 1.8 ng/dL.
T4 (Thyroxine) Total 8.3 range 4.5 to 12.5 mcg/dL
T3, Free 361 range 230 to 420 pg/dL.
Ferritin 88 range 20 to 380 ng/ml.
Folate Serm. >24 normal > 5.4 ng/mL
Estradiol 21 range 13 to 54 pg/ml
IGF-1 146 range 75 to 228 mg/ml.
None of my Testosterone labs came back was still in process.
Hear are the numbers from 8 weeks ago.
Total T 831 range 250 to 1100 ng/dL.
Free T 173.1 range 46 to 224 pg/mL.
Bio. T 333.4 range 110 to 575 ng/dL.
SHBG 23 range 17 to 54 nmol/L.It does look like your FT3 is a little low for the level of RT3 you are carrying. When I figure your FT3/RT3
ratio by the method Dr. Holtorf uses, I get 100*3.61/380 = 0.95. Holtorf says you need to be over 2.0 to be well by his definition. Your ferritin level looks good. How are your cortisol levels? It’s possible you might feel even better if that RT3 came down some.
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