This test is inexpensive and readily available in the U.S. Unfortunately, the same is not true in Germany, where only one lab offers VLCFA testing. Additionally, very few doctors, including general practitioners and specialists, are willing to include this test in their diagnostic process.
Saw the paper on VLCFA quickly. My interest was only what kind of chain length and the paper says C22 plus. What is the source of such fatty acids in our body ? Does the body produce them, what for ? Given the common knowledge that our source of fatty acids are the fats and oils we consume, directly or indirectly from foods that contain oils ( e.g. nuts)and the fact almost all common oils and fats of either plan origin or animal origin, including dairy fats, contain only upto C-18 chain and some oils (e.g) low percentages of C-20 ( very rarely traces of C-22 in sparsely used oils), how do we get C-22+ chains for one to become prone to this fatigue presentations. Can you give further inputs on these questions. Three fourths of what we consume from different sources are C16 and C18, whether saturated, mono unsaturated, diunsaturated or triunsaturated. The exceptions on either end are those consuming a lot of coconut oil and palm kernel oil ( predominantly C-12) or fish ( polyunsaturated from C-18/C-20).
Nice summary of amine acids. Thanks. Would go through them over and over again. But my query remains unanswered, the source of VLCFA in the body, when very little of it is available from the fats and oils we consume. VLCFAs ( C 22 and plus) are normally found in natural waxes ( bees wax etc) which we don’t eat and in Jojoba Oil, which though edible, is not normally eaten. These are all not triglycerides, but esters of long chain fatty acids and long chain fatty alcohols.
Thanks. Some good updating of knowledge. Do you consider phytanic acid very long chain ? It is only a C 16 chain ( palmitic acid) with 4 methyl side chains. Makes it only C 20. It is a multiple branched acid. I am, for the first time, reading that such a branched chain acid is present in the food sources mentioned. Or is it a metabolic product in the body - if so the metabolism of what from these food source ? By the way, if this acid is available industrially, it will be an excellent lubricant in many industrial applications. I am going by the example of isostearic acid, which has a single methyl side group,in the middle of a normal fatty chain.
Isostearic acid, with its branched structure, interacts with VLCFAs by altering membrane properties, potentially interfering with enzyme function, and being metabolized differently than straight-chain VLCFAs. This can have significant implications in the context of diseases where VLCFA metabolism is impaired, as branched-chain fatty acids may exacerbate these conditions or lead to altered fatty acid dynamics. (my research in progress)
More serious complications arise when managing a patient with VWD Type II and V, Celiac disease, and elevated phytanic acid levels, as these conditions require careful coordination of both diet and medications. Since the combination of all three conditions is rare, few patients are diagnosed with this complex overlap, making treatment even more challenging and highly individualized.
I read. I listened. I listened again. Then I took 600mg of TRU NIAGEN. Within an hour, my muscle pain has eased and I can sit still without squirming in pain and move without wincing.
I'm already on a CIRS chronic inflammation treatment program, but so far the muscle pain has been resistant to exercise (makes it worse), stretching, massage gun, physio, remedial massage, magnesium, etc. Phototherapy is like being plugged into a power socket - couldn't move without it, but even though it stimulates my mitochondria it does nothing for the muscle pain (maybe even makes it worse).
Thank you for the missing link ❤️. Maybe it will get me through until I can achieve a longer-term solution. 😊
Let us hope this assessment holds true, opening the prospects of some clinically correct treatment. This long covid or more appropriately long vax is a nagging, even treacherous condition and there could be more routes to its occurrence, often a combination of them. It is necessary to keep exploring. Whatever, I would underscore on fundamental. It is certainly the lingering virus spike proteins, vax spike segments and the cationic LNPs that are driving the persistence of these presentations. As root causes, they need to be flushed out, to render other treatments effective. I am surprised and even concerned that in the dozens and dozens of substack presentations I have seen, including Dr. McMillan’s, this flushing out has not been discussed at all, let alone as a focus. Without it, there will not be complete light on this disease conditions. Could this residuals be treated as a virus infection by themselves and be addressed by classical covid treatments with repurposed drugs - the off label anti virals, anti histamines, anti inflammatories etc ?
Increasingly looking like a chicken and egg syndrome - which came first ? If the spike is the root cause, then inflammation comes next, so should we not expel the spikes first, wherever they have taken residence ?
the true explanation is understanding basic human physiology, which is not that simple but covid 19 messes with the bodies electricity, like every serious disease, hence oxygen distribution is not optimal, hence fatigue and all the other symptoms. I wrote in my latest article with great examples how to save life in critically ill patients, which nobody did in protocols for covid , all backed by scientific papers:)
Hi Dr., thank you for this post. The audio is especially helpful as I am very symptomatic with LC and ME/CFS.
Was wondering if you have seen Rob Wust’s recent webinar on his study results of skeletal muscle in LC? I’ll link it here.
I tried supplementing with carnitine and niacin a few years back but I think my inflammation was just too high for it to make a difference. I’m a bit better now, but I am loathe to spend any more money on supplements as it always feels like a shot in the dark.
The whole purpose of the post was to highlight that simple supplementation without addressing the root cause of inflammation is unlikely to bring long term benefit.
If you have symptoms of CFS/ME, (almost indistinguishable from long Covid symptoms) it might be that your symptoms are actually due to intracellular hypothyroidism (IH) – you can look up IH at “research gate”. Anyway, check your thyroid 3 and reverse thyroid 3 levels – if FT is less than 4.0, maybe you have IH.
If you do have IH (a.k.a. “low T3 syndrome”), oral DHEA will help a bit, but the correct prescription is slow-release Triiodothyronine (Liothyronine), titrated to produce a serum free T3 between 4.5 and 6.2.
If you decide not to check this recommendation, no sweat!
If you do decide to check it, please let me know the outcome.
Thank you for this. I’ve had Hashimoto’s and hypothyroidism for decades now. My levels were all stable until about two years into long COVID, when my TSH started jumping all over the place. I’m working with a great endocrinologist and for a while she had me on liothyronine in addition to Synthroid, but my T3 levels were never a problem and I didn’t feel any different on the liothyronine, so she took me off of it. She incrementally titrates my Synthroid and retests me every six weeks. It’s been kind of a tiresome situation because just when it stabilizes, then the next time I have bloodwork, I become either hypo- or hyperthyroid yet again. Long COVID has really messed with my body metabolically. Pre-diabetes and high LDL and total cholesterol too, out of nowhere and not diet related. It’s been quite a ride.
Hashimoto's causes true hypothyroidism (TH), in which T3 is in short supply because the thyroid gland's output of T4 is reduced. True hypothyroidism is nicely treated with Eltroxin or Synthroid (T4), providing that your cells are converting T4 into T3, as they normally do.
Under stress conditions however, increased cortisol production blocks T4 – to – T3 conversion, along with increased conversion of T3 to reverse T3 and what you have been is intracellular hypothyroidism (IH) – you can look that up either in SUBSTACK, or via Research Gate.
You can have both conditions together. If you do, and you try to treat your TH with T4, the T4 you take won't convert to normal T3: it will convert to reverse T3, which does not work.
As an example, I checked my Reverse T3 for the first time back in 2013, and was shocked to find that it was 34 (it should be <13). I tried treating it with desiccated thyroid (DT contains70% T4 and 30% T3) and when I rechecked the reverse T3, it had shot up to 54! ..... I got good relief of my symptoms by taking T3, instead of Eltroxin and the reverse T3 went down to 7.
I have been taking compounded, slow-release T3 since 2014: my current dose is 50 µg and I take it at 4 AM, to mimic the normal diurnal surge of T3.
If the ratio is less than 20, you have IH, not TH and you need to be treated with slow-release T3 (Triiodothyronine, or "Liothyronine").
NOTE:
(1) Cytomel, the proprietary T3 preparation, is in a quick-release tablet and adequate dosage tends to produce a "spike – and – crash" phenomenon, which can be quite unpleasant.
(2) when taking T3, the TSH tends to go way, way down, because the T3 filters through into the pituitary gland and the pitcher forgets so "happy" that it stops producing TSH. That is not a problem: it is simply a sign that the pituitary is happy with the amount of T3 is getting.
I agree - supplementing with nicotinamide riboside didn't make enough difference, sadly. Having an extremely restricted diet (established via scientific process) has been essential but has reached its limit of helpfulness. Anti inflammatories are also invaluable - NAC (brain), ubiquinol (muscles), etc. Not sure yet how much PEA is helping.
I consult with a functional medicine nutritionist who is following the CIRS Shoemaker Protocol (the nicotinamide riboside wasn't part of this). It involves supplements and lots of expensive tests, but she is obtaining the only insights into causes and mechanisms. My life is on complete hold (with my bank account draining), waiting for our Western medical system to catch up and help. If only doctors would even acknowledge functional medicine practitioners it would be a start, as GP's are the gatekeepers to our health system (the ones that apply functional medicine practice are few and hard to access, but also are not nutritionists). Most GP's seem to be following standardised protocols (some sort of rule book) and seem adverse to applying a scientific approach in wielding their medical knowledge. I've heard it a disturbing number of times - "They didn't teach us that at med school, therefore it doesn't exist". Learning shouldn't stop at the end of school, but I'm sensing that our medical system doesn't reward initiative.
Hey Karen! Take your PEA with 200 mg of Pregnenolone (Progesterone is a better idea if you are in menopause), at night: you will sleep better, your memory will improve
(Watch out – maybe you will remember your dreams and if you tend to have nightmares, you will remember them and blame the supplements) – there are no other side effects, but I did notice that when I put my progesterone dose up to 200 mg, my heart rhythm irregularity went away.
Sorry! – That first paragraph should read "you will sleep better, your memory will improve and you will get the full effect of the PEA" ........... in answer to your next question, PEA does its "magic" by encouraging conversion of pregnenolone (or progesterone) to Allopregnanolone – you can look that up in "Aging and your hormones".
YES. "They didn't teach us that at med school, therefore it doesn't exist". This attitude is so tiresome. It’s really something that research scientists fully expect to be wrong about hypotheses and to be learning new things their whole careers, and doctors whose work is based upon such research can be so closed off to the idea that they don’t - can’t possibly - know it all. I feel fortunate to have eventually landed on more humble practitioners, but I had to kiss a lot of frogs to find these princes and princesses.
Thanks for your note: you are not alone! Since retiring (which I deeply regret), I have had huge difficulty finding a practitioner who is willing to even think about my views.
What that means is that I can't find someone to help the friends and relatives who have problems with metabolic aberrations.
Are you in Canada? - If you are, I'd love to hear who you are seeing.
One question: in my opinion, all patients with "long Covid" should be checked for the low T3 syndrome (LT3S), which is known to be a factor in the symptomatology of all severe illness and many chronic diseases.
The point is that if the patient has low T3 syndrome, therapy with slow-release Triiodothyronine (Liothyronine) will safely and reliably relieve those symptoms which are due to LT3S. This is a huge boon for people with Long Covid.
I have written a post with regard to this: please see
I think that everyone with severe, or chronic disease should be checked for LT3S and I would be most interested in hearing your opinion regarding this post.
I am the old guy, sitting by himself, over in the corner!
Due respect, to all, especially to Dr. McMillan, who (I suspect) is as Jamaican as I am!
I think that Long Covid symptoms are mostly due to Intracellular Hypothyroidism, a.k.a. "the Low T3 Syndrome" but the explanation is a bit complicated!
So, rather than asking you to read a long "writeup" here, if you are interested, please see
A comment on a possible mechanism for reduced tryptophan absorption in the gut in long COVID: "A deficiency of intestinal ACE2 impairs the absorption of the essential amino acid tryptophan" https://drgalland.com/
Dr. McMillan,
I sincerely appreciate your attention to this issue.
I have been raising the possibility that muscle weakness might be linked to VLCFAs since 2018.
To explore this further, I personally funded a test in the U.S., which is available here:
"Very Long-Chain Fatty Acids (VLCFAs), X-ALD, and Spinal Muscular Atrophy (SMA): Exploring the Connection."
https://swaresearch.blogspot.com/2024/10/very-long-chain-fatty-acids-vlcfas-and.html
However, no neurologist or researcher made the connection until the release of this recent paper:
https://www.sciencedirect.com/science/article/abs/pii/S0960896624003353
This test is inexpensive and readily available in the U.S. Unfortunately, the same is not true in Germany, where only one lab offers VLCFA testing. Additionally, very few doctors, including general practitioners and specialists, are willing to include this test in their diagnostic process.
Thank you again for your time and consideration.
Sincerely,
SWA
Fundamentally you are aiming to try and improve symptoms without addressing the underlying issues.
It may have some benefit, but carries other risks in the medium to longer term.
Best used as a short term strategy but still limited by mitochondrial access to carnitine.
In my case the underlining issue is X-ALD - Refsum Disease.
https://swaresearch.blogspot.com/2024/10/phytanic-acid-and-refsum-disease.html
Saw the paper on VLCFA quickly. My interest was only what kind of chain length and the paper says C22 plus. What is the source of such fatty acids in our body ? Does the body produce them, what for ? Given the common knowledge that our source of fatty acids are the fats and oils we consume, directly or indirectly from foods that contain oils ( e.g. nuts)and the fact almost all common oils and fats of either plan origin or animal origin, including dairy fats, contain only upto C-18 chain and some oils (e.g) low percentages of C-20 ( very rarely traces of C-22 in sparsely used oils), how do we get C-22+ chains for one to become prone to this fatigue presentations. Can you give further inputs on these questions. Three fourths of what we consume from different sources are C16 and C18, whether saturated, mono unsaturated, diunsaturated or triunsaturated. The exceptions on either end are those consuming a lot of coconut oil and palm kernel oil ( predominantly C-12) or fish ( polyunsaturated from C-18/C-20).
Would you like to read: https://swaresearch.blogspot.com/2024/10/the-20-standard-amino-acids-plus.html
Nice summary of amine acids. Thanks. Would go through them over and over again. But my query remains unanswered, the source of VLCFA in the body, when very little of it is available from the fats and oils we consume. VLCFAs ( C 22 and plus) are normally found in natural waxes ( bees wax etc) which we don’t eat and in Jojoba Oil, which though edible, is not normally eaten. These are all not triglycerides, but esters of long chain fatty acids and long chain fatty alcohols.
The cornerstone of managing elevated phytanic acid is a low-phytanic acid diet. This involves restricting or eliminating foods high in phytanic acid:
Dairy products (milk, cheese, butter),
Fatty fish (cod, herring),
Ruminant fats (from beef, lamb, etc.).
More details at: Elevated Phytanic Acid: Causes, Genetic Factors, and Treatment Approaches https://swaresearch.blogspot.com/2024/10/phytanic-acid-and-refsum-disease.html
Thanks. Some good updating of knowledge. Do you consider phytanic acid very long chain ? It is only a C 16 chain ( palmitic acid) with 4 methyl side chains. Makes it only C 20. It is a multiple branched acid. I am, for the first time, reading that such a branched chain acid is present in the food sources mentioned. Or is it a metabolic product in the body - if so the metabolism of what from these food source ? By the way, if this acid is available industrially, it will be an excellent lubricant in many industrial applications. I am going by the example of isostearic acid, which has a single methyl side group,in the middle of a normal fatty chain.
Isostearic acid, with its branched structure, interacts with VLCFAs by altering membrane properties, potentially interfering with enzyme function, and being metabolized differently than straight-chain VLCFAs. This can have significant implications in the context of diseases where VLCFA metabolism is impaired, as branched-chain fatty acids may exacerbate these conditions or lead to altered fatty acid dynamics. (my research in progress)
More serious complications arise when managing a patient with VWD Type II and V, Celiac disease, and elevated phytanic acid levels, as these conditions require careful coordination of both diet and medications. Since the combination of all three conditions is rare, few patients are diagnosed with this complex overlap, making treatment even more challenging and highly individualized.
https://swaresearch.blogspot.com/2024/10/managing-patient-with-von-willebrand.html
I read. I listened. I listened again. Then I took 600mg of TRU NIAGEN. Within an hour, my muscle pain has eased and I can sit still without squirming in pain and move without wincing.
I'm already on a CIRS chronic inflammation treatment program, but so far the muscle pain has been resistant to exercise (makes it worse), stretching, massage gun, physio, remedial massage, magnesium, etc. Phototherapy is like being plugged into a power socket - couldn't move without it, but even though it stimulates my mitochondria it does nothing for the muscle pain (maybe even makes it worse).
Thank you for the missing link ❤️. Maybe it will get me through until I can achieve a longer-term solution. 😊
Excellent.
The article referenced is now 3 years old.surely more data that is relevant is available?
Depends on the approach to research.
My view is that the answer to long Covid lies in understanding MECFS and Fibromyalgia.
Therefore I always correlate new studies with prior research to reduce the risk of being too focused on just Covid.
Very broad perspective.
Let us hope this assessment holds true, opening the prospects of some clinically correct treatment. This long covid or more appropriately long vax is a nagging, even treacherous condition and there could be more routes to its occurrence, often a combination of them. It is necessary to keep exploring. Whatever, I would underscore on fundamental. It is certainly the lingering virus spike proteins, vax spike segments and the cationic LNPs that are driving the persistence of these presentations. As root causes, they need to be flushed out, to render other treatments effective. I am surprised and even concerned that in the dozens and dozens of substack presentations I have seen, including Dr. McMillan’s, this flushing out has not been discussed at all, let alone as a focus. Without it, there will not be complete light on this disease conditions. Could this residuals be treated as a virus infection by themselves and be addressed by classical covid treatments with repurposed drugs - the off label anti virals, anti histamines, anti inflammatories etc ?
The spike remnants are located primarily in long lived immune cells.
Therefore the solution is to reduce inflammation first, prior to targeting the spike.
No quick and easy answers.
Increasingly looking like a chicken and egg syndrome - which came first ? If the spike is the root cause, then inflammation comes next, so should we not expel the spikes first, wherever they have taken residence ?
the true explanation is understanding basic human physiology, which is not that simple but covid 19 messes with the bodies electricity, like every serious disease, hence oxygen distribution is not optimal, hence fatigue and all the other symptoms. I wrote in my latest article with great examples how to save life in critically ill patients, which nobody did in protocols for covid , all backed by scientific papers:)
Hi Dr., thank you for this post. The audio is especially helpful as I am very symptomatic with LC and ME/CFS.
Was wondering if you have seen Rob Wust’s recent webinar on his study results of skeletal muscle in LC? I’ll link it here.
I tried supplementing with carnitine and niacin a few years back but I think my inflammation was just too high for it to make a difference. I’m a bit better now, but I am loathe to spend any more money on supplements as it always feels like a shot in the dark.
https://youtu.be/uQiv0zSveA8?feature=shared
Thank you Amy.
The whole purpose of the post was to highlight that simple supplementation without addressing the root cause of inflammation is unlikely to bring long term benefit.
This is a marathon to wellness.
One step at a time.
If you have symptoms of CFS/ME, (almost indistinguishable from long Covid symptoms) it might be that your symptoms are actually due to intracellular hypothyroidism (IH) – you can look up IH at “research gate”. Anyway, check your thyroid 3 and reverse thyroid 3 levels – if FT is less than 4.0, maybe you have IH.
You can prove IH by checking the T3/rT 3 ratio (See https://gervaisharry.substack.com/p/t3rt3-ratio-diagnoses-low-t3-syndrome) – you can simply locate your T3/rT 3 on the chart below.
If you do have IH (a.k.a. “low T3 syndrome”), oral DHEA will help a bit, but the correct prescription is slow-release Triiodothyronine (Liothyronine), titrated to produce a serum free T3 between 4.5 and 6.2.
If you decide not to check this recommendation, no sweat!
If you do decide to check it, please let me know the outcome.
Thank you for this. I’ve had Hashimoto’s and hypothyroidism for decades now. My levels were all stable until about two years into long COVID, when my TSH started jumping all over the place. I’m working with a great endocrinologist and for a while she had me on liothyronine in addition to Synthroid, but my T3 levels were never a problem and I didn’t feel any different on the liothyronine, so she took me off of it. She incrementally titrates my Synthroid and retests me every six weeks. It’s been kind of a tiresome situation because just when it stabilizes, then the next time I have bloodwork, I become either hypo- or hyperthyroid yet again. Long COVID has really messed with my body metabolically. Pre-diabetes and high LDL and total cholesterol too, out of nowhere and not diet related. It’s been quite a ride.
Hi Amy.
Hashimoto's causes true hypothyroidism (TH), in which T3 is in short supply because the thyroid gland's output of T4 is reduced. True hypothyroidism is nicely treated with Eltroxin or Synthroid (T4), providing that your cells are converting T4 into T3, as they normally do.
Under stress conditions however, increased cortisol production blocks T4 – to – T3 conversion, along with increased conversion of T3 to reverse T3 and what you have been is intracellular hypothyroidism (IH) – you can look that up either in SUBSTACK, or via Research Gate.
You can have both conditions together. If you do, and you try to treat your TH with T4, the T4 you take won't convert to normal T3: it will convert to reverse T3, which does not work.
As an example, I checked my Reverse T3 for the first time back in 2013, and was shocked to find that it was 34 (it should be <13). I tried treating it with desiccated thyroid (DT contains70% T4 and 30% T3) and when I rechecked the reverse T3, it had shot up to 54! ..... I got good relief of my symptoms by taking T3, instead of Eltroxin and the reverse T3 went down to 7.
I have been taking compounded, slow-release T3 since 2014: my current dose is 50 µg and I take it at 4 AM, to mimic the normal diurnal surge of T3.
So don't worry about TSH or and/or FT4: check your T3 and rT3, go to https://gervaisharry.substack.com/p/t3rt3-ratio-diagnoses-low-t3-syndrome and figure out your T3/rT3 ratio by consulting the conversion table.
If the ratio is less than 20, you have IH, not TH and you need to be treated with slow-release T3 (Triiodothyronine, or "Liothyronine").
NOTE:
(1) Cytomel, the proprietary T3 preparation, is in a quick-release tablet and adequate dosage tends to produce a "spike – and – crash" phenomenon, which can be quite unpleasant.
(2) when taking T3, the TSH tends to go way, way down, because the T3 filters through into the pituitary gland and the pitcher forgets so "happy" that it stops producing TSH. That is not a problem: it is simply a sign that the pituitary is happy with the amount of T3 is getting.
I agree - supplementing with nicotinamide riboside didn't make enough difference, sadly. Having an extremely restricted diet (established via scientific process) has been essential but has reached its limit of helpfulness. Anti inflammatories are also invaluable - NAC (brain), ubiquinol (muscles), etc. Not sure yet how much PEA is helping.
I consult with a functional medicine nutritionist who is following the CIRS Shoemaker Protocol (the nicotinamide riboside wasn't part of this). It involves supplements and lots of expensive tests, but she is obtaining the only insights into causes and mechanisms. My life is on complete hold (with my bank account draining), waiting for our Western medical system to catch up and help. If only doctors would even acknowledge functional medicine practitioners it would be a start, as GP's are the gatekeepers to our health system (the ones that apply functional medicine practice are few and hard to access, but also are not nutritionists). Most GP's seem to be following standardised protocols (some sort of rule book) and seem adverse to applying a scientific approach in wielding their medical knowledge. I've heard it a disturbing number of times - "They didn't teach us that at med school, therefore it doesn't exist". Learning shouldn't stop at the end of school, but I'm sensing that our medical system doesn't reward initiative.
Hey Karen! Take your PEA with 200 mg of Pregnenolone (Progesterone is a better idea if you are in menopause), at night: you will sleep better, your memory will improve
(Watch out – maybe you will remember your dreams and if you tend to have nightmares, you will remember them and blame the supplements) – there are no other side effects, but I did notice that when I put my progesterone dose up to 200 mg, my heart rhythm irregularity went away.
Sorry! – That first paragraph should read "you will sleep better, your memory will improve and you will get the full effect of the PEA" ........... in answer to your next question, PEA does its "magic" by encouraging conversion of pregnenolone (or progesterone) to Allopregnanolone – you can look that up in "Aging and your hormones".
Thank you so much, Dr Harry!
YES. "They didn't teach us that at med school, therefore it doesn't exist". This attitude is so tiresome. It’s really something that research scientists fully expect to be wrong about hypotheses and to be learning new things their whole careers, and doctors whose work is based upon such research can be so closed off to the idea that they don’t - can’t possibly - know it all. I feel fortunate to have eventually landed on more humble practitioners, but I had to kiss a lot of frogs to find these princes and princesses.
Hi Amy,
Thanks for your note: you are not alone! Since retiring (which I deeply regret), I have had huge difficulty finding a practitioner who is willing to even think about my views.
What that means is that I can't find someone to help the friends and relatives who have problems with metabolic aberrations.
Are you in Canada? - If you are, I'd love to hear who you are seeing.
Thanks again.
Hi doc - no, I’m in NY. A different flavor of a broken medical system than you have in Canada, from what Canadian friends tell me.
https://rumble.com/v4nz8eo-artificial-intelligent-transformation-of-humanity-nano-and-micro-robots-in-.html Might be worth looking into this.
Hi Dr. McMillan,
Excellent article!
One question: in my opinion, all patients with "long Covid" should be checked for the low T3 syndrome (LT3S), which is known to be a factor in the symptomatology of all severe illness and many chronic diseases.
The point is that if the patient has low T3 syndrome, therapy with slow-release Triiodothyronine (Liothyronine) will safely and reliably relieve those symptoms which are due to LT3S. This is a huge boon for people with Long Covid.
I have written a post with regard to this: please see
https://gervaisharry.substack.com/p/long-covid-and-ih.
I think that everyone with severe, or chronic disease should be checked for LT3S and I would be most interested in hearing your opinion regarding this post.
Hi everybody!
I am the old guy, sitting by himself, over in the corner!
Due respect, to all, especially to Dr. McMillan, who (I suspect) is as Jamaican as I am!
I think that Long Covid symptoms are mostly due to Intracellular Hypothyroidism, a.k.a. "the Low T3 Syndrome" but the explanation is a bit complicated!
So, rather than asking you to read a long "writeup" here, if you are interested, please see
(1) https://gervaisharry.substack.com/p/long-covid-and-ih
(2) https://gervaisharry.substack.com/p/undiagnosed-hypothyroidism
A comment on a possible mechanism for reduced tryptophan absorption in the gut in long COVID: "A deficiency of intestinal ACE2 impairs the absorption of the essential amino acid tryptophan" https://drgalland.com/