Does anyone know why Ray Peat said hypothyroid patients have low blood sugar?

kimbriel

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I read a Peat article today where he mentioned hypothyroidism suppresses blood sugar. Does anyone have any links to the science behind that? It's the first I've heard of that. I'm interested because after being on T3 for a number of months, my A1c went up to 5.3, which is higher than my typical baseline of 4.9 or 5. When I read the patient insert for T3 medication, it stated that the med could raise blood sugar. So - just a peculiar point of interest for me. I admit a lot of Ray's writings are way over my head.
 

Elie

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I remember him saying the opposite at one point, that diabetics tend to be hypothyroid.
Thyroid hormone signals glucose breakdown (to produce energy).
Low thyroid means less glucose is oxidized for energy, so less is taken up by cells, which means that more remains in circulation.

I'd love to hear more nuanced views.
 

Peatful

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Mechanism is mitochondrial respiration possibly?






Great resource / website if you’re not familiar:

 

xeliex

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I read a Peat article today where he mentioned hypothyroidism suppresses blood sugar. Does anyone have any links to the science behind that? It's the first I've heard of that. I'm interested because after being on T3 for a number of months, my A1c went up to 5.3, which is higher than my typical baseline of 4.9 or 5. When I read the patient insert for T3 medication, it stated that the med could raise blood sugar. So - just a peculiar point of interest for me. I admit a lot of Ray's writings are way over my head.
There is also the Broda Barnes observation that he wrote a book on.

hope for hypoglycemia: it's not your mind, it's your liver

The liver does not store glycogen well in these states (edit: low thyroid state), causing stress responses in an attempt to raise blood glucose back to baseline.
 

mostlylurking

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I read a Peat article today where he mentioned hypothyroidism suppresses blood sugar. Does anyone have any links to the science behind that? It's the first I've heard of that. I'm interested because after being on T3 for a number of months, my A1c went up to 5.3, which is higher than my typical baseline of 4.9 or 5. When I read the patient insert for T3 medication, it stated that the med could raise blood sugar. So - just a peculiar point of interest for me. I admit a lot of Ray's writings are way over my head.
If you are hypothyroid your liver won't be working very well so it has a harder time of storing sugar for release when you need it.
 
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kimbriel

kimbriel

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If you are hypothyroid your liver won't be working very well so it has a harder time of storing sugar for release when you need it.
I am very hypothyroid (unfortunately) and you are correct - my liver wasn't working well. It turned out I had fatty liver. I don't know if I still have it, but I'll find out in a few days because I have to have a follow up CT for lung carcinoid (ugh) in which case it will show up. I take 54mcg of T3 throughout the day. It's entirely a possibility that that has resolved my fatty liver along with the 48 lbs of weight loss I've seen in the last 4 months.
 
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kimbriel

kimbriel

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I remember him saying the opposite at one point, that diabetics tend to be hypothyroid.
Thyroid hormone signals glucose breakdown (to produce energy).
Low thyroid means less glucose is oxidized for energy, so less is taken up by cells, which means that more remains in circulation.

I'd love to hear more nuanced views.
It's entirely possible that both could be true.
 
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kimbriel

kimbriel

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There is also the Broda Barnes observation that he wrote a book on.

hope for hypoglycemia: it's not your mind, it's your liver

The liver does not store glycogen well in these states (edit: low thyroid state), causing stress responses in an attempt to raise blood glucose back to baseline.
Ooh! I love Broda Barnes - I'll have to check that out.
 
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kimbriel

kimbriel

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Mechanism is mitochondrial respiration possibly?






Great resource / website if you’re not familiar:

Thank you so much for this. I clearly do have mitochondrial issues.
 

mostlylurking

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I am very hypothyroid (unfortunately) and you are correct - my liver wasn't working well. It turned out I had fatty liver. I don't know if I still have it, but I'll find out in a few days because I have to have a follow up CT for lung carcinoid (ugh) in which case it will show up. I take 54mcg of T3 throughout the day. It's entirely a possibility that that has resolved my fatty liver along with the 48 lbs of weight loss I've seen in the last 4 months.
I think it would be very helpful to include thiamine status/function in the equation. The thyroid needs thiamine to function. So does the liver. Thiamine resolved my fatty liver (early stages).

links:
Nutrition in the Management of Cirrhosis and its Neurological Complications a search for "thiamine" yields this:

Vitamin B1​

Thiamine (vitamin B1) in the form of its diphosphate ester, is an enzyme cofactor involved in glucose and amino acid metabolism and is also, as its triphosphate ester, a component of neuronal membranes. Thiamine deficiency is common in many forms of cirrhosis particularly alcoholic liver disease where it is caused by inadequate dietary intake, decreased hepatic storage, and impairment of intestinal thiamine absorption by ethanol.39 Wernicke's encephalopathy is a seriously under-diagnosed metabolic encephalopathy with severe neurological symptoms and region-selective neuronal cell death caused by thiamine deficiency is often encountered in chronic alcoholism.40,41 A neuropathologic study examining brain tissue from patients with autopsy-proven cirrhosis revealed evidence of both acute and chronic hemorrhagic lesions in thalamus and mammillary bodies that are typical of Wernicke's encephalopathy as well as mild-to-severe cerebellar degeneration in cirrhotic patients, suggesting a role of chronic liver disease per se on brain thiamine status, a finding that has been attributed to a loss of liver thiamine stores.42 Unsuspected and irreversible thalamic and cerebellar lesions due to thiamine deficiency could explain the incomplete resolution of neuropsychiatric symptoms following the use of treatment strategies or liver transplantation in patients with end-stage liver failure.
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"Objectives: In a previous study on fatigue and related disorders in inflammatory bowel disease (IBD), we observed that IBD patients improved after treatment with high-dose thiamine. We hypothesized that the chronic fatigue accompanying inflammatory and autoimmune diseases is the clinical manifestation of a mild thiamine deficiency that is probably due to a dysfunction of the intracellular transport or to enzymatic abnormalities. Hashimoto's thyroiditis is both a common automimmune disease and cause of hypothyroidism. Although levothyroxine, a thyroid hormone, is the treatment of choice for hypothyroidism, a significant number of patients on thyroid hormone replacement therapy report not feeling well despite having thyroid function tests within the healthy range. Based on our hypothesis, we started treating the fatigue in patients affected by Hashimoto's thyroiditis and taking a thyroid hormone with thiamine. This is a report of the outcomes of three cases in which the fatigue component reported by patients with Hashimoto's thyroiditis was treated with thiamine.

Design: Three patients on thyroid hormone replacement because of Hashimoto's thyroiditis were treated for the fatigue component of the disease from May to July 2011. Fatigue was measured using the Fatigue Severity Scale. Free thiamine in the serum and thiamine pyrophosphate in red cells were tested before and after the therapy. All three patients received oral (600 mg/day) or parenteral (100 mg/ml every four days) doses of thiamine.Results: Treatment with thiamine led to partial or complete regression of the fatigue within a few hours or days.

Conclusion: As the administration of thiamine led to a partial or complete regression of the fatigue and related disorders, it is reasonable to infer that the administration of large quantities of thiamine restores thiamine-dependent processes. The mild thiamine deficiency suggested by fatigue and related disorders may be due a dysfunction of the intracellular transport of thiamine or to enzymatic abnormalities most likely related to the autoimmune process of the disease."
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David PS

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Answer from Peatbot -
User: is hypothoid related to low blood sugar

Peatbot: Yes, hypothyroidism can be related to low blood sugar. When the thyroid gland does not produce enough thyroid hormone, it can lead to a decrease in metabolism and a decrease in the body's ability to oxidize glucose. This can put the body in a stress state, which can lead to an increase in cortisol production. High levels of cortisol can interfere with the body's ability to regulate blood sugar, potentially causing low blood sugar levels. Additionally, the liver, which plays a role in converting inactive thyroid hormone to active thyroid hormone, may also be affected by low blood sugar, further contributing to hypothyroidism. Therefore, addressing the underlying cause of high blood sugar, such as hypothyroidism, is important in managing blood sugar levels effectively.

the quickest way to break out of this cycle is to eat... a well-balanced natural diet, but emphasizing a lot of fruits. Orange juice, for example, because of the high potassium content, which lets you handle and absorb blood sugar without disturbing your insulin. The potassium itself handles the sugar without triggering the insulin. And when your liver is receiving enough sugar... from the combination of potassium and sugar in the fruit, it is able to activate the thyroid hormone, restoring the poisoned function of your mitochondria and letting you use oxygen efficiently. So it can bring you out of a chronic allergic hypoglycemic state and get you back to a steady blood sugar, sometimes just in a day or two. Yeah, I think you mentioned a couple of things that most people are not aware of. Number one is that orange juice has potassium in it. Everybody thinks about eating bananas, but if you're low in potassium you can drink orange juice and get it increased much quicker. You also mentioned something about the liver, which is an area where the thyroid is converted from active to inactive to active form. Most people don't understand. Many years ago wrote a very good book called hypoglycemia. It's your liver not your mind and He was one of the first people To emphasize that most of the active thyroid about 70% of it Is produced in your liver rather than in the thyroid gland the gland Itself in your neck produces about 30% of the active hormone, but anytime your blood sugar falls If you go without eating for eight hours, for example, your blood sugar is likely to fall and that your liver doesn't want to convert your tissues to food and so your liver stops making thyroid so your metabolism decreases, your temperature goes down at some point when you have stopped eating so that you don't burn up your body too fast as you would if your metabolic rate stayed high without eating. Yeah, now we mentioned that the thyroid is produced by the thyroid, it's also produced by the liver and are converted there. Doesn't that conversion also take place at the cellular level as well? Several tissues produce quite a bit of it. The pituitary gland can detect T4 because the inactive form of the thyroid......thyroxin, and since it can convert it, it doesn't distinguish very strongly between whether you're taking T4 or T3, it turns off its activity whenever it sees T4 or T3. And
Source: kkvv-081031-ray-peat.mp3-transcript.txt

and proposed other kinds of so-called diabetes, like pregnancy diabetes, I think these are just medical inventions to sell products and services. And it's based way back in the 1940s. Research on the pituitary, pancreas, thyroid, adrenal interactions showed that the insulin was only a very tiny part of the blood sugar regulatory system. And yet, doctors almost always fail to check what's going on with your endocrine system known to regulate blood sugar. They just call it diabetes and leave it at that. Give you something that directly lowers the blood sugar, even though it's achieved at the cost of damaging your mitochondrial respiratory system so that you go into an inefficient glucose wasting condition. And a traditional side effect problem of this treatment of diabetes has been increased lactic acid production with serious, even deadly lactic acidosis being a result. But the principle has continued to be damage the respiratory use of glucose so that you waste glucose and lower the blood sugar. I think the problem should be approached by looking first for what is causing the high blood sugar. Often it's just a chronically high level of cortisol production or of another hormone. And if you find out why your cortisol is high, often that's a reaction simply to hypothyroidism. The lack of thyroid hormone makes you unable to oxidize glucose. And that puts you in a stress state. The stress state amplifies to raise the blood sugar. It keeps the cells from using it and shifts you over, forcing you to run on fats. And putting fats into your bloodstream. Free fatty acids are the other essential blood test for anyone diagnosed with so-called type 2 diabetes. Cortisol and free fatty acids, and if possible, checking on your lactic acid level. Your lactic acid should be at the very bottom of the so-called acceptable normal range. And is it true that simple angst or worry or fear can raise cortisol levels? Right, right. As well as lowering thyroid. Just a very sudden onset of worry, anxiety or fear can give you a surge of free fatty acids, which will block your ability to use glucose. There's a direct antagonism when your blood fats rise in the free fatty acid form. That blocks use of glucose, and so you can instantly create the appearance of type 2 diabetes. In other words, just high blood sugar is all they diagnose it on. Hi, Dr. Ray Peters with us. We are
Source: 03.02.21 Peat Ray [997481839].mp3-transcript.txt
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kimbriel

kimbriel

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Thank you all. So my A1c has indeed gone up since being on T3, and I take, essentially, a replacement dose of it daily. But having said that, it's still far below even pre-diabetes still.
 
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