RP Says Glucose Helps T4 To T3, Then Why Fructose?

khan

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haidut said:
sueq said:
If 100g cooked chard only has 29 ug K2 and an ounce of liver only has 0.9 ug K2 (crono) and we're talking 15mg as a goal, is there no practical dietary alternative to supplementing?

You could try high dose CoQ10 or idebenone. I have not seen what Ray has written on those, but there are studies showing benefit for NAFLD from CoQ10. The doses were in the range of 300mg-500mg daily. Also, there are studies using 1,200mg and 2,400mg of CoQ10 for diabetes type II, which some people believe to be just another name for liver disease. Finally, 1,200mg-2,400mg of CoQ10 are currently in humans trials for Parkinson disease, so there must be something to the quinones like CoQ10 and K2.

Which version of CoQ10 is fine in your opinion? Any product suggestion?
 

haidut

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khan said:
haidut said:
sueq said:
If 100g cooked chard only has 29 ug K2 and an ounce of liver only has 0.9 ug K2 (crono) and we're talking 15mg as a goal, is there no practical dietary alternative to supplementing?

You could try high dose CoQ10 or idebenone. I have not seen what Ray has written on those, but there are studies showing benefit for NAFLD from CoQ10. The doses were in the range of 300mg-500mg daily. Also, there are studies using 1,200mg and 2,400mg of CoQ10 for diabetes type II, which some people believe to be just another name for liver disease. Finally, 1,200mg-2,400mg of CoQ10 are currently in humans trials for Parkinson disease, so there must be something to the quinones like CoQ10 and K2.

Which version of CoQ10 is fine in your opinion? Any product suggestion?

I think the plain ubiquinone is best, ubiquinol has some studies showing bad effects. Just get whatever product has the least additives. If you look at the studies with Coq10 they all used pretty generic stuff, sometimes buying it from the local drug store. But, Coq10 won't match the effectiveness of K2 as far as I know. In doses of 2,400mg per day it may be as effective for mitochondrial health as K2 but won't be as effective for liver health. I just suggested it for alternative for people that absolutely cannot get their hands on K2 at doses of 15mg or more.
 
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I think Ray Peat is fine with any insulin, it is just the resistant state brought on by free fat and polyunsaturated fat which leads him to define what is an undesirable level of insulin.
 

haidut

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Such_Saturation said:
I think Ray Peat is fine with any insulin, it is just the resistant state brought on by free fat and polyunsaturated fat which leads him to define what is an undesirable level of insulin.

So, what we should be doing is asking the doctor to do a blood test for iodine since that is a measure of a person's PUFA status. Low iodine means low PUFA and then insulin levels won't matter much. High iodine and high insulin would imply insulin resistant state brought about by fat oxidation. Right?
 

khan

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haidut said:
khan said:
haidut said:
sueq said:
If 100g cooked chard only has 29 ug K2 and an ounce of liver only has 0.9 ug K2 (crono) and we're talking 15mg as a goal, is there no practical dietary alternative to supplementing?

You could try high dose CoQ10 or idebenone. I have not seen what Ray has written on those, but there are studies showing benefit for NAFLD from CoQ10. The doses were in the range of 300mg-500mg daily. Also, there are studies using 1,200mg and 2,400mg of CoQ10 for diabetes type II, which some people believe to be just another name for liver disease. Finally, 1,200mg-2,400mg of CoQ10 are currently in humans trials for Parkinson disease, so there must be something to the quinones like CoQ10 and K2.

Which version of CoQ10 is fine in your opinion? Any product suggestion?

I think the plain ubiquinone is best, ubiquinol has some studies showing bad effects. Just get whatever product has the least additives. If you look at the studies with Coq10 they all used pretty generic stuff, sometimes buying it from the local drug store. But, Coq10 won't match the effectiveness of K2 as far as I know. In doses of 2,400mg per day it may be as effective for mitochondrial health as K2 but won't be as effective for liver health. I just suggested it for alternative for people that absolutely cannot get their hands on K2 at doses of 15mg or more.
Thank you haidut for clarifying. I will go for vitamin K2 and caffeine.
 
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haidut said:
Ben said:
Geeze, this hasn't been answered yet? Fructose keeps glucose in the bloodstream and this inhibits cortisol, which is the primary inhibitor of T4-T3 conversion. Basic facts, people.

So, assuming one keeps a steady dietary supply of sucrose (or some other type of sugar), wouldn't the constant presence of glucose in the blood stream keep insulin chronically elevated too? I have read various, and often contradictory, statements from Peat about the whole blood sugar and insulin thing. Often, he says that it is important to always keep blood glucose up to keep cortisol at bay and metabolism high. Of course, this means insulin would be elevated chronically too. On insulin, Ray sometimes says it is a good hormone responsible for anabolism and keeping tumor growth under control. At other times he has said that elevated insulin is not a good thing. So, I am bit confused about the overall dietary guidelines. Should we try to keep blood sugar elevated all the time but at a certain stable (and reasonable) level, which would imply higher (but stable insulin), or should we do pulse feeds which would temporarily bring insulin up to shuttle the glucose to the muscles and then insulin goes down and the body runs on glycogen from the liver?
I suspect a number of people on the forum struggle with this issue as evidenced by several posts of rapid weight gain, elevated blood glucose and insulin on blood tests and worried doctors making recommendations to cut down on sugar, blood pressure rising in people who did not have blood pressure issues before, etc. Some of these things could be beneficial, but there was a post by one person who said her blood pressure went from 120/80 to 150/90 after adopting the higher sugar diet and after some back and forth with her doctor she decided to quit the Peat diet. Then she reported her blood pressure normalizing after reducing sugar intake. Btw, it is well known in the bodybuilding community that cutting carbs works just like diuretics. I am not an advocate of this, but wouldn't people prone to edema and having thyroid problems get their water-retention problems exacerbated if they increase sugar/carbs intake? I guess that would happen at least initially and the theory is that as their metabolism normalizes they should be able to better utilize glucose and then lose all the excess water. So, the million dollar question is how long does one have to re-feed higher carbs diet (and suppress fatty acid oxidation through the Randle effect) until their insulin sensitivity is restored?
Finally, there have been a number of reports on Peatarian and occasionally on this forum of people experiencing proteinuria (protein in the urine) when increasing sugar intake above 200g daily. If you are eating 80g+ of protein then you probably strive to eat at least as many carbs. Peat has said that this proteinuria is due to people burning PUFA, which makes albumin leak in the urine and show up on the tests but as far as I can tell, these people were actually burning fat before adopting the higher sugar diet and only experienced proteinuria after increasing sugar intake. Of course, they could have had this issue all along and only realized it after switching and measuring their urine but there are several reports of this so I doubt it's a random thing. Somebody also posted a study on thousands of university employees and those who consumes the most sugary drinks reported the highest incidence of proteinuria.
It would be nice if we can get some guidelines on this. Personally, I use caffeine to increase the utilization of sugar and don't really have issues with it, but in theory there should be a way to handle sugar from diet without relying on sugar burning aids like caffeine and/or thyroid. Thyroid does not seem to be a good option for me, and I have tried all kinds of supplementing schedules and dosages. As I have posted on other threads, my experience with sugar only improved after I took serious measures to "normalize" my liver function through caffeine and vitamin K2, BUT my liver enzymes were NORMAL according to the standard lab ranges. If the stats are true and over 80% of people over 30 have some degree of fatty liver, which is the real cause behind type II diabetes, then I think many people adopting the Peat diet will likely experience stress reduction through the lower cortisol, but may end up making their fatty liver worse, especially is supplementing niacinamide and aspirin. Such_Saturation and I posted about this in another thread.
So, my main point is that burning sugar is definitely preferable to burning fat based on both Peat's writings and all the studies I have seen about liver disease being caused by increased lipid peroxidation byproducts, and cirrhosis (in alcoholic rats) being easily and succesfully treated by feeding about 60g-70g of saturated fat like butter or coconut oil for a week, while the rats kept drinking alcohol at the same time! So, on the point of burning sugar I think the question is settled that it is preferable to burning fat.
However, the point is to actually BURN the sugar rather than simply feeding ourselves more of it. For people with sluggish livers, many of whom also take niacinamide and aspirin, this is likely to make the metabolism situation worse by fattening the liver even more, even though admittedly the fat synthesized will be saturated since it is made from sugar. But fatty liver will increase your estrogen no matter how saturated the fat is that you are synthesizing. So, fattening up the liver even more probably won't do much good for metabolism. Another suggestion from Peat would be to increase protein intake to at least 80g a day which should support liver function, lower estrogen and increase conversion of T4 into T3. However, that will likely also not work very well in people with sluggish and fatty livers since underperforming liver will convert a lot of that extra protein into ammonia. Even Peat is clear on this point in one of his articles where he says that "hyperammonemia can be caused by exhaustive exercise or hypothyroidism". This is also evidenced by a number of studies showing that people in their late 30s, 40s, and 50s experience chronic fatigue issues that are greatly helped by giving them ammonia-reducing agents like ornithine or sodium benzoate. And those people consume nowhere near the 80g of protein Peat recommends. So, if they are having ammonia issues imagine how would the people loading up on extra protein would feel.
Which brings us to the point that for many people over the age of 30, simply increasing sugar and/or protein will likely not solve the metabolic issues. Thus, the Peat diet, while the correct way to eat, may not be a solution to the issues of hypothyroidism, but rather a way to avoid the worse option of running on cortisol and adrenalin, which while energizing in the short run will ruin you in the longer run.
Considering the Barnes book "Hypoglycemia: It's not your brain, it's your liver", which I read, it seems that restoring optimal liver function is also a key to improving metabolism. Yes, thyroid function is important too, but I think Peat's recommendation on supplementing thyroid even in the presence of normal thyroid labs may cause issues for a number of people. Charlie, and at least 20 other people have posted on struggling with supplementing thyroid. If they take it, they develop teeth issues, skin issues, anxiety or some other unpleasant symptoms. If they don't take it, their digestion slows down to a crawl or they start getting hypothyroid symptoms like brain fog or muscle issues, etc.
So, if the stats are true and the evidence I have seen is legit, then eating according to the peat guidelines is a great strategy AFTER metabolism is fixed. But if 80% of people over 30 are having liver issues or some other problems with metabolism, then the diet will be certainly supportive, but likely not "curative". And for some people with particularly bad liver problems the situation may end up getting worse in a way due to even more fatty liver issues or higher ammonia levels. Just ask anybody over the age of 40 if they are having trouble maintaining (let alone building) muscle mass.
Then the question becomes, what will aid metabolic recovery, other than blindly supplementing thyroid even in the presence of normal thyroid labs? I guess the answer Peat will give is that one needs to wait at least 4 years and get rid of the PUFA before starting to see solid results. There is some solid evidence in favor of lower PUFA fixing metabolic issues. But I wonder if working on liver health or trying to build more muscle will also help while waiting out the PUFA detox period? Uncoupling agents are probably also key, but they should probably be other than aspirin since it may make fatty liver issues worse for many people if used in the doses needed for mitochondrial uncoupling. Finally, increasing CO2 production or intake somehow will also likely have a key role. Just throwing things out there that seem to be cardinal methods for improving metabolism.
Sorry about the long rant, I just felt like this deserves some attention since a number of threads pop on the forum asking the same questions and I have been thinking about this for some time. If someone knows about Peat's definitive opinion on this issue please share it. Maybe I missed it in his articles. IMHO, after reading pretty much all of his published stuff, reading people's testimonies/complaints, cross-referencing this with studies, and my own experience, I think a number of chicken/egg question still remain.
Anybody care to comment?
There are many questions raised here, haidut, but for me they all hinge on looking at the body though the (mis)conceptions of medical literature, rather than from the perspective of Peat and Ling. Peat and Ling share a world view of long range electronic effects on adsorbed proteins in structured water that is very different from the (foolish) membrane pumps and genetic receptors of the medical literature. The difference is profound and for me, life-changing.

Basically, for Peat and Ling, the goal of "diet" is simply to increase oxidation of glucose by having a steady supply of the cardinal adsorbents that make oxidation of glucose efficient: CO2 (increased by phosphorylation uncoupling with T3, aspirin and caffeine), progesterone, ATP/insulin (co-dependent on phosphorylation of sugar), magnesium/calcium, NAD+ (made from B3/niacinamide), potassium/sodium, ubiquinone (for which Vitamins E and K2-MK4 can substitute), as well as GSH/GSSG redox balancers (thiamine and methylene blue) and a balance of keto and amino acids, especially glycine to reduce methylation.

If you look at the complaints from members on this forum, you can see that the problem is very simple, from Peat and Ling's perspective: people here are deficient in one or more of these cardinal adsorbents or redox balancers and it's forcing their metabolism to rely on glycolysis or lipolysis for less efficient energy generation, which in turn forces their bodies to take on lesser organized structures -- everything from impaired liver, brain, guts and skeleton to weaker muscle and swollen adipose tissue.

Supplementing these cardinal adsorbents and redox balancers is relatively cheap, harmless and easy, but it does need to be done on a continuous basis throughout the day, which it seems to me few if any of the members here do (other than me?)

I'm trying to make it easy by developing "RDAs" here: viewtopic.php?f=13&t=5551&start=30#p66013
In fairness, I shouldn't leave Gilbert Ling out, so maybe they should be GRDAs!

Comments are welcome!

PS. Just to give a short answer to at least one of your questions, haidut (I counted 12!): "Insulin resistance" occurs when fatty acids are being burned. Put another way, insulin is used up for promoting the oxidation of glucose, but not used during the oxidation of fatty acids. Thus, insulin levels increase when fatty acids are being burned.

Put another way, when you burn fat, you increase insulin, and when you increase insulin you increase the storage of fat, which in turn leaves more fatty acids available for you to burn. Ray Peat after me: burning fat is what makes you fat!

In the case of fatty liver, fat is stored in the liver tissue in response to high insulin from fatty acid oxidation in the liver tissue itself.

This is why you need to stop the vicious cycle of the oxidation of fatty acids as much as possible. Keep up a constant supply of sugar/fructose, and of niacinamide and aspirin, which can suppress fatty acid oxidation in the cells that have already degenerated and begun relying on lipolysis. (Whatever you and Such may have written to the contrary, notwithstanding.)

How much PUFAs are stored in your fat is actually much less important, as long as you are not burning them!

The safe way to get rid of polyunsaturated fatty acids from the body is to glucuronidate them and excrete them in the urine, or bound to albumin in the liver, but NOT through oxidation! (At least this is what Peat thinks.)
 
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haidut said:
Such_Saturation said:
I think Ray Peat is fine with any insulin, it is just the resistant state brought on by free fat and polyunsaturated fat which leads him to define what is an undesirable level of insulin.

So, what we should be doing is asking the doctor to do a blood test for iodine since that is a measure of a person's PUFA status. Low iodine means low PUFA and then insulin levels won't matter much. High iodine and high insulin would imply insulin resistant state brought about by fat oxidation. Right?

If that is a reliable method to establish the saturation of one's fats, then why not, I think. Some good indicators for issues would be darkening of the skin around joints and just the reaction to sugary water for example. However I don't think Ray Peat would ever feel liable for any bad reactions to sugar eaten without potassium, since he has never claimed that to be safe, I don't think.
 
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Such_Saturation said:
haidut said:
Such_Saturation said:
I think Ray Peat is fine with any insulin, it is just the resistant state brought on by free fat and polyunsaturated fat which leads him to define what is an undesirable level of insulin.

So, what we should be doing is asking the doctor to do a blood test for iodine since that is a measure of a person's PUFA status. Low iodine means low PUFA and then insulin levels won't matter much. High iodine and high insulin would imply insulin resistant state brought about by fat oxidation. Right?

If that is a reliable method to establish the saturation of one's fats, then why not, I think. Some good indicators for issues would be darkening of the skin around joints and just the reaction to sugary water for example. However I don't think Ray Peat would ever feel liable for any bad reactions to sugar eaten without potassium, since he has never claimed that to be safe, I don't think.
I'm afraid fatty acid oxidation may not be evenly systemic but occurring more in any swollen, degenerated tissues, such as an overworked liver, estrogenic gut, breasts and testicles, or swollen muscles and foggy brain.

Would the iodine test for FFAs be tissue specific?
 

narouz

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visionofstrength said:
In the case of fatty liver, fat is stored in the liver tissue in response to high insulin from fatty acid oxidation in the liver tissue itself.

This is why you need to stop the vicious cycle of the oxidation of fatty acids as much as possible. Keep up a constant supply of sugar/fructose, and of niacinamide and aspirin, which can suppress fatty acid oxidation in the cells that have already degenerated and begun relying on lipolysis. (Whatever you and Such may have written to the contrary, notwithstanding.)

I've really enjoyed this thread.
It is interesting, these different theories about fatty liver and metabolism.
I really like the way, VoS, that you present an electric-centered perspective.
You may've outlined it earlier,
but would you give a notion of how you eat,
separate from the supplements?
I'm just trying to picture it.

So on this fatty liver thing:
you think niacinamide and aspirin are good?

How do you get protein in your diet, personally?

I take it you are a proponent like Peat and Barnes of liberal thyroid supplementation?
or do you think there's something to haidut's and Such's leanings toward it
being maybe not really necessary
a lot of the time...hope I'm not mis-interpreting them :) ...?
 

SQu

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VoS I am one who is trying to divide up food and thyroid at intervals. I take T3 with food (fruit jelly/milk/cottage cheese/fruit) hourly or close to it. sometimes 2 hourly. always sugar with protein. Certainly feeling benefits but long way to go. Recent improvement - bumpy fingernails growing out smoother. (terrible Beau's lines for many years). I've updated my log "an almost fat free starch free experiment" if relevant
Fixing glucose metabolism would be such a breakthrough.
 
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sueq said:
VoS I am one who is trying to divide up food and thyroid at intervals. I take T3 with food (fruit jelly/milk/cottage cheese/fruit) hourly or close to it. sometimes 2 hourly. always sugar with protein. Certainly feeling benefits but long way to go. Recent improvement - bumpy fingernails growing out smoother. (terrible Beau's lines for many years). I've updated my log "an almost fat free starch free experiment" if relevant
Fixing glucose metabolism would be such a breakthrough.
You are the very first person to publish the phrase "fat free starch free experiment" on the web, according to this google search:
https://www.google.com/search?q=%22fat+ ... eriment%22

Says something about how messed up the world of diet and nutrition is.

Great work, sueq! Anything you can do to increase CO2 should help reduce fatty oxidation. I use a magnesium-calcium-bicarbonate water which can be homemade for pennies.
 
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narouz said:
I take it you are a proponent like Peat and Barnes of liberal thyroid supplementation?
or do you think there's something to haidut's and Such's leanings toward it
being maybe not really necessary
a lot of the time...hope I'm not mis-interpreting them :) ...?
Anyone suffering from the rampant excess of estrogenic contaminants should be helped immediately by thyroid and progesterone. And unless you somehow live in abundance on a mountaintop, who isn't suffering?

Careful, though, the tiny dose of a few micrograms of T3 every hour or two (and with a tiny speck of DHEA for men) is crucial.

If anyone here is dosing more T3 than that like some kind of street drug, as Such Saturation has hinted, please don't. Too much may well be worse than too little.
 
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It lost effect while taking four micrograms every few hours I think it was.
 

narouz

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Such_Saturation said:
It lost effect while taking four micrograms every few hours I think it was.

This is an interesting theory:
that T3 is not effective long term,
or that T3 doesn't work with some.
Isn't the answer to raising metabolism in some situations.
 
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narouz said:
Such_Saturation said:
It lost effect while taking four micrograms every few hours I think it was.

This is an interesting theory:
that T3 is not effective long term,
or that T3 doesn't work with some.
Isn't the answer to raising metabolism in some situations.
I guess I don't see how it can lose effect, any more than caffeine can lose effect, unless you're not getting enough fructose.

The product itself could be inconsistent in its ingredients, due to poor batch control.
 

narouz

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visionofstrength said:
(and with a tiny speck of DHEA for men) is crucial.

The place of DHEA in PeatDom is unsettled.
Peat has said recently he takes like 2 mg per day,
and experiences a mildly euphoric result.

Are you associating DHEA with thyroid for some reason...?

I like your train of thought VoS...not trying to be inquisitorial here...!
 
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My reading of Peat is that it needs to be used (at least by men) in small amounts, always in balance with thyroid and progesterone.

I also read that the place of pregnenolone is unsettled, since there are many conditions under which it is not effective, or worse, has side effects of increasing cortisol.
 

tara

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visionofstrength said:
narouz said:
Such_Saturation said:
It lost effect while taking four micrograms every few hours I think it was.

This is an interesting theory:
that T3 is not effective long term,
or that T3 doesn't work with some.
Isn't the answer to raising metabolism in some situations.
I guess I don't see how it can lose effect, any more than caffeine can lose effect, unless you're not getting enough fructose.

The product itself could be inconsistent in its ingredients, due to poor batch control.

Is there a possibility that supplementing T3 and/or T4 at a rate that tries to drive the metabolism higher than there are resources to sustain could result in the body defending itself by converting some of the T4 that is around into reverse T3, which has the effect of opposing T3?
VoS mentions fructose, which seems reasonable, but I wonder if it applies to other essential nutrients too, not just fructose and/or glucose? Perhaps protein supply could also be such a bottle neck? Or some of the micronutrients? And not just what goes into your mouth, but what is absorbed in a usable form by your digestion, in whatever state it is currently in?
 
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