[Non Peat] Undermethylators, Ketogenesis

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kineticz

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My dietary calcium intake is negligible. Magnesium and mitochondrial output limit calcium and cortisol problems. I eat stone age meat and veg diet. Sugar, like the EFAs, should only be used strategically in my view, and only when your cells are efficiently producing ATP via ketogenesis, in order to prevent low blood sugar and increase LDL cholesterol for pregnenolone.

I have come to the conclusion that it is best to become a fat burner for ATP, but use sugar to limit ACTH and cortisol, which increases pregnenolone. Mitchondrial DNA is from your mothers side and I can say with some certainty my mother is NOT a sugar burner. I don't think you can alter DNA in this manner. So my diet is ketogenic. Sugar is also troublesome in relation to SIBO and fermentation generating lactic acid when your cells are very low in generating ATP.
 
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Agent207 said:
post 112816 Thaks for your insight. I guess proper thyroid function is needed before attempting to fix any methylation issue. Can I ask whats is your dietary calcium intake aprox?

Regarding thyroid, I have high T3, but low T4. I have attributed low T4 to kidney weakness since tyrosine is made in the kidneys. T4 downregulates when cells are not generating ATP. Simply taking more thyroid does not automatically fix issues of methylation and heart, brain, liver, kidney health.

"Thyroid function" is more to do with cell performance than whether your thyroid can make thyroid hormone in my opinion. There are a small number of exceptions.

I take 50mcg T4 at night now before bed along with 100mg aspirin and 1000mg taurine. Stress hormones and therefore fatty acid liberation need to be throttled the most during sleep.
 
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Agent207

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Looking at typical thyroid values, TSH, T3, T4, Antibodies... is possible to determine when the root of the problem relies on hormonal (thyroid) or cellular impairment?
 
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Agent207 said:
post 112820 Looking at typical thyroid values, TSH, T3, T4, Antibodies... is possible to determine when the root of the problem relies on hormonal (thyroid) or cellular impairment?

High TSH implies low mitochondrial respiration in general, so cellular impairment.
Low T4 implies nutrient or amino acid deficiency. I think T4 is highly linked to kidney function, so as we have discussed the kidney's role in angiotensin, could also be a sign of cellular impairment. I also read that low T4 will reduce the physical size of the kidneys which reduces their ability to filtrate.
Low T3 implies conversion enzyme deficiency in the gut/liver. In my case I had high TSH, high cortisol and high T3 so I knew it was definitely not a conversion issue. High reverse T3 usually goes in hand with high cortisol for this reason.
 
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Agent207

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Ubclinical hipothyrodism is low mithochondrial function, even when high antibodies? Interesting, I always thought bad thyroid caused mitochondrial impairment, not the opposite. This is crucial if you attempt to fix the root.

And did you restore TSH levels down to normal with that simple protocol? How was TSH level before and after?
 
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Hypothyroidism does not cause problems, it reacts to problems. However, I do believe thyroid receptor resistance exists, due to prolonged unused thyroid hormone in serum. But again, this is due to cellular impairment.
 
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Agent207 said:
post 112823 Ubclinical hipothyrodism is low mithochondrial function, even when high antibodies? Interesting, I always thought bad thyroid caused mitochondrial impairment, not the opposite. This is crucial if you attempt to fix the root.

And did you restore TSH levels down to normal with that simple protocol? How was TSH level before and after?

I restored TSH by a ketogenic diet to yield increased ATP. Low ATP, whether regional or systemic, is the root of all degeneration. Ketogenesis blocks out all problems with glucose and lactic acid. Limit fatty acid liberation from the liver, efficiently burn the ones that are liberated to generate ATP, and keep cell membrane fats healthy. Use sugar sparingly only during incidences of increased stress on the adrenals.
 
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This is extremely interesting and paradoxical at the same time. There have bee cases when hipothyroid symtoms and thyroid impairment happened after long term cetogenic or low carb diets. You reversed it with it, in a way you think you couldn't with carbs, right? Maybe theres no rule set in stone nor a unique optimum pathway for ATP generation for everyone.

You still following low carb after you restored thyroid and mitochondrial function? Did you use any uncouplers... Q10, PQQ, ALA...etc?
 
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Agent207 said:
post 112823 Ubclinical hipothyrodism is low mithochondrial function, even when high antibodies? Interesting, I always thought bad thyroid caused mitochondrial impairment, not the opposite. This is crucial if you attempt to fix the root.

And did you restore TSH levels down to normal with that simple protocol? How was TSH level before and after?

Antibodies and autoimmunity occur because high cortisol suppresses proper immune function. So the immune system invades the thyroid.

High cortisol occurs due to angiotensin and undermethylation. The thyroid will gain access if the cells can both perform and recycle.
 
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Agent207 said:
post 112831 This is extremely interesting and paradoxical at the same time. Theres been cases when hipothyroid symtoms and thyroid impairment after long term cetogenic or low carb diets. You reversed it with it, in a way you think you couldn't with carbs, right?

Ketogenesis directly produces acetyl coenzyme A and bypasses all the problems with glucose but due to it's requirement for fatty acids to generate ATP is highly reliant on a healthy liver, kidneys and the adrenal hormone adrenaline. What is adrenaline made out of? Tyrosine. What is thyroxine made out of? Tyrosine.

Because ketogenesis is extremely efficient but energy intensive, it relies on healthy liver methylation to mop up potential stray fatty acids that become damaged, and the adrenals and kidneys must sustain tyrosine and adrenaline in order to match the fat burning shuttle into ATP.

Hence I still support Ray's views on limiting PUFAs and using sugar, albeit diligently. Sugar is helpful to lighten the load of the adrenals in providing the fatty acids and ketones to generate ATP without becoming hypoadrenal and therefore hypothyroid.

There is nothing better than a ketogenic body using coconut oil for energy and healthy brain cell membranes retaining magnesium reducing any chance of angiotensin and cortisol raising blood sugar causing diabetes, alongside healthy kidneys retaining sodium and producing glycine and tyrosine.

Sugars job should be to protect overwork of the kidneys and adrenals so that tyrosine can be sustained, and such efficient burning of fats will work in combination with sugar reducing the risk of excessive fatty acid liberation causing oxidative stress.
 
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Agent207 said:
post 112831
You still following low carb after you restored thyroid and mitochondrial function? Did you use any uncouplers... Q10, PQQ, ALA...etc?

I eat veg which helps digestive transition and provides a slow release of carbohydrates. I do believe in the term complex carbohydrates. Spinach is a great source of K2 and vit A.

Meat provides various pro-methylation nutrients:

carnitine
zinc
tyrosine
magnesium
copper
iron
etc etc

I do take PQQ before I go in the gym. I stopped taking ALA as I read it can chelate mercury. I also take brewers yeast, great for gut health. Pregnenolone originates in the gut.
 
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Agent207 said:
post 112831Maybe theres no rule set in stone nor a unique optimum pathway for ATP generation for everyone

I believe this is possible. As mentioned earlier, mitochondrial DNA is based on your mother. So it might be interesting to look back over her diet and how long she lived, body composition etc. I've done this with my mother and she's most suited to burning fats efficiently through a lower number of mitochondria.

Also, my grandmother had kidney failure, so I know that potentially some glucose enzymes I have inherited are deficient. The kidneys when weak will prefer a highly efficient ketogenic state and sodium retention over high cortisol and poor glucose control/insulin sensitivity any day.

The three nutrients most deficient in kidney disease are zinc, magnesium, selenium, zinc being crucial for insulin sensitivity. So if you have genetic kidney problems my view is that you will have insulin and therefore sugar problems. So I cut all that risk out with a ketogenic stone age diet.

What is set in stone is that fat burning is the most direct way of generating ATP. This is fact. The issues occur because fatty acids readily increase stress on the liver when unused for ATP.

But again I revert to my theory that while we should limit fatty acid liberation, the main issue is not whether to burn fats, it's whether our cells ARE ABLE TO burn fats EFFICIENTLY. The heart loves burning fats. Again this is fact.

Cell maintenance is performed by the process of methylation, driven by ATP. Methylation is diverted to ammonia when brain, and only brain, ATP is dwindling. Finally, high histamine is highly stimulatory to cortisol, and inhibitory to the effects/benefits of adrenaline. This can also factor into the calcium influx of undermethylation. Remethylation needs strong sodium potassium pumps.
 
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fwiw, I had good success with much more glucose and fructose for a while, due to it's many sparing effects, but I did find it didn't produce ATP like my meat and veg diet does, and I put on so much weight which I could never foresee be offset by metabolism.

Also, worth noting that I was for a long time successfully ketogenic before starting to consume more glucose. So now I just see glucose as something to gently spare the stress response so adrenal and kidney output is maximised while the liver methylates using the high levels of fat-burning ATP. This is hand in hand with my gym aims.

(An)aerobic exercise is highly adrenal and kidney taxxing but you cannot doubt the detoxification and cardio benefits of sweating your nipples off on treadmills.

Become a lean fat burner and use glucose around exercise and before bed. Glucose is essential in these smaller quantities because certain sections of the brain cannot function on ketones alone.

People on the forum consume great quantities of sugar and if lucky report increases in metabolism and sex drive after a while putting on weight. Instead I view that you should use sugar in relation to ketogenesis to do the same. A more measured approach, similar to my points on replenishing brain fats with EFAs in small doses.

Serotonin is only bad if it is not matched or exceeded by dopamine.
Fatty acids are only bad if they are not matched or exceeded by cellular conversion and output into ATP. Highly oxidized fats consumes your glutathione and in the end your body resorts to localised angiotensin in lungs and kidneys. The severity of angiotensin determines calcium and cortisol toxicity.

Moderators, sorry for posting so many separate replies.
 

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Love conficting information lol. But what you say has a lot of sense, and in part I see myself indentified since I started a more oriented "raypeatforum" diet.

Before I used to eat almost everything, quality/real food, without giving much attention to low PUFAS (although i didnt consume much), lots of starches and MUFAs oils from olive, avocados, oats, sugar from honey for workouts... and moderate protein for gym (around 2gr/kg). Actually I was pretty good, maybe a bit of tiredness lately and then i read about thyroid and R.Peat and this forum and i moved to consuming more fruit sugars, orange juices, 2 quarts of milk (before i barely take milk, mostly cheese and whey)... almost no starches, etc.

And while Im not gonna say t was detrimental, there were no improvement either. I reduced exercise since i think it was part of the problem, overtraining... and even with that my tsh went from 3 to 3.40 in a year.

I think theres no point on labelling diets wrong or optimal, lowcarb, highcarb, zero grain... etc becouse things are complex. As you say sugar and carbs have their roles, the same as fats, and blaming either one for generating atp just becouse you read the "perfect diet" say so is absurd. What it is importat is researching, looking good sources of information, even conflicting between them, and trying to grow knowlesge to understand the whole whole picture better.

As Peat wisely said, the only valid protocol is "perceive, think, act".
 
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The most efficient way to produce ATP is ketogenesis if your body can sustain it.

Life is too short to spend so long reading conflicting information. I have done this for four years, spent £8,000, and the above advice combined with my high levels of education is the best advice I can give, and will certainly be spending no more time experimenting or researching,
 

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Btw Kinectz, I imagine the main dietary fat you use for ATP comes from coconut oil, right? Some minimun O6/O3 for brain, but regarding energy I guess you'll use CO mainly and some sugar.

i've read too about lots of people on "paleo" diets increasing insulin resistance and leaving with elevated blood gucose after long term very low carb. Whats your take on this?
 

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kineticz said:
post 112854 The most efficient way to produce ATP is ketogenesis if your body can sustain it.

Life is too short to spend so long reading conflicting information. I have done this for four years, spent £8,000, and the above advice combined with my high levels of education is the best advice I can give, and will certainly be spending no more time experimenting or researching,
You have some very interesting arguments kineticz; a fresh re-breathe from dogmatism.
 
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Agent207 said:
post 112855 Btw Kinectz, I imagine the main dietary fat you use for ATP comes from coconut oil, right? Some minimun O6/O3 for brain, but regarding energy I guess you'll use CO mainly and some sugar.

The main use of fats comes from carnitine and my meat diet. Whichever fat I have stored in my body is burned. The process is more important than the source. It doesn't really matter what type of fat, it matters how well the cells burn fat. The type of fat matters only when replenishing cell membranes in the brain.

I use coconut oil because it has low chance of oxidative stress and contains enzymes that produce pregnenolone directly.

You seem to have reverted back to Peat norms out of context again by trying to target and nail down exacts. What conflicting information do you refer?
 
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kineticz said:
The most efficient way to produce ATP is ketogenesis if your body can sustain it.

Life is too short to spend so long reading conflicting information. I have done this for four years, spent £8,000, and the above advice combined with my high levels of education is the best advice I can give, and will certainly be spending no more time experimenting or researching,
There may be a significant increase in ATP and other benefits from ketones, which can be synthesized or consumed.
http://www.coconutketones.com/pdfs/Veec ... ations.pdf

Whether a "ketogenic" (or other) diet is working for you can be predicted by an MRI, which would measure (among other things) your visceral obesity. If an MRI is not practical, a measurement of waist-to-hip ratio can give an approximation. A waist-to-hip ratio of less than .9 for a man, or less than .85 for a woman, is considered safe, and lower ratios are likely better.
 

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kineticz said:
The main use of fats comes from carnitine and my meat diet. Whichever fat I have stored in my body is burned. The process is more important than the source. It doesn't really matter what type of fat, it matters how well the cells burn fat. The type of fat matters only when replenishing cell membranes in the brain.

I use coconut oil because it has low chance of oxidative stress and contains enzymes that produce pregnenolone directly.

You seem to have reverted back to Peat norms out of context again by trying to target and nail down exacts. What conflicting information do you refer?

You're right. The conflicting information would be wether glycolisis vs ketogenesis to be the most efficient way to produce ATP. Specially in a context of very active lifestyle and high intensity training.

Also, I'm concerned about the insulin-glucose impairment and resistance developing reported on most cases under long term ketogenic diets. Whats your take on this? Did you check this on yourself?
 
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