Improving Liver Function Before Going Full Peat? Dealing With Abdominal Fat

[Spondive]

I have to add that Glycine has reduced my inflammation.. My crp went from 6.6 down to 0.8 in a few months

 

[visionofstrength]

I agree with you and Peat that is why I am reluctant to use choline and Betaine. I figured if my metabolism increases with the use of T3 and uncouplers I would require more choline etc. the choline seems to lower my liver enzymes whether that is healthy or not is a different story and whether it is liberating to much free fatty acids because of this could be detrimental

Yes, uncouplers (including progesterone/DHEA) are one way to slow down fatty acid oxidation. The carbon dioxide that's generated by uncoupling is used to activate the PDH complex, which in turn promotes the oxidation of glucose to even more carbon dioxide. A healthy cycle!

 

[narouz]

I have to add that Glycine has reduced my inflammation.. My crp went from 6.6 down to 0.8 in a few months

Interesting, Spondive.
What kind & how much glycine?

 

[Spondive]

Pure bulk about 5000mg a day

 

[visionofstrength]

Pure bulk about 5000mg a day

There are 6,300 mg glycine in 3 tablespoons of gelatin. I use at least 6 tablespoons of gelatin a day.

narouz, you asked somewhere about my protein source. This is a big part of it along with nonfat milk and cottage cheese.

 

[Spondive]

I have been using casein from pure bulk and gelatin the green can and mixing it in juice to get more protein in for my liver with little extra fat multiple times aday based on what visionofstrength has said in previous posts also

 

[narouz]

Pure bulk about 5000mg a day

There are 6,300 mg glycine in 3 tablespoons of gelatin. I use at least 6 tablespoons of gelatin a day.

narouz, you asked somewhere about my protein source. This is a big part of it along with nonfat milk and cottage cheese.

Thanks, VoS.
How many grams, roughly, you shoot for per day?

 

[visionofstrength]

Pure bulk about 5000mg a day

There are 6,300 mg glycine in 3 tablespoons of gelatin. I use at least 6 tablespoons of gelatin a day.

narouz, you asked somewhere about my protein source. This is a big part of it along with nonfat milk and cottage cheese.

Thanks, VoS.
How many grams, roughly, you shoot for per day?

42 gelatin
64 nonfat milk/cottage cheese
14 liver or eggs
-----
120 total

Though I have (in)famously consumed up to 300 grams per day on my 6,000 calorie diet of uncouplers, when I was rebuilding muscle and lean body mass.

 

[BingDing]

Betaine and choline are described as methyl donors. Though conventional medical literature may curry to corporate interests as proproprietors of methyl donors, I think Peat is clear that reducing methylation from methyl donors is important:

Methionine and choline are the main dietary sources of methyl donors. Restriction of methionine has many protective effects, including increased average (42%) and maximum (44%) longevity in rats (Richie, et al., 1994). Restriction of methyl donors causes demethylation of DNA (Epner, 2001). The age accelerating effect of methionine might be related to disturbing the methylation balance, inappropriately suppressing cellular activity. Besides its effect on the methyl pool, methionine inhibits thyroid function and damages mitochondria.

If you need to treat fatty liver, Peat's answer is to stop fatty acid oxidation, which has systemic benefits in the liver and the body.

When free fatty acid levels are elevated, the metabolism of glucose to carbon dioxide becomes impaired, and glucose is rerouted to lactate instead.

I tried to write more about this in the post that I linked to above, in response to what haidut calls his long rant.

I think you are mistaken once again, Vision. RP has written conflicting things about DNA methylation.

RP- "With aging, DNA methylation is increased (Bork, et al., 2009). I suggest that methylation stabilizes and protects cells when growth and regeneration aren't possible (and that it's likely to increase when CO2 isn't available). Hibernation (Morin and Storey, 2009) and sporulation (Ruiz-Herrera, 1994; Clancy, et al., 2002) appear to use methylation protectively.

And a methylation step is used in many metabolic pathways. There is a discussion here.

 

[visionofstrength]

Betaine and choline are described as methyl donors. Though conventional medical literature may curry to corporate interests as proproprietors of methyl donors, I think Peat is clear that reducing methylation from methyl donors is important:

Methionine and choline are the main dietary sources of methyl donors. Restriction of methionine has many protective effects, including increased average (42%) and maximum (44%) longevity in rats (Richie, et al., 1994). Restriction of methyl donors causes demethylation of DNA (Epner, 2001). The age accelerating effect of methionine might be related to disturbing the methylation balance, inappropriately suppressing cellular activity. Besides its effect on the methyl pool, methionine inhibits thyroid function and damages mitochondria.

If you need to treat fatty liver, Peat's answer is to stop fatty acid oxidation, which has systemic benefits in the liver and the body.

When free fatty acid levels are elevated, the metabolism of glucose to carbon dioxide becomes impaired, and glucose is rerouted to lactate instead.

I tried to write more about this in the post that I linked to above, in response to what haidut calls his long rant.

I think you are mistaken once again, Vision. RP has written conflicting things about DNA methylation.

RP- "With aging, DNA methylation is increased (Bork, et al., 2009). I suggest that methylation stabilizes and protects cells when growth and regeneration aren't possible (and that it's likely to increase when CO2 isn't available). Hibernation (Morin and Storey, 2009) and sporulation (Ruiz-Herrera, 1994; Clancy, et al., 2002) appear to use methylation protectively.

And a methylation step is used in many metabolic pathways. There is a discussion here.

He's saying that if your tissue would be injured or excitatory, but low metabolic rate/CO2 prevents it from actually growing or regenerating, then methyl (electron) donors will be protective by shifting things in a more reduced direction -- that's what a donor is, it has a low ionization potential and can donate an electron causing a shift in the redox potential in the more reduced direction. The lower the ionization potential the greater the shift.

The same thing could be said of estrogen, under excitatory conditions when cell division is needed, such as growth of the embryo, estrogen can be protective by shifting tissues in a more reduced direction during the growth. And progesterone reverses the effect of estrogen by shifting in a more oxidized direction.

As Peat explains it here:

Progesterone is able to regulate the cell's metabolism, so that the oxidative pathway, forming estrone from estradiol, predominates. Estrogen-dominated tissues are likely to have a balance in the direction of reduction rather than oxidation, increasing the amount of the active estradiol.

The examples of hibernation and sporulation are particularly apt. If you need to go into hibernation, then you should suppress your metabolic rate/CO2 in a more reduced direction, and take methyl donors.

Otherwise, you'll want to increase metabolic rate/CO2 in the more oxidized direction, with uncouplers and redox balancers that shift in the oxidized direction (and decrease methyl donors).

It took me a while but I feel like I have a least a basic understanding of redox potential itself, which goes something like the really simple explanation that Peat gives here:

Koch’s understanding of the oxidative apparatus of life, as a matter of electron balances, involved the idea that molecules with a low ionization potential, making them good electron donors, amines specifically, interfered with respiration, while quinones, with a high affinity for electrons, making them electron acceptors, activated respiration. The toxic effects of tryptophan derivatives, indoles, and other amines related to the behavior of their electrons. (Serotonin wasn’t known at the time Koch was doing his basic research.) Koch believed that similar electronic functions were responsible for the effects of viruses.

 

[BingDing]

That's another flunk, Vision. In a methylation reaction a methyl group, CH3, gains a fourth covalent bond with the carbon atom. That is why a specific methyltransferase enzyme is required. It has nothing to do with electron donors or redox reactions. I really wish you would go away, or at least quit posting BS in RP's name.

But the bigger issue is whether methyl donors like betaine or methylcobalamin (active form of b12) are healthy aside from the DNA methylation issue. RP has said methylcobalamin can be helpful, regardless of the MTHFR mutation, see the post I linked to above.

 

[visionofstrength]

That's another flunk, Vision. In a methylation reaction a methyl group, CH3, gains a fourth covalent bond with the carbon atom. That is why a specific methyltransferase enzyme is required. It has nothing to do with electron donors or redox reactions. I really wish you would go away, or at least quit posting BS in RP's name.

But the bigger issue is whether methyl donors like betaine or methylcobalamin (active form of b12) are healthy aside from the DNA methylation issue. RP has said methylcobalamin can be helpful, regardless of the MTHFR mutation, see the post I linked to above.

For Peat, everything has to do with redox balance and ionization potential. The body is a kind of liquid crystal structure held together by electronic redox potential, not membranes.

University training, which ignores Ling's work, cannot understand how this could be so. And so Peat's biophysics is really a difference of night and day from university curricula.

Peat says that a good explanation of pH and redox is here:
http://www.molecularhydrogeninstitute.c ... nceptions/

Please be nice. There are many views in the world, and being open to others is good. For example, you can write to Peat to ask him, but you already know he's going to suggest that you avoid betaine and choline. You are just doubting his biophysics, it seems, which is great. Keep disagreeing and keep exploring!

I don't mean to be flip, Peat is saying that, "The age accelerating effect of methionine might be related to disturbing the methylation balance, inappropriately suppressing cellular activity." [Emphasis mine.]

He is again saying, in nearly the same words, that it is sometimes useful for methyl donors to shift this balance when needed for appropriately suppressing cellular activity, as in the case of hibernation or sporulation. I hope that helps?

Takeaway: If you want to shift your methylation balance to suppress your cellular activity, perhaps in order to hibernate, then ingest significant quantities of methyl donors.

 

[BingDing]

I try to be nice, but you are so full of ***t that it is impossible.

 

[visionofstrength]

Sorry to disappoint! Please let me know if there are Peat references you have in mind. Always eager to learn more about Peat!

 

[BingDing]

No good, Vision. You are wrong so often that I'm loathe to have a conversation with you. I'll make some remarks on your past threads.

I really do wish you would go away.

 

[visionofstrength]

No good, Vision. You are wrong so often that I'm loathe to have a conversation with you. I'll make some remarks on your past threads.

I really do wish you would go away.

I don't doubt that I'm wrong, I'd just like to know where you have references to Peat that make you think I am. I also wonder how I offended you by expressing my views, wrong though they may be. I've looked at your other posts -- which go back to 2012! -- and you've never been offended by anyone else, even if you disagreed with them, that I can see.

We're all essentially on the same team here, as a very small group of people who read and appreciate Ray Peat's work, and try to promulgate it to others. Let's work together!

If you feel like methylation balance is not a kind of redox balance, here's another way to describe methylation balance, in terms of the structural temperature of the cells:

Temperature regulation apparently involves some nerve cells that sense temperature very accurately, and change their activity accordingly. Water has a remarkably high heat capacity, meaning that it takes a relatively large amount of heat to change its temperature. The "disappearing heat" is being consumed by structural changes in the water. Proteins have the same sort of structural complexity as water, and together they can make effective temperature transducers, "thermometers." (Other substances tend to undergo major structural changes only as they melt or vaporize. The famous "liquid crystals" have a few distinct structural phases, but cytoplasm is like a very subtle liquid crystal.) The "thermostat cells" are actually responding to a degree of internal structure, not to the temperature in the abstract. So things that change their internal structure will modify their temperature "set-point."

Increased estrogen causes an animal to lower its temperature, and it probably does this by increasing the "structural temperature" of the thermostat cells, "melting" their internal structure. Progesterone causes the animal to increase its temperature, and it apparently does this by increasing the structure/decreasing the structural temperature of the thermostat cells. If you put ice in the thermostat, the room gets hot.

A cell's internal structure is equivalent to its readiness to work. Fatigue represents a slightly "melted" state of the cell, in which structure appears to have been consumed along with the chemical energy reserves. Experiments that demonstrated this effect were very clear, but they were ignored because they didn't fit people's stereotyped idea of the cell. With a very sensitive thermometer, it's possible to measure the heat produced by a nerve when it is stimulated. That's not surprising. But it's surprising that, when the nerve is recovering from the stimulation, it absorbs heat from its environment, lowering the temperature locally. That even violated some people's conception of "entropy," but it can easily be demonstrated that changing the form of some materials changes their heat capacity, as when a rubber band is stretched (it gets hot), or contracts (it gets cooler).

The excitants, estrogen and cortisol, slow the conduction of nerves, because they cause its internal structure to be dissipated. They create a "pre-fatigued" state in the cell.

In experiments with rabbit hearts, Szent-Gyorgyi showed that estrogen decreased the heart's readiness to work, and that progesterone increased its readiness to work, and he said it did this by "building structure." He pointed out that, for a given drug or other stimulus, cells have a characteristic response, becoming either more activated or more inhibited, but he showed that, outside the normal concentration or intensity range of the stimulus, a cell's response is often reversed.

If this is the situation in the nerves in MS, it explains the strange behavior, in which warming the nerve reduces its function. The implication is that internal structure (and energy) must be restored to the nerves. In experiments that I have described in previous newsletters, increasing sodium, ATP, carbon dioxide, and progesterone, and increasing the ratio of magnesium to calcium, have been found to increase cellular energy and structure. The thyroid hormone is ultimately responsible for maintaining cells' energy and structure, and responsiveness, but if it is increased suddenly without allowing all the other factors to adjust, it will raise the temperature too suddenly. It needn't take a long time, but all the factors have to be present at the same time.

Serotonin, melatonin, estrogen, and polyunsaturated fats all tend to lower body temperature. Since estrogen and the unsaturated fats are cellular excitants, the actual decrease in body temperature helps to offset their excitatory effects.

Shifting methylation balance with methyl donors to a lower redox potential or higher "structural temperature" (if you prefer) works in the same way, helping to offset the excitatory effects of growth or regeneration that is stymied by hibernation or sporulation.

 

[tara]

University training, which ignores Ling's work, cannot understand how this could be so. And so Peat's biophysics is really a difference of night and day from university curricula.

I don't doubt that university training has it's deficiencies, and Peat has drawn attention to some of them. But to write it all off seems to me to undervalue the information and learning that can be available through universities, and strikes me as disrespectful to people who do in fact know things that they learned there. I'm fairly sure that a good many of the studies Peat refers to are conducted either in universities or by university-trained scientists. They provide a great deal of relevant evidence about physical functioning, even if they often also display some systematic inconsistencies with reality in some areas.

Please be nice. There are many views in the world, ...

It is fine to express your opinion, and to speculate, and to sometimes be wrong. In my opinion it is not OK to repeatedly attribute your interpretations, extended inferences and speculations to Peat. That you continue to do this after it has been repeatedly drawn to your attention by several people strikes me as systematically disrespectful to Peat, and to the people here who are trying to learn from Peat.

I don't doubt that I'm wrong, ...

If you understand, as you say above, that you are sometimes wrong, and as you have said elsewhere, that you have limited understanding of biochemistry etc, then please exercise some restraint, and replace 'Peat thinks' and 'Peat feels' in front of your thoughts with 'I think' , and stop referring misleadingly to 'the RDAs' all over the forum. It is not 'being nice' or in my book to continue with these phrases.

It is also problematic, from my PoV, when you present solutions that seem to have worked well for you personally, as though they are guaranteed to have exactly the same beneficial (or 'miraculous') effect for other people (especially problematic if you preface this with 'Peat thinks ...' etc, but problematic even without that). You run the risk of seriously misleading people who come here in good faith trying to learn about Peat's approach. If something has worked for you, that's great. Sharing it is great. If you've read much of the forum, you'll be aware that people do not always react the same way to various things. Confidently and repeatedly stating that your solution will work for everyone else does not seem to correspond to a reasonable understanding of how things work, as acquired from reading either Peat or this forum. In fact, it seems to invalidate a great deal of the experience other posters generously report here.

It seems I am not the only one who has these concerns. If you could adapt your posting to avoid these problems, I think that would go a ways towards us all being able to work together more harmoniously for the purposes of the forum, without you having to constrain your own good creative thinking, and without others feeling the frustratingly repeated need to defend Peat and other forum readers from your misrepresentations.

On the positive side, VoS, you often find and present relevant quotes from Peat, you often synthesise imaginative (in a good way) lines of thought, you have generously shared some really interesting information about your own personal experiments, and you make efforts to encourage people. I would be pleased if you would continue with these aspects of your postings.

 

[moss]

"A man convinced against his will is of the same opinion still"....

 

[Spondive]

I am trying to figure out why you guys are saying that VoS is not in line with Peat or misinterpreting etc.? He is suggesting all the the things Peat says in his writings and talks. High protein low PUFA lower fat, high sugar, progesterone, T3, low amounts of dhea etc etc.

What specifically are you at odds with? Just for my own interest

 

[panda]

Well, the K2 is here (Carlson 5mg), so I took one around 1PM, was planning to take another one at night, but not sure if I should start easily with the K2 or if it doesn't matter if I start with 1,5,10,25 or 45mg?
I felt some fatigue after taking it, but of course I don't know if it's the K2, especially since I'm tapering benzodiazepines (clonazepam), and the fing withdrawal process of the benzos creates all kind of strange symptoms. I'm pretty sure the benzos are a big part of the problem, but I'm doing what I can at the same time, tapering (and getting rid of them eventually) while doing some other things with supplements/food to improve my health, seems like a good strategy. I know improving my sugar intake has helped a lot with my anxiety and stress levels.
I have been increasing my caffeine intake to near 400mg levels (but not coffee, is it the same as long as I increase caffeine?), and I feel better. My hope is that now with the K2, things will be even better, but I'll wait 2 weeks to report.
Any advise about the caffeine and K2 levels will be appreciated. Any other supplement/food that may help with this process?