Tyw. Said Something That Makes Alot Of Sense!

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beachbum

beachbum

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I don't want to make this back and forth discussion worse, I hope what I post makes it better. First I have gotten alot of good information from Tyw, and there is a dispute or whatever you want to call it with pufa. Below is from what RP has said:

Essential fatty acids (EFA) are, according to the textbooks, linoleic acid and linolenic acid, and they are supposed to have the status of "vitamins," which must be taken in the diet to make life possible. However, we are able to synthesize our own unsaturated fats when we don't eat the "EFA," so they are not "essential." The term thus appears to be a misnomer. [M. E. Hanke, "Biochemistry," Encycl. Brit. Book of the Year, 1948.]


Just saying
 
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m_arch

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Sorry if it led you down a bad path. Those massive doses actually did help me in terms of recovering liver health. It was just a part of the picture for me and when I stopped seeing benefit I stopped doing it. But yeah, I am wrong about many things, no doubt about it. That's why I don't like to argue, and just try to find what works. Here is one link where gbolduev talks about Wilson and his craziness. I was wrong, it was Wilson and not Eck apparently.
Bicarbonate Vs. PaCO2 Blood Tests
"...Check out Wilsons article where he tells people to have sex in kitty litter box for modesty)) or how you need to clean your woman 5 times a day , since women are dirty entities))) HE lOST it totally, may be he interprets his tests not correctly."
From what I have seen, Eck is not much better. I have not done much digging on Eck/Wilson, beyond a few quick readings. Interesting stuff but I did not think it addresses may of the prime causes of disease.

Who is this Wilson and Eck guy? What do I google to read more about them?
 
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Read just two pages and I am now insulin resistant
 
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Yep like this..:hairpull:crazy::rolling

resource.gif
 

michael94

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Who is this Wilson and Eck guy? What do I google to read more about them?
Their work is based on mineral balancing... They have a lot of good ideas and insights but trying to correct mineral imbalances by taking more minerals usually leads to worse problems ( some exceptions ). There are some very real issues they bring up like copper and iron overload but their solutions are not the best. For example, the way your body rids itself of excess copper is through the bile but I never read them mentioning this nor its implications. I actually contacted gbolduev about half a year ago and he recommended swimming in the ocean, fasting, and liver flushes.
 
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@tyw

Peter has talked about oleic being more carb friendly, as you know

So, could you eat a mixed diet of MUFA and glucose and get some of the benefits that mono-macronutrient diets have?

High oleic sunflower oil + starch for example.

I imagine glucose would have to higher than fat, and that fructose would mess things up.

It should still allow unobstructed flow of energy.

But maybe MUFA creates too much superoxide.

And MUFA being incorporated into cell structures could be pretty benign or perhaps beneficial.
 
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Amazoniac

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The Randle cycle/effect seems like a perfectly natural response to mixed fuel substrate. When there's 100% of any micronutrient, you burn 100% of that macronutrient.

When there's mixed fuel, you burn a mix of the fuels in whatever ratio that cell sees fit.

It seems fine and I'm not sure exactly what it's even supposed to prove or mean when brought up.

Yeah, FFA might inhibit glucose oxidation, but that's because beta-oxidation is now taking place, the cell can only handle so much at one time.

And with the knowledge we have now on the differences in fat saturation and their effect on insulin signalling/glucose oxidation, the Randle effect seems to broad and outdated to be used meaningfully anymore.

But I strongly suspect I don't understand it as well as I should.
 
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Amazoniac

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The Randle cycle/effect seems like a perfectly natural response to mixed fuel substrate. When there's 100% of any micronutrient, you burn 100% of that macronutrient.

When there's mixed fuel, you burn a mix of the fuels in whatever ratio that cell sees fit.

It seems fine and I'm not sure exactly what it's even supposed to prove or mean when brought up.

But perhaps I'm not understanding exactly what it actually means.
Still pertinent because there's a link there discussing how a variation on the type of fat interferes with the use of glucose, related to your questionings. On top of that, a study in which dairy fat, despite being significantly saturated, interfered less than expected.
 
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Still pertinent because there's a link there discussing how a variation on the type of fat interferes with the use of glucose, related to your questionings. On top of that, a study in which dairy fat, despite being significantly saturated, interfered less than expected.

Okay I'll read everything and get back to you.

That's interesting though.
 

tyw

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@tyw

Peter has talked about oleic being more carb friendly, as you know

So, could you eat a mixed diet of MUFA and glucose and get some of the benefits that mono-macronutrient diets have?

High oleic sunflower oil + starch for example.

I imagine glucose would have to higher than fat, and that fructose would mess things up.

It should still allow unobstructed flow of energy.

But maybe MUFA creates too much superoxide.

And the benefit of eating mostly MUFA as fat is that even if it gets incorporated into any structures, it's fine.

Ref: hyperlipid post on MUFA and the FADH2:NADH ratio -- Hyperlipid: Protons: FADH2:NADH ratios and MUFA

A F:N ratio above 0.47 generates a lot of superoxide through Reverse Electron Chain Transport (RET) through Complex 1. Ratios below this 0.47 number do not. This is value achieved through experimental data, and one can check the entire (40+ post long) Protons series on Peter's site fro the experimental data.

Also note that if RET occurs, it will dominate superoxide production by far -- http://www.biochemj.org/content/417/1/1.long . Also see references 71, 79, and 95 from that paper. We are taking about 10x Superoxide production as compared to Complex 3 superoxide production.​

His calculation for palmitoleic acid (16:1) gives 14 FADH2 and 31 NADH upon full beta oxidation, and thus a F:N ratio of 14/31 = 0.4516. Oleic acid (18:1) gives 16 FADH2 and 35 NADH, and thus a F:N ratio of 16/35 = 0.4571, which still allows forward flow dominance.

Regarding the point about substrate use, the case for "100% use of a substrate" only applies under cases of acute overloading, and still depends on tissue level differences and prior context. For example: have an experienced lifter go do a 1 hour full body workout, then feed them a gallon of full fat ice cream -- what likely happens is that skeletal muscle uptakes glucose very readily, while still using both a mix of fatty acids and glucose for fuel, whereas the liver is completely overload with the fructose load, and is forced to upregulate carbohydrate use to nearly 100%.

SIDENOTE 1: the Randle effect in the liver is reversed => if carbs are present, they are used instead of fatty acids. Almost everywhere else (other than brain), it is the reverse => if fatty acids are too high, carb use is displaced.

SIDENOTE 2: yet another reason why I don't like the fructose-containing-Sugar + SFA overload condition.​

However, even in very high carb diets, there will always be a mix of fuels. This was addressed here, and note the proportionate change in RQ to almost exactly match fuel intake (and slightly more fatty acids were always used, eg: 30% fatty acid use on a 25% fat diet, up until a point of very low fat) -- How The Sugar Industry Shifted Blame To Fat

In that sense, Peter's mechanics are very valid, since mitochondria are going to see that sort of mixed carb/fat fuel use for the majority of the time.

Specific to the "carbosis" state, whereby you have maximum insulin sensitivity and lack of interference of fatty acids, requires at most a 10-15% fat intake. This alone means that you cannot add much fat of any kind, though of course, SFA intake is even worse at maintaining carbosis.

But yet, a high-oleic oil (like olive oil), used in small amounts, is probably not going to interfere with superoxide mechanics, and thus allow maintenance of carbosis. "Small amounts" literally means like "1 tablespoon a day at most", since for many people, "10% fat" is something like 25g of fat a day.


In terms of benefits, the few that come to mind are probably better assimilation of fat soluble vitamins. Of course, whole food sources which also contain said vitamins are probably preferred, but I can see an argument for say having a little olive oil in a salad in concurrence with Vit K supplementation (which could be in the form of high-Vit-K foods), but otherwise follow a low fat diet.

There have also been some cases where people just feel better having a little bit more fat, especially later in the day.

.....
 

tyw

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Okay I'll read everything and get back to you.

That's interesting though.
Still pertinent because there's a link there discussing how a variation on the type of fat interferes with the use of glucose, related to your questionings. On top of that, a study in which dairy fat, despite being significantly saturated, interfered less than expected.

That study is a comparison of single meal glucose rise and insulin secretion, of a very high fat meal. Study is here -- https://www.researchgate.net/public...e_Metabolic_Response_to_Ingested_Carbohydrate

The important characteristics were:

- After a 12-hour overnight fast => there were was no "second meal effect" at play, and this was in the morning, when glucose clearance was the highest, and systemic insulin sensitivity was the best (at least 33% better, as per Bill Lagakos post -- “Afternoon diabetes” and nutrient partitioning).

- 50g carbs from potato, 25g fat from various sources. In terms of macronutritional ratios, this is 52.9% fat by calories. A far far cry from what is considered a low fat diet (which as mentioned above, is more like 25g fat in an entire day)

This is a known effect, whereby adding fat to a meal "lowers the GI" of that meal. I view this as a separate, acute effect, applicable only to single-meal scenarios, which should be discussed separately to overall daily intake of macronutrients.

.....
 

Amazoniac

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That study is a comparison of single meal glucose rise and insulin secretion, of a very high fat meal. Study is here -- https://www.researchgate.net/public...e_Metabolic_Response_to_Ingested_Carbohydrate

The important characteristics were:

- After a 12-hour overnight fast => there were was no "second meal effect" at play, and this was in the morning, when glucose clearance was the highest, and systemic insulin sensitivity was the best (at least 33% better, as per Bill Lagakos post -- “Afternoon diabetes” and nutrient partitioning).

- 50g carbs from potato, 25g fat from various sources. In terms of macronutritional ratios, this is 52.9% fat by calories. A far far cry from what is considered a low fat diet (which as mentioned above, is more like 25g fat in an entire day)

This is a known effect, whereby adding fat to a meal "lowers the GI" of that meal. I view this as a separate, acute effect, applicable only to single-meal scenarios, which should be discussed separately to overall daily intake of macronutrients.

.....
Thanks! But I meant the other discussion linked.
 
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Drareg

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Thanks, but I don't find the genetic condition example convincing, neither the observational evidence of some species favoring PUFA through feeding. We don't know what else is dysregulated in Barth syndrome. A mutation is never an isolated event. As you know, even a single mutation has effects on transcription across multiple genes. Always more than one often affecting the silencing/activation of hundreds if not thousands of genes.
Like I said, I interact with EFA deficient people on a daily basis and they do not have any gross pathology detectable as structural abnormality on scans or anything showing up on blood tests that would constitute a pathology. Perhaps most notably, even though less applicable to systemic health, they do not have the famous scaly skin or wasting reported by the Burr studies. Of course, absence of evidence is not evidence of absence. Maybe these people do have a little EFA synthesized through those alternative pathways. In a completely EFA deficient cell culture, humans cells can be maintained indefinitely and are not subject to the Hayflick limit.
Fat-free Cultured Cells: No Need For PUFAS; Where Are The Studies ?

To this day we do not have a proper replication of the Burr experiment in humans, including groups fed B6, zinc and biotin, which supposedly takes care of the deficiency symptoms. If you are aware of anything that addresses this as an actual experiment please let me know. We had a very similar situation up until very recently - blaming saturated fat based on a single (possibly fraudulent) study from the 1960s. And now the official stance on saturated fat and cholesterol has been reversed.

Do the patients with Barts syndrome avoid linoleic acid? I'm guessing they eat food at times and probably get linoleic acid at some point,by the research quoted by tyw barts syndrome should not exist by this logic.
 
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