tyw
Member
@Westside PUFAs roped me into the thread .... so I guess peeps will have to deal with my rantingz.
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Glucose and Fatty Acids Used at the Same Time
First, to address Westside's claim that "We're always burning both glucose and fatty acids" .....
We ignore the case of extreme anaerobic exercise, whereby pure carb utilisation can occur, but never for long. Thus, we deal with average energy expenditure during daily free-living conditions.
In the case of resting fuel use, the above statement is generally true, unless given the context of very high carbohydrate feeding in excess of caloric needs. Even then, Respiratory Quotient (RQ) drops below 1.0 (pure carb metabolism) very quickly (study link). In children, who are arguably "more eagerly carbohydrate metabolising", RQ still only climbed to a max of 0.91 in this study, when the kids were fed a 25% fat diet. See table 4 for breakdown -- an RQ of 0.91 reflects about 70% energy from carbs, and 30% from fat.
Therefore, yes, in almost all circumstances, both glucose and fatty acids are used.
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PUFA does not hinder recovery in Roy Swank's Multiple Sclerosis (MS) Patients, so long as fat intake is generally low
This was highlighted in Denise Minger's article on very low fat diets -- In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)
In Peat terms, Swank's "Small amounts of polyunsaturated vegetable oils and fish oil (10 – 40 grams per day)", is not low. And yet, he had multi-decade studies of patients recovering from MS despite this sort of PUFA consumption. In fact, he observed worse outcomes with both increased fat consumption, and increased saturated fat consumption.
As a clarifying note, the PUFAs did not seem strictly necessary on Swank's protocol -- McDougall Interview with Dr. Roy Swank, MD | Dr. McDougall's Health & Medical Center
Now, we must separate these concepts, and clarify each concept INDEPENDENTLY . There shall be no lazy thinking about whether a compound like PUFA is "good" or "bad" unless context is sufficiently qualified.
First, saturated fat supports a low-carb diet, and can impair signalling in a high carb diet.
If you want details, I have cited Peter @ Hyperlipid many times, especially his "Protons (38)" article -- Hyperlipid: Protons (38) and ultra low fat once more
I have gone through the mechanics many times on this forum, and regardless of whether we are talking about high Free Fatty Acids inhibiting glucose uptake (this is the Randle Effect, and is applicable to all tissues except the liver, brain, and heart), or if we are talking about Peter's mechanic of saturated fat causing mitochondrial insulin resistance via decreased membrane potential / delta-psi ...... it can be said that both the availability of Saturated fat reduces the potential ability for cells in the body to use glucose.
Peter's described mechanics also show that PUFAs provide the opposite signal when metabolised, allowing for continued insulin function, and unaffected carbohydrate metabolism.
Be clear about mechanic please => mitochondrial beta oxidation of PUFA does not hurt on-going carbohydrate metabolism.
This says nothing about whether PUFAs are good for the rest of the body in general. All it says is that if you eat a meal of PUFA + Starch/Sugar, both the PUFA and Starch or Sugar can be digested and used at the same time.
This is not true for a meal of SFA + Starch/Sugar. I've mentioned the observation in this post -- Need Thyroid Med HELP! , and in particular, this study, where it is clear that the more Unsaturated a fat is, the faster it gets oxidised for energy. There is even a statement:
Again, if we look at the mechanics of the FADH2:NADH ratio that Peter has mentioned ad-nauseam, this makes sense during the immediate post-prandial phase where nutrients are competing for utilisation. Then, in the case of fatty acid mobilisation, that last thread I linked to explained the relative ease of mobilisation of PUFA vs SFA.
Again, back to Swank's patients. We have the observations that, in the context of a High Carb, Low Fat diet:
(1) Add more Saturated Fat => patients get moar MS
(2) Add too much overall fat => patients get MOAR MS
(3) Add limited PUFA => patients recover from MS
One simplistic explanatory model becomes obvious: avoid stuff that screws with carbohydrate metabolism, and MS patientz get better
Again, PUFA isn't necessary . But it doesn't stop carbohydrates from being used => cells have enuf energy, and don't screw things up.
As an aside, Minger did mention Walter Kempner, and his diet was truly almost zero fat, and his patients (while not MS patients), also saw good things happen.
If we believe in the "more cellular energy => more cellular intelligence" theory, and the mechanics I have described above (PUFA allows carb metabolism to continue), then this makes perfect sense.
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However, we must not ignore the seemingly positive results of people like Terry Wahls, who takes the exact opposite dietary approach to MS, and instead, promotes ketosis.
IMO, this is still perfectly logical -- in the case of ketosis, you have unhindered FFA access, plus ketones, without having any carbs to screw with the metabolism of fat.
If all goes well, we still end up with a case whereby cellular energy requirements can be fulfilled, albeit through a separate mechanism. The success of such a strategy depends on the ability of the patient to process and use all that incoming fatty acids. Some seem to have more success than others.
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Note the Theme here: DO NOT DISRUPT THE USAGE OF THE PRIMARY FUEL SOURCE
When dealing with raw energetics, we aren't talking about "carbs good" or "fat bad", but rather, what is the correct balance of each energetic substrate for a particular person's idiosyncratic way of partitioning and dealing with these substrates.
I have stated my opinion before, whereby one triangulates this balance by starting at one extreme. ie: either exclusively Very Low Fat (<10% fat), or Very Low Carb (<50g carb), and then add more of the "opposing nutrient", until a balance is reached.
In that sense, I am not "anti-fat", nor "anti-carb" , but am of the opinion that one needs to "pick sides" when it comes to a primary nutrient, and lean on it pretty hard. ie: I am biased to say that >15% fat is not good if carbs are thy choice, and >100g carbs are not good if fat is thy poison . Of course, the standard diet that people eat inevitably ends up in limbo territory, where neither of the 2 macronutrients are high or low. Body is confused ......
I have also stated my bias, having found success at the very low fat end of the spectrum (which also happens to fall into my ancestral patterns of eating), and with lots of starch as opposed to sugar.
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[RANT_OVER]
....
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Glucose and Fatty Acids Used at the Same Time
First, to address Westside's claim that "We're always burning both glucose and fatty acids" .....
We ignore the case of extreme anaerobic exercise, whereby pure carb utilisation can occur, but never for long. Thus, we deal with average energy expenditure during daily free-living conditions.
In the case of resting fuel use, the above statement is generally true, unless given the context of very high carbohydrate feeding in excess of caloric needs. Even then, Respiratory Quotient (RQ) drops below 1.0 (pure carb metabolism) very quickly (study link). In children, who are arguably "more eagerly carbohydrate metabolising", RQ still only climbed to a max of 0.91 in this study, when the kids were fed a 25% fat diet. See table 4 for breakdown -- an RQ of 0.91 reflects about 70% energy from carbs, and 30% from fat.
Therefore, yes, in almost all circumstances, both glucose and fatty acids are used.
----
PUFA does not hinder recovery in Roy Swank's Multiple Sclerosis (MS) Patients, so long as fat intake is generally low
This was highlighted in Denise Minger's article on very low fat diets -- In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)
In Peat terms, Swank's "Small amounts of polyunsaturated vegetable oils and fish oil (10 – 40 grams per day)", is not low. And yet, he had multi-decade studies of patients recovering from MS despite this sort of PUFA consumption. In fact, he observed worse outcomes with both increased fat consumption, and increased saturated fat consumption.
As a clarifying note, the PUFAs did not seem strictly necessary on Swank's protocol -- McDougall Interview with Dr. Roy Swank, MD | Dr. McDougall's Health & Medical Center
Swank: We have found over the years that the vegetable oils can be added, from 10 to 30 grams a day, unless one is overweight.
JM: What do you think about adding vegetable oils to your diet?
Swank: Well, I think it’s worthwhile. We have looked at this over a number of years, and have found that the skin and the hair seem better in women. There is also some reserve of calories for energy. Best of all, however, is the fact that the patients can follow the diet more easily if they can have some oil. It makes it more palatable for them.
JM: What do you think about adding vegetable oils to your diet?
Swank: Well, I think it’s worthwhile. We have looked at this over a number of years, and have found that the skin and the hair seem better in women. There is also some reserve of calories for energy. Best of all, however, is the fact that the patients can follow the diet more easily if they can have some oil. It makes it more palatable for them.
Now, we must separate these concepts, and clarify each concept INDEPENDENTLY . There shall be no lazy thinking about whether a compound like PUFA is "good" or "bad" unless context is sufficiently qualified.
First, saturated fat supports a low-carb diet, and can impair signalling in a high carb diet.
If you want details, I have cited Peter @ Hyperlipid many times, especially his "Protons (38)" article -- Hyperlipid: Protons (38) and ultra low fat once more
I have gone through the mechanics many times on this forum, and regardless of whether we are talking about high Free Fatty Acids inhibiting glucose uptake (this is the Randle Effect, and is applicable to all tissues except the liver, brain, and heart), or if we are talking about Peter's mechanic of saturated fat causing mitochondrial insulin resistance via decreased membrane potential / delta-psi ...... it can be said that both the availability of Saturated fat reduces the potential ability for cells in the body to use glucose.
Again, the exception are the tissues of the brain and heart. The brain will demand glucose, and the heart will demand fatty acids, and their fuel use behaviours will barely change unless in ketosis and/or starvation.
Peter's described mechanics also show that PUFAs provide the opposite signal when metabolised, allowing for continued insulin function, and unaffected carbohydrate metabolism.
Be clear about mechanic please => mitochondrial beta oxidation of PUFA does not hurt on-going carbohydrate metabolism.
This says nothing about whether PUFAs are good for the rest of the body in general. All it says is that if you eat a meal of PUFA + Starch/Sugar, both the PUFA and Starch or Sugar can be digested and used at the same time.
This is not true for a meal of SFA + Starch/Sugar. I've mentioned the observation in this post -- Need Thyroid Med HELP! , and in particular, this study, where it is clear that the more Unsaturated a fat is, the faster it gets oxidised for energy. There is even a statement:
Cooper et al. found that 80–100% of dietary 18:1 was oxidized within 24 h of feeding the labeled meal, while 10–25% of dietary 16:0 was oxidized over the same time frame [51].
Again, if we look at the mechanics of the FADH2:NADH ratio that Peter has mentioned ad-nauseam, this makes sense during the immediate post-prandial phase where nutrients are competing for utilisation. Then, in the case of fatty acid mobilisation, that last thread I linked to explained the relative ease of mobilisation of PUFA vs SFA.
Sidenote: for those interested in another explanation of SFA vs PUFA oxidation and FADH2:NADH mechanics, expand the quoted section that immediately follows.
TYW email response on some random topic said:The mechanism by which insulin sensitization takes place, is the maintenance of an elevated Mitochondrial Inner Membrane Charge Potential. This is measured in volts, and is what Peter calls "Delta-Psi" (notation is ΔΨ, which is purely for convenience sake).
Insulin requires high delta-psi to signal. The oxidation of fatty acids will enable or disable the maintenance of high delta psi, depending on the FADH2:NADH ratio achieved from full beta oxidation of a fatty acid. (Assume that beta oxidation is taken to completion, which isn't always the case, but let's assume that anyway).
NOTE: the FADH2:NADH ratio is simply a way of determining relative Complex 1 to Complex 2 activity. FADH2 enters at Complex 2, and NADH enters at Complex 1. No matter what substrate is used, mitochondria will always oscillate between Complex 1 and Complex 2 activity. Overall low level mechanics depend both on total electron flow, as well as the relative activity of Complex 1 vs Complex 2.
Then, it is much more Complex 2 activity relative to Complex 1 activity, that causes reverse electron flow through Complex 1, and the subsequent production of ROS and reduction in delta psi.
This is achieve through proportionately more FADH2 than NADH -- ie: a HIGH FADH2:NADH ratio.
The more un-saturated the fatty acid, the lower the FADH2:NADH ratio. Low FADH2:NADH ratios support Complex 1 forward flow; they keep delta-psi High, and allow insulin to continue to function.
This is an Active process. The moment that there is no substrate pouring through mitochondria, none of this is applicable. In the context of the analysis of single meals and their impact these low level mechanics, we must strictly apply this to the post-prandial state.
This is not a simple analysis, and will depend on various factors. Once a potato with fat is eaten, the carbohydrates are going to be digested relatively quickly compared to the fat, and will hit the bloodstream within 20-30 mins of eating the meal (assuming that there was no meal already present and still digesting beforehand).
The fat will take maybe at 1 hour or 2 hours to be available to cells, and this is still within the overlap period of when carbohydrates from a meal may be digesting. This is when the mechanics apply.
Again, back to Swank's patients. We have the observations that, in the context of a High Carb, Low Fat diet:
(1) Add more Saturated Fat => patients get moar MS
(2) Add too much overall fat => patients get MOAR MS
(3) Add limited PUFA => patients recover from MS
One simplistic explanatory model becomes obvious: avoid stuff that screws with carbohydrate metabolism, and MS patientz get better
Again, PUFA isn't necessary . But it doesn't stop carbohydrates from being used => cells have enuf energy, and don't screw things up.
As an aside, Minger did mention Walter Kempner, and his diet was truly almost zero fat, and his patients (while not MS patients), also saw good things happen.
If we believe in the "more cellular energy => more cellular intelligence" theory, and the mechanics I have described above (PUFA allows carb metabolism to continue), then this makes perfect sense.
NOTE: it is NEVER so simple that "more of the right food => more cellular energy". I have touched on the topic of cellular efficiency before, phrased with the question, "Metabolism stimulates Cell Intelligence, and Cell Intelligence permits better metabolism. Yet metabolism is Broken. WTF? " -- Metabolic Efficiency And Metabolic Rate - Doubt
If there isn't anything fundamental that is breaking this virtuous Metabolism<=>Intelligence feedback loop, then it may be possible that "more of the right food => more cellular energy".
If there isn't anything fundamental that is breaking this virtuous Metabolism<=>Intelligence feedback loop, then it may be possible that "more of the right food => more cellular energy".
----
However, we must not ignore the seemingly positive results of people like Terry Wahls, who takes the exact opposite dietary approach to MS, and instead, promotes ketosis.
IMO, this is still perfectly logical -- in the case of ketosis, you have unhindered FFA access, plus ketones, without having any carbs to screw with the metabolism of fat.
If all goes well, we still end up with a case whereby cellular energy requirements can be fulfilled, albeit through a separate mechanism. The success of such a strategy depends on the ability of the patient to process and use all that incoming fatty acids. Some seem to have more success than others.
----
Note the Theme here: DO NOT DISRUPT THE USAGE OF THE PRIMARY FUEL SOURCE
When dealing with raw energetics, we aren't talking about "carbs good" or "fat bad", but rather, what is the correct balance of each energetic substrate for a particular person's idiosyncratic way of partitioning and dealing with these substrates.
I have stated my opinion before, whereby one triangulates this balance by starting at one extreme. ie: either exclusively Very Low Fat (<10% fat), or Very Low Carb (<50g carb), and then add more of the "opposing nutrient", until a balance is reached.
In that sense, I am not "anti-fat", nor "anti-carb" , but am of the opinion that one needs to "pick sides" when it comes to a primary nutrient, and lean on it pretty hard. ie: I am biased to say that >15% fat is not good if carbs are thy choice, and >100g carbs are not good if fat is thy poison . Of course, the standard diet that people eat inevitably ends up in limbo territory, where neither of the 2 macronutrients are high or low. Body is confused ......
I have also stated my bias, having found success at the very low fat end of the spectrum (which also happens to fall into my ancestral patterns of eating), and with lots of starch as opposed to sugar.
====
[RANT_OVER]
....
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