How The Sugar Industry Shifted Blame To Fat

[tyw]

@Westside PUFAs roped me into the thread .... so I guess peeps will have to deal with my rantingz.

----
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.​

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.

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".​

----

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]

....

 

[Ewelina]

@Westside PUFAs roped me into the thread .... so I guess peeps will have to deal with my rantingz.

----
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.​

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.

​

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".​

----

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]

....

I used to be on a so called "Optimal Diet" created by dr. Kwasniewski which stipulated that the worst thing anybody can do is to mix energy sources, i.e. one can be only a fat burner or a sugar burner and anything in between will cause havoc and disease.

 

[Mito]

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 .....

In your opinion, can the "side you pick" for the primary nutrient be varied (by meal or day or week) if a person finds that both high carb-low fat & low carb-high fat work equally well? For example could you eat a low carb-high fat breakfast and lunch and then switch to high carb-low fat for the last meal of the day. Or do we need to "pick a side" long term to attain optimal energy metabolism?

 

[tyw]

In your opinion, can the "side you pick" for the primary nutrient be varied (by meal or day or week) if a person finds that both high carb-low fat & low carb-high fat work equally well? For example could you eat a low carb-high fat breakfast and lunch and then switch to high carb-low fat for the last meal of the day. Or do we need to "pick a side" long term to attain optimal energy metabolism?

I used to be on a so called "Optimal Diet" created by dr. Kwasniewski which stipulated that the worst thing anybody can do is to mix energy sources, i.e. one can be only a fat burner or a sugar burner and anything in between will cause havoc and disease.

First, no matter what you do, fatty acids will have to be used at some stage through each person's circadian cycle. In terms of fuel availability, fatty acids are always in much larger amounts in the body, and will constantly be mobilised to some degree.

Circadian cycling of fuel use should always be the norm, and proper entrainment to the cycles of the sun will also come with relative changes in fuel use through the day. A simplified stance will be:
- During wakeful (daylight) hours, more fuel use, and more carbohydrate use
- During sleeping (night time) hours, less fuel use, and proportionately more fatty acid use

The technically-minded out there (like Bill Lagakos), may like to break this down into further supporting mechanics like relative SIRT1 expression in governing tissues like the liver, whereby increased SIRT1 activity (along with increased fatty acid use) occurs during the night time hours, and that this is essential in order to reset particular substrate pools (eg: total adenine nucleotide pool requires this sort of "SIRT1 reset mechanism". And as a sidenote, caffeine at night time prevents this sort of recycling, and disrupts circadian cycling)

Regardless, the generalised theme of "Light time => carbs. Night time => fat" remains true.

What the relative balance of various substrate should be depends on the person and their context. Innate insulin sensitivity will differ, innate fatty acid oxidation capacity will differ, etc .... Again, it comes down to self experimentation.

Personally, I will eat a high carbohydrate low fat diet, and eat all of my calories during daylight hours, and almost always with 50% or more of that before solar noon. I am a lean individual (<10% body fat), who has experimented with a very low fat and very low PUFA diet for a year (ie: combination of low body fat and chronic PUFA depletion diet => stored PUFA already low), and who has good insulin sensitivity, very good carbohydrate tolerance, and can mobilise fatty acids well (I will test myself occasionally for morning Beta-hydroxybutyrate levels, and they are always a moderate 0.3 - 0.6mM even with carbohydrates in my diet). This will automatically shift the balance of substrate throughout the day, and always require a larger degree of fatty acid use during the night time hours.

Some people cannot make the transition to a low carb diet even with days of adaptation. Some people cannot do the same for a low fat diet. Experiment as required.

----

As another aside, I have seen this false reasoning pop up in several Peat-related facebook groups, whereby the statement, "During stress, more fatty acids are used", is then taken to mean "fatty acid use is not ideal".

More accurate is the idea that during Stress any and all substrate is mobilised in order to provide as much energy to stressed tissues as possible. The stress state is the one state in which the Randle Effect does not hold -- see the section 'Stress Overrides Fatty Acid Inhibition of Glucose Metabolism' of the paper The Randle cycle revisited: a new head for an old hat

The operative term is "Stress", with fatty acids simply being provided in greater quantities during that state. Using fatty acids is not inherently harmful .... We can just as well say that more carbs are oxidised during the stress state, and therefore causing uncontrolled amounts of Reactive Oxygen Species in mitochondrial. Again, the problem is a systemic state which is demanding more and more energy to cells. The type of substrate isn't the primary issue here.

.....

 

[Ewelina]

You are wise beyond your years, tyw!

Great post!

 

[m_arch]

First, no matter what you do, fatty acids will have to be used at some stage through each person's circadian cycle. In terms of fuel availability, fatty acids are always in much larger amounts in the body, and will constantly be mobilised to some degree.

Circadian cycling of fuel use should always be the norm, and proper entrainment to the cycles of the sun will also come with relative changes in fuel use through the day. A simplified stance will be:
- During wakeful (daylight) hours, more fuel use, and more carbohydrate use
- During sleeping (night time) hours, less fuel use, and proportionately more fatty acid use

The technically-minded out there (like Bill Lagakos), may like to break this down into further supporting mechanics like relative SIRT1 expression in governing tissues like the liver, whereby increased SIRT1 activity (along with increased fatty acid use) occurs during the night time hours, and that this is essential in order to reset particular substrate pools (eg: total adenine nucleotide pool requires this sort of "SIRT1 reset mechanism". And as a sidenote, caffeine at night time prevents this sort of recycling, and disrupts circadian cycling)

Regardless, the generalised theme of "Light time => carbs. Night time => fat" remains true.

What the relative balance of various substrate should be depends on the person and their context. Innate insulin sensitivity will differ, innate fatty acid oxidation capacity will differ, etc .... Again, it comes down to self experimentation.

Personally, I will eat a high carbohydrate low fat diet, and eat all of my calories during daylight hours, and almost always with 50% or more of that before solar noon. I am a lean individual (<10% body fat), who has experimented with a very low fat and very low PUFA diet for a year (ie: combination of low body fat and chronic PUFA depletion diet => stored PUFA already low), and who has good insulin sensitivity, very good carbohydrate tolerance, and can mobilise fatty acids well (I will test myself occasionally for morning Beta-hydroxybutyrate levels, and they are always a moderate 0.3 - 0.6mM even with carbohydrates in my diet). This will automatically shift the balance of substrate throughout the day, and always require a larger degree of fatty acid use during the night time hours.

Some people cannot make the transition to a low carb diet even with days of adaptation. Some people cannot do the same for a low fat diet. Experiment as required.

----

As another aside, I have seen this false reasoning pop up in several Peat-related facebook groups, whereby the statement, "During stress, more fatty acids are used", is then taken to mean "fatty acid use is not ideal".

More accurate is the idea that during Stress any and all substrate is mobilised in order to provide as much energy to stressed tissues as possible. The stress state is the one state in which the Randle Effect does not hold -- see the section 'Stress Overrides Fatty Acid Inhibition of Glucose Metabolism' of the paper The Randle cycle revisited: a new head for an old hat

The operative term is "Stress", with fatty acids simply being provided in greater quantities during that state. Using fatty acids is not inherently harmful .... We can just as well say that more carbs are oxidised during the stress state, and therefore causing uncontrolled amounts of Reactive Oxygen Species in mitochondrial. Again, the problem is a systemic state which is demanding more and more energy to cells. The type of substrate isn't the primary issue here.

.....

Great post!!

So carbs + sat fat is bad because it interupts the body from using the carbs. Thus low fat high carb or low carb high fat is recommended.

If you eat high carb low fat for breakfast and then low carb high fat for lunch (lets say 4hrs later), will this interupt the body from using the fuel - or is it fine as long as the previous meal is fully metabolized?

It seems like i tolerate fat better than carbs (especially sugar) but ive been eating fatty meat and rice which doesn't sound optimal.

I'm guessing pufa doesn't effect saturated fat metabolism?

 

[tyw]

Great post!!

So carbs + sat fat is bad because it interupts the body from using the carbs. Thus low fat high carb or low carb high fat is recommended.

If you eat high carb low fat for breakfast and then low carb high fat for lunch (lets say 4hrs later), will this interupt the body from using the fuel - or is it fine as long as the previous meal is fully metabolized?

It seems like i tolerate fat better than carbs (especially sugar) but ive been eating fatty meat and rice which doesn't sound optimal.

I'm guessing pufa doesn't effect saturated fat metabolism?

Peter @ Hyperlipid had summed up the scenario of SFA + Carbs very well. I quote him:

I believe this is what Denise Minger might be describing using "carbosis" as the corollary of ketosis. Under both of these conditions there is minimal insulin secretion but under carbosis there is enough insulin sensitivity working through mtG3Pdh to accurately regulate a near pure glucose metabolism. Fructose is no problem as there is plenty of "exchangeable" glucose for use in a substitution manner.

Fatty acids have to be very low for "carbosis" to occur at all and it will be degraded far more easily by saturated fats than by PUFA, as per the ETC diagrams above and as per Denise’s examples.​

This boils down to simple flow mechanics of Complex 1 vs Complex 2 dominance during active oxidative metabolism. I will agree with Peter's assessment fully.

As a quick aside, he shows mechanically why Fructose "is no problem" under carbosis, but is very much a problem under conditions of excess SFA + Fructose. Again, quoting from the same article:

I suppose we also ought to think of the situation under a large, uncontrolled fructose input through mtG3Pdh occurring at the same time as saturated fatty acids are being oxidised.

Having two inputs reducing the CoQ couple (as well as a little input from SDH) is a perfect recipe for driving extreme reverse electron transport through complex I with the production of completely unreasonable quantities of superoxide and H2O2. This is the scenario of free radical mediated damage combined with serious insulin resistance.

The problems are less severe with PUFA fats but this leaves us with a different set of problems, not for today. OK.​

This is part of the reason why I do not support high sugar consumption (along with the higher level mechanics that put the liver as a bottleneck). This is also why all the high carb advocates over the decades have found increasing SFA consumption to lead to worse and worse outcomes.

Glucose does not suffer as much from this problem, because it can be seen as a "pure Complex 1" fuel. Still, overload conditions are not good.

As an aside to that aside, "problems are less severe with PUFA" is a statement purely scoped upon active oxidative metabolism, and assumes full beta-oxidation of fats, and saturated flow of both carbohydrate and fatty acid derived inputs. All this statement can be taken to mean, is that PUFA do not disrupt the forward flow through ECT as much as SFA. There are still issues concerning overload, which PUFA will permit more so than SFA -- insulin is allowed to continually function, substrate input is continually allowed, and cells are forced to deal with oversupply of nutrients, and possibly excess stress further down the chain of ECT (complex 3 and 4).

An example of higher problems with PUFA that can bubble up from the mitochondrial level, are excess insulin sensitising of the wrong tissues. "Insulin Sensitising" can be taken to mean "primed for further energy uptake". Adipose tissue that is insulin sensitive is primed to uptake more energy, and become fatter if further energy is supplied. Skeletal tissue that is insulin sensitive is primed to uptake more energy, and be forced to either store it (as glycogen or Intra-muscular triglycerides), or burn it off as quickly as possible.

In fact, the case of excess adipose tissue insulin sensitivity was just discussed by Peter -- Hyperlipid: Musing about linoleic acid ..... I will agree with his assessment, provided that caloric excess is the case. Chronic eucaloric intake could also lead to the scenario which he discussed, especially on a mixed-fuel diet that doesn't put one in carbosis or ketosis.

That is why the ideal weight loss scenario is one of Adipose Tissue insulin resistance, with Insulin sensitivity in all other tissues. This is described by Lyle McDonald -- http://www.bodyrecomposition.com/fat-loss/insulin-resistance-fat-loss.html/

Again, context matters, and if we ignore genetic defects (whole other topic which I do not have time to discuss, and only applies to the people who have those defects anyway) ..... then largest factors are:

(1) Total caloric intake
(2) Circadian timing of caloric intake

Regarding (1), statements from Peter, like:

- Linoleic acid produces excessive whole body insulin sensitivity.
- Adipocytes distend under this effect.​

applies primary to cells in which linoleic acid has undergone beta-oxidation (and produced the resultant NADH and FADH2). Which is to say, these mechanics apply the most to the most metabolically active tissues, and especially so when energetic excess is present (be it locally or globally).

ie: Adipocytes will only distend under the effect of insulin sensitisation if there is excess energy floating around. These conditions required for adipocyte distention is going to be the case with almost people eating a caloric-adequate standard diet all over the world (and most people are in calorie excess, given the rising rates of obesity in so many countries). However, understanding the mechanics allows for potential manipulation of them.

Also, while adipose tissue is metabolically active, needless to say, other tissues are way more metabolic active, and therefore, much more sensitive to the sides effects of linoleic acid oxidation.

If we understand the way that fat is digested (link to a prior paper -- http://pubmedcentralcanada.ca/pmcc/articles/PMC3588585/), we know that the fat that you eat in a meal:

- Takes at least 1-2 hours to reach the bloodstream
- Is often stored around the intestine, and only released after another meal (this is called the "second meal effect")
- Or is released from the intestine after no food for awhile, ie: during sleep

Which is to say, unless you have eaten a boat load of fat during the night before, the first meal of the day is the closest to being composed purely of the consumed food (from the perspective of available fuel to tissues); fat eaten during earlier meals during the day tends to be released later into the day, and usually upon stimulation of subsequent meals.

Which is to say, if one eats a high fat breakfast, and then a high carb lunch, that lunch is actually effectively a "high carb high fat lunch" from the perspective of available fuel in the bloodstream.

Of course, the overriding factor is still caloric demands -- eg: relatively small (wrt to future caloric demands) high fat breakfast, followed by 2 hour endurance run, followed by 3 more hours before lunch => not much left of meal to affect lunch digestion mechanics.

Firstly, it is clear that even from the above simple mechanics, that fatty acid use rises through the day, and reaches a high at night time during sleep. This is completely normal, and should be maintained. But now we need to complicate things more, by adding number (2), the circadian component.

As we know, both adipose tissue and muscle tissue insulin sensitivity start out high in the morning, and then both drop off as the day goes on.

Skeletal tissue insulin sensitivity can be modulated by exercise though, and this was the genesis of John Keifer's idea of exercising at night, and then pounding carbs, which would go to the insulin-sensitised and GLUT-4 transporter primed skeletal tissue, instead of the now-insulin-resistent adipose tissue. I do not personally like this idea in practice, but I can see where the logic arises from.

But back to the original point, unless a boat-load of PUFA and calories was eaten during a night time meal (another reason to avoid eating big at night), eating during the morning, even with some fat, will in general lead to PUFA not having proportionately large action on adipocytes. NOTE that this assumes that PUFA intake is controlled to begin with, and any PUFA from the previous day has been oxidised (which is possible, given the studies on 18-hr oxidation rates of fatty acids, and showing that almost all consumed PUFA is oxidised under non-calorie excess conditions).

If PUFA is eaten in the morning, when the PUFA is actually released later in the day, insulin sensitivity of adipose tissue is already decreasing, while PUFA use is more localised to day-time active expensive tissues like the muscles, the heart, the liver, etc ......

ie: PUFA is causing insulin sensitisation of these metabolically active tissues ... whereas the metabolically lazy adipose tissue isn't as affected.

If you combine the above with relative caloric deficit, what we have in the later part of the day, is pressure to mobilise fat stores, blunting any nonsense about PUFA-metabolic effect on adipose tissues, whereas other tissues still need to sustain a baseline activity (eg: liver still needs to work when you sleep), and those get insulin-sensitised by the late-day release of PUFA.

If you combine the above with a caloric surplus, all bets are off .......

SIDENOTE: in the case of SFA + PUFA consumption, even without carbs, we need to ask what overall energetic burden is. PUFA oxidation will still give a mixed effect on Complex 1 vs Complex 2 activity, making mitochondrial oxidation more Complex 1 dominant (compared to pure SFA derived metabolism), effects are probably minimal at low doses of PUFA, but slowly scale up with increasing intake to resemble the SFA + Glucose scenario.

Again, total energetic input to a cell is the largest factor, since access to ECT is predicated upon the fatty acids actually being transported into the mitochondria to begin with.

Another aside would be that PUFA are more likely transported into the mitochondria for use in beta-oxidation, meaning that concurrently eaten SFA are more likely stored.

Will the scenario happen whereby insulin sensitised adipose tissue eagerly uptake more saturated fat and become fat as hell? Dunno, but it is plausible that in this way, PUFA helps make existing fat cells fatter.​

The above mechanics can explain why Roy Swank's eucaloric-high-carb-with-PUFA diet didn't cause much harm, but we MUST qualify the context in which energetic substrate is consumed.


Again, IMO:

(a) a person needs to pick either fat or carbs, and make either of them a primary energetic substrate.
(b) caloric excess must be avoided as much as possible.
(c) as a corollary to (b), caloric excess from either entirely Glucose (NOT fructose) or entirely SFA is the "safest excess". Excess is still not preferred.
(d) if a mixed diet is to be consumed (which is contrary to (a)) -- carbs during the day, fat at night. Experiment to see how much of each is best, and at what times.

....

 

[m_arch]

Peter @ Hyperlipid had summed up the scenario of SFA + Carbs very well. I quote him:

I believe this is what Denise Minger might be describing using "carbosis" as the corollary of ketosis. Under both of these conditions there is minimal insulin secretion but under carbosis there is enough insulin sensitivity working through mtG3Pdh to accurately regulate a near pure glucose metabolism. Fructose is no problem as there is plenty of "exchangeable" glucose for use in a substitution manner.

Fatty acids have to be very low for "carbosis" to occur at all and it will be degraded far more easily by saturated fats than by PUFA, as per the ETC diagrams above and as per Denise’s examples.​

This boils down to simple flow mechanics of Complex 1 vs Complex 2 dominance during active oxidative metabolism. I will agree with Peter's assessment fully.

As a quick aside, he shows mechanically why Fructose "is no problem" under carbosis, but is very much a problem under conditions of excess SFA + Fructose. Again, quoting from the same article:

I suppose we also ought to think of the situation under a large, uncontrolled fructose input through mtG3Pdh occurring at the same time as saturated fatty acids are being oxidised.

Having two inputs reducing the CoQ couple (as well as a little input from SDH) is a perfect recipe for driving extreme reverse electron transport through complex I with the production of completely unreasonable quantities of superoxide and H2O2. This is the scenario of free radical mediated damage combined with serious insulin resistance.

The problems are less severe with PUFA fats but this leaves us with a different set of problems, not for today. OK.​

This is part of the reason why I do not support high sugar consumption (along with the higher level mechanics that put the liver as a bottleneck). This is also why all the high carb advocates over the decades have found increasing SFA consumption to lead to worse and worse outcomes.

Glucose does not suffer as much from this problem, because it can be seen as a "pure Complex 1" fuel. Still, overload conditions are not good.

As an aside to that aside, "problems are less severe with PUFA" is a statement purely scoped upon active oxidative metabolism, and assumes full beta-oxidation of fats, and saturated flow of both carbohydrate and fatty acid derived inputs. All this statement can be taken to mean, is that PUFA do not disrupt the forward flow through ECT as much as SFA. There are still issues concerning overload, which PUFA will permit more so than SFA -- insulin is allowed to continually function, substrate input is continually allowed, and cells are forced to deal with oversupply of nutrients, and possibly excess stress further down the chain of ECT (complex 3 and 4).

An example of higher problems with PUFA that can bubble up from the mitochondrial level, are excess insulin sensitising of the wrong tissues. "Insulin Sensitising" can be taken to mean "primed for further energy uptake". Adipose tissue that is insulin sensitive is primed to uptake more energy, and become fatter if further energy is supplied. Skeletal tissue that is insulin sensitive is primed to uptake more energy, and be forced to either store it (as glycogen or Intra-muscular triglycerides), or burn it off as quickly as possible.

In fact, the case of excess adipose tissue insulin sensitivity was just discussed by Peter -- Hyperlipid: Musing about linoleic acid ..... I will agree with his assessment, provided that caloric excess is the case. Chronic eucaloric intake could also lead to the scenario which he discussed, especially on a mixed-fuel diet that doesn't put one in carbosis or ketosis.

That is why the ideal weight loss scenario is one of Adipose Tissue insulin resistance, with Insulin sensitivity in all other tissues. This is described by Lyle McDonald -- http://www.bodyrecomposition.com/fat-loss/insulin-resistance-fat-loss.html/

Again, context matters, and if we ignore genetic defects (whole other topic which I do not have time to discuss, and only applies to the people who have those defects anyway) ..... then largest factors are:

(1) Total caloric intake
(2) Circadian timing of caloric intake

Regarding (1), statements from Peter, like:

- Linoleic acid produces excessive whole body insulin sensitivity.
- Adipocytes distend under this effect.​

applies primary to cells in which linoleic acid has undergone beta-oxidation (and produced the resultant NADH and FADH2). Which is to say, these mechanics apply the most to the most metabolically active tissues, and especially so when energetic excess is present (be it locally or globally).

ie: Adipocytes will only distend under the effect of insulin sensitisation if there is excess energy floating around. These conditions required for adipocyte distention is going to be the case with almost people eating a caloric-adequate standard diet all over the world (and most people are in calorie excess, given the rising rates of obesity in so many countries). However, understanding the mechanics allows for potential manipulation of them.

Also, while adipose tissue is metabolically active, needless to say, other tissues are way more metabolic active, and therefore, much more sensitive to the sides effects of linoleic acid oxidation.

If we understand the way that fat is digested (link to a prior paper -- http://pubmedcentralcanada.ca/pmcc/articles/PMC3588585/), we know that the fat that you eat in a meal:

- Takes at least 1-2 hours to reach the bloodstream
- Is often stored around the intestine, and only released after another meal (this is called the "second meal effect")
- Or is released from the intestine after no food for awhile, ie: during sleep

Which is to say, unless you have eaten a boat load of fat during the night before, the first meal of the day is the closest to being composed purely of the consumed food (from the perspective of available fuel to tissues); fat eaten during earlier meals during the day tends to be released later into the day, and usually upon stimulation of subsequent meals.

Which is to say, if one eats a high fat breakfast, and then a high carb lunch, that lunch is actually effectively a "high carb high fat lunch" from the perspective of available fuel in the bloodstream.

Of course, the overriding factor is still caloric demands -- eg: relatively small (wrt to future caloric demands) high fat breakfast, followed by 2 hour endurance run, followed by 3 more hours before lunch => not much left of meal to affect lunch digestion mechanics.

Firstly, it is clear that even from the above simple mechanics, that fatty acid use rises through the day, and reaches a high at night time during sleep. This is completely normal, and should be maintained. But now we need to complicate things more, by adding number (2), the circadian component.

As we know, both adipose tissue and muscle tissue insulin sensitivity start out high in the morning, and then both drop off as the day goes on.

Skeletal tissue insulin sensitivity can be modulated by exercise though, and this was the genesis of John Keifer's idea of exercising at night, and then pounding carbs, which would go to the insulin-sensitised and GLUT-4 transporter primed skeletal tissue, instead of the now-insulin-resistent adipose tissue. I do not personally like this idea in practice, but I can see where the logic arises from.

But back to the original point, unless a boat-load of PUFA and calories was eaten during a night time meal (another reason to avoid eating big at night), eating during the morning, even with some fat, will in general lead to PUFA not having proportionately large action on adipocytes. NOTE that this assumes that PUFA intake is controlled to begin with, and any PUFA from the previous day has been oxidised (which is possible, given the studies on 18-hr oxidation rates of fatty acids, and showing that almost all consumed PUFA is oxidised under non-calorie excess conditions).

If PUFA is eaten in the morning, when the PUFA is actually released later in the day, insulin sensitivity of adipose tissue is already decreasing, while PUFA use is more localised to day-time active expensive tissues like the muscles, the heart, the liver, etc ......

ie: PUFA is causing insulin sensitisation of these metabolically active tissues ... whereas the metabolically lazy adipose tissue isn't as affected.

If you combine the above with relative caloric deficit, what we have in the later part of the day, is pressure to mobilise fat stores, blunting any nonsense about PUFA-metabolic effect on adipose tissues, whereas other tissues still need to sustain a baseline activity (eg: liver still needs to work when you sleep), and those get insulin-sensitised by the late-day release of PUFA.

If you combine the above with a caloric surplus, all bets are off .......

SIDENOTE: in the case of SFA + PUFA consumption, even without carbs, we need to ask what overall energetic burden is. PUFA oxidation will still give a mixed effect on Complex 1 vs Complex 2 activity, making mitochondrial oxidation more Complex 1 dominant (compared to pure SFA derived metabolism), effects are probably minimal at low doses of PUFA, but slowly scale up with increasing intake to resemble the SFA + Glucose scenario.

Again, total energetic input to a cell is the largest factor, since access to ECT is predicated upon the fatty acids actually being transported into the mitochondria to begin with.

Another aside would be that PUFA are more likely transported into the mitochondria for use in beta-oxidation, meaning that concurrently eaten SFA are more likely stored.

Will the scenario happen whereby insulin sensitised adipose tissue eagerly uptake more saturated fat and become fat as hell? Dunno, but it is plausible that in this way, PUFA helps make existing fat cells fatter.​

The above mechanics can explain why Roy Swank's eucaloric-high-carb-with-PUFA diet didn't cause much harm, but we MUST qualify the context in which energetic substrate is consumed.


Again, IMO:

(a) a person needs to pick either fat or carbs, and make either of them a primary energetic substrate.
(b) caloric excess must be avoided as much as possible.
(c) as a corollary to (b), caloric excess from either entirely Glucose (NOT fructose) or entirely SFA is the "safest excess". Excess is still not preferred.
(d) if a mixed diet is to be consumed (which is contrary to (a)) -- carbs during the day, fat at night. Experiment to see how much of each is best, and at what times.

....

Damn. Thanks for the reply. My diet experiment continues.

 

[Shredder2]

The rice diet will provide you with a nice norwood 6, just as it did Kempner.

 

[m_arch]

The rice diet will provide you with a nice norwood 6, just as it did Kempner.

doesn't appear to be doing that for TYW

 

[Wagner83]

Again, IMO:

(a) a person needs to pick either fat or carbs, and make either of them a primary energetic substrate.
(b) caloric excess must be avoided as much as possible.
(c) as a corollary to (b), caloric excess from either entirely Glucose (NOT fructose) or entirely SFA is the "safest excess". Excess is still not preferred.
(d) if a mixed diet is to be consumed (which is contrary to (a)) -- carbs during the day, fat at night. Experiment to see how much of each is best, and at what times.

....

That is interesting, my knowledge is very limited and yet given the positive anecdotical feedback on ketogenic diets (+ some studies) , and the positive anecdotical feedback on some for high carb and lowish fat diets, as well as the apparent competition between sugar and fats (randle cycle) I've been wondering for some time if going all fats or all carbs wouldn't be both beneficial. Around here fatty acids oxidation is associated with a few negative things like tumor growth and cancer, do you have anything t say on that? Does the fact high fat diets are usually high PUFAs diet play a major role ?
Also the idea of muscles burning fat at rest made me wonder about the value of two high carbs meals during the day and a high fat one for dinner,

 

[m_arch]

That is interesting, my knowledge is very limited and yet given the positive anecdotical feedback on ketogenic diets (+ some studies) , and the positive anecdotical feedback on some for high carb and lowish fat diets, as well as the apparent competition between sugar and fats (randle cycle) I've been wondering for some time if going all fats or all carbs wouldn't be both beneficial. Around here fatty acids oxidation is associated with a few negative things like tumor growth and cancer, do you have anything t say on that? Does the fact high fat diets are usually high PUFAs diet play a major role ?
Also the idea of muscles burning fat at rest made me wonder about the value of two high carbs meals during the day and a high fat one for dinner,

It seems a 'healthy' ketogenic diet is high in saturated fats like broth / tallow etc, and tries to avoid PUFA (although it would still probably be higher than is achievable with a low fat high carb diet) - but it looks like from TYW's explination that it doesn't matter that much, as long as your calories are not in excess.

 

[Wagner83]

Yeah well of course the idea that oxidizing mainly PUFAs is ok is completely against Ray's ideas (doesn't mean it's wrong) . TYW seems to suggest relying on PUFAs as a source of energy could lead to more weight gain as fat.

As an aside I see for a lot of Americans weight is the one thing that needs to be controlled and is the holy grail of health but as an ever lean guy I can say there's much more to health than weight. I find it annoying to see the vast majority of health and dietary advice is geared towards fat loss.

 

[damngoodcoffee]

Who the heck would want to eat zero carbs. Laaaaame.

 

[m_arch]

Who the heck would want to eat zero carbs. Laaaaame.

Taste wise i think it would taste better to eat zero carbs than zero fat

 

[damngoodcoffee]

Taste wise i think it would taste better to eat zero carbs than zero fat

Meat, eggs, cheese
VS
Good fruit, good potatoes, jasmin rice, pasta

I couldn't eat one meal without carbs!

 

[Westside PUFAs]

The rice diet will provide you with a nice norwood 6, just as it did Kempner.

Rice eaters the world over have perfect hair. Africa, Asia, India, etc.

.

 

[Strongbad]

As an aside I see for a lot of Americans weight is the one thing that needs to be controlled and is the holy grail of health but as an ever lean guy I can say there's much more to health than weight. I find it annoying to see the vast majority of health and dietary advice is geared towards fat loss.

Being lean doesn't mean being bone-skinny. Why does everything here has to be interpreted in extreme? Either being boney or being fat? There's a thing called being moderate aka balance.

Being fat also means being estrogen dominant. Since one of Peater's campaigns is to reduce as much estrogen as possible, it's in our best interest to stay lean.

Being lean also improve our insulin sensitivity. Great preventive measure against diabetes and insulin resistance.

Meat, eggs, cheese
VS
Good fruit, good potatoes, jasmin rice, pasta

I couldn't eat one meal without carbs!

That's subject to personal taste. Everyone's difference.

The rice diet will provide you with a nice norwood 6, just as it did Kempner.

The entire east and southeast Asia disagree with you:

Hideo Kojima, 53 years old. Worked like a slave during his tenure in Konami especially within the past few years. A very lean guy.

Hayao Miyazaki, the Studio Ghibli genius, 76 years old.

Shigeru Miyamoto, Nintendo genius, creator of Mario, 64 years old.



Jackie Chan, 62 years old.

The rest:
Jung Woo-sung, 43 years old
Lee Beom-soo, 47 years old
Ahn Sung-ki, 65 years old
Ahn Gil-Gang, 50 years old
Choi Il-Hwa, 57 years old

As seen in this trailer:



Notice how most of them are lean?

If you've traveled to Japan, South Korea, Taiwan, Vietnam, Philippine, Thailand you know what I'm talking about. Hairloss is much less prevalent there compared to US or western countries. And if you've been to Tokyo you know that they eat way less calories than us. Small portion. And lots of walking and catching trains.

 

[tyw]

It seems a 'healthy' ketogenic diet is high in saturated fats like broth / tallow etc, and tries to avoid PUFA (although it would still probably be higher than is achievable with a low fat high carb diet) - but it looks like from TYW's explination that it doesn't matter that much, as long as your calories are not in excess.

The best keto diets are those that are low in PUFA, with the primary fuel source being saturated fats. "PUFA upper limit" may be higher on a ketogenic diet due to the overall high oxidation of fat, but nonetheless, you want to be insulin resistant on a ketogenic diet.

(In Peter @ Hyperlipid's words) Physiological insulin resistance is required on a ketogenic diet, to:

limit the ingress of glucose when glucose is in short supply and it's best not to waste it on non-glucose dependent tissues.​

PUFA is not good for a ketogenic metabolism.

----

Next, ketogenic diets should be thought of as a therapeutic diet. ItsTheWoooo! is one such example of a person who is forced into a ketogenic diet due to various genetic and prior-life circumstance. Even she will tell you that ketosis is medicine:

- *The Scribble Pad*: I don't like having to be keto.
- *The Scribble Pad*: Ketosis: some myths and facts
- *The Scribble Pad*: My life depends on ketosis, true fact.

----

Next, it should be obvious that not all low carb diets are ketogenic diets.

When I say "All carb, or All fat", that really is just a simple rule of thumb for thinking in the correct direction, and not a fact.

More accurately, I have said: Start from an extreme of either very low carb or very low fat, and then slowly add more of the reduced macronutrient until balance is reached.

"Balance" is going to be difficult to define positively, so it has to be found through negative heuristics -- One example scenario: upon starting at a very low carb of 25g a day, food intolerances and lethargy start coming up after around 120-150g of carbs a day. It is then simple enough to come up with a "100g carbs a day" heuristic for this person.

Again, the underlying principle is: Do not interfere with energy use from the primary nutrient (exclusively fat or carb).

What level of the opposing nutrient constitutes "interference" is the variable that must be discovered for oneself. A heavy exercising "keto athlete" may still require 150g of carbohydrate to maintain overall glucose levels. Likewise, some people may still be in "carbosis" while eating 20% of their calories from fat, due to very fast fatty acid clearance (for whatever reason).

(NOTE: tolerance levels for Carbs-interfere-Fat are listed in grams, while tolerance levels for Fat-interfere-Carbs are listed as percentages of total. This seems to be the most accurate way of assessing things, though "grams of tolerated fat a day" is also useful when doing a primarily carbohydrate-based diet)

====

As a final aside, remember that all of this is merely Information . Knowledge has no power in decision making -- Ancient Civilisations Considered Advanced-AF. Modern Day Health Implications

....

 

[Westside PUFAs]

Next, ketogenic diets should be thought of as a therapeutic diet. ItsTheWoooo! is one such example of a person who is forced into a ketogenic diet due to various genetic and prior-life circumstance. Even she will tell you that ketosis is medicine:

Except that she takes it beyond her personal condition and perpetuates the Gary Taubes dogma, which is her prerogative but just sayin':

"I guess people really really like carbs. IDK. Pretty sure if anyone proclaimed this omniscient mastery of any other subject, we would spit water at our smartphones in disbelief of the audacity and arrogance."

*The Scribble Pad*: The insulin hypothesis: still valid and alive in science

I wonder what she would say about all of these carbohydrate addicts: Thoughts On Starch

"I don't care about seizures or any of that. I only care about weight loss. Should I aim for maximum ketosis?"

She says:

IMO? No. Not at all.

If your goal is weight loss, you should not be racing to get the darkest ketone pee, because as I stated earlier ketosis DOES NOT CAUSE WEIGHT LOSS, it is merely a sign of weight loss sometimes, and it is not an absolute sign of weight loss. This is the mistake jimmy moore made and that's part of the reason he regained so much weight : he ate a lot of dietary fat to try to increase ketosis, but increasing ketosis does not translate into decreasing body weight."

Except in water only fasting, one does indeed lose weight, both water and fat, and some muscle but mostly water and fat tissue. I know she was talking about no energy being swallowed but her statement had an exception.

.