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Old 02-20-2014, 07:36 AM   #31
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I have been wanting to do an experiment with this, see if in absence of carbs (as close to zero as possible with fat intake with tiny bit of protein) one would gain weight or not.

Each time, I talk myself out of it for some reason. I am thinking of trying this for 3 weeks and see what happens. I know everyone is different but I am curious for myself I guess.
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Old 02-20-2014, 09:51 AM   #32
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I have been wanting to do an experiment with this, see if in absence of carbs (as close to zero as possible with fat intake with tiny bit of protein) one would gain weight or not.

Each time, I talk myself out of it for some reason. I am thinking of trying this for 3 weeks and see what happens. I know everyone is different but I am curious for myself I guess.
It sounds like you are describing a fat fast (depending on what you mean by a "tiny bit of protein"), which should not be done for long periods. After 3-5 days max of mostly fat you need to make sure you each enough protein each day to support your lean body mass or you will start losing muscle.
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Old 02-20-2014, 12:09 PM   #33
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AnneK, What Mistizoom said! over a few days of that, you'd almost assuredly LOSE weight if you'd been eating any significant amount of carbs before. just the loss of glycogen in the liver and muscles causes water weight loss from storage. But you do need a minimum of protein each day, not for muscle building, but for muscle maintenance. If you follow what is essentially a protein sparing fast, you'd be eating only enough protein to maintain your body without harm and getting the balance of your calories from fat.

if CICO is true, then eating the same amount of calories, you'd neither gain, nor lose, but I'll bet that with min protein and majority fat and the same number of calories, you'd probably lose some weight.

Some folks lose eating high fat in excess of their "maintenance" calories, and that's confusing to those who gain weight just by adding a couple tablespoons of coconut oil, for example.

If you plan to try this for 3 weeks, just use a calculator to determine your min protein needs and don't go below that for extended period of time. Fat fast for 3-5 days is okay cause there is still protein in the menu in the form of bacon and beef and eggs.
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Old 02-22-2014, 06:46 AM   #34
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It sounds like you are describing a fat fast (depending on what you mean by a "tiny bit of protein"), which should not be done for long periods. After 3-5 days max of mostly fat you need to make sure you each enough protein each day to support your lean body mass or you will start losing muscle.
^This!!!

This discussion is not intended to be a diet or weight loss plan. It is important that we get enough protein to fulfill our needs and those are individual. A few days here and there are likely fine but not chronic.

I do think it is interesting (at least to me) that if you try to think of what one might eat as pure fat (no carbs or protein), it becomes a less than satisfying menu. For instance, I love butter but I could not make a meal out of it. Same for bacon fat.... it is fabulous to cook with but a meal? Me thinks not.

The closest I come to a purely fat 'meal' is bpc and even that has trace carbs and although it is very satiating for a long time, I tend to want something else come the end of the day. Is this because my physiology is reminding me that fat is not enough in terms of nutrition? Is this the new level of defense (after carb restriction)? It appears that it is carbs and protein that are the insulin provokers and fat.... not much, if at all.

I get very tired of hearing the message that fat is bad and too high a fat woe is a stall maker and on and on. It seems to me that is really inaccurate.
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Old 02-28-2014, 06:51 AM   #35
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Cathy


Fatty acids are absorbed from the gut and transported into the cells as triglycerides(TG) by lipoprotein lipase and -insulin-.
When needed, they are released by mobilizing lipase, glycogOn, and -adrenalin- to the liver and the muscles cells, and converted back to fatty acids..(Glycogon also releases glycogen from muscles)
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Old 02-28-2014, 11:45 AM   #36
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Hi there Drjlo! How are things?

So is that process (including insulin ) the same on a kstogenic woe?
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Old 03-02-2014, 06:51 AM   #37
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Responses of adipose tissue lipoprotein lipase to weight loss affect lipid levels and weight regain in women | Endocrinology and Metabolism


JCI - Increase of adipose tissue lipoprotein lipase activity with weight loss.
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Old 03-02-2014, 07:07 AM   #38
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While interesting neither address the question which is can dietary fat (in isolation - no carbs and no protein) cause weight gain? If so what is the mechanism. Lack of insulin seems to say that is would be impossible.

The reason I was thinking about it was because of a mouse study published recently whose conclusion was that ketogenic diets are bad long term. It was a faulty conclusion and was 'disected' properly by a group of researchers.

The thing about that study was that the mice did not gain on a diet of 100% vegetable oil (they didn't lose either). It raises the question for me.... can dietary fat cause weight gain?
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Old 03-02-2014, 07:15 AM   #39
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High-cholesterol diet-induced lipoproteins stimulate lipoprotein lipase secretion in cultured rat alveolar macrophages


http://www.jlr.org/content/50/6/1109.abstract

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Old 03-02-2014, 07:50 AM   #40
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I know Cathy, I was just gathering info for everyone to read.

Insulin is ONE of the stimulators of this enzyme, but we are never without insulin in our systems. If that were the case, we would be T1. Insulin stimulates LPL, but that doesn't mean it isn't working in the absence of insulin either. It looks like the presence of LDLs, triglycerides, etc also stimulate LPL.

The LPL is needed for the circulating fat to get into the cells to be used for energy. Are we able to pull as much into storage as we are into muscle cells or any cell for that matter? Are our fat cells overloaded with receptors for this enzyme?

Just because you are not eating carbs doesn't mean you don't have high blood insulin levels. Insulin resistance will cause your body to produce more insulin than needed. Will having ketones available for energy fix that??

The best way to determine if you still have high insulin levels is to get blood insulin levels checked. This has been on my mind for a long time. I have been wondering if that may be my problem and yours.

Keyword; hyperinsulinemia
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Old 03-02-2014, 08:46 AM   #41
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Yes, I have wondered about this as well. Problem is, what to do to treat it? It seems that a vlc and moderate protein is almost the only treatment aside from metformin.
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Old 03-02-2014, 02:10 PM   #42
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I've been thinking about this....the actual mechanism.

Getting right to the meat; Glucose in excess is broken down and made into fatty acids which are formed into the fat that we can store in those fat cells, (that is just to simplify and assume that all the other processes are complete).

Dietary fat is broken down into fatty acids, as well. The same fatty acids.
At that point, can our bodies identify excess fatty acids made from one or the other and make the decision to store one and not the other?

Just some food for thought...or fat.
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Old 03-02-2014, 06:58 PM   #43
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Glucose is not broken down into fatty acids.

Lipids are broken down into fatty acids in order to be absorbed from the intestines. In order for these fatty substances to be soluble in the water medium, which is the blood, they must be made into a water soluble molecule. Sugars and starches are digested and glucose is directly absorbed from the intestines.
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Old 03-02-2014, 07:51 PM   #44
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The liver turns various carbohydrate into glucose which is turned to a combination of phosphorus/glucose then to trigs, fatty acids or used up as energy.
Remaining is stored as body fat.

My only point is that fatty acids are ultimately stored as fat and maybe that is what happens to the fatty acids from fat.

I have not studied chemistry or physiology in a very long time but I remember some of the basics.
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Old 03-06-2014, 06:44 AM   #45
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I am probably beating a dead horse (where ever did that expression come from... it is terrible!) but I have not found a reliable source to explain how dietary fat in isolation of other nutrients can be stored in adipose tissue. It seems that it is accurate that things like bullet proof coffees because of their composition can provide fuel but will not add to adipose tissue stores.

It also appears to be accurate to say that dietary fat in isolation of other nutrients can boost energy by providing a dietary source that is quickly converted to ketones (i.e. mct oil) and again, does not convert to stored body fat.

I think it is not really discussed much because it is difficult to eat just fat. It almost always comes with protein at least and carbs to a lesser degree. It is also important that is cannot provide for protein requirements. We can go a few days without protein but not without risking some lean body loss.

So I guess it comes back to the fat fast. If done properly, the calorie restriction that Atkins puts on it, really should not be necessary provided it is actual fat (with no protein or carbs in the mix). Truth be known, it would not be a very satisfying. Apparently we crave some of the things we need, like protein.
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Old 03-06-2014, 04:40 PM   #46
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New Role For Protein In Fat Cells May Improve Understanding Of Obesity And Diabetes -- ScienceDaily


Lipolysis, Fat Mobilization, Fatty Acid (beta, alpha, omega) Oxidation, Ketogenesis





The glucose-fatty acid cycle represents the interactions between glucose uptake and metabolism and the consequent inhibition of fatty acid oxidation and the effects of fatty acid oxidation on the inhibition of glucose utilization. The reciprocal regulation is most prevalent in skeletal muscle and adipose tissue. When glucose levels are high it is taken into cells via the GLUT4 transporter and phosphorylated by hexokinase. The reactions of glycolysis drive the carbon atoms to pyruvate where they are oxidized to acetyl-CoA. The fate of the acetyl-CoA is complete oxidation in the TCA cycle or return to the cytosol via citrate for conversion back to acetyl-CoA via ATP-citrate lyase (ACLY) and then into into malonyl-CoA and subsequent long-chain fatty acid (LCFA) synthesis. The synthesis of malonyl-CoA is catalyzed by acetyl-CoA carboxylase (ACC) and once produced will inhibit the import of long-chain fatty acyl-CoAs (LCFacyl-CoA) into the mitochondria via inhibition of carnitine palmitoyltransferase 1 (CPT-1). This effectively blocks the oxidation of fatty acids leading to increased triacylglyceride synthesis (TAG). The equilibrium between malonyl-CoA synthesis and breakdown back to acetyl-CoA is determined by the regulation of ACC and malonyl-CoA decarboxylase (MCD). As long as there is sufficient capacity to divert glucose carbons to TCA cycle oxidation and fatty acid synthesis there will be limited acetyl-CoA mediated inhibition of the pyruvate dehydrogenase complex (PDHc).

This second part may help Cathy.


On the other hand, when fatty acid levels are high they enter the cell via one of several fatty acid transporter complexes [fatty acid translocase (FAT)/CD36 is shown since this transporter has a preference for LCFAs], and are then transported into the mitochondria to be oxidized. The large increase in fatty acid oxidation subsequently inhibits the utilization of glucose. This is the result of increased cytosolic citrate production from acetyl-CoA and the inhibition of phosphofructokinase-1 (PFK1). The increased acetyl-CoA derived from fat oxidation will in turn further inhibit glucose utilization via activation of PDH kinases (PDKs) that will phosphorylate and inhibit the PDHc. Although not shown, PDKs are also activated by increased mitochondrial NADH/NAD+ ratios in response to increased fatty acid β-oxidation. Under conditions where fat oxidation is favored ACC will be inhibited and MCD will be activated ensuring that LCFA that enter the cell will be able to be transported into the mitochondria. PS is pyruvate symporter responsible for mitochondrial uptake of pyruvate. TCAT is tricarboxylic acid transporter.
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Old 03-07-2014, 07:06 AM   #47
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Originally Posted by drjlocarb View Post
New Role For Protein In Fat Cells May Improve Understanding Of Obesity And Diabetes -- ScienceDaily


Lipolysis, Fat Mobilization, Fatty Acid (beta, alpha, omega) Oxidation, Ketogenesis





The glucose-fatty acid cycle represents the interactions between glucose uptake and metabolism and the consequent inhibition of fatty acid oxidation and the effects of fatty acid oxidation on the inhibition of glucose utilization. The reciprocal regulation is most prevalent in skeletal muscle and adipose tissue. When glucose levels are high it is taken into cells via the GLUT4 transporter and phosphorylated by hexokinase. The reactions of glycolysis drive the carbon atoms to pyruvate where they are oxidized to acetyl-CoA. The fate of the acetyl-CoA is complete oxidation in the TCA cycle or return to the cytosol via citrate for conversion back to acetyl-CoA via ATP-citrate lyase (ACLY) and then into into malonyl-CoA and subsequent long-chain fatty acid (LCFA) synthesis. The synthesis of malonyl-CoA is catalyzed by acetyl-CoA carboxylase (ACC) and once produced will inhibit the import of long-chain fatty acyl-CoAs (LCFacyl-CoA) into the mitochondria via inhibition of carnitine palmitoyltransferase 1 (CPT-1). This effectively blocks the oxidation of fatty acids leading to increased triacylglyceride synthesis (TAG). The equilibrium between malonyl-CoA synthesis and breakdown back to acetyl-CoA is determined by the regulation of ACC and malonyl-CoA decarboxylase (MCD). As long as there is sufficient capacity to divert glucose carbons to TCA cycle oxidation and fatty acid synthesis there will be limited acetyl-CoA mediated inhibition of the pyruvate dehydrogenase complex (PDHc).

This second part may help Cathy.


On the other hand, when fatty acid levels are high they enter the cell via one of several fatty acid transporter complexes [fatty acid translocase (FAT)/CD36 is shown since this transporter has a preference for LCFAs], and are then transported into the mitochondria to be oxidized. The large increase in fatty acid oxidation subsequently inhibits the utilization of glucose. This is the result of increased cytosolic citrate production from acetyl-CoA and the inhibition of phosphofructokinase-1 (PFK1). The increased acetyl-CoA derived from fat oxidation will in turn further inhibit glucose utilization via activation of PDH kinases (PDKs) that will phosphorylate and inhibit the PDHc. Although not shown, PDKs are also activated by increased mitochondrial NADH/NAD+ ratios in response to increased fatty acid β-oxidation. Under conditions where fat oxidation is favored ACC will be inhibited and MCD will be activated ensuring that LCFA that enter the cell will be able to be transported into the mitochondria. PS is pyruvate symporter responsible for mitochondrial uptake of pyruvate. TCAT is tricarboxylic acid transporter.
Drjlo, thank you for having the confidence that I could possibly understand both these links you provided. I am sad to have to admit that they are beyond my very limited abilities. In other words,

What I may have taken from them is that some cells do not operate as they should due to a lack of cholestreryl ester and that results in poor transport of fatty acids. I interpret this to mean is that some body fat is next to impossible to 'utilize'. Permanent body fat. Also known as a zucker rat?

The second is again far too technical for my scope but seems to be framed in a context that included glucose uptake and wonder how relevant it is to a situation where glucose would be very low (little to no insulin)?

I hope you can clarify for me as I would really like to understand despite my very limited background.

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Old 03-08-2014, 05:48 AM   #48
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Drjlo, thank you for having the confidence that I could possibly understand both these links you provided. I am sad to have to admit that they are beyond my very limited abilities. In other words,

What I may have taken from them is that some cells do not operate as they should due to a lack of cholestreryl ester and that results in poor transport of fatty acids. I interpret this to mean is that some body fat is next to impossible to 'utilize'. Permanent body fat. Also known as a zucker rat?

The second is again far too technical for my scope but seems to be framed in a context that included glucose uptake and wonder how relevant it is to a situation where glucose would be very low (little to no insulin)?

I hope you can clarify for me as I would really like to understand despite my very limited background.
No problem Cathy. I wouldn't expect you ( or most people ) to be able to digest it as written. The problem with questions like the one you asked is the biochemical process of our bodies are so complex that you have to dig deep into all the pathways in order to get the full picture. The reason you are having a hard time getting an answer to your question on a public forum such as ours, is that when you Google a question like yours, you get a laymans answer according to their limited knowledge of the few pathways that are dicussed the most.

I wanted to get these links posted as I was in a hurry, but knew I would have to come back and discuss it.

As LC'ers we have trained ourselves to think outside the box. Let's think about it.

We already understand that when the blood glucose is high because we are absorbing the carbs we just put in our mouths. We digest and absorb all the glucose and have to deal with it. Right? Insulin is released to lower those levels as they are dangerous to our bodies. This inhibits the release of fat because we don't need them for energy.

Maybe what our question should be is, "What happens when we put mostly fat in our mouths?" All the fat is digested and absorbed and enters our blood stream. What happens to clear the extra fat from the bloodstream? Does it make sense to assume it just floats around in large quantites until it is all used for energy? Does it make sense that we would only absorb what we need and the rest just sits in our gut and gets absorbed as we need it or gets wasted if we don't?

Let's assume you were starving (in ketosis) and suddenly came upon a cup of coconut oil. If you ate that cup of coconut oil, would your body just absorb and use what little it needed for the next 12 hours and waste the rest? Or, would the great machine, that is the human body, have a way to store that extra energy for later?

The idea that without insulin the body cannot store fat becomes a little to simplistic. It may be the major pathway, but what are the minor pathways?
Even Gary Taubes admits that the insulin hypothosis is too simplistic. It is the main player in weight loss, but not the only player. And that concept works for most who trust it.


*posting this before I do something stupid to delete it, will be back with more*
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Old 03-08-2014, 06:35 AM   #49
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No problem Cathy. I wouldn't expect you ( or most people ) to be able to digest it as written. The problem with questions like the one you asked is the biochemical process of our bodies are so complex that you have to dig deep into all the pathways in order to get the full picture. The reason you are having a hard time getting an answer to your question on a public forum such as ours, is that when you Google a question like yours, you get a laymans answer according to their limited knowledge of the few pathways that are dicussed the most.

I wanted to get these links posted as I was in a hurry, but knew I would have to come back and discuss it.

As LC'ers we have trained ourselves to think outside the box. Let's think about it.

We already understand that when the blood glucose is high because we are absorbing the carbs we just put in our mouths. We digest and absorb all the glucose and have to deal with it. Right? Insulin is released to lower those levels as they are dangerous to our bodies. This inhibits the release of fat because we don't need them for energy.

Maybe what our question should be is, "What happens when we put mostly fat in our mouths?" All the fat is digested and absorbed and enters our blood stream. What happens to clear the extra fat from the bloodstream? Does it make sense to assume it just floats around in large quantites until it is all used for energy? Does it make sense that we would only absorb what we need and the rest just sits in our gut and gets absorbed as we need it or gets wasted if we don't?

Let's assume you were starving (in ketosis) and suddenly came upon a cup of coconut oil. If you ate that cup of coconut oil, would your body just absorb and use what little it needed for the next 12 hours and waste the rest? Or, would the great machine, that is the human body, have a way to store that extra energy for later?

The idea that without insulin the body cannot store fat becomes a little to simplistic. It may be the major pathway, but what are the minor pathways?
Even Gary Taubes admits that the insulin hypothosis is too simplistic. It is the main player in weight loss, but not the only player. And that concept works for most who trust it.


*posting this before I do something stupid to delete it, will be back with more*
I am going to wait for the rest before commenting. I am so pleased that we can have this discussion!
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Old 03-09-2014, 08:03 AM   #50
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glycerol-3-phosphate and hormone sensitive lipase

Hormone regulated pathways -insulin/glucogon (hormones)

I'm Back. Sorry for the delay. Life sometimes gets in the way.

If you go the second link, there is a section titled "Cellular Uptake of Fatty Acids".

There is a list of 8 fatty acid transporters. This tells me there are mulitple ways to store fat. The text says interaction with fatty acids with these transporters is a transmembrane concentration gradient driven process. That means the higher levels of fatty acids in the blood are driving the acitvity(opening) these transporters to allow fat to go into the cells. No insulin involved.

Another quote from that article..
"In addition to sparing glucose for the brain, fatty acid oxidation (use by the cells) also preserves pyruvate and lactate which are important gluconeogenesis substrates. The effects of fatty acids on glucose utilization can also be observed in the well fed state after a high fat meal and during periods of exercise."

This tells me that when we are using FAs, we are also saving subrtates for gluconeogenisis(GNG). You and I are both VERY good at GNG.
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Old 03-09-2014, 08:44 AM   #51
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This second part may help Cathy.


On the other hand, when fatty acid levels are high they enter the cell via one of several fatty acid transporter complexes [fatty acid translocase (FAT)/CD36 is shown since this transporter has a preference for LCFAs], and are then transported into the mitochondria to be oxidized. The large increase in fatty acid oxidation subsequently inhibits the utilization of glucose. This is the result of increased cytosolic citrate production from acetyl-CoA and the inhibition of phosphofructokinase-1 (PFK1). The increased acetyl-CoA derived from fat oxidation will in turn further inhibit glucose utilization via activation of PDH kinases (PDKs) that will phosphorylate and inhibit the PDHc. Although not shown, PDKs are also activated by increased mitochondrial NADH/NAD+ ratios in response to increased fatty acid β-oxidation. Under conditions where fat oxidation is favored ACC will be inhibited and MCD will be activated ensuring that LCFA that enter the cell will be able to be transported into the mitochondria. PS is pyruvate symporter responsible for mitochondrial uptake of pyruvate. TCAT is tricarboxylic acid transporter.
The first part of post we all kinda understand, so I will comment on this half.
* my interpretation*

After a high fat meal, the high levels of fatty acids encourage the transport into the cells. Does that mean because glucose is spared, there are more glycerol backbones available for triglycerides to be packaged and moved into the fat cells?

We know there is constant flux of fat moving into and out of the fat cells all the time. When energy is plentiful, whether that is glucose and/or fat, some energy is stored after a meal as the food we ate is digested and absorbed from the intestines. We now know about the many transporters for FAs. It doesn't look like insulin is involved in these pathways. That tells me that after a meal, excess fat nor immediately used for energy has to be removed from the blood when it reaches a critical level.


I am not saying this is correct, but it seems to be a reasonable assumption.

And, yes, it is an assumption. I don't think the research is out there to answer your question. Or maybe that no one has asked that question of the people who would know.

If we could ask the people who know spend their lives researching these processes, they probably know your answer. They are just not thinking like that because they have never heard of a fat fast. They would just think you were trying to commit suicide by coconut oil.


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Old 03-09-2014, 09:03 AM   #52
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Quote:
Originally Posted by clackley View Post

What I may have taken from them is that some cells do not operate as they should due to a lack of cholestreryl ester and that results in poor transport of fatty acids. I interpret this to mean is that some body fat is next to impossible to 'utilize'. Permanent body fat. Also known as a zucker rat?



I hope you can clarify for me as I would really like to understand despite my very limited background.
YES! That's what I got too.

Good job Cathy. See, you can read between the lines and pull the "jist" from this without having a working vocabulary of the "big words".
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Old 03-09-2014, 02:11 PM   #53
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A great big THANK YOU!!! For taking the time and effort to explain to a simpleton like me!

Love the death by coconut oil!! Better that then some other dietary deaths!!

I am looking forward and hoping I am still around for the science to progress - particularly that which is framed in a ketogenic woe. I think many things change in that state and so much of the available science is not in that framework. This however may not be one of them.

Thanks again my GNG sister!
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Old 03-10-2014, 05:32 AM   #54
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You are so welcome.

I am also learning by researching your questions. I really wish the "in the know" LC gurus would lurk around here and help us out sometimes.
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Old 03-10-2014, 05:35 AM   #55
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It really s#cks when your super hero power is GNG!
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Old 03-10-2014, 05:51 AM   #56
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Love that!!

I did pose the question to Jimmy Moore for his book that he is currently writing (keto clarity). He has the ear of lots of those in the know. So who knows???
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Old 03-12-2014, 09:26 AM   #57
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Cathy, I'm so glad you asked this question. What a great thread.

I have experimented with keeping foodstuffs the same, protein and carb levels constant, and testing what happens if I eat more butter or beef fat drippings.

For example, going along rather constantly for a few days at ca. 60-65g PRO and 25g CHO, I do well at 110-130g FAT, if I stick to the primary foods in my food plan. No trigger foods. If I up the fat to even 140-150, using butter or beef dripping fat, something switches in my brain and metabolism. I feel off, go into weight-gaining mode, triggered appetite, thinking of eating things not in my primary food group, etc. (Using hwc is worse. But my tests with hwc have been with ultra-pasteurized commercial hwc, containing carrageenan. Raw hwc might be different.) Upping the fat grams to Dr. Kwasniewski's 3 or 3.5 times the grams of protein dramatically exacerbates that unpleasant direction of weight-gain, feeling unwell, and triggering appetite for foods not in my primary food list. I just do better at about 1.5 - 2 FAT grams per gram of PRO, keeping carbs under 30.

Keeping the black tea intake restricted is vital for me, too.

For me, it is not only how much of each of P, F, and C, but very much what kind of protein, what kind of fat, what kind of carb.

Also, if I eat ca. 12 g PRO at a time and one Tablespoon of butter or CLO, that seems to keep my brain feeling smooth, clear and cheery, and, the small amounts of meat don't trigger that insulin surge near or at the end of the meal, or thereafter. Four tiny meals, lots of fat in the morning, and my gelatin-and-yoghurt snacks in between, seem to be a good food timing for me.

Thank you for a very helpful thread!

I find what Jem51 posted about the Critical Fat Level to be true.
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Last edited by Auntie Em; 03-12-2014 at 09:33 AM.. Reason: clarification
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Old 03-12-2014, 10:50 AM   #58
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I'm curious to see how this thread plays out.

Medi Weightloss recommends lean proteins, but I will sometimes buy the full fat versions when they have less carbs.
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Old 03-12-2014, 01:57 PM   #59
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You know, I was listening to an interview with Phinny where he said that a certain type of fat could only be used for energy or disposed of (pooped)... The example was coconut oil, so I while I am not remembering exactly the exact phrase, coconut oil is medium chain triglyceride, so that may have been the type.

I think it was somewhere in here:
https://www.youtube.com/watch?v=OFD2q5iqevY

but I'm not sure and it is a long video...It is good if you have time. I have listened to it a few times while working. I am also about halfway through The Art and Science of Low Carb. Living" So I wonder if it was in the Triglyceride metabolism section?

I will try to find something a little more specific and a little less "I remember something about something" wishy washy
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Old 03-13-2014, 06:31 AM   #60
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I believe the fate of excess MCT's, that are not used for immediate energy by the cells, is that they are used to make ketones.

Coconut oil is high in MCT, but contains a fair amount of saturated fat as well.
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