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  #1   ^
Old Mon, Dec-18-17, 11:46
dcc0455 dcc0455 is offline
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Default I'n going to quit worrying about ketone levels

Link:
https://optimisingnutrition.com/201...e-relationship/

summary:
OPTIMAL KETONE AND BLOOD SUGAR LEVELS FOR KETOSIS
JULY 20, 2015 MARTY KENDALL
A low carb helps reduce blood sugars and insulin levels and helps improve common metabolic diseases (e.g. diabetes, heart disease, stroke, cancer, Parkinson’s and Alzheimer’s).
We become insulin resistant when our adipose tissue becomes full and can’t store any more energy. Excess energy is then stored in the liver, pancreas, heart, brain and other organs that are more insulin sensitive.
Endogenous ketosis occurs when we don’t eat, and we burn our own body fat (e.g. fasting). While insulin and blood sugar levels are low, we may have lower blood ketones flowing from our fat stores.
Exogenous ketosis occurs when we eat lots of and/or take exogenous ketones. Our blood ketones may be higher, but our insulin levels will also rise because we have an excess of energy coming from our diet.
Most of the good things associated with ketosis occur due to endogenous ketosis.
Most people following a ketogenic diet have lower blood ketone values than Phinney’s ‘optimal ketosis’ chart, especially once they become fat adapted and are not trying to drive high blood ketones through the consumption of excess energy from refined fat.
If your goal is blood sugar control, longevity or weight loss then endogenous ketosis with lower blood sugars and lower ketones is likely a better place to be than chasing higher blood ketones via lots of added dietary fat.
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  #2   ^
Old Mon, Dec-18-17, 21:26
M Levac M Levac is offline
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From my point of view, there's a few errors in that text. A few corrections, also from my point of view.

Exogenous ketones cause both insulin and blood glucose to drop. This is due to an otherwise normal feedback loop where ketones regulate themselves through activation of liver insulin receptors. In turn, this triggers a sequence of steps, the first is inhibition of ketogenesis (self-regulation of ketones production), the second is inhibition of glycogenolysis (regulation of glucose release from the liver), last step is insulin degradation with insulin-degrading enzyme (don't need the insulin, it's done its job). The liver and the brain have the insulin-degrading enzyme, all other tissues do not.

Recently, I read another text that tried to explain this topic. In it, I found something that adds to my paradigm. By activating liver insulin receptors, ketones are the key to what's been called insulin resistance. In essence, lack of ketones is the primary cause of insulin resistance - the insulin receptors do not get activated. A chain of events follows. Ketones are needed for the last step of insulin degradation. Thus, even though insulin still inhibit ketogenesis - blood ketones drop to zero - insulin remains higher than otherwise, and acts on all other tissues accordingly, i.e. fat tissue especially. Since this condition is primarily caused by dietary carbs, this then also stuffs the liver with glycogen, through insulin's second step of inhibiton of glycogenolysis. At some point, it's possible that the liver just can't store any more glycogen, in spite of ample insulin, blood glucose lingers, diabetes type 2. Here, we can easily see that diabetes type 2 must be described as hyperglycemia, hyperinsulinemia, and total absence of ketones. If the liver truly became insulin resistant, there would be plenty of ketones in the blood, since that's the first thing insulin acts on when it hits the liver.

Incidentally, insulin's second step - inhibition of glycogenolysis - is the primary means by which excess glucose is cleared from the blood. All other ideas, i.e. cells use up glucose as some turbo fuel or whatever, is just BS. If there's carbs coming in, there's insulin going up, there's ketones dropping to zero. Cells require a specific balance of various substrates, namely glucose and ketones, for proper cellular function. For glucose to be used up, it must be accompanied by ketones. The lower the ketones, the slower glucose gets used up. Glucose gets used slowly enough already, there's basically a tiny reserve of it. Excess is primarily stored, not used. Excess must be stored, and quickly, for normal metabolism to resume.

In effect, when carbs come in, they disrupt normal ketones metabolism, that feedback loop of self-regulation of ketones production. Without carbs, ketones metabolism remains virtually constant even throughout a meal. No disruption. Protein also disrupts this, but to a lesser extent. Protein does not provide a single calorie of energy. The primary pathways for dietary protein is structure, enzymes, etc - building blocks.

Eating a lot of additional fat is absolutely self-regulating. Try it for yourself. Eat a stick of butter, tell me about it. Personally, when I tried it, it was very hard the first time, easier later on but still not easy. When I played golf, that was often my lunch, a stick of butter. No adverse effect I can even think of, including any difficulty in maintaining my weight (I had reached the limit of the possible at that point).

As for it being hard to achieve any degree of ketosis, that's not merely a question of diet. As Taubes often says, carbs is the primary cause, not the only cause. Always, always, always keep that distinction in mind when talking about how hard it is to get into ketosis. If carbs can do it, and if carbs is just the biggest thing, then there must be other things capable of doing the same, let's see what they are.

Anecdotally, I had tons of ketones coming out the wazoo when I was the most physically active of my life. So, that last paragraph is a lie from my point of view.

You can't possibly manage your energy balance. It's impossible to know what Eout is at any point.

OK, I skimmed the article. There's too many errors from my point of view. I won't read it in detail. I won't take any advice from it. Maybe there's still some good stuff in there, I won't know.
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  #3   ^
Old Tue, Dec-19-17, 08:20
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WereBear WereBear is offline
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I've got so many other things to worry about

As always, a great deal of good info, M Levac!
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  #4   ^
Old Tue, Dec-19-17, 11:30
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teaser teaser is online now
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Exogenous ketones--assuming they're bad makes as much sense as assuming they're good. When people talk about exogenous ketones increasing insulin, so preventing weight loss, one big thing missing is any data showing that this is so. Sprinkling ketone salts on your french fries, I'd probably bet against. Supplemental ketones added to a low carb diet? I wouldn't waste money on that as an individual, but I think it's worth studying and I can't pretend to know what the outcome will be without the actual studies being done.

As fat as ketones-->insulin goes, it depends on context. Replace sugar with ketones? Probably the insulin response will be reduced. The same is true of fat. Add fat to a given sugar load, the insulin response will be higher. Replace sugar with fat, it will be lower. Without context, ketones can secretes the insulin doesn't mean much.

Now never mind dietary load of glucose, just look at exogenous glucose. If exogenous ketones reduce blood glucose--the "basal" glucose that the beta cells are exposed to is reduced, some of the ketones are replacing glucose in the blood, rather than just being plopped on top.

Quote:
Effects of ketone bodies on insulin release and islet-cell metabolism in the rat.
Biden TJ, Taylor KW.
Abstract
Ketone bodies promote insulin secretion from isolated rat pancreatic islets in the presence of 5 mM-glucose, but are ineffective in its absence. At concentrations of 10 mM or less, the relative abilities of the ketone bodies to potentiate release are in the order D-3-hydroxybutyrate greater than DL-3-hydroxybutyrate greater than acetoacetate. The response curve relating insulin release to D-3-hydroxybutyrate concentration displays a threshold at 1 mM and a maximum at 10 mM. D-3-Hydroxybutyrate (5 mM, but not 10 mM) promotes insulin secretion in the presence of 5 mM concentrations of both L-arginine and DL-glyceraldehyde, but not with L-leucine, L-alanine, L-glutamate or 4-methyl-2-oxopentanoate. The oxidation rates of the exogenous ketone bodies do not correlate well with their capacities to promote insulin release. Moreover, the oxidation of 5 mM-D-3-hydroxybutyrate can be inhibited by 25% with methylmalonate (10 mM) without any diminution of release. The potentiation with D-3-hydroxybutyrate occurs without an observable increase in total islet cyclic AMP. However, a small net efflux matches the relative abilities of the ketone bodies to promote insulin release. With islets from 48 h-starved animals the insulin response is both diminished and less sensitive than in fed animals, since insulin secretion is not significantly raised until a threshold of 5 mM-D-3-hydroxybutyrate is reached. These results suggest that, in the rat at least, there should be a reappraisal of the physiological role of ketone bodies in the promotion of insulin release.


At least one context where ketones aren't that insulinogenic--those 24 hour starved animals. It's a context where glucose is fairly scarce. But it's in islets, not the whole animal.

Quote:
Suppression of glucose production and stimulation of insulin secretion by physiological concentrations of ketone bodies in man.
Miles JM, Haymond MW, Gerich JE.
Abstract
To determine the mechanism by which ketone bodies decrease plasma glucose in man, seven normal postabsorptive volunteers were infused for 3 h with beta-hydroxybutyrate. Total plasma ketone bodies (beta-hydroxybutyrate plus acetoacetate) increased to levels (approximately 2.5 mM) observed after a 2- to 3-day fast in normal subjects. Plasma glucose decreased 10% concomitant with decreases of 25% and 10%, respectively, in the rates of glucose production and glucose utilization determined isotopically with [3-3H]glucose. Plasma insulin and glucagon concentrations were unaltered, but plasma C-peptide levels increased from 2.6 +/- 0.1 ng/ml to a maximum of 3.9 +/- 0.2 ng/ml at 30 min (P < 0.01) and remained significantly increased for more than 2 h. Plasma alanine decreased approximately 14% (P < 0.05), while plasma lactate increased 25% (P < 0.01) so that there was no net decrease in the combined levels of these gluconeogenic substrates. These results demonstrate that physiological increments in circulating ketone body concentrations decrease plasma glucose in normal man by suppressing glucose production, an effect which can be explained by the stimulation of insulin secretion being reflected only in changes in plasma C-peptide. Thus, changes in pancreatic B cell function not sufficient to alter peripheral plasma insulin levels may cause significant changes in hepatic glucose production.


And that's why the whole animal matters, not to mention the species. An increased rate of insulin secretion that the increase in c-peptide implies might be offset by increased insulin clearance by the liver. The decrease in glucose production by the liver makes for less of a signal for further insulin secretion. Systemic regulation is what matters, not what happens in a petri-dish. An islet that secretes insulin in the body results in reduced glucose, an islet sitting in a puddle of glucose and ketones does not. An increase in insulin that can be handled by the liver, is that so bad?
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  #5   ^
Old Tue, Dec-19-17, 14:06
M Levac M Levac is offline
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Teaser, I think it's not so bad when the liver can handle insulin properly. Normally, that's precisely what it must do, it's the primary site for insulin degradation. Imagine several feedback loops, not all the same length. The shortest is pancreas-to-liver for insulin. The longest is liver-to-liver for ketones. Within these loops are points of regulation, the liver, the pancreas, fat tissue, the gut, etc.

When all is well, the liver handles any insulin fluctuation for whatever reason promptly, it's the shortest loop. If all continues to be well, the liver should handle insulin promptly still for a time, i.e. an occasional bolus of carbs or lean protein for example. Cells that rely on insulin and other hormones signaling for growth and repair for example, adjust their receptors rather than calling for more or less of those hormones, i.e. they become more or less sensitive through activation of certain enzymes like lipoprotein lipase for example.

The long loop invokes the short loop to regulate ketone production. When ketones drop, less insulin is secreted, ketogenesis goes up, ketones go back up. When ketones go up, more insulin is secreted, ketogenesis goes down, ketones go back down. To be fair, insulin stimulation by ketones is very low compared to dietary carbs or protein. Long loop homeostasis is prompt because it invokes the short loop. The important thing here is that insulin level is different - most likely higher - in the short loop than it is in the long loop, because it is degraded in the liver at the end of the short loop, it's done its job.

Description of the main disruption helps to explain benefit of drinking ketones.

We eat carbs, insulin goes up, should all be handled by the liver - within the short loop - before it ends up in the long loop, causing all kinds of nasty things like growing fatter beyond what a normal meal would do. But, there's no way to produce that much glucose in such a short time, the system can't handle that, disruption, short loop is overwhelmed, insulin and glucose leak out to the long loop, we can measure it at the arm. Simultaneously, ketogenesis shuts down through that bolus of insulin from the pancreas.

At this point there's a problem of regulation of both short and long loop, strictly due to shut down of ketogenesis, because ketones are the true master molecule, not insulin, insulin is merely invoked by ketones. Cells require a specific balance of substrates, balance is disrupted, substrates are used less quickly than otherwise, glucose lingers longer than otherwise, BG goes up in the long loop. Until ketogenesis picks up again, until ketones flow in the long loop again, insulin must drop for that, glucose must drop for that, but it gets used less quickly than otherwise because of lack of ketones.

At this point, drink ketones.

Now we got ketones activating liver insulin receptors, short loop gets better, insulin drops through insulin-degrading enzyme, glucose drops in the short loop through inhibition of glycogenolysis, gets stored as glycogen, less glucose leaks out to the long loop, BG drops in the long loop, ketogenesis remains shut down for now, but there's ketones flowing so that's not a problem. Long loop gets better, cells begin to get proper balance of substrates, glucose gets used more quickly because ketones are flowing, BG drops in the long loop. Back in the short loop, insulin drops through lower stimulation by lower glucose coming back from the long loop to the pancreas, in turn insulin drops further in the long loop, less of it leaks out.

That's the benefit of drinking ketones in the context of disruption by a bolus of dietary carbs. In a short time, we're going from disrupted on the high side, to back down to normal on the comparatively low side. It's a short time because the system is already driving that way, we're just giving it what it's missing for overall normal regulation - ketones. Conversely, from a normal level, drinking ketones provides a much lesser benefit - the system is already normal, ketones are already flowing, regulation normal across the board. In effect, we're going from normal, to lower than normal, which is much harder to do - the system is fighting back to return to normal.

So, the increase in insulin from drinking ketones, from disruption-to-normal is much lower than the increase in insulin from normal-to-below-normal, because of all the other points of regulation along the short and long loops. So yeah, I'm not worried about a bit more insulin from drinking ketones either way.
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  #6   ^
Old Wed, Dec-20-17, 18:52
dcc0455 dcc0455 is offline
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Quote:
Originally Posted by M Levac
OK, I skimmed the article. There's too many errors from my point of view. I won't read it in detail. I won't take any advice from it. Maybe there's still some good stuff in there, I won't know.


Thanks for your feedback. I can't really speak to the technical aspects of the article, but there is so much conflicting information ranging from body builders who try to drive ketones as high as possible and bloggers who say the number doesn't matter. I'll still check to confirm if something kicked me out of ketosis, but I won't worry what the number is as long as there are ketones.
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  #7   ^
Old Wed, Dec-20-17, 19:00
dcc0455 dcc0455 is offline
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Quote:
Originally Posted by teaser
Systemic regulation is what matters, not what happens in a petri-dish. An islet that secretes insulin in the body results in reduced glucose, an islet sitting in a puddle of glucose and ketones does not.


I enjoy reading the research, but to be honest, I take it all with a grain of salt. I am somewhat doing my own research on myself, taking cues from posts here and other sites. For example, I did up my fat % after reading your response to my question in another post. We'll see how that goes.
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  #8   ^
Old Wed, Dec-20-17, 20:41
M Levac M Levac is offline
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When measuring ketones, or any single parameter, context is most important. Take blood pressure for example. White coat syndrome - BP goes through the roof. Measuring BP at that point is meaningless and can lead to unnecessary treatment. We just discussed this not long ago on this forum. Even with standard medical care, context is important. They talk about ketoacidosis in conjunction with hyperglycemia, in the context of diabetes type 1 especially.

So what's going on with ketones, what's the context that makes it mean something? In that article that I won't read, there's still lots we can take from it to answer that question. For example, it says that ketones level should go really high after a reasonably lengthy fast (which I agree). Well, that gives us a tool we can use to determine if ketones metabolism, especially in the liver, works as it should. Measure ketones, fast for a day or two, measure ketones again, see the difference. See? Context.

Now that we're aware that context is important, and we're aware that certain contexts give us certain expectations or predictions, we can use that to control what happens to ketones, or even better we can use it to find out if something's going on that we don't know about yet.

Take that fasting context again and see what we can do with that. We expect ketones to rise much higher than otherwise, right? Now what if they don't? Right then we know there's something else going on we don't yet know about. Let's find it, fix it, done.

So, ketones isn't something to worry about, instead it's something that speaks to us. Personally when my ketones numbers were through the roof coming out my wazoo, it was telling me all is quite well thank you very much. I didn't really need to know the ketones number, I had a bunch of other things that were telling me the same thing, all together all at once. For example, blood glucose was 3.5 (67mg/dl), at the very limit of low BG. BP, the same, low enough to diagnose low BP - 90/60. Not bragging, just illustrating context. I'm certainly not bragging now when I say that at some point everything went south. My health took a bad turn, still trying to figure it out. The point is, if then a fast would shoot up my ketones, today it will not - something else is going on that interferes with normal ketones metabolism. Now because the context of fasting predicts that ketones rise significantly, if at some point they do, then I will have figured out - and fixed - what's wrong with me. But then so will everything else that speaks to me, tell the same story ketones do.

In essence, I'm trying to make diet become the only thing that has any effect on ketones, by fixing and eliminating all other causes.
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  #9   ^
Old Thu, Dec-21-17, 06:46
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thud123 thud123 is online now
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how tight do you guys think the correlation between ketones expressed in the breath as acetone and ketones measured in the blood is? I have some interesting and confusing observations tracking period it extremely high carbohydrate intake and ketone in breath measurements. I can share here if open for discussion or speculation or start another thread.

And to the original posters point (I have not read the article yet) I find that tracking ketones in novel and interesting not to say confusing. I do not use a current snapshot reading as very meaningful - kind of like a snapshot of a scale weight. Together with snapshots of other things tracked over time might be more meaningful but I'm still constantly in a state of wonder and confusion
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  #10   ^
Old Thu, Dec-21-17, 08:28
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teaser teaser is online now
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737348/?report=reader#!po=14.0000

Page 4, figure 2 in this study on fat loss and acetone, there is a strong relationship between breath acetone and beta-hydroxybutyrate in the blood. The big "but" is that around .5 mM bhb, from lowest to highest readings there's a greater than tenfold difference, as you go higher for bhb, the range seems to narrow, but there are far less data points.

You see the same thing here;


http://ajcn.nutrition.org/content/7....expansion.html

Quote:
Breath acetone is a reliable indicator of ketosis in adults consuming ketogenic meals


Very strong relation. You can predict the relationship in a group, but there can be wide variations in blood ketones with the same level of breath acetone, and vice versa, in individuals.

The diagnostic usefulness of acetone doesn't have to end at blood ketones. BHB 2.0, high vs. low breath acetone, what does it mean, metabolically?

I've been looking at acetone after seeing your posts about it. Maybe as simple as an organic energy molecule can get, but look at what you can do with zeros and ones.
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  #11   ^
Old Thu, Dec-21-17, 10:20
dcc0455 dcc0455 is offline
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Quote:
Originally Posted by thud123
how tight do you guys think the correlation between ketones expressed in the breath as acetone and ketones measured in the blood is? I have some interesting and confusing observations tracking period it extremely high carbohydrate intake and ketone in breath measurements. I can share here if open for discussion or speculation or start another thread.

And to the original posters point (I have not read the article yet) I find that tracking ketones in novel and interesting not to say confusing. I do not use a current snapshot reading as very meaningful - kind of like a snapshot of a scale weight. Together with snapshots of other things tracked over time might be more meaningful but I'm still constantly in a state of wonder and confusion


In my experience, the trends track, even if the numbers don't. The problem I have had with the breathalyzer is at the low end. For example, yesterday I had .6mmol/L blood; trace (.5) urine and 0 breath. However, when I do read .3 on the breathalyzer (which the manufacturer says is ketosis) , I know my blood ketones will be closer to 1 mmol/L and the urine will show trace (.5) or small (1.5). If I ignore the number and just look at the trend, they do all correlate and I can probably just rely on the breathalyzer since it was a one time cost.

Update: Checked again this morning and got .2g/l on breathalyzer and .4mmol/L on blood. I can assume the urine will show negative ketones. As I mentioned, the low end is unreliable, but higher up the scale I do see correlation.

Last edited by dcc0455 : Thu, Dec-21-17 at 10:29.
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