Insulin and effects when practicing ketosis

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(Mg ) #1

So I’m hearing about insulin spikes.
Some say any carb can spike your insulin.
Spiking of insulin works diffrent for everyone.
How does one gauge insulin spike?
How does insulin assist or temper your weight loss goals?
Is there a certain spike you must watch out for because your weight-loss goal will be inhibited due to the spike?
Is there a sweet spot with insulin when practicing ketogenic lifestyle? (Does this in fact affect everyone the same or is it diffrent for everyone?)

I believe that my plateau is difficult because of insulin.
That’s kinda where my doctor is going. We’ve reached this conclusion. Via blood work, however he doesn’t get specific because he isn’t knowledgable in ketosis.
Difficult to find a doctor who is.

Thank you

#2

Not quite in order, but I think this pretty much covers your questions:

You can’t track your insulin in real time but you can often deduce from what happens to your blood sugar (the insulin kicks in when your blood sugar rises), and in general if you keep your blood sugar low, you’ll improve your insulin sensitivity (keeping it low overall and improving its effectiveness when it’s needed).

Anything that raises your blood sugar will provoke an insulin response. Carbs raise blood sugar, protein does (more in some folks than in others), fat barely does.

Insulin is a fat storage hormone. Its job is to get the blood sugar down, and it does this by signaling our cells to store the extra energy. When insulin is high we don’t have access to our own fat stores because we’re actually in a fat storage state rather than a fat-burning state. So weight loss in Keto works like this: keep insulin low (by restricting carbs and by limiting the number of times/day that we eat) so that when your body needs fuel, it can just tap into your own stored energy.

Fat adaptation is the adjustment to using fat as a primary energy source, so the mechanism I just described isn’t always this straightforward (in the beginning) if your body has been used to burning sugar and carbs for energy.

(Mg ) #3

Um WOWZA! YOU’RE BETTER THAN MY DOCTOR!
It’s technical.
Hard to figure out but you described it amazingly! Wish you could pin this. So many people new to keto don’t realize the significance of this and how seriously important it is.
Guess it’s like the transmission in your car. If the transmission fails the entire engine fails. If you’re doing keto for weight-loss like I am.
That insulin is serious stuff. It determines everything.
I believe not nearly enough attention is paid to it.
It should be right up there with learning carbs and Micros because they all three totally tie in together.
Very important info you gave. Thank you honey

#4

I’m glad it was useful!

(Bunny) #5

Some other interesting and amazing things about non-insulin uptake of glucose:

image

[1] “… The glucose transport proteins (GLUT1 and GLUT4) facilitate glucose transport into insulin-sensitive cells. GLUT1 is insulin-independent and is widely distributed in different tissues. GLUT4 is insulin-dependent and is responsible for the majority of glucose transport into muscle and adipose cells in anabolic conditions. We suggest the hypothesis that insulin resistance is dependent on whether glucose is entering through GLUT1 or GLUT4 and on the two functional compartments of glucose 6-phosphate formation within the cell. Glucose entering the muscle cell through GLUT4 and phosphorylated by hexokinase II is mainly directed to glycogen synthesis and glycolysis. If glucose is entering through GLUT1 and phosphorylated by hexokinase I, the glucose 6-phosphate so formed is available for all metabolic pathways, including the hexosamine pathway. Hexosamines have a negative feedback effect on GLUT4, and reduced GLUT4 activity decreases insulin-mediated glucose uptake. Thus, insulin-independent glucose transport through GLUT1 can meet the basal needs of the muscle cell. If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance. …” …More

[2] “…We found that by using a method of extrapolation to determine NIMGU (non-insulin mediated glucose uptake), the calculated value in individuals with NGR (normal glucose regulation) was identical to that determined in previous studies using somatostatin-induced insulinopenia. NIMGU was increased in individuals with type 2 diabetes and was related to percent body fat. Furthermore, NIMGU was an independent predictor of EE. These results indicate that increasing adiposity and associated insulin resistance result in upregulation of insulin independent alternative pathways of glucose uptake potentially as a compensatory measure to ensure sufficient glucose flux into the cell. …” …More

[3] “…However one should recall that about 75% of whole body glucose uptake (GU) is operated through pathways which are non-insulin dependent. …” …More

[4] “…Only 25% of glucose uptake occurs in insulin-sensitive tissues, primarily skeletal muscle, during fasting conditions (6). During the postabsorptive state, tissue glucose uptake is closely matched by HGP…” …More

(Mg ) #6

Wow! This is serious stuff. Don’t you think it’s absolutely pivotal?
Here is what I think… Researching a bit now.
People fail miserably and feel extremly down about it. Ketogenic lifestyle is brutal until you learn it.
I have concluded, almost everyone who fails, fails for two reasons.

  1. Not staying under 20 carbs just to be safe. No brainer.
  2. Insulin spikes!
    Seriously, very little attention is placed on this.
    People knowledgable speak on it, however it’s not focused on because perhaps it’s so techie, people would zone out.
    The 75 percent and 25 percent you posted… Is the damn key here.
    I think a ton of people would really succeed easily if a genius just came up with an easy, quick theory that civilians could comprehend.
    Sincerely believe that.
    Thank you so much! Looking at the 75-25 ratio
(Gregory - You can teach an old dog new tricks.) #7

I would venture most people fail because they have trouble getting over the hurdle of getting past sugar cravings.
This is exacerbated by all the "Keto"diet plans that feature " Keto Desserts "…

It is much like any addiction that is not easy to overcome.
A lot ( most? ) of people want an easy fix for something they have spent years breaking…

(Mg ) #8

Totally agree old dog but… Cravings have everything to do with insulin spikes? No? That’s what I mean. Everything centers around insulin. The entire platform of ketogenic

(Bunny) #9

To me it almost sounds like it has to do with the way protein and bile interact and determines if insulin will be launched in the blood stream to activate GLUT 4 pathway rather than GLUT 1 and so strange how it is connected to my other post on estrogens and glucuronidase.

This makes me wonder if eating only protein is activating the GLUT 1 pathway?

Here is another observation: what does ammonia have to do with it? Hexosamine is ammonia the word amino acid is derived from Amine also Ammonia?

•Amino Acid - Amino = Amine ==>Ammonia (sulfur bonds in cysteine and methionine keeps it from being toxic)

image

[1] ”…Amines are formally derivatives of ammonia, wherein one or more hydrogen atoms have been replaced by a substituent such as an alkyl or aryl group[4] (these may respectively be called alkylamines and arylamines; amines in which both types of substituent are attached to one nitrogen atom may be called alkylarylamines). Important amines include amino acids, biogenic amines, trimethylamine, and aniline; see Category:Amines for a list of amines. Inorganic derivatives of ammonia are also called amines, such as monochloramine …” …More

[2] “…Glutamate is the one amino acid that undergoes oxidative deamination to liberate free ammonia for the synthesis of urea. Once free ammonia is formed in peripheral tissues, it must be transferred to the liver for the conversation to urea. This is carried out by the 'glucose-alanine cycle”. …” …More

[3] The results show that in acutely diabetic and normal rats, L-tryptophan administration reduced striatal dopamine and increased striatal serotonin release, whereas in chronically diabetic rats, the release of both biogenic amines was decreased. The findings indicate that the progression of diabetes is associated with an impaired ability to release primary neurotransmitter biogenic amines. …” …More

[4] “…The results obtained in these experiments suggest that high levels of glucose may have an inhibitory effect on the metabolism of NE (norepinephrine) and 5-HT (5 - hydroxytryptamine receptors) resulting in increases in the level of both amines. They also suggest that brain insulin is independent of the pancreatic one since high blood glucose did not influence the central level. …” …More

[5] “…1. Moderate bleeding, performed with care, does not affect essentially the blood sugar level in rabbits.
2. Subcutaneous injections of ammonium carbonate or urease solution tend to produce hyperglycemia.
3. Hyperglycemia may be considered as a means of protection against increases in ammonia in the blood. This forms a basis for the use of glucose in cases of ammonia intoxication.
4. The blood sugar level may be partly regulated by ammonia.
5. In the aeration method some “extra urea” is formed in blood filtrates, thus giving falsely high figures.
6. The effect of ammonium hydroxide on insulin is still open to question. …” Source: AMMONIA AND BLOOD SUGAR. BY A. A. HORVATH.
(From the Department of Medicine, Peking Union Medical College, Peking, China.)
(Received for publication, August 3, 1926.)

[6] Amine: CHEMICAL COMPOUND …More

[7] Metabolism and Interactions: The Chemistry and Biology of Compounds edited by Endre A. Balazs, Roger W. Jeanloz: “…The ability of muscle to yield ammonia from the hexosamine substrates was quite limited, suggesting relatively low levels of deaminase activity, whereas yeast was able to catalyze rapid degradation of the…”

(Mg ) #10

It’s crazy bunny.
The more one researches the more you find how critical it is.
I looked for a dummy guide to insulin.

It speaks about some things but nothing related to ketogenic lifestyle.
Very very interesting to me, all this.
Thank you

(Tracy) #11

I agree OldDog. Getting past that sugar addiction is tough. When you’ve been eating sugar in the form of grain and regular sugar your entire life, you almost need professional help to overcome it.

MG1 - I agree with people not keeping it under 20. There’s a difference in Keto and low carb. I have found most people won’t take the time to read up on what Keto. They want to do their own thing and when it doesn’t work they throw in the towel. All of my free time is used reading up or watching videos on Keto and everyday I learn something new that I can improve on.

(Tracy) #12

Excellent explanation.Thanks!

#13

Did they happen to figure out how to increase the use of the glut1 pathway. My guess would be it must be demand driven ie exercise and things that make your muscles ask for more?

(Bunny) #14

They injected peeps with Somatostatin at the Phoenix Indian Hospital in Arizona to activate the GLUT1 pathway.

Somatostatin suppresses insulin and glucagon, but you would not want to mess with that stuff, if you don’t know what your doing.

Somatostatin is produced by the pancrease.

What is really crazy about what I posted above is that hexosamines are a type of amino sugar.

Something like a table sugar IV is used to disable or neutralize e.g. ammonia poisoning?

What is even more suspicious is that the research in this area is like rare or non-existent? (conspiracy theories are running through my head at great speeds at this point i.e. population control?)

A further in depth observation is that the alkalinic prostatic fluid of males smells like ammonia (a bleachy type odor) but is a sugar that powers the tail of the sperm and inside the head of the spermatozoon is the mitochondria which I imagine is generating lots of ATP and phosphorylation (subatomic nuclear radiation[4])? (example of cross comparison on mitochondrial burning or oxidation of glucose, amino acids and fatty acids)

Footnotes:

[1] Hexosamines are amino sugars created by adding an amine group to a hexose.

Examples include:

[2] AMMONIA AND BLOOD SUGAR: …Similar results were obtained when ammonia was added to an aqueous solution of glucose dissolved in an aqueous phosphate mixture of pH = 7.40.” These suggestive findings led us to study the effect of ammonia on blood sugar in vivo as well as the effect of glucose on blood urea in vitro. …” …More

[3] “…August 7, 1965: A new imidazole compound was isolated as crystalline form from the reaction mixture of glucose and ammonia, and identified as 4(5)-(DL-glycero-2,3-dihydroxypropyl)imidazole. From the results the authors suggested that pentose may be formed in the reaction mixture not by direct fission of C-C bond of glucose but by recombination of glucose fragments, for example, of triose and glycolic aldehyde. 4(5)-[D-(-)-Glycero-2,3 dihydroxypropyl]imidazole was also newly prepared from D-xylose via 3-deoxy-D pentosone. …” …More

[4] “…When in vitro DNA in test tubes was exposed to coherent laser light, the laser light spiralled along the DNA helix as if it was guided by the structure of the DNA molecule. The most amazing effect was noticed when the DNA itself was removed and the laser light kept spiralling! The vacuum of the space that was just previously occupied by the DNA had changed and something caused the laser light to keep spiralling. These effects have been measured and remained for quite some time after the DNA was removed. The effect is now becoming well known as the DNA phantom effect. …” …More