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Question regarding Ketones and Insulin

Answered on May 16, 2016
Created December 07, 2011 at 5:33 PM

I am trying to get my head around the more intricate elements of the body's metabolism and I have a question.

From what I understand, elevated blood sugar triggers an increase in insulin which tells the body to start storing that carbohydrate and to down regulate the body's lipid metabolism.

This Wikipedia article prompted a question about an obvious hole in my understanding: http://en.wikipedia.org/wiki/Ketoacidosis#Pathophysiology

"In healthy individuals this (ketoacidosis) normally does not occur because the pancreas produces insulin in response to rising ketone/blood glucose concentration."

So, does insulin go up with increased levels of ketones (thereby telling the body to lay off further ketone production because the body has "enough") in the same way as insulin's relationship with sugar?

Thanks in advance for your answers.

Best regards

Nick Kinsella

33d79be41042b7e6f62191ccfa9fde8d

on December 08, 2011
at 11:37 AM

Thank you Lucas for your highly eloquent answer. "Insulin inhibits ketogenesis. Ketone bodies stimulate insulin." clicked everything into place for me :-)

B4e1fa6a8cf43d2b69d97a99dfca262c

(10255)

on December 07, 2011
at 05:54 PM

ketones are produced when energy is needed and there is no glucose available; no? so maybe its the presence of glucose which triggers insulin that halts the production of ketones?

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8 Answers

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Medium avatar

(10611)

on November 06, 2015
at 04:09 PM

For what it's worth, here's Guyenet's reading of Hall's study. He considers this definitive disproof of the carbohydrate insulin theory:

http://wholehealthsource.blogspot.com/2015/08/a-new-human-trial-seriously-undermines.html?m=1

In this ward study of obese patients isocaloric high fat and high carb diets were consumed. Despite a 22% reduction in insulin in the high fat group, the body fat loss was half that of the high carb group. Clearly insulin suppression has not generated the effect of aiding body fat loss postulated in the CI theory. The author goes further, projecting that a high carb diet maintains a metabolic advantage over a high fat diet for weight loss over a period of months.

This question appears to be based on an assumption that CI theory is valid for predicting effects of insulin, based on the "carbs are stored" and "lipids are downregulated" statements. In light of evidence that CI is false, all the corrolary theories (calories don't matter, exercise is unimportant, lipid theory is invalid, etc.) stemming from CI need to be rejected if and until they can be demonstrated in ward studies.

It's important that Guyenet brought this to the fore, since he is in favor of low carb and Paleo for weight loss and lifestyle. He is a scientist who favors Good Science over Bad Science too. The Paleo community needs to root out false assumptions when they are identified. For instance, nonsense like the following is based on CI theory:

http://www.diabetes-book.com/insulin-fat-connection/

And deservedly belongs in the recycle bin. Despite how much Dr. Bernstein wishes it, carbohydrates are NOT the major source of body fat. Whether anything else he says in his book is true, it is mooted and reduced to quackery because he has rejected all the studies proving that dietary fat is stored as body fat within hours of eating. He's based his entire book on a false assumption.

12
68f2734a5078a7106f560a7079df45fd

on December 07, 2011
at 07:20 PM

Insulin inhibits ketogenesis. Ketone bodies stimulate insulin. Oxymoron? No. Negative feedback. Ketones are good, too much ketones is bad. Ketones and FFA regulate their own levels by stimulating the release of inhibitory molecules, such as insulin. Remember that normal basal insulin levels are ESSENTIAL for the body.

During fasting, there is no exogenous stimuli for insulin secretion. If you don't have "back-up" mechanisms to maintain a normal level of insulin, you would die. Because fat stores are high, and ketogenesis is stimulated by the level of FFA in the liver, without insulin you would have uncontrolled ketogenesis (ketoacidosis). So the role of insulin is supressing the precursors of ketone bodies (FFA) and the conversion of acetyl CoA to ketone bodies. Thus, the insulin release following FFA and ketone body stimulation serves to control the rate of ketogenesis, and prevent the development of abnormal levels of both FFA and ketones.

The relationship between ketones-insulin is not the same as glucose-insulin. Physiologically, ketones rise when blood glucose is low. If ketones would have the same influence on insulin secretion as glucose, you would die of hypoglycemia.

The body is in a dynamic equilibrium; not static.

33d79be41042b7e6f62191ccfa9fde8d

on December 08, 2011
at 11:37 AM

Thank you Lucas for your highly eloquent answer. "Insulin inhibits ketogenesis. Ketone bodies stimulate insulin." clicked everything into place for me :-)

5
A968087cc1dd66d480749c02e4619ef4

(20436)

on December 07, 2011
at 06:20 PM

http://diabetes.diabetesjournals.org/content/48/3/577.full.pdf

In a word, yes. Turns out quite a few things stimulate insulin release - which is not to say that the effects are equal. Free fatty acids, protein, ketones, glucose. the point is that insulin helps maintain energy balance. All of these provide energy.

About ketoacidosis - there is always a basal level of insulin in healthy people, even in most T2 diabetics - which is why they typically don't run into ketoacidosis all the time. T1 diabetics have 0 insulin, which is why they can have this problem.

2
Dfada6fe4982ab3b7557172f20632da8

(5332)

on December 07, 2011
at 06:23 PM

Far be it for me to question a quote from wikipedia, but it's possible there's some confusion there. For the most part ketoacidosis is a risk for diabetics, who by definition have problems regulating insulin levels.

Ketone production is a byproduct (initially at least) of gluco-neogenisis as fat is used to fuel the breakdown of protein to create glucose, which in healthy individuals will only occur if there is not enough glucose available. This maintains a manageable glucose level for the few criticial functions that require it, while providing energy for the rest of the body and keeping everything ticking along nicely. This is good honest ketosis which we all engage in regularly.

Ketoacidosis is a completely different mechanism which can occur despite high blood sugar becuase of a problem with the pancreas resulting in no insulin being released. So in healthy individuals, the normal insulin response to rising blood glucose prevents ketone production happening at the same time so this state never occurs. That is what I think the article is referring to.

0
322a2783dfe4086591f323c6d2c086d6

on May 16, 2016
at 06:45 PM

Regarding the Kevin Hall study. I did not see any specific references to actual menu items and so I posit a confounder... "INSULIN-Like Growth Factor" in dairy. I know that when I am very-low-carb, actually IN ketosis, dairy will always screw me over! (hey! I like my whole-milk, cheese and heavy cream! ;-p ) I never lose weight while in ketosis if I include dairy.

0
4d20b9a0585c79d853f3531e6f2369ce

on October 25, 2014
at 05:50 AM

 

Hi there,

 

I am type 1 diabetic and struggle with this immensely.

 

I have been Paleo for quite some time and have recently begun intermittent fasting (only having 500calories twice a week).

 

I am massively struggling with it at the moment as I fast between 6am - 6pm and throughout the day I measure my blood glucose and blood ketone levels. BGL stays stable for the morning and I think its going great, then towards mid-day I begin to become hypoglycaemic - inevitably I decrease my rate of insulin as I really don’t want to eat sugar to fix the hypo. Then in the afternoon my ketones increase to quite a high level and to the point I feel sick. Following this my BGL begins to rise and rise and I have to increase my insulin a fair amount, in fact I end up having to put a lot of insulin in to correct the high BGL (it takes quite a while, almost like a resistance to my insulin). Following this my levels again stabilise and i eat a low/no carb dinner. Then again the process happens all over again and become hyperglycaemia and highly ketotic. I find it extremely interesting as I continuously monitor by BGL and ketones and also satisfying as I can see that I am burning fat. But I do not understand if the increase in insulin requirements defeat the purpose? I am a nurse and have a rather in depth understanding of the body's metabolism but can't figure this one out. Also I do not believe being a diabetic makes it any more dangerous. I believe that the difference is I have control over the release of insulin, which anyone else's body would be doing automatically. What’s more, is that I know exactly what my BGL and ketone blood levels are and exactly how much insulin is being released. Please share your thoughts on the matter!

 

Ceca3cd1934aa5c8301c4ff077635bd6

(0)

on November 06, 2015
at 03:03 AM

Bakerducky, my guess would be that the action of glucagon is causing your issues.  Glucose is stable in the morning but begins to fall.. glucagon will be stimulated to raise it again.  Glucagon also upregulates the flow of free fatty acids from adipose tissue, which in turn upregulates ketogenesis.  Because you've also lowered available insulin (instead of eating sugar) there's less insulin available to offset FFA flow and ketone production..and glucagon is active.. Hence acidosis symptoms and accelerated gluconeogenesis in the afternoon necessitating extra insulin injection.

0
8f246f4cfc73364ec6b9a4849a67c18f

on July 21, 2014
at 06:56 PM

Hello,

Mr. Lucas Tafur (or anyone who has an opinion on this),

What happens in the case of a diabetic type 1 who follows a ketogenic diet? Will he need to inject additional insulin to manage ketone levels (besides glucose levels) ? What do you think will happen if the ketone levels start rising and-theoritically-insulin reasease from the pancreas is needed ? Will the glucose levels ,of the diabetic T1, start rising in the absence of endogenous insulin to control ketone levels?

I`m looking forward to your replies and opinions.

@Lucas Tafur

@Dave S.

@AndyM

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