Low carb - but high sugars - advice please!

[Oldvatr]

Does the processing of ketones "use up" any insulin?

I know in a "normal person" ketones results in a very small insulin response hence the ketones cycle can't get out of control if someone can produce any insulin of their own.

Yes insulin is involved in regulating ketones.
https://en.wikipedia.org/wiki/Ketosis

Edit: inaulin is used, but not necessarily used up. The brain and nervous system cannot use fat as a fuel but muscle cells can, So ketones replace glucose in powering the brain during ketosis and get used up. Ketones that are not burnt up get excreted in the urine, sweat and breath.

In diabetic DKA the ketones do not get burnt up because our bodies have a preference to burn glucose instead, so fats and ketones do not get burnt when there is ample blood glucose around, and thus build up to dangerous levels.

 

[ringi]

But does this "use up" insulin, or is the insulin just a message remaining in the blood until the liver breaks it down?

 

[Oldvatr]

But does this "use up" insulin, or is the insulin just a message remaining in the blood until the liver breaks it down?

Think insulin is just a switch. It is called the storage hormone. We do not burn insulin.

<<<Insulin that is secreted by the pancreas has a circulating half-life of approximately 6 minutes, which is to say that every 6 minutes, the amount of insulin in the blood declines by 50%. In fact, after it is released from the pancreas, insulin is no longer detectable in the bloodstream within 30 minutes. Insulin is removed from the body by enzymes in the kidney and the liver, as well as by its interaction with insulin receptors<<<

 

[ickihun]

Does the processing of ketones "use up" any insulin?

I know in a "normal person" ketones results in a very small insulin response hence the ketones cycle can't get out of control if someone can produce any insulin of their own.

Type2s producing useless insulin or insufficient insulin can go DKA and SGLT-2 inhibitors can cause DKA too in type2s.

 

[ringi]

Type2s producing useless insulin or insufficient insulin can go DKA and SGLT-2 inhibitors can cause DKA too in type2s.

I may be missing something, but I thought the risk with SGLT-2 inhibitors is that someone can have a "normal" BG reading while being in DKA, not that they cause DKA.

 

[ringi]

So back to the original question:

Is it everyone's view that a low level of ketones does not effect how much insulin is needed for a given number of grams of carbs or protein? (I am thinking if someone is changing between ketones and none ketones depending on what they do on a given day.)

 

[ickihun]

I may be missing something, but I thought the risk with SGLT-2 inhibitors is that someone can have a "normal" BG reading while being in DKA, not that they cause DKA.

Cause. Due to incorrect meter readings so no insulin injection corrections. Hence DKA.

 

[ickihun]

So back to the original question:

Is it everyone's view that a low level of ketones does not effect how much insulin is needed for a given number of grams of carbs or protein? (I am thinking if someone is changing between ketones and none ketones depending on what they do on a given day.)

I don't know but someone must. @Brunneria might know?

 

[Oldvatr]

I may be missing something, but I thought the risk with SGLT-2 inhibitors is that someone can have a "normal" BG reading while being in DKA, not that they cause DKA.

They increase the risk. The additional danger that the bgl levels can be low on A&E admission may mean that paramedics discount the DKA and thus do not treat for DKA.

 

[Oldvatr]

I don't know but someone must. @Brunneria might know?

There is a Sticky thread in the meds section that carries the FDA warnng and the news item. If you read this thread, then you will find people reporting actual events and it is a real risk.

 

[kokhongw]

From this SGLT2 "euglycemic DKA" case report:-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5446101/

In summary, reduced serum glucose, reduced insulin doses, increased glucagon release, and reduced clearance of ketone bodies are contributors to euDKA in patients taking SGLT2 inhibitors.11

My interpretation..."The definition of euglycemic DKA is glucose < 250mg/dl ~ 13.8 mmol/L with high level of ketones > 3 mmol."

The patient was admitted with glucose level around 200mg/dl~ 11 mmol/L. A level not usually associated with DKA.

Recommended treatment

For patients diagnosed with euDKA while taking SGLT-2 inhibitors, the following steps are essential: stopping the SGLT2 inhibitor, starting long-acting insulin (or increasing insulin doses for those already taking it), increasing carbohydrate intake (if possible), and serial monitoring of electrolytes and ketones. Importantly, short-acting sliding scale insulin may not be sufficient to correct the metabolic acidosis. While mild cases of euDKA can be treated in the ambulatory setting, patients should be admitted in case of vomiting, infection, systemic illness, inability to eat, dyselectrolytemia, or acute changes in the kidney function

 

[ickihun]

There is a Sticky thread in the meds section that carries the FDA warnng and the news item. If you read this thread, then you will find people reporting actual events and it is a real risk.

My reply was regarding if ketosis was a result of IR or rather IR as a result of ketosis?
I don't know because I don't measure my ketones. Many do hou. Brunneria, I believe does or at least used to.

 

[tim2000s]

Hi @Odin004 - as others have mentioned, both type 1s and type 2s eating a low carb or very low carb can and do experience what's known as "physiological insulin resistance" after a period of low carbing, which is a mechanism whereby the GLUT4 transporters in the cells are effectively turned off to allow any glucose produced to be used by the brain first (as the brain is the main organ that has a minimum requirement for glucose, no others do). In terms of T1, as most of the exogenous insulin we take is taken up by muscles rather than the liver (very little injected insulin makes it to the liver), having fewer active GLUT4s means that we don't process insulin as effectively. This also means that glucose production from the liver is less likely to be reduced.

Metformin works by decreasing the glucose production of the liver in response to both protein and to the natural requirements, while alcohol achieves the same thing because the liver is single tracked and can't produce glucose whilst processing alcol. That demonstrates one mechanism for dealing with physiological insulin resistance.

When I have been low carb, I have also done it in combination with resistance training, which depletes glycogen stores from the muscles and liver. This has the secondary effect of re-enabling GLUT4s in the muscles as they try to replenish those glycogen stores, meaning that they are there when exogenous insulin is applied, and I haven't, therefore, experienced an increase in insulin resistance.This is also a mechanism used in the "body transformation" world, where a low carb diet in combination with a resistance training programme is used to cut body fat and maintain low insulin requirements in non-diabetics.

In order to try and handle what you are seeing, it may be as simple as hitting the gym for weights sessions two or three times a week. What I've measured in terms of insulin sensitivity, when not low carb, is that for the 36 hours after a weight training session, my insulin sensitivity increases by up to 30%, so it's certainly something worth taking a look at as a way of dealing with it. Hope that helps.

 

[ringi]

Thanks @tim2000s

Yet another reason way I should join a gym and do some resistance training rather than just doing power walking and swimming. As a Type2 I have no way to measure insulin resistance but clearly should reduce it as much as possible, so I have to learn from people with Type1 who measure it everyday.

 

[Odin004]

According to Phinney and Volek the normal level for a LC keto diet is <0.6 mmol/l, for light ketosis, but for Optimal ketosis, the levels need to be between 1 and 3 mmol/l, The important thing to note is that the bgl levels for dietary ketosis will be low, whereas for diabetic DKA they will be high (> 15 mmol.l usually) so as an insulin dependant, then the signs of DKA comes from having HIGH bgl levels. then testing for ketones. I think the level of 5 mmol.l I quoted came from Tim Noakes, who was talking about diabetic athletes in HIT training.

<<<<According to Volek and Phinney in their best-selling book "The Art and Science of Low-Carbohydrate Living", nutritional ketosis is defined by serum ketones ranging from 0.5 to 3.0 mM. ... The level of ketones in ketoacidosis are 3-5 times higher than in ketosis resulting from a ketogenic diet.>>>>>


And from Tim Noakes trial transcript
http://www.openfuture.biz/evidence/InsulinResistance-Ketones.html

I see what you mean; it's true that blood sugars are a relevant factor (except in the case of euglycemic ketoacidosis). For example, an insulin dependent diabetic might have ketones of say 2.0 - but this could be quite a normal response to a low carb or "ketogenic" diet, especially if the person is also exercising, and therefore, nothing to worry about - however, another diabetic could have ketones of 1.7 (lower) - but this *could* indicate that there is insufficient insulin in the system - which if left unchecked could be the beginnings of DKA. So it's not just the level of ketones that's relevant - it's the reason for those ketones too; and blood sugar levels help identify the root cause of the issue (i.e. can point to lack of insulin in the system). It really is tricky sometimes being diabetic

 

[Odin004]

Hi @Odin004 - as others have mentioned, both type 1s and type 2s eating a low carb or very low carb can and do experience what's known as "physiological insulin resistance" after a period of low carbing, which is a mechanism whereby the GLUT4 transporters in the cells are effectively turned off to allow any glucose produced to be used by the brain first (as the brain is the main organ that has a minimum requirement for glucose, no others do). In terms of T1, as most of the exogenous insulin we take is taken up by muscles rather than the liver (very little injected insulin makes it to the liver), having fewer active GLUT4s means that we don't process insulin as effectively. This also means that glucose production from the liver is less likely to be reduced.

Metformin works by decreasing the glucose production of the liver in response to both protein and to the natural requirements, while alcohol achieves the same thing because the liver is single tracked and can't produce glucose whilst processing alcol. That demonstrates one mechanism for dealing with physiological insulin resistance.

When I have been low carb, I have also done it in combination with resistance training, which depletes glycogen stores from the muscles and liver. This has the secondary effect of re-enabling GLUT4s in the muscles as they try to replenish those glycogen stores, meaning that they are there when exogenous insulin is applied, and I haven't, therefore, experienced an increase in insulin resistance.This is also a mechanism used in the "body transformation" world, where a low carb diet in combination with a resistance training programme is used to cut body fat and maintain low insulin requirements in non-diabetics.

In order to try and handle what you are seeing, it may be as simple as hitting the gym for weights sessions two or three times a week. What I've measured in terms of insulin sensitivity, when not low carb, is that for the 36 hours after a weight training session, my insulin sensitivity increases by up to 30%, so it's certainly something worth taking a look at as a way of dealing with it. Hope that helps.

Hi @tim2000s

Thanks very much for this information - the GLUT4 explanation does make sense, as glucose is being prioritised for the brain. Interesting also re Metformin - from what you say, it doesn't actually decrease insulin resistance, rather it just decreases an "extra" source of sugar (from the liver).

In terms of resistance training, I've done this on and off for some years - although not since a bad hypo after exercise about a year ago. I have been thinking about starting again, and slowly getting back into it; it's certainly true that after previous exercise sessions, my bolus for my next meal could be reduced by 50%. One question if I may - if the GLUT4 transporters are desensitised in order to spare glucose for the brain - but we're then re-enabling them with exercise - won't the brain be at risk, unless the carb intake also increases? - otherwise, won't this just mean that glucose is redirected away from the brain via GLUT4?

 

[tim2000s]

Hi @tim2000s

Thanks very much for this information - the GLUT4 explanation does make sense, as glucose is being prioritised for the brain. Interesting also re Metformin - from what you say, it doesn't actually decrease insulin resistance, rather it just decreases an "extra" source of sugar (from the liver).

In terms of resistance training, I've done this on and off for some years - although not since a bad hypo after exercise about a year ago. I have been thinking about starting again, and slowly getting back into it; it's certainly true that after previous exercise sessions, my bolus for my next meal could be reduced by 50%. One question if I may - if the GLUT4 transporters are desensitised in order to spare glucose for the brain - but we're then re-enabling them with exercise - won't the brain be at risk, unless the carb intake also increases? - otherwise, won't this just mean that glucose is redirected away from the brain via GLUT4?

Not really. Whilst you still want the GLUT4 sensitised for insulin use, as long as you are keto, your body is using lipids as your fuel source, and not glucose. Essentially, you have partially active GLUT4 rather than fully active GLUT4.

 

[Odin004]

Not really. Whilst you still want the GLUT4 sensitised for insulin use, as long as you are keto, your body is using lipids as your fuel source, and not glucose. Essentially, you have partially active GLUT4 rather than fully active GLUT4.

I see, thankyou, that also makes sense - so hopefully, with exercise, my muscles can just use some of that sugar circulating in the blood (that is currently proving difficult to shift). Could I please ask if you have any advice on appropriate sets and reps, and intensity of exercise, in this context? I know that going too intense/low reps does make me less insulin sensitive for a while after.

 

[tim2000s]

I see, thankyou, that also makes sense - so hopefully, with exercise, my muscles can just use some of that sugar circulating in the blood (that is currently proving difficult to shift). Could I please ask if you have any advice on appropriate sets and reps, and intensity of exercise, in this context? I know that going too intense/low reps does make me less insulin sensitive for a while after.

Not really, it's one of those things that you have to find out for yourself. For me, super intense ones that properly cause exhaustion lower sensitivity, while 5x5s with the last set being tough seem to be okay. It's a bit of find your own level.

 

[Odin004]

Not really, it's one of those things that you have to find out for yourself. For me, super intense ones that properly cause exhaustion lower sensitivity, while 5x5s with the last set being tough seem to be okay. It's a bit of find your own level.

Thanks Tim, I shall experiment.