Some thoughts about Insulin Resistance

[LittleGreyCat]

Reading my copy of Volek and Phinney again, and one thing I noted was that there is a very strong relationship between the insulin level in the blood and the ability of cells to metabolise fat.

Apparently Lipase is key to metabolising fats and its action is inhibited by insulin. The graph shown is the traditional hockey stick curve

This cut from a screen print from my Kindle programme.

The diagram assumes that if you are on a low carbohydrate diet then you are running low insulin levels and so you can metabolise fats relatively easily.

This did make me wonder if there are people who are strongly insulin resistant and therefore perforce are running higher insulin levels despite being on a low carbohydrate diet. This in turn would make it much harder to metabolise fats and thus much harder to lose weight. Perhaps they are forced to metabolise proteins to release glucose because they can't effectively metabolise fats.

I also wonder if there is always a correlation between losing weight, nutritional ketosis and insulin levels. From the graph it would seem that if you aren't eating much carbohydrate then you must be living on fat and in turn you must have lower insulin levels. Of course, everyone is different and perhaps some people at higher insulin levels just break the fat down less efficiently and more slowly.

On the "thinking of design reasons" front, insulin seems a logical switch between burning fat and storing fat.

Assume that insulin secretion is driven by glucose in the blood, derived from dietary carbohydrates.

If there is plentiful carbohydrate you want to store it away as fat against the hard times and not burn any fat stores. Maximise the storage of fat. So you secrete a lot of insulin.

If the availability of carbohydrate drops, then you think about mobilising your fat stores. You secrete less insulin. However you don't switch fully over to fat burning for a few weeks in case this is just a blip in the carbohydrate supply and there is more on the way. [I think this is not directly controlled by insulin but by the modification of metabolic pathways in the tissues.]

Oh, and if your insulin concentration goes through the roof but you are massively insulin resistant then you can't get glucose into the cells, you also can't metabolise fats for energy, and your body starts to break down protein because it thinks that is all that is left. So DKA. Which would explain one thing that has puzzled me about DKA. I have always wondered why DKA came about if you can metabolise ketones. Perhaps all the metabolic pathways are slightly screwed up. Then again you can get DKA if you stop producing insulin.

Oh, and that reminds me. V&P say that you only really burn ketones in the muscles when you first start to keto adapt. Once you are keto adapted then most of your body is burning fats directly, not blood ketones. The ketones are mainly reserved for the brain and other parts of the central nervous system.

I must keep reading these books (Art and Science of Low Carbohydrate Living & Performance) as I keep missing key facts.

 

[Brunneria]

Yes.
I have always assumed that my body’s stubborn refusal to access its own fat reserves is due (at least in part) to my high insulin resistance (PCOS, RH, obesity, prolactinoma and medication for the prolactinoma which has a side effect of raising insulin resistance further. I am also nearing menopause, so things are due to get even more fun then).

 

[Guzzler]

I find that I have to reread or review stuff that I miss first time around. It doesn't help that I am borderline inumerate so graphs etc mean little to me, and that my memory is so poor. Still, it keeps me out of trouble... mostly.

 

[ziggy_w]

Fascinating, @LittleGreyCat.

It also seems that it can take a while after switching to low carb for insulin level to lower. I remember that @CherryAA did a fasting insulin test quite a while into her low carb diet and it was still slightly elevated.

Just wondering -- Would it be possible that a fatty liver will release more glucose trying to rid itself of the fat, which then causes an insulin response, thus keeping insulin levels higher than normal? (At least for some time.) This would explain why it might take a while until we see the weight dropping. I also seem to remember reading that some argue that the more fundamental problem with T2D is the increased release of glucose from the liver.

Just thought I throw this out there. Curious about your thinking.

 

[Guzzler]

Fascinating, @LittleGreyCat.

It also seems that it can take a while after switching to low carb for insulin level to lower. I remember that @CherryAA did a fasting insulin test quite a while into her low carb diet and it was still slightly elevated.

Just wondering -- Would it be possible that a fatty liver will release more glucose trying to rid itself of the fat, which then causes an insulin response, thus keeping insulin levels higher than normal? (At least for some time.) This would explain why it might take a while until we see the weight dropping. I also seem to remember reading that some argue that the more fundamental problem with T2D is the increased release of glucose from the liver.

Just thought I throw this out there. Curious about your thinking.

Interesting points. My experience was that I lost weight almost within days of starting LCHF (water?) and carried on until I had to take steps to stop it. I have also read that this approach will see a quick response by the liver to rid itself of fats, again, within days. The pancreas however takes much longer and I wonder about the chemical messages between the two organs needing longer to readjust.

 

[ziggy_w]

Hi @Guzzler,

Agree -- my experience is similar to yours -- I have to admit, though, that my HbA1c was very high at diagnosis, so maybe my insulin production was already compromised, making it easier to lose weight.

I remember reading that some members here initially had trouble losing weight. So, maybe some have higher insulin levels for longer. Too bad that insulin is rarely measured. I bet we would learn a lot if it was.

 

[ringi]

This did make me wonder if there are people who are strongly insulin resistant and therefore perforce are running higher insulin levels despite being on a low carbohydrate diet. This in turn would make it much harder to metabolise fats and thus much harder to lose weight. Perhaps they are forced to metabolise proteins to release glucose because they can't effectively metabolise fats.

Enter Dr Jason Fung, he covers this in his fasting book.

Also, VERY low carb where protein is limited along with adding lots of good fat, but most people can't do this without a lot of support, enter Volek and Phinney new company, https://www.virtahealth.com

This week I am trying bulletproof coffee for breakfast, along with one meal a day (dinner) to see if it speeds up my weight loss.

Oh, and if your insulin concentration goes through the roof but you are massively insulin resistant then you can't get glucose into the cells, you also can't metabolise fats for energy, and your body starts to break down protein because it thinks that is all that is left. So DKA. Which would explain one thing that has puzzled me about DKA. I have always wondered why DKA came about if you can metabolise ketones. Perhaps all the metabolic pathways are slightly screwed up.

It needs a little insulin to allow ketones to enter cells when the insulin level is close to nothing, the cells can't use ketones.

 

[Guzzler]

Hi @Guzzler,

Agree -- my experience is similar to yours -- I have to admit, though, that my HbA1c was very high at diagnosis, so maybe my insulin production was already compromised, making it easier to lose weight.

I remember reading that some members here initially had trouble losing weight. So, maybe some have higher insulin levels for longer. Too bad that insulin is rarely measured. I bet we would learn a lot if it was.

Kraft would agree with you. The five hour insulin measure would be problematic, though, with our cash strapped NHS.

 

[Biggles2]

Kraft would agree with you.

Following up on that thought @Guzzler, here is a link to a really great guest-post on hyperinsulinemia by Nick Mailer. He describes Dr. Kraft’s contribution to our knowledge base rather nicely:

"Sugar Sugar Baby, Get On Down The Line, Part 2":​

https://baby.botherer.org/2018/01/sugar-sugar-baby-get-on-down-the-line-part-2/

 

[Guzzler]

Following up on that thought @Guzzler, here is a link to a really great guest-post on hyperinsulinemia by Nick Mailer. He describes Dr. Kraft’s contribution to our knowledge base rather nicely:

"Sugar Sugar Baby, Get On Down The Line, Part 2":​

https://baby.botherer.org/2018/01/sugar-sugar-baby-get-on-down-the-line-part-2/

I get the 'Web page not available' message on the link you give. I did see FatEmperor's interview with Dr. Kraft and many of the boffins cite his work.

 

[Biggles2]

I get the 'Web page not available' message on the link you give. I did see FatEmperor's interview with Dr. Kraft and many of the boffins cite his work.

Give it another try @Guzzler, I tried just now and it works. It is a brilliant piece, well worth a read! Here is a small snippet:

"This is why people who smugly conclude that the way to deal with diabetes, or PCOS, or any other related disease, is “to lose weight” have got it quite the wrong way round. Putting on weight is a symptom of hyperinsulinaemia: your body starts crazily sequestering energy in its fat cells."​

 

[first14808]

I kinda agree with Biggles I think. As I understand it..

Pancreatic beta cells are our natural glucometers. If they detect high glucose in blood, they produce insulin and suppress the alpha cells from producing glucagon. Fat cells will still take up glucose, but if we're insulin resistant, presumably at a lower rate as that rate is increased normally by the effect of insulin on those cells. But if our BG stays high, the alpha cells stay pretty much suppressed and don't produce the glucagon needed to suppress glucose uptake, and trigger the glycogenolysis needed to get fat cells releasing glycogen for the liver to convert back to glucose.

That kinda fits with what I learned when I used to train hard. Muscles store their own energy, but to burn adipose fat, it needed hefty carb reduction to trigger glycogenolysis.. and then eat protein and fats to avoid gluconeogenisis burning muscle instead of fat. And I think that might be why different people have different experiences, ie if we're insulin resistant rather than insulin deficient.

 

[LittleGreyCat]

Fascinating, @LittleGreyCat.

It also seems that it can take a while after switching to low carb for insulin level to lower. I remember that @CherryAA did a fasting insulin test quite a while into her low carb diet and it was still slightly elevated.

Just wondering -- Would it be possible that a fatty liver will release more glucose trying to rid itself of the fat, which then causes an insulin response, thus keeping insulin levels higher than normal? (At least for some time.) This would explain why it might take a while until we see the weight dropping. I also seem to remember reading that some argue that the more fundamental problem with T2D is the increased release of glucose from the liver.

Just thought I throw this out there. Curious about your thinking.

Not 100% sure about this.

Breaking down fats, especially triglycerides, does release some glycerol which can be converted into glucose. Apart from that there is a finite amount of glucose which can be stored in the liver (although, again, I don't know if an enlarged liver can store more glucose or if it has the same glucose storage ability and the increase in size is purely due to the amount of fat). So in general I think that once LCHF is under way the glucose/glycogen stores in the liver and other tissues will become depleted quite quickly.

I wonder if insulin resistance drives the body to create more carbohydrate (for example by gluconeogenesis) to try and maintain glucose supply to the brain but I am by no means sure.

The main thing is that even if you are fully keto adapted and only need a small amount of blood glucose for red blood cells and some bits of the brain I suspect that you still have to run higher than usual insulin levels if you still have any IR. I have had a test recently and I have quite low (but normal) insulin levels but at the time of the fasting test my BG was elevated so I do still have some IR. The big question is why, and how can I lower it?

My bete noir is fat in my belly, which probably means fat in and around my organs. January (and beyond) is aimed at getting my waist measurement down.

 

[ickihun]

I still find my no weight loss on lchf but weight loss in low carb, low fat very very interesting. As well as taking insulin injections and metformin and then less thyroid med. When losing weight; I didn't really know why i was, considering I was having 100g carb on some days but less in others.
I only lost weight when my bgs were in the 4-7mmol/l range constantly!!!!!! With insulin.

 

[Guzzler]

Following up on that thought @Guzzler, here is a link to a really great guest-post on hyperinsulinemia by Nick Mailer. He describes Dr. Kraft’s contribution to our knowledge base rather nicely:

"Sugar Sugar Baby, Get On Down The Line, Part 2":​

https://baby.botherer.org/2018/01/sugar-sugar-baby-get-on-down-the-line-part-2/

Still can't get it to work, possibly due to my steam driven tablet. A shame as my interest is piqued.

 

[Bluetit1802]

Following up on that thought @Guzzler, here is a link to a really great guest-post on hyperinsulinemia by Nick Mailer. He describes Dr. Kraft’s contribution to our knowledge base rather nicely:

"Sugar Sugar Baby, Get On Down The Line, Part 2":​

https://baby.botherer.org/2018/01/sugar-sugar-baby-get-on-down-the-line-part-2/

Wonderful post! Very readable, amusing, and informative.

Right at the end - not just carbs causing insulinaemia but also omega 6 seed oils.

 

[first14808]

My bete noir is fat in my belly, which probably means fat in and around my organs. January (and beyond) is aimed at getting my waist measurement down.

I think that's explained in Part 1:-

https://baby.botherer.org/2017/08/sugar-baby-get-on-down-the-line/
"So we eat food that promotes insulin. Our body is locked in storage mode. We literally cannot burn any of the fat that lies copious on our body while insulin’s about."

So the insulin supressing the alpha cell's glucagon signal to start converting fat. But now I'm curious how we could measure that. I guess in theory, a combination of fasting and/or low carb should get to a point where we start burning fat. I've noticed a few times that my BG goes up between first reading and pre-meal, which is usually 6-8hrs later at least. So for example today, I was 4.9 in the morning, then 6.6 before dinner and <10g carbs in between samples.

 

[Guzzler]

Finally! Googled the URL and accessed it, no bother. I hadn't realised that Ivor had brought Kraft's work back from the brink of oblivion. Thanks @Biggles2 I enjoyed this piece not least because it is aimed at us laypeople in plainspeak. I would suggest that the link be added to daisy1 info pack for newcomers, it is so readily digestible (you see what I did there? ).

 

[Shiba Park]

Fascinating, @LittleGreyCat.

I also seem to remember reading that some argue that the more fundamental problem with T2D is the increased release of glucose from the liver.

But the liver needs to recharge from somewhere... I thought that this was primarily from glucose in the blood but could be synthesised from other energy sources if necessary?

 

[ziggy_w]

Hi @LittleGreyCat and @Shiba Park,

Mind you, I am by no means an expert on this. I am sure others know a lot more about this.

This is, however, what I seem to remember (provided I understood it correctly). One of the functions of insulin (apart from pushing glucose into the cells) is to shut off glucose production in the liver. However, if the liver is resistant to insulin (as in T2D and fatty liver), this doesn't work (or not sufficiently well) and the liver keeps producing and releasing glucose into the blood either from its own stores or, if depleted, through gluconeogenesis, even though there is already sufficient glucose in the blood stream. This then leads to even higher blood glucose levels, which in turn trigger the release of more insulin from the pancreas. More insulin in the blood furthermore leads to increased fat storage (part of which will be stored in the liver) and insulin resistance, setting into motion a self-reinforcing process. Thus, the essential problem might be insulin resistance of the liver due to too much fat in the liver.

Anyway -- I am curious as to your thoughts on this.