Before Ivor, there was also this post by Prof Grant Schofield about Kraft and his PhD student Catherine Croft's work: https://profgrant.com/2013/08/16/joseph-kraft-why-hyperinsulinemia-matters/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?).
Before Ivor, there was also this post by Prof Grant Schofield about Kraft and his PhD student Catherine Croft's work: https://profgrant.com/2013/08/16/joseph-kraft-why-hyperinsulinemia-matters/
So great that Kraft's work was re-discovered, his data passed on, his book published and Ivor was able to film those fabulous interviews before he passed away.
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.
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?
great article that is, thank you for positing - really well written - such a shame that this type of information cannot seem to penetrate into mainstream mediaFollowing 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/
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/
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/
"first-phase insulin response" is a VERY rapid increase in insulin level when a little glucose to injected. This stops if the bete cells are finding it impossible to control BG. The "first-phase insulin response" is close to normal in most people with pre-diabetes, but nearly none existent in most people with full Type2.
Insulin resistance results in a very high "background" insulin level that does not change much in response to food etc (assuming high carb diet).
They also tracked the great reduction of Insulin Resistance due to losing liver fat in the first few weeks of the diet, but that was not "new science" therefore gets very little space in their research papers. They were the first research group to prove that "first-phase insulin response" could be returned to normal in someone with Type2 other than by surgery.
"first-phase insulin response" is a VERY rapid increase in insulin level when a little glucose to injected. This stops if the bete cells are finding it impossible to control BG. The "first-phase insulin response" is close to normal in most people with pre-diabetes, but nearly none existent in most people with full Type2.
Insulin resistance results in a very high "background" insulin level that does not change much in response to food etc (assuming high carb diet).
They also tracked the great reduction of Insulin Resistance due to losing liver fat in the first few weeks of the diet, but that was not "new science" therefore gets very little space in their research papers. They were the first research group to prove that "first-phase insulin response" could be returned to normal in someone with Type2 other than by surgery.
By looking at the RATE of increase of insulin, they can separate the effects of the beta-cells "waking up" from the effects of losing liver fat.
Its a test I would like to see done on some people who have "reversed" their Type2 with very low carb, as it would confirm if the beta cells recover with very low carb, or if, very low carb is just a great way to live with broken beta cells.
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
View attachment 24859
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.
I guess at the moment I am an example of a large person who uses low carb to get a healthy hba1c whilst maintaining .Me too. I'd also be fascinated to compare the test results between someone who has used low carbs to get a healthy HbA1c while maintaining weight, and someone who has used low carbs to get a healthy HbA1c while losing weight. I think it's an important distinction and the most impressive result would be a large person who packs themselves full of calories on low carbs just to maintain weight but nevertheless gets greatly improved results in tests for insulin resistance and glucose tolerance.
That said, I totally respect people who have adopted a low-carb diet, enjoy it, see their HbA1c's get down to safe levels, don't get dangerous spikes from their food, and who have no interest whatsoever in knowing about the potential of their metabolism to deal with carbs. It's more a curiosity thing for me, plus I'd like to have an idea about what foods I could safely eat because I do like a variety and I do very much like foods with carbs.
I guess at the moment I am an example of a large person who uses low carb to get a healthy hba1c whilst maintaining .
I decided my goal was to focus on the insulin rather than the weight because I wanted to see if I could maintain my weight whist controlling hba1c but effectively eat more foods as opposed to being ' on a diet" . For me personally I have found that I can with classic LCHF 60% fat 20% protein 15% carbs 5% whiskey lol
I have maintained for a year now during which time hba1c went from 44 to 36.
I guess at the moment I am an example of a large person who uses low carb to get a healthy hba1c whilst maintaining .
I decided my goal was to focus on the insulin rather than the weight because I wanted to see if I could maintain my weight whist controlling hba1c but effectively eat more foods as opposed to being ' on a diet"
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