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.
).
