Half-Marathon 7. Deliberately running into ketoacidosis
Everything has been going so well so far that one run seems to blend into another with ease. Training is fun. Glucose control is good, injuries are non-existent and times are improving. I am feeling good. I have without doubt shown that carbohydrates are not necessary if one can get the insulin dose correct. I have shown that fat burning allows fasting to be done safely. It makes exercising so much more fun as planning is a doddle. I am on a roll down Easy Street! In fact I did this 7 th run in cruise control.
I got away with minimal training and ran with my friend, Joanne. She is a fellow low-carber and a tireless campaigner for the cause. She does not have diabetes but as a clinician she was interested in ketogenic diets in Type 1. In fact the run was a long natter about all things low carb and was the best meeting in the best location of low hills and coast. What a great day at the office! All days should be like this.
The Plan for the Run.
I was on another 13 hour fast, I find it the easiest way to prepare. But there was a variation in the preparation this time. You see, I have become pretty much obsessed with insulin resistance. I have been looking it up and it is not just my unique view. There was a study on fit young people who did not have diabetes but were given intravenous infusions of insulin. [*] The glucose levels were controlled with intravenous doses of glucose as needed. The result was that there was evidence of insulin resistance after just 40 hours compared to controls. 40 hours! I have been over-injecting insulin for nearly 22 years in an attempt to balance the carbs, which I now know I didn’t need to do. That adds up to 191,555 hours of possibly avoidable insulin resistance. In spite of that I have been lucky so far. Insulin has prolonged my life and quality of life beyond all measure compared to a century ago. If I were around then, I would barely have lasted a year, with recurrent episodes of ketoacidosis that would eventually cause my demise. But, as they say. If I knew 21 years ago what I know now I would have done differently. I didn’t. I did what I was told, and did to others what I was taught. I believed in carb counting, DAFNE, statins. I swallowed it all, hook, line and sinker. Once you ‘get it’ of course, it is a lightbulb moment and you wonder how it was possible to see things any other way. But that remains a minority view. I am eternally grateful to have googled into Richard Bernstein. He changed my life, possibly saved me from future problems. We will have to see. Of course, the diabetes is still there. That’s going nowhere. And I feel lucky to have found fellow clinicians who also ‘get’ low carbing and are sharing knowledge in the hope that one day we can do better for all people with diabetes. But, I still reckon that there are plenty of clinicians who think I am completely bonkers. They will listen politely, then say something like, ‘Well, good for you if it works,for you. I do see genuine enthusiasm sometimes, but I guess you are only truly interested if you have the condition. All clinicians are truly interested in something. That keeps us going.
For us that have Type 1, it is more of a desperate search to survive. We have to be interested. And we need quality information. Thank God for the internet. Change will come from the ground up, not top down. And this run was done to raise funding for the Public Health Collaboration who are campaigning to make that change happen https://phcuk.org/.
To find that I have 0.2 million hours of insulin resistance is not only a nerdy fact, it is chilling!
Type 1 managed by keto is pretty straight forward. I instinctively think that there is more to learn about therapy, but keto is good for now. It frees me up, makes me feel good and, most significantly I now feel in control of my diabetes. But where Type 1 seems straight forward, what about Type 2? No one wants Type 2! There is a view out there that somehow taking tablets over insulin makes it less of a condition. Threatening to add insulin (why, in 99% of cases I don’t know, but go with it) in people with Type 2 really wakes those people up. Some people think it is really serious then. Actually adding insulin in type 2 is really serious, but for a different reason. But we are Type 1’s. I don’t want to indulge myself by ranting. The metabolic mayhem caused by insulin resistance is such a profound change in the body because it affects so much. The complex inter-dependent hormonal and chemical reactions are altered by insulin resistance. So, insulin resistance is a metabolic state caused by diet that started possibly with genetic vulnerability. In type 2 insulin resistance is caused when the body produces it’s own insulin. In Type 1 it is caused by injected insulin over and above what is essential replacement that Type 1 will always need. Insulin resistance, if sustained, will eventually cause true disease. Once the blood vessels start popping and the nerves get damaged, things get very tricky indeed. I have finally controlled my glucose levels well and am approaching the optimal doses of insulin that I will need for life. But I know that things could be even better if I could get round insulin resistance. Timing of injections, stubborn slightly highs, slow to come down glucoses. This is all insulin resistance, I’m sure.
So for this run I would start the process of estimating insulin resistance. The plan for this run was to reduce my insulin injection to a level which would not be able to cope with my internal glucose production (gluconeogenesis). Then the blood glucose would rise relentlessly and not peak because there would be insufficient insulin to do this. That would stimulate unregulated fat burning because insulin reduces glucose levels partly by stimulating the cells to take in glucose and partly by making fat from excess carbohydrate. The opposite happens if there is insufficient insulin. Glucose cannot enter cells so stays in the blood, and glucose levels rise. The body then has to burn fat for energy. Unregulated fat burning because of insufficient insulin will generate more ketones eventually into the ketoacidosis zone. Regulated fat burning with sufficient insulin would never cause ketoacidosis, just nutritional ketosis. So, if I could get into unregulated fat burning I would know that I had injected too little insulin. Extreme diabetes in one way. But, in the bad old days when I was getting my carb-counting wrong, this was undoubtably going on all the time but not bad enough to qualify for a hospital bed. Plus I was never offered ketone testing so never knew whether I had early ketoacidosis or not.
On the morning of the run I woke with a good glucose of 6mmol/l which had been steady at 4mmol/l through the night. I would normally go for 10 units of long-acting insulin here, and possibly one unit of rapid-acting insulin, maybe two if the insulin after one hour of being awake showed signs of climbing. But this morning glucose was stable. 10 units of long -acting insulin is the current figure for combined Type 1 and 2 and this keeps glucose levels stable. But I want to try to estimate how much of this dose is for Type 1. And how much for Type 2. This is practical diabetes, Lemming-style. I’m going for 6 units. But I wanted to do this safely so took the rapid-acting insulin with me on the half-marathon. Just in case. For me the rapid-acting insulin is now working at around 40 minutes compared to 3 hours before I decided to go keto. So I hope that this represents less insulin resistance now. What actually happened was that the glucose rose at about half the rate compared to eating glucose tablets so was probably representing internal glucose production, gluconeogenesis, not quite controlled by 6 units. I had the luxury of continuous monitoring so total control.) CGM really should be available to all Type 1’s. Sign the petition https://petition.parliament.uk/petitions/151064 ).
At a glucose level of 14mmol/l, I baled out and injected 4 units of rapid-acting insulin half way through. At 2.2mmol/l reduction per unit of insulin which I know is the particular rate for me, that should get to around 6mmol/lit. It did after 3 hours. So with 10 units of long-acting insulin giving good control and sometimes slight hypo, and 6 units showing a tendency to ketoacidosis, I reckon that 7-9 units twice a day represents Type 1 and the rest is due to acquired insulin resistance. Less than I thought but I am pleased. The less resistance the better. I now have a target. But after all that experimentation, I reckon that sensitivity to insulin action is just as good in practically. Getting from 3 hours for rapid-acting to act to currently 40 mins is a good enough measure of resistance. If I keep on the ketogenic diet, I am hoping eventually to get back to true Type 1 and get rid of the insulin resistance for ever.