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 a doubt, shown that carbohydrates are not necessary if one can get the insulin dose correct. I have confirmed 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! 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. The run was a long natter about all things low carb and was the best meeting in the best location of small 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 hours 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. Despite 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 mine is 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, 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 genuinely interested if you have the condition. All clinicians are genuinely 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. The change will come from the ground up, not top-down. And this run was done to raise funding for the Public Health Collaboration who is 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 wakes those people up. Some people think it is severe then.
Actually, adding insulin in Type 2 is 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. Thus, insulin resistance is a metabolic state caused by a diet and started possibly with a genetic vulnerability. In Type 2, insulin resistance is caused when the body produces its own insulin. In Type 1, it is caused by injected insulin over and above what is an essential replacement that Type 1 will always need. Insulin resistance, if sustained, will eventually cause actual 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 around insulin resistance. Timing of injections, stubborn, slightly highs, slow to come down glucose. It 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 that 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 uncontrolled fat burning because insulin reduces glucose levels partly by stimulating the cells to take in the glucose and partly by making fat from excess carbohydrates. With 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 create uncontrolled fat burning, I would know that I had injected too little insulin. It is extreme diabetes experimentation in one way. But, in the bad old days when I was getting my carb-counting wrong, this was undoubtedly going on all the time but not bad enough to qualify for a hospital bed. Plus, I was never offered ketone testing, so I never knew whether I had early ketoacidosis or not. I am responsibly testing my limits. No access to a ketone meter is, in my view, irresponsible management practice.
On the morning of the event, I woke with glucose of 6mmol/l. It had been steady at 4mmol/l through the night. I would usually 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 my 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 I 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 happened was that the glucose rose at about half the rate compared to eating glucose tablets, so it was probably representing internal glucose production, gluconeogenesis, not entirely controlled by 6 units. I had the luxury of continuous monitoring, so I was in total control.) CGM really should be available to all Type 1’s.
At a glucose level of 14mmol/l, I baled out and injected 4 units of rapid-acting insulin halfway 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 excellent 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. Since going keto, my action tie of rapid-acting insulin has reduced from 3 hours to currently 40 mins. I think that is also is a good measure of improvement of insulin resistance. If I remain on the ketogenic diet, I am hoping eventually to get back to actual Type 1 and get rid of the insulin resistance forever.