In the previous post, I described the unleashing of diabetic complications that resulted from starting insulin therapy for my type 1 diabetes (T1D). Fortunately, all but one of the complications slowly resolved after 2.5 years of insulin therapy: a big relief. Of course, I had to continue dealing with the daily management of blood glucose (BG) and hypoglycemic episodes (low blood glucose). These episodes occurred around 2-5 times/week. Learning new strategies to minimize them had always been one of my top priorities. One of my earliest strategies to minimize hypoglycemia was carbohydrate counting.
Carbohydrate Counting, Not Very Effective
I learned about carb counting from the American Diabetes Association (ADA) website. They also stated that by counting carbohydrates, I could exchange some sweets for other carb containing foods and still keep my BGs on track. This was good news to me has I had always had a sweet tooth and this seemed like a way to “have my cake and eat it too,” literally! So for the next two years, I measured, weighed, and calculated the grams of carbohydrate in each meal, and then used that to determine how much mealtime insulin to inject. In retrospect, it don’t understand why I continued doing it for two years because it never actually worked. I guess I figured if the ADA thought it was a good idea, I should also.
So why did carb counting not work for me. Well, there are several reasons none of which are unique to me. First, estimation of the carbohydrate content of foods is quite error prone. It has been estimated to have a 50% error rate (Waldron S: Controversies in the dietary management of diabetes in childhood and adolescence. Br J Hosp Med 1996, 56(8):450–454.). So, for example, if you measure your dinner carb intake as 120 grams, it could actually result in the absorption of anywhere from 60 to 180 grams of carbohydrate (which is ultimately broken down to glucose). If one then calculates their insulin dose based on 120 grams of carbs, that dose could be just right, way too much, or a lot less than actually needed. Thus, the post-meal BG could be just right, very low, or very high. But the important point is that it is unpredictable. So the more carbohydrate that is eaten, the larger the variability in BG. And that’s just one of the sources of error.
Variability of Insulin Absorption & Action
Insulin absorption from the injection site is another. Regular insulin used for meals has a 30% variation in the amount of insulin absorbed into the bloodstream from one injection to the next. For insulin analogs, the variation is somewhat better at 10-20% (study here). So this variation is multiplied by the error in the carbohydrate content of the meal. This variability of insulin absorption occurs at all levels of carbohydrate intake, but the degree of variability is dependent on how much carbohydrate is in the meal. Thus, a high carbohydrate intake requires a larger mealtime insulin dose and therefore more variability in insulin absorption and effect, and more variability in BG.
Insulin Analogs, Improved Pharmacokinetics
Understand that I was unaware of these factors until after 2012. My next strategy to improve management of BG was to try different insulin preparations. So I replaced NPH with Ultralente as my basal insulin. I won’t spend much time describing what happened because Ultralente was taken off the market (due to lack of sales). Suffice it to say it was an improvement over NPH. In my case, I took NPH twice daily (morning and dinnertime or bedtime) and since it had a peak of activity, it frequently caused hypoglycemia either in the afternoon (due to the morning dose) or during the night while sleeping (due to the evening or bedtime dose). Ultralente had a more subtile peak and reduced the occurrence of hypoglycemia.
I also replaced regular human insulin with lispro (Humalog) insulin at mealtimes. Although, exogenously injected insulin will never mimic endogenously produced insulin by the pancreatic beta cells, Humalog was a great improvement over regular human insulin in my case. Humalog has a faster onset of action, is more potent (thus requiring a smaller dose), and a shorter duration of action compared to regular insulin. The timing of Humalog’s action more closely mimics the timing of the absorption of the nutrients that require insulin (mainly carbohydrates and protein).
In 2005, an endocrinologist suggested changing my Ultralente to glargine insulin (Lantus) as my basal insulin. Again, this resulted in further improvement in my BG control with nighttime hypoglycemic episodes becoming less common. I continue to use Lantus to this day (although I did try detemir insulin (Levimer), more on that in a future post).
These changes in insulin preparations improved my BG control, although I do not have actual BG and insulin data to show you from prior to 2007. The oldest data I have is from April 2007 shown below to compare to March 2010 and July 2011. What happened in 2007? Exercise.
Exercise Improves Sensitivity to Insulin
In July 2007, I took up the sport of triathlon. I thought despite my best efforts to control my BG, that adding regular exercise to my regimen might lower my risk of heart disease. Besides, I had always enjoyed cycling and running, and was interested in learning to swim. I don’t mean I couldn’t swim, but I had never learned an efficient stroke or attempted to swim any long distance before. I quickly learned that exercise has a significant effect on BG. Apparently, my muscles were using glucose and with insulin already injected, there was no way to turn off the absorption of insulin from the injection site. In persons without diabetes, that is exactly what the pancreas does, it decreases or stops insulin production/secretion during exercise to maintain a normal BG. Therefore, I quickly learned to consume sports gels (which are essentially just sugar) in various amounts and measure my BG with a glucose meter during exercise. Well, exercise has another effect that can cause elevated BG. Other hormones including cortisol, epinephrine, growth hormone, and glucagon can be released during exercise which increases BG. Of course, insulin can override these hormones and result in hypoglycemia at any time. So my efforts to minimize hypoglycemia during exercise by taking sugar combined with the hormones that raise BG, resulted in more hyperglycemia that ever before.
Finally, exercise improves ones sensitivity to insulin (a good thing) so that insulin doses can be lowered. So in summary, exercise improved my strength, endurance, fitness, sense of well-being, and reduced my insulin doses, but also resulted in more hyperglycemia, and some overuse injuries as well (more on that in a future post). The chart below summarizes the effect of exercise on BG control and insulin doses.
By May of 2011, I had decided I wanted to complete an ironman distance triathlon which consists of a 2.4 mile swim, 112 mile bike ride, and a 26.2 mile marathon all in one day. I thought if I could do it, it would demonstrate to myself at least that I could accomplish a physical feat that most people could not, or would not want to, despite having T1D. But I realized that my BG control had deteriorated since starting triathlon and was still fearful of developing hypoglycemia during the event and while training for it. At that same time, I had come across the world of podcasts and was listening to podcasts on IM Talk during bike rides on an indoor trainer. The podcast that turned on a lightbulb in my brain was an interview with Loren Cordain, PhD. He had spent many years researching and writing about the Paleo Diet. During the podcast, he explained that what you eat has a big influence on your health and development of numerous chronic diseases. Believe it or not, that concept is really not taught in medical school in the US, or at least it wasn’t in the early 1980’s when I attended Emory University School of Medicine. So, now very curious to learn more about this, I read his book, “The Paleo Diet.” In the next blog post, I’ll talk about what happened after starting the Paleo Diet.