#27 July 2016 Update on My T1D Management

In July 2016, my glycemic control was similar to prior months with a slightly higher mean blood glucose (BG), but with less hypoglycemia and hyperglycemia. With no travel this month, I was back to my usual exercise routine and low carb ketogenic eating plan.

The summary table of current and previous mean BG and insulin doses is shown below. Compared to June 2016, my exercise time increased to an average of 10 hrs/week. The mean BG increased from 97 to 101 mg/dl, but my mean total daily insulin dose decreased from 28.5 IU/day to 28.1 IU/day due to a decrease in basal insulin (from a mean of 23.0 to 21.2 IU/day Lantus) and an increase in rapid-acting insulin (from a mean of 5.5 to 6.9 IU/day Humalog). I had 5 of 129 (4%) BG readings < 51 mg/dl, but all were without symptoms due to either nutritional ketosis or hypoglycemia unawareness (see blog post #12 for more details). I had 92 of 129 (71%) BG readings between 51 and 120 mg/dl, 29 of 129 (23%) between 121 and 200 mg/dl, and 3 of 129 (2%) > 200 mg/dl.

Post 27 Means Table

Below are my BG readings along with exercise type and time so you can see how the type and duration of exercise and rest days affect my glycemic control.

Post 27 Blood Glucose and Exercise

The table below shows the summary of current and previous BG variability results. All of the results were improved compared to previous months and years with improvement in the following variability measures: standard deviation = 38, coefficient of variation = 37%, mean BG Δ per hour = 9, mean daily BG range = 66, mean time of hyperglycemia = 5.1 hr/day, mean time of hypoglycemia = 0.4 hr/day, interquartile range BG = 46. The measures of BG variability were defined and explained in blog post #10.

Post 27 Variability Table

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below.

Post 27 Insulin Doses

The Ketonix breath ketone (acetone) monitor results beginning June 2015 are shown below (see blog post #19 for more details). I have been in continuous nutritional ketosis due to my low carbohydrate ketogenic diet.

Post 27 Ketonix Breath Ketones

The graphs below show the change in BG that results from mealtime rapid-acting insulin. On the x-axis is the Breakfast and Dinner mealtime insulin dose (Humalog) plotted against the change in BG, i.e. Post meal BG minus Pre meal BG on the y-axis. Thus positive values represent an increase in BG and negative values represent a decrease in BG after the meal. Also, note that I removed 5 of 31 Breakfast points and 10 of 31 Dinner points from the graphs where the Post meal BG was not in the range of 51-120 mg/dl. The rationale for this is to eliminate graphing mealtime doses that were “incorrect” so to speak. This way the graph shows both that larger doses of insulin reduce BG more (obvious), but more importantly even when the resulting Post BG was in an acceptable range, that there is a wide variation in the amount of BG reduction for any given dose of insulin. This variation can be due to varying absorption of injected insulin, variation in insulin sensitivity from exercise, or variation in food consumed during the meal. Reducing this variation is an important goal of mine.

Post 27 Breakfast Dinner BG changes

The graph below shows the change in BG due to weightlifting. On the y-axis, positive values represent an increase in BG due to weightlifting. There were five negative values representing a reduction in BG and ten positive values representing an increase in BG due to weightlifting. The main feature is than this exercise results in both increases and decreases in BG which cannot be predicted in advance.

Post 27 BG change due to weightlifting

I required quite a few doses of rapid-acting insulin (Humalog) to correct hyperglycemia this month. The resulting change in BG is shown in the graph below. Negative values represent a decrease in BG. Note that I removed 7 of 20 correction doses from the graphs where the Post meal BG was not in the range of 51-120 mg/dl. The rationale for this is to eliminate graphing correction doses that were “incorrect” so to speak. Again, the main feature is variability and unpredictability of the BG response to insulin injections.

Post 27 Humalog Correction Doses

In August, I will continue weightlifting and aerobic exercise, but on alternate days. This will result in a decrease in weightlifting to 3.5 – 4 days/week and in increase in aerobic exercise to 2 – 2.5 days/week and one rest day. The olympic weightlifting now consists of only 4 exercises (snatch, clean and jerk, snatch overhead squat, front squat) which take 1.5 – 2 hours to complete including warmup, cool down, and stretching to maintain mobility. The aerobic exercise consists of swimming or cycling at low intensity for 0.5 – 2 hours. The goal is to exercise consistently to maintain insulin sensitivity while avoiding injury and overtraining.

The goal of glycemic management in type 1 diabetes is to keep BG as close to normal (83 mg/dl) as is safely possible (i.e. avoiding hypoglycemia) to avoid both diabetic complications and a reduction in lifespan. Glycemic management in type 1 diabetes is analogous to walking down a narrow path with sloping cliffs on either side. One cliff is hypoglycemia with its potential symptoms and fatal outcomes and the other cliff is hyperglycemia with its potential for longterm diabetic complications and reduced lifespan. Frequently a gust of wind blows across this path pushing one onto one or the other cliff. Why that gust comes is not always clear, but consistency in food, exercise, and frequency of BG monitoring minimizes them and keeps one on the narrow path to health.

For me, a nutrient-dense whole food low carbohydrate ketogenic diet (see blog post #9 for more details) combined with insulin analogs (Humalog/Lantus) have been the best tools so far in accomplishing this goal. I also feel, but cannot prove, that this eating plan and the resulting nutritional ketosis reduces the symptoms of hypoglycemia and protects the brain from the consequences of mild degrees of hypoglycemia (see blog post #12 for more details). Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult, but I both enjoy it and feel exercise has other health and lifespan extending benefits. Hopefully, my BG values are close enough to normal to avoid both a reduction in lifespan and diabetic complications. Only time will tell.

Till next time ….



    • Keith Runyan, MD

      I haven’t measured BHB at the same time as breath acetone. My recollection is that they do not correlate according to Michel Lundell. He thinks they are measuring different things, literally and functionally. I also have not graphed acetone reading with blood glucose readings. Since I have type 1 diabetes, my glucose regulation is not normal. My liver does not get nearly as much insulin as normal since I inject it subcutaneously compared to a pancreas that secretes insulin directly to the liver through the portal vein. My liver also receives an abnormal amount of glucagon via the same route. Therefore, I doubt ketone production by the the liver is comparable to normal either. The idea that glucose production is lower when ketone production is higher makes sense when you look at the Krebs cycle. Ketones are produced when oxaloacetate levels are low as a result of gluconeogenesis and acetyl-CoA levels rise. Acetyl-CoA is the substrate for ketogenesis. In other words, ketone production coincides with gluconeogenesis. I’m not sure, but I suspect that when adequate ketones are being made, less glucose is needed, thus lower levels of blood glucose is the result. Dr. Dominic D’Agostino has said that when he gives mice/rats exogenous ketones or MCTs, the blood glucose falls as well presumably due to less need for glucose.
      As for me, I noticed no correlation between blood BHB levels and lack of symptoms of hypoglycemia which was why I was measuring ketones in the first place. Admittedly it wasn’t a proper experiment to test the idea, but given the cost of BHB strips and doing well regarding blood glucose control and lack of symptoms of hypoglycemia, I saw no reason to keep testing BHB in the blood. For more information see my blog posts #6, #11, and #12. If I that doesn’t answer your question, ask again. Cheers.

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      • Robert Simms

        Thank you for the ‘heads up’ that yours is a more tightly managed situation. I was thinking of comparing acetone to glucose, using glucose as a proxy for BHB, since glucose and BHB should be roughly complementary.
        I’m curious about the idea that artificially raising ketones may bypass some benefits, like possibly normalization of gluconeogenesis. Alison Gannett said in her talk at Low Carb Vail (at 5:30) that she found coconut oil suppressed her acetone measure. (That at least would interfere with using breath acetone as a proxy for glucose monitoring.) And in a recent interview with Brian Williamson, Michel Lundell suggested that 1/ acetone corresponds directly with ‘being in ketosis’ and 2/ that acetone and blood BHB are related with a time delay dependent with the magnitude of acetone in the breath. (Ketovangelist episode 66, question at 13:10, answer at 14:35 “Ketosis is the level of acetone in your breath. BHB is a product of ketosis and time.”)