This is a monthly update on my glycemic management of type 1 diabetes (T1DM) using Humalog and Lantus insulin injections with resistance exercise and a low carb ketogenic diet as described in my book, The Ketogenic Diet for Type 1 Diabetes also available on Amazon in print. My other book, Conquer Type 2 Diabetes with a Ketogenic Diet, is also available on Amazon in print. See below.
Although glycemic management in T1DM will always be challenging, the low carb ketogenic whole-food diet definitely improves it by reducing average blood glucose (BG) and variations in BG as well as insulin requirements. Those with T1DM who also have insulin resistance, called double diabetes, can reverse their insulin resistance with a low carb ketogenic diet, exercise, and other lifestyle changes. The low carbohydrate ketogenic whole-food diet directly improves both insulin resistance and endogenous hyperinsulinemia in T2DM and exogenous insulin requirements in T1DM (i.e. reduced insulin doses).
June 2018 was the fourth full month of taking metformin at a dose of 2000 mg/day (started that dose on Feb. 15, 2018). I am tolerating it without any side effects. As you may know metformin is the first-line medication for T2DM, but can also be useful for those with T1DM who also have insulin resistance. Although I do not have any signs of insulin resistance (excess body fat, increased waist circumference, hypertriglyceridemia, low HDL-C, high blood pressure), I was interested to see if my insulin requirements could be further reduced by taking metformin. Metformin acts on the liver to reduce glucose production by suppressing both gluconeogenesis and glycogenolysis. I think this may be useful for those with T1DM on a low carbohydrate diet because the reduction in dietary carbohydrate reduces insulin requirements which in turn stimulates glucagon secretion by the alpha cells in the pancreas which in turn increases glucose production by the liver. This increase in glucose production occurs primarily from increased gluconeogenesis, but also some increase in glycogenolysis is suggested in some studies. In addition, metformin stimulates muscle uptake of glucose independent of insulin. Hopefully over time, I will be able to determine if taking metformin either reduces my insulin requirements. So far, it is not clear that it is doing much due to the baseline variation in insulin doses over time that I have experienced over the years. I am estimating that I will need to take it for at least 6 months to be able to make a before and after comparison as far as the insulin dose comparison is concerned. There is a possibility that metformin could increase the incidence and severity of hypoglycemia while on a ketogenic diet, so caution should be exercised. A possible mechanism for this is the fact that gluconeogenesis plays a more important role in maintaining BG in those on a ketogenic diet than on a balanced macronutrient diet. If metformin reduces gluconeogenesis, then hypoglycemia could result if insulin doses are not appropriately reduced.
My June glycemic results were significantly improved compared to previous time periods and I did reach my desired BG goal of >70% time spent with a BG value between 61 and 110 mg/dl. I had less hypoglycemia this month with no symptoms of hypoglycemia. Below are my mean BG values, mean insulin doses, and BG frequency distribution for June 2018 compared to previous time periods. The predicted HbA1c uses the formula: AUC mean BG plus 88.55 divided by 33.298. This formula is the least squares fit using my own personal mean BG versus measured HbA1c over many years. My particular HbA1c values are higher than many other individuals with the same mean BG. This is referred to as being a “high glycator.”
As discussed previously, exogenous insulin cannot mimic normal insulin secretion, so persons with T1DM should not expect to have truly normal BG values at all times. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms or less common, yet more dangerous, consequences including brain damage, seizure, injury, coma, or death. I have set my target BG range at 61-110 mg/dl because values in this range are not likely to lead to harm or complications of T1DM. Your target BG range should be determined with your physician because one size does not fit all. Normal BG is 96 ± 12 mg/dl (mean ± standard deviation (SD)) and coefficient of variation is 13% which is the weighted mean from two studies of continuous glucose monitoring in healthy subjects (see references at the end). The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. Clinical outcomes in T1DM (i.e. microvascular and macrovascular complications) have only been documented to correlate with measures of mean BG, particularly HbA1c. This does not mean that BG variability is not important, but it just has not been documented to correlate with outcomes and complications of T1DM. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy (injected or pumped). Monitoring the standard deviation and/or coefficient of variation and finding ways to improve them to the best of one’s ability is desirable in my opinion. Following a low carb whole-food ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. A ketogenic diet may also provide an alternate or additional brain fuel in the form of ketones to protect the brain when BG does go low. The alternative energy that ketones supply to the brain may prevent or blunt the sympathoadrenal response to hypoglycemia which in turn reduces or eliminates the symptoms of and harm from hypoglycemia. This hypothesis needs to be tested before it can be stated as fact. Having mild asymptomatic hypoglycemia adapts the brain to lower BG and reduces the symptoms of mild hypoglycemia and potentially the harm from hypoglycemia due to lack of activation of the sympathetic nervous system by reducing sympathoadrenal-induced fatal cardiac arrhythmia (see references at the end).
Below are my BG readings along with the Humalog (rapid-acting insulin) doses in June 2018. I adjust the breakfast (blue circles), post-workout lunch (black circles), and dinner (purple circles) meal-time doses based on the pre-meal BG reading and take extra correction Humalog doses (red circles) for high BG readings as needed. I continued my previous pattern of higher BG readings after weightlifting which I correct with my lunch-time Humalog dose.
The table below shows the BG variability results for current and previous time periods. The percentiles (10th, 25th, 75th, 90th) on the right show the spread of the BG readings about the median. The interquartile range, the difference between the 75th and 25th percentiles, is a measure of BG variability. In the middle of the table are the %Time in three BG ranges: %Time BG < 61 mg/dl (hypo) and the mean BG during that time, then %Time BG 61-110 mg/dl (target) and the mean BG during that time, and %Time BG > 110 mg/dl (hyper) and the mean BG during that time. Both the %Time with hypoglycemia and hyperglycemia are probably overestimates because they do not account for the corrections with glucose tablets for hypoglycemia or rapid-acting insulin (Humalog) for hyperglycemia. Measuring my BG more frequently than 5 times per day or using an accurate CGM would result in a more accurate estimate.
The total basal (Lantus), meal-time rapid-acting (Humalog), and total insulin doses along with the BG readings and are shown in the graphs below for June 2018. You can see I had to gradually increase the basal insulin (Lantus) dose during June to control my fasting BG. This may have been a result of a reduction in the intensity of my weightlifting in June due to some muscle and joint niggles although that is simply a guess.
The daily insulin dose totals for 2018 are shown in the graph below. You can see a reduction in insulin doses since the peak at the beginning of January 2018. The measures I have taken to reduce this variation in insulin dose have included keeping meals and exercise as constant as possible and adding metformin to suppress liver glucose production. Specifically, I try to keep all meals constant in terms of portion size, macronutrient composition and timing of my meals. In addition, I try to keep exercise constant including frequency (daily), type (the type of weightlifting exercises, mainly compound movements), intensity (gradually increasing weight over time as tolerated), and volume (repetitions). That said, keeping exercise intensity constant from day to day is quite difficult.
The graph below illustrates the distribution of BG values in the ranges indicated at various times of day. This could be useful to point out problems (hypoglycemia and/or hyperglycemia) at different times of day.
The graph below illustrates the percentage of time spent in three BG ranges for each day of the month of June. The numeric percentage is shown on top of the green bars for the % of time BG was between 61 and 110 mg/dl.
The graph below is new and simply shows the change in BG that occurs after weightlifting during the month. I think the variability in the BG response to exercise from day to day is quite remarkable. That said, some of the variation is related to the fact that my basal (Lantus) insulin dose was changing (increasing) during the month. The current basal insulin dose influences BG between meals.
In July, I will continue olympic weightlifting every day with 2 exercises per day. I will also continue metformin 2000 mg daily (1000 mg every twelve hours).
My goal of glycemic management in T1DM with a ketogenic diet is to keep BG as close to normal i.e. 96 ± 12 mg/dl (mean ± SD) as is safely possible (i.e. avoiding hypoglycemia) to avoid diabetic complications, a reduction in lifespan, and unpleasant symptoms of as well as injury and death from hypoglycemia. For me, a well-formulated whole-food nutrient-dense ketogenic diet, daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. My basic diet philosophy is to avoid processed foods especially those containing refined carbohydrates, sugar, and vegetable (seed) oils while enjoying whole foods (with just one ingredient) as close to their original state as possible. I think just knowing the guidelines in this paragraph would be a good start for those wanting to improve their diet. To treat diabetes, the additional step is to eliminate all foods with significant amounts of carbohydrate to keep the net carbohydrate total < 50 grams/day. Some may do better with < 30 grams/day, while others who exercise a lot may do well with < 100 grams/day. Each person needs to determine their own level of carbohydrate tolerance to optimize their BG.
What I Cook & Eat
What I Drink
Water (filtered by reverse osmosis), Unsweetened Tea & Coffee
What I Don’t Eat
What I Don’t Drink
My exercise regimen often results in post-exercise hyperglycemia which is a normal response to intense exercise. However due to having T1DM, my body is unable to correct this without taking exogenous rapid-acting insulin (Humalog). The exercise I choose negatively affects my glycemic control to some extent. I’m sure I could find an exercise that has less impact on glycemia, but I enjoy weightlifting and feel it has health-span and life-span extending benefits which may compensate for the temporary increase in BG during/after exercise. Hopefully my BG values and variability as well as the relatively lower insulin doses that result from my ketogenic diet, exercise, and possibly metformin (yet to be determined) are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia.
Both books are available as a PDF ebook and as a print book from Amazon. Note: Clicking on the links above will take you to the website of Ellen Davis, MS, my coauthor. Her website is ketogenic-diet-resource.com.
If you would like to consult with me about managing your diabetes or other metabolic conditions discussed on this website, you may send me an email to discuss your needs, receive a patient history form to complete, and schedule a Skype meeting. After we have scheduled a meeting, you can use the payment button below. There is an email form on the Contact page.
If you like the information provided and have benefited from it, please support my efforts by purchasing a book or making a voluntary donation below.