May 2017 was my first personal experience with taking the medication metformin. I developed two common side effects: diarrhea and fatigue. I did not follow my own advice of slowly increasing the dose over time which is likely responsible for these side effects. After quickly increasing the dose to 1000 mg twice daily and developing these side effects, I stopped it for a few days and restarted at 500 mg once daily at dinnertime. So far, so good. I will increase more slowly from this point forward. I think it is too early to understand whether or not it has a beneficial effect, so I did not attempt to make that assessment.

Glycemic Management Results for June 2017 

June 2017 glycemic results were noteworthy for more hyperglycemia requiring increasing insulin doses during the month. Fortunately, I had quite a bit less hypoglycemia with no symptomatic hypoglycemia. Hypoglycemia in a person with T1DM who is conscientiously trying to control blood glucose (BG) is a real danger that should be minimized by slightly underestimating the insulin dose (e.g. by 0.5 IU) to be administered (in my opinion). Additional insulin correction doses can always be given later to correct hyperglycemia.

Below are my mean blood glucose (BG) values, mean insulin doses, and BG frequency distribution for June 2017 compared to previous time periods. I have changed two columns to indicate the AUC mean BG and predicted HbA1c. AUC mean BG is the mean BG by calculating the area under the curve (AUC) of BG versus time. 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 most other individuals with the same mean BG. This is referred to as being a “high glycator.”

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with T1DM should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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 these two studies (here and here) of continuous glucose monitoring in healthy subjects. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. However, be advised that clinical outcomes in type 1 diabetes (i.e. microvascular and macrovascular complications) have only been documented to correlate with measures of mean BG, particularly HbA1c. This does not mean 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). I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG variability and thus the standard deviation and coefficient of variation. I plan to get the FreeStyle Libre CGM as soon as it becomes available in the U.S. 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 carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. A ketogenic diet may also provide an alternate/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 BG close to normal most of the time (some of which are hypoglycemic) also minimizes the symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time for June 2017. You can see below that most of the hyperglycemia occurred after weightlifting (at 2 pm – black circles or at 6 pm – magenta circles). I have explained in prior blog posts that this may be related to stress hormones which are normally released during intense exercise that serve to increase both BG and fatty acid levels in the blood to provide exercising muscles with additional energy. Because those with type 1 diabetes (T1DM) cannot make insulin, BG can rise with intense exercise and will need to be corrected with exogenous insulin. I don’t like the fact that my BG increases so much with weightlifting. However, it beats the alternative of hypoglycemia and loss of performance during the workout. I have not used exogenous insulin prior to a workout in anticipation of hyperglycemia for fear of hypoglycemia. Hopefully, any adverse effects from these temporary rises in BG will be mitigated by the benefits of the exercise itself.

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. The other measures of BG variability were defined and explained in blog post #10.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. You can see that I had to increase my insulin doses progressively during the month from 27 IU/day to 45 IU/day. I have yet to understand why my doses vary so much over time other than the simple fact that exogenous insulin therapy does not mimic endogenous insulin secretion. Nor have I found a way to make the insulin doses more stable while still enjoying the exercise that I know contributes to glycemic variability. I had to take multiple extra rapid-acting insulin doses to correct hyperglycemia and I had to increase both basal and mealtime bolus insulin doses during the month.

I did not measure blood or breath ketones in June.

In July, I will continue olympic weightlifting every other day. I am taking a break from regular aerobic exercise and instead I am stretching and foam-rolling every other day as well as doing rotator cuff exercises to rehab my left shoulder which I injured in March 2017. The foam-rolling has been effective in resolving trigger points (along with two rounds of trigger point dry needling) in my IT bands which has resolved the IT band syndrome in my right knee.

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. My current version of ketogenic diet has changed slightly since I last wrote about it in detail in blog post #9.

My current diet looks like this.

What I Cook & Eat

•Beef, grass-fed, including meat (85% lean), heart, liver, and kidney (liverwurst)

•Fish, mainly wild Alaskan salmon

•Canadian bacon (uncured pork loin)

•Lamb occasionally

•Chicken & Turkey occasionally

•Chicken Eggs

•Non-starchy vegetables (about 5% carbohydrate content by weight) including Cabbage (Red, Green, Napa), Kale, Collard Greens, Spinach, Bell Peppers, Raw Carrots, Leeks, Onions, Brussels sprouts, Home-made Sauerkraut from Red Cabbage, Bok-Choy, Broccoli, Cauliflower, Yellow Squash, Zucchini, Cucumber, Lettuce (Iceberg & Romaine), and some others.

•Fruit – Avocado, Tomatoes, Olives, Strawberries, Blueberries, Blackberries, lemon juice on fish and salads

•Nuts & Seeds – Pepitas, Macadamia, Brazil, Pecan, Walnut, Pistachio, Cashew.

•Note: I developed an intolerance to milk prior to my diagnosis of T1D. I did try heavy whipping cream after starting my KLCHF diet, but am also intolerant of it. I do tolerate butter, but wanted to decrease my fat intake, so eliminated all dairy including cheese and yogurt.

What I Drink

Water (filtered by reverse osmosis), Unsweetened Tea & Coffee

What I Don’t Eat

•Grains – Wheat, Corn, Rice, Oats (there are many more) or anything made from them, which is too numerous to list here. Gluten is a protein present in a number of grains (all varieties of wheat including spelt, kamut, and triticale as well as barley and rye.) which can cause a number of medical problems for a significant portion of the population with gluten sensitivity or celiac disease. In my case, I avoid them due to their carbohydrate content.

•Starchy vegetables – potatoes, sweet potatoes, yams, most root vegetables (turnip root okay), peas

•Legumes – peas, beans, lentils, peanuts, soybeans

•High sugar fruits – includes most fruits except berries, see above.

•Sugar and the fifty other names used to disguise sugar.

•Vegetable Oils (really seed oils) – Canola, Corn, Soybean, Peanut, Sunflower, Safflower, Cottonseed, Grape seed, Margarine & Butter substitutes, Shortening.

•All Processed Food-like Substances i.e., most of what is in the grocery store.

•I avoid restaurants except when traveling, and then order fish or steak with plain steamed non-starchy vegetables (no gravy or sauces that typically contain sugar, cornstarch, or flour) or salad.

•Refined, but healthy, Fats – I have eliminated refined fats from my diet including butter, coconut & olive oils.

What I Don’t Drink

•Colas (both sweetened, artificially sweetened, and unsweetened).

•Fruit Juice except small amounts of lemon juice.

•Alcohol (can cause hyperglycemia or hypoglycemia in persons with diabetes).

•No artificial sweeteners, don’t need or like them.

A large part of my fat intake comes from nuts & seeds which hypothetically could result in potential adverse consequences from omega-6 polyunsaturated fats in the opinion of some low carb advocates. However, I have yet to see any studies that show harm from eating nuts & seeds. As a reference, the average fat breakdown of the seven nuts & seeds that I eat daily is 33% polyunsaturated, 52% monounsaturated, and 15% saturated fat. However, when my entire diet is analyzed, 26% of my fat intake is from polyunsaturates, 56% is from monounsaturates, and 18% is from saturated fats. When my diet is broken down by macronutrients, I consume 170 grams of fat (or 68% of my total daily calories), 70 grams of carbohydrate, 30 grams of which is dietary fiber (or 12% of my total daily calories), and 110 grams of protein (or 20% of my total daily calories). In calories, it totals to 2,250 kcal/day.

My exercise regimen and its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my lower insulin doses that result from my ketogenic diet and exercise are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

I would expect that the majority of those with diabetes, including type 1 diabetes (T1DM), have at least heard of the medication, metformin. It is primarily used to lower blood glucose (BG) in those with type 2 diabetes (T2DM), but does so by addressing insulin resistance, the primary defect in T2DM. However in recent years, it has been used “off-label” for persons with insulin resistance that leads to other conditions including pre-diabetes, severe obesity, polycystic ovarian syndrome (PCOS), cancer, and T1DM.

Its use in T1DM has been targeted to those with signs of insulin resistance which include hypertension, elevated serum triglycerides (>150 mg/dl), reduced HDL-C (<40 mg/dl in males or <50 mg/dl in females), overweight/obesity or elevated waist-to-height ratio (>0.5) (which includes about 25% of those with T1DM). Although any of these signs can be associated with insulin resistance, the more signs one has, the higher the risk of having insulin resistance. The term “double diabetes” has been used to describe those with T1DM who are also insulin resistant. Insulin resistance as has been reviewed in detail in my blog post #22 primarily in the context of prediabetes and type 2 diabetes. But you may ask, “How does a person with T1DM become insulin resistant?” You probably won’t hear very many provide an explanation for it, but here is mine. I think it is a combination of a diet high in refined (processed) carbohydrates and sugar with the use of exogenous insulin to cover those carbohydrates. Exogenous insulin is far from physiologic and there are many hours of the day or night where there is insufficient insulin to suppress hepatic (liver) glucose production leading to elevated BG (glucotoxicity): one of the proposed mechanisms of insulin resistance in T1DM. Additionally, there are hours of the day or night where insulin levels are excessive which can also contribute to insulin resistance. But most importantly the combination of taking lots of dietary carbohydrate, to which those with T1DM are intolerant, with lots of exogenous insulin, directly leads to insulin resistance just as it would in a person with prediabetes or T2DM (in their case the insulin would be endogenous in response to the dietary carbohydrate).

The use of metformin for cancer is still in the animal research arena primarily, but originates from the observation in population studies that patients with T2DM taking metformin was associated with reduced incidence and mortality rates of cancer compared to those not taking metformin.

As far as drugs go, metformin is particularly useful in addressing the problem of insulin resistance. Metformin improves insulin resistance by decreasing hepatic glucose production and intestinal glucose absorption and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. There have been numerous small studies of using metformin in patients with T1DM. A systematic review from 2010 found that “Metformin was associated with reductions in: (1) insulin-dose requirement (5.7–10.1 U/day in six of seven studies); (2) HbA1c (0.6–0.9% in four of seven studies); (3) weight (1.7–6.0 kg in three of six studies); and (4) total cholesterol (0.3–0.41 mmol/l in three of seven studies). Metformin was well tolerated, albeit with a trend towards increased hypoglycaemia.” A meta-analysis of eight randomized-controlled trials published in 2015 came to similar conclusions: “Metformin was associated with a reduction in daily insulin dosage, body weight, total cholesterol level, low-density lipoprotein level, and high-density lipoprotein level but an increase in risk of gastrointestinal adverse effects compared with placebo treatment in T1DM patients. No significant difference was found between the metformin group and the placebo group in HbA1c level, fasting plasma glucose level, or triglycerides level. No significant difference was found between the metformin group and the placebo group in the risk of severe hypoglycemia or diabetic ketoacidosis.” Note: I had access only to the abstract so I can’t give you any more details from this meta-analysis.

I hope it goes without saying that insulin resistance is expressed in those with a genetic tendency who are also exposed to an adverse environment, in this case, dietary carbohydrate consumption, particularly refined (processed) carbohydrates and sugars, in excess of one’s tolerance. This may also require excess calorie consumption as well. However, there is good evidence to suggest that refined (processed) carbohydrates and sugars stimulate appetite and fat deposition (via the signal of increased insulin). Thus, there is a link between refined (processed) carbohydrate and sugar consumption and excess calorie consumption. It has also long been known that physical activity affects insulin resistance. Other things being equal, sedentary behavior increases the likelihood of insulin resistance whereas regular physical activity decreases it. Thus, the first-line treatment for insulin resistance should be carbohydrate restriction, shedding of excess body fat (if needed), and regular physical activity before initiating any drug therapy.

Personally, I have been contemplating trying metformin for my T1DM for many years, but have not done so because I have never had any signs of insulin resistance (see above). More recently however, I have decided to give it a try primarily for the purpose of seeing if metformin might further reduce my insulin requirement which could, in turn, further reduce the frequency of hypoglycemia. Since my insulin requirements do fluctuate significantly over time, I estimate that it could take many months (up to 6 months possibly) to understand whether or not metformin has reduced my insulin requirement. I might be surprised sooner if the effect is more dramatic than I anticipate of course. However, if I am already insulin sensitive, metformin may not improve it much further. So on June 1, I will start metformin at 250-500 mg twice daily with meals and possibly eventually increase to a maximum of 1,000 mg twice daily to see if there is any reduction in insulin doses or hypoglycemia. Needless to say, anyone contemplating a similar experiment with metformin should discuss that with their own physician.

Glycemic Management Results for May 2017

May 2017 glycemic results were rather typical despite travel and a back strain that eliminated exercise for 6 days this month. This also changed my exercise to a less insulin-sensitizing activity (walking instead of weightlifting) for several more days which in turn affects BG and insulin doses. My total daily insulin dose ranged from a high of 42 IU/day to a low of 24 IU/day. It still remains baffling how my insulin dose can vary so much in the span of one month. These changes in insulin doses are in response to both hypoglycemia (leading to a reduction in insulin doses) and hyperglycemia (leading to increases in insulin doses), but I had more hypoglycemia this month resulting in insulin dose reductions for most of the month. Fortunately, none of the hypoglycemic episodes were symptomatic. I also checked blood ketones twice this month, both values happened to be the same at 1.2 mM beta-hydroxybutyrate. I did not measure breath ketones this month.

Below are my mean blood glucose (BG) values, mean insulin doses, and BG frequency distribution for April 2017 compared to previous time periods.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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 these two studies (here and here) of continuous glucose monitoring in healthy subjects. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. However, be advised that clinical outcomes in type 1 diabetes (i.e. microvascular and macrovascular complications) have only been documented to correlate with measures of mean BG, particularly HbA1c. This does not mean 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). I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG variability and thus the standard deviation and coefficient of variation. I plan to get the FreeStyle Libre CGM as soon as it becomes available in the U.S. 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 carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. A ketogenic diet may also provide an alternate/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 BG close to normal most of the time (some of which are hypoglycemic) also minimizes the symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time for May 2017.

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 and the mean BG during that time, then %Time BG 61-110 mg/dl and the mean BG during that time, and %Time BG > 110 mg/dl and the mean BG during that time. The other measures of BG variability were defined and explained in blog post #10.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. I had to take multiple extra rapid-acting insulin doses to correct hyperglycemia and the breakfast and dinner rapid-acting insulin doses increased during the first week of the month. Then BG began decreasing with more hypoglycemia require progress reductions in rapid-acting insulin doses. I made small changes in my basal insulin doses based on the fasting BG results as usual. I still find it interesting that my insulin doses vary so much over time for reasons that I largely do not understand. Again, this is due to the very nature of exogenous insulin therapy and the effect of my exercise on insulin sensitivity.

I am omitting my Ketonix breath acetone results this month since I did not take any measurements in May.

In June, I will continue olympic weightlifting most days while trying to avoid injury and overtraining (by adjusting the load (intensity times repetitions) up or down) and do aerobic exercise (swimming, rowing, walking, or cycling at low intensity for ≈ 0.5 – 2 hours) the remainder of the days.

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. My current version of ketogenic diet has changed slightly since I last wrote about it in detail in blog post #9. Since that post, I have eliminated dairy and decreased my fat intake to further improve my body composition so as to be able to compete in masters olympic weightlifting in the 77 kg weight class without having to think about when and how much I eat before weigh-in.

My current diet looks like this.

What I Cook & Eat

•Beef, grass-fed, including meat (85% lean), heart, liver, and kidney (liverwurst)

•Fish, mainly wild Alaskan salmon

•Canadian bacon (uncured)

•Lamb occasionally

•Chicken & Turkey occasionally

•Eggs (from chicken)

•Non-starchy vegetables (about 5% carbohydrate content by weight) including Cabbage (Red, Green, Napa), Kale, Collard Greens, Spinach, Bell Peppers, Raw Carrots, Leeks, Onions, Brussels sprouts, Home-made Sauerkraut from Red Cabbage, Bok-Choy, Broccoli, Cauliflower, Yellow Squash, Zucchini, Cucumber, Lettuce (Iceberg & Romaine), and some others.

•Fruit – Avocado, Tomatoes, Olives, Strawberries, Blueberries, Blackberries, lemon juice on fish and salads

•Nuts & Seeds – Pepitas, Macadamia, Brazil, Pecan, Walnut, Pistachio, Cashew.

•Note: I developed an intolerance to milk prior to my diagnosis of T1D. I did try heavy whipping cream after starting my KLCHF diet, but am also intolerant of it. I do tolerate butter, but wanted to decrease my fat intake, so eliminated all dairy including cheese and yogurt.

What I Drink

Water (filtered by reverse osmosis), Unsweetened Tea & Coffee

What I Don’t Eat

•Grains – Wheat, Corn, Rice, Oats (there are many more) or anything made from them, which is too numerous to list here. Gluten is a protein present in a number of grains (all varieties of wheat including spelt, kamut, and triticale as well as barley and rye.) which can cause a number of medical problems for a significant portion of the population with gluten sensitivity or celiac disease. In my case, I avoid them due to their carbohydrate content.

•Starchy vegetables – potatoes, sweet potatoes, yams, most root vegetables (turnip root okay), peas

•Legumes – peas, beans, lentils, peanuts, soybeans

•High sugar fruits – includes most fruits except berries, see above.

•Sugar and the fifty other names used to disguise sugar.

•Vegetable Oils (really seed oils) – Canola, Corn, Soybean, Peanut, Sunflower, Safflower, Cottonseed, Grape seed, Margarine & Butter substitutes, Shortening.

•All Processed Food-like Substances i.e., most of what is in the grocery store.

•I avoid restaurants except when traveling, and then order fish or steak with plain steamed non-starchy vegetables (no gravy or sauces that typically contain sugar, cornstarch, or flour) or salad.

•Refined, but healthy, Fats – I have eliminated refined fats from my diet including butter, coconut & olive oils.

What I Don’t Drink

•Colas (both sweetened and unsweetened).

•Fruit Juice except small amounts of lemon juice.

•Alcohol (can cause hyperglycemia or hypoglycemia in persons with diabetes).

•No artificial sweeteners, don’t need or like them.

A large part of my fat intake comes from nuts & seeds which hypothetically could result in potential adverse consequences from omega-6 polyunsaturated fats in the opinion of some low carb advocates. However, I have yet to see any studies that show harm from eating nuts & seeds. As a reference, the average fat breakdown of the seven nuts & seeds that I eat daily is 33% polyunsaturated, 52% monounsaturated, and 15% saturated fat. However, when my entire diet is analyzed, 26% of my fat intake is from polyunsaturates, 56% is from monounsaturates, and 18% is from saturated fats. When my diet is broken down by macronutrients, I consume 170 grams of fat (or 68% of my total daily calories), 70 grams of carbohydrate, 30 grams of which is dietary fiber (or 12% of my total daily calories), and 110 grams of protein (or 20% of my total daily calories). In calories, it totals to 2,250 kcal/day.

My exercise regimen and its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my lower insulin doses that result from my ketogenic diet and exercise are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time …

Whereas February 2017 was one of my best months in terms of glycemic control to date and March was rather typical of the previous two years or so, April was quite lack luster with more high and low blood glucose (BG) readings than the previous two months. This occurred despite no travel or major changes in exercise patterns. Fortunately, none of the hypoglycemic episodes were symptomatic, I feel well, and weightlifting performance is on par.

Glycemic Management Results for April 2017

Below are my mean blood glucose (BG) values, mean insulin doses, and BG frequency distribution for April 2017 compared to previous time periods.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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 these two studies (here  and here) of continuous glucose monitoring in healthy subjects. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. However, be advised that clinical outcomes in type 1 diabetes (i.e. microvascular and macrovascular complications) have only been documented to correlate with measures of mean BG, particularly HbA1c. This does not mean 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). I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG variability and thus the standard deviation and coefficient of variation. I plan to get the FreeStyle Libre CGM as soon as it becomes available in the U.S. 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 carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. A ketogenic diet may also provide an alternate/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 BG close to normal most of the time (some of which are hypoglycemic) also minimizes the symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time for April 2017.

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 and the mean BG during that time, then %Time BG 61-110 mg/dl, and %Time BG > 110 mg/dl and the mean BG during that time. The other measures of BG variability were defined and explained in blog post #10.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. I had to take multiple extra rapid-acting insulin doses to correct hyperglycemia and the breakfast and dinner rapid-acting insulin doses increased during the month. I made small changes in my basal insulin doses based on the fasting BG results as usual. I still find it interesting that my insulin doses vary so much over time for reasons that I largely do not understand. Again, this is due to the very nature of exogenous insulin therapy and the effect of my exercise on insulin sensitivity.

I am omitting my Ketonix breath acetone results this month since I did not take many measurements in April.

In May, I will continue olympic weightlifting most days while trying to avoid injury and overtraining (by adjusting the load (intensity times repetitions) up or down) and do aerobic exercise (swimming, rowing, walking, or cycling at low intensity for ≈ 0.5 – 2 hours) the remainder of the days.

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. My current version of ketogenic diet has changed slightly since I last wrote about it in detail in blog post #9. Since that post, I have eliminated dairy and decreased my fat intake to further improve my body composition so as to be able to compete in masters olympic weightlifting in the 77 kg weight class without having to think about when and how much I eat before weigh-in.

My current diet looks like this.

What I Cook & Eat

•Beef, grass-fed, including meat (85% lean), heart, liver, and kidney (liverwurst)

•Fish, mainly wild Alaskan salmon

•Canadian bacon (uncured)

•Lamb occasionally

•Chicken & Turkey occasionally

•Eggs (from chicken)

•Non-starchy vegetables (about 5% carbohydrate content by weight) including Cabbage (Red, Green, Napa), Kale, Collard Greens, Spinach, Bell Peppers, Raw Carrots, Leeks, Onions, Brussels sprouts, Home-made Sauerkraut from Red Cabbage, Bok-Choy, Broccoli, Cauliflower, Yellow Squash, Zucchini, Cucumber, Lettuce (Iceberg & Romaine), and some others.

•Fruit – Avocado, Tomatoes, Olives, Strawberries, Blueberries, Blackberries, lemon juice on fish and salads

•Nuts & Seeds – Pepitas, Macadamia, Brazil, Pecan, Walnut, Pistachio, Cashew.

•Note: I developed an intolerance to milk prior to my diagnosis of T1D. I did try heavy whipping cream after starting my KLCHF diet, but am also intolerant of it. I do tolerate butter, but wanted to decrease my fat intake, so eliminated all dairy including cheese and yogurt.

What I Drink

Water (filtered by reverse osmosis), Unsweetened Tea & Coffee

What I Don’t Eat

•Grains – Wheat, Corn, Rice, Oats (there are many more) or anything made from them, which is too numerous to list here. Gluten is a protein present in a number of grains (all varieties of wheat including spelt, kamut, and triticale as well as barley and rye.) which can cause a number of medical problems for a significant portion of the population with gluten sensitivity or celiac disease. In my case, I avoid them due to their carbohydrate content.

•Starchy vegetables – potatoes, sweet potatoes, yams, most root vegetables (turnip root okay), peas

•Legumes – peas, beans, lentils, peanuts, soybeans

•High sugar fruits – includes most fruits except berries, see above.

•Sugar and the fifty other names used to disguise sugar.

•Vegetable Oils (really seed oils) – Canola, Corn, Soybean, Peanut, Sunflower, Safflower, Cottonseed, Grape seed, Margarine & Butter substitutes, Shortening.

•All Processed Food-like Substances i.e., most of what is in the grocery store.

•I avoid restaurants except when traveling, and then order fish or steak with plain steamed non-starchy vegetables (no gravy or sauces that typically contain sugar, cornstarch, or flour) or salad.

•Refined, but healthy, fats – I have eliminated refined fats from my diet including butter, coconut & olive oils.

What I Don’t Drink

•Colas (both sweetened and diet i.e. artificial sweeteners).

•Fruit Juice except small amounts of lemon juice.

•Alcohol (can cause hyperglycemia or hypoglycemia in persons with diabetes).

•No artificial sweeteners, don’t need or like them.

A large part of my fat intake comes from nuts & seeds which hypothetically could result in potential adverse consequences from omega-6 polyunsaturated fats in the opinion of some low carb advocates. However, I have yet to see any studies that show harm from eating nuts & seeds. As a reference, the average fat breakdown of the seven nuts & seeds that I eat daily is 33% polyunsaturated, 52% monounsaturated, and 15% saturated fat. However, when my entire diet is analyzed, 26% of my fat intake is from polyunsaturates, 56% is from monounsaturates, and 18% is from saturated fats. When my diet is broken down by macronutrients, I consume 170 grams of fat (or 68% of my total daily calories), 70 grams of carbohydrate, 30 grams of which is dietary fiber (or 12% of my total daily calories), and 110 grams of protein (or 20% of my total daily calories). In calories, it totals to 2,250 kcal/day.

My exercise regimen and its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my lower insulin doses that result from my ketogenic diet and exercise are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

Whereas February 2017 was my best one month glycemic control to date, March was rather typical of the previous two years or so. This was in part due to changing insulin doses, both increases and decreases, which continue for reasons not altogether clear to me since I am just responding to and correcting high and low blood glucose (BG) readings. Another factor in BG fluctuations in March was travel for a week that was also highlighted with a symptomatic hypoglycemic episode: the first one in 2017. Travel has always resulted in more hypoglycemia and hyperglycemia due to changes in diet, exercise, sleep patterns, time zones, and possibly stress. During my trip I also participated in my second olympic weightlifting meet on March 26th in San Diego, CA where I lifted 72 kg in the snatch and 95 kg in the clean & jerk for a total of 167 kg, an 8 kg improvement compared to my first meet total of 159 kg. I made 5 of 6 lifts to achieve that total. The hypoglycemic episode mentioned above occurred after dinner on the day of the weightlifting meet.

Glycemic Management Results for March 2017

Below are my mean blood glucose (BG) values, insulin doses, and BG frequency distribution for March 2017 compared to previous time periods.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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 these two studies (here and here) of continuous glucose monitoring in healthy subjects. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. However, be advised that clinical outcomes in type 1 diabetes (i.e. microvascular and macrovascular complications) have only been documented to correlate with measures of mean BG, particularly HbA1c. This does not mean BG variability is not important, but just that measuring BG variability over long periods of time in numerous individuals with T1DM is more difficult so very few trials have attempted to measure it. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG control. I plan to get the FreeStyle Libre CGM as soon as it becomes available in the U.S. 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 carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. The ketogenic diet may also provide an alternate/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 BG close to normal most of the time also minimizes symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time for March 2017.

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 and the mean BG during that time, then %Time BG 61-110 mg/dl, and %Time BG > 110 mg/dl and the mean BG during that time. The other measures of BG variability were defined and explained in blog post #10.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. I had to take multiple extra rapid-acting insulin doses to correct hyperglycemia and the breakfast and dinner rapid-acting insulin doses increased in the second half of the month. I made small changes in my basal insulin doses based on the fasting BG results as usual. I still find it interesting that my insulin doses vary so much over time for reasons that I largely do not understand. Again, this is IMO due to the very nature of exogenous insulin therapy.

I am omitting my Ketonix breath acetone results this month since I did not take many measurements in March.

In April, I will continue olympic weightlifting most days by adjusting the load (intensity times repetitions) to avoid injury and overtraining and do aerobic exercise (swimming, rowing, or cycling at low intensity for ≈ 0.5 – 2 hours) the remainder of the days.

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. 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 moderate degrees of hypoglycemia (see blog post #12 for more details). I also think that hypoglycemia unawareness (due to my frequent asymptomatic hypoglycemic episodes) contributes to my lack of symptoms of hypoglycemia. As pointed out in blog post #29, this may not necessarily be a bad thing. Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my insulin doses are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

The Ketogenic Diet For Type 1 Diabetes: Reduce Your HbA1c and Avoid Diabetic Complications

has been available as an ebook since 2014 at ketogenic diet resource.com, but is now available in print on Amazon here. Ellen Davis, MS and I wrote this book as a practical guide for those with type 1 diabetes and the parents of children with the condition to utilize the ketogenic diet to improve glycemic control reducing both hyperglycemia and hypoglycemia and thus diabetic complications all with reduced insulin doses. Additional benefits described in the book include reduction in inflammatory markers, improvement in dyslipidemia, high blood pressure, insulin resistance, overweight, and obesity. Also included is the effect of exercise on glycemic control in those with type 1 diabetes and how to deal with the added glycemic fluctuations brought on by exercise.

Conquer Type 2 Diabetes with a Ketogenic Diet: A Practical Guide to Reducing Your HbA1c and Avoiding Diabetic Complications

has been available as an ebook since 2014 at ketogenic diet resource.com, but is now available in print on Amazon here. Ellen Davis, MS and I wrote this book as a practical guide for those with type 2 diabetes, pre-diabetes, glucose intolerance, insulin resistance, or metabolic syndrome to utilize the ketogenic diet to improve glycemic control reducing both hyperglycemia and hypoglycemia and thus diabetic complications all with reduced medications and/or insulin doses. Additional benefits described in the book include reduction in inflammatory markers, improvement in dyslipidemia, high blood pressure, insulin resistance, overweight, and obesity. Also included is the effect of exercise on glycemic control in those with type 2 diabetes and how to deal with the added glycemic fluctuations brought on by exercise.

 

February 2017 turned out to be the best one month glycemic control that I have achieved to date. Another highlight was my first olympic weightlifting meet on Feb. 12th in Palmetto, FL where I lifted 70 kg in the snatch and 89 kg in the clean & jerk for a total of 159 kg. I made 5 of 6 lifts to achieve that total. I have another meet scheduled later this month.

Glycemic Management Results for February 2017

Below are my mean blood glucose (BG) values, insulin doses, and BG frequency distribution for February 2017 compared to previous time periods. I had the least hypoglycemia so far with 11% of BG values < 61 mg/dl this month vs 23% last month. None of these hypoglycemic values were associated with symptoms. My goal is less than 10%. The decrease in hypoglycemia was accompanied by an increase in hyperglycemia with 33% of BG values > 110 mg/dl this month vs 21% last month. My goal is less than 20%.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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. As mentioned last month, normal mean BG is 96 ± 12 mg/dl (mean ± standard deviation (SD)) and coefficient of variation is 13% as a frame of reference. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG control. I plan to get the FreeStyle Libre CGM as soon as I becomes available in the U.S. Monitoring the standard deviation and/or coefficient of variation and finding ways to improve them to the best of one’s ability is desirable. Following a low carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. The ketogenic diet may also provide an alternate/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. And as I mentioned last month, having BG close to normal most of the time also minimizes symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time for February 2017.

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 and the mean BG during that time, then %Time BG 61-110 mg/dl, and %Time BG > 110 mg/dl and the mean BG during that time. The other measures of BG variability were defined and explained in blog post #10. Compared to last month, glycemic variability decreased and frequency of as well as %Time with BG < 61 mg/dl decreased, to record low levels. Overall, I hope this continues next month.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. I had to take multiple extra rapid-acting insulin doses to correct hyperglycemia and the breakfast and dinner rapid-acting insulin doses increased in the second half of the month. I made small changes in my basal insulin doses based on the fasting BG results as usual. I still find it interesting that my insulin doses vary so much over time for reasons that I largely do not understand. Again, this is IMO due to the very nature of exogenous insulin therapy.

My Ketonix breath acetone results since June 1, 2015 are shown below. There has been a gradual reduction in breath ketones. I suspect, but cannot prove, that this is related to an increased carbohydrate content of my meals. I have gradually increased the amount of berries, nuts, and seeds that I eat to help increase diet variety and add nutrients while at the same time decreasing added fats including coconut oil, olive oil, and butter. I occasionally supplement with MCT oil to help increase ketones and keep total calories about the same: 2,250 kcal/day due to the reduction in coconut oil, olive oil, and butter. I estimate I am now eating about 70 grams of carbohydrate per day of which 30 grams is fiber i.e. 40 grams of net carbs per day, 110 grams protein/day, and 170 grams of fat/day which is referred to as a 1:1 ketogenic diet. This is terminology used by neurologists who treat adults and children with epilepsy with ketogenic diets. They often use 4:1 or 3:1 ketogenic diets for epilepsy. The ratio indicates grams of fat divided by the grams of carbohydrate plus protein. For me, for example, 170 grams fat ÷ (70 grams carbohydrate + 110 grams protein) ≈ 1:1.

In March, I will continue to exercise daily but will try olympic weightlifting six days a week and aerobic exercise (swimming, rowing, or cycling at low intensity for ≈ 0.5 – 2 hours) one day a week.

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. 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 moderate degrees of hypoglycemia (see blog post #12 for more details). I also think that hypoglycemia unawareness (due to my frequent asymptomatic hypoglycemic episodes) contributes to my lack of symptoms of hypoglycemia. As pointed out in blog post #29, this may not necessarily be a bad thing. Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my insulin doses are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

January’s post was delayed because I attended and spoke at the Metabolic Therapeutics Conference on February 3rd in Tampa, Florida on The Management of Type 1 Diabetes with a Ketogenic Diet. My talk was videoed and I will post a link when it is available on YouTube. It was an excellent conference and I would highly recommend it to anyone interested in ketogenic diets.

Glycemic Management Results for January 2017

Below are my mean BG values, insulin doses, and BG frequency distribution for January 2017 compared to previous time periods. I am always aiming for less hypoglycemia, but I had more this month 23% vs 15% of BG values were < 61 mg/dl last month. My goal is less than 10%. The increase in hypoglycemia was I suspect related to the increase in insulin doses that began last month to treat hyperglycemia. Thus, most of this month I had to reduce the insulin doses to address the hypoglycemia. Fortunately, none of the hypoglycemia was associated with symptoms.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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. As mentioned last month, normal mean BG is 96 ± 12 mg/dl (mean ± standard deviation (SD)) and coefficient of variation is 13% as a frame of reference. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG control. I plan to get the FreeStyle Libre CGM as soon as I becomes available in the U.S. Monitoring the standard deviation and/or coefficient of variation and finding ways to improve them to the best of one’s ability is desirable. Following a low carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. The ketogenic diet may also provide an alternate/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. And as I mentioned last month, having BG close to normal most of the time also minimizes symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time.

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 and the mean BG during that time, then %Time BG 61-110 mg/dl, and %Time BG > 110 mg/dl and the mean BG during that time. The other measures of BG variability were defined and explained in blog post #10. Compared to last month, glycemic variability increased and frequency of as well as %Time with BG < 61 mg/dl increased, but I do not expect this to persist next month. Overall, satisfactory.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. The decline in my insulin requirements that began on 12/22/2016 continued in the month of January. The total daily insulin dose came back down to my prior level in the low 30’s IU/day by the end of the month.

My Ketonix breath acetone results since June 1, 2015 are shown below. There has been a gradual reduction in breath ketones. I suspect, but cannot prove, that this is related to an increased carbohydrate content of my meals. I have gradually increased the amount of berries, nuts, and seeds that I eat to help increase diet variety and add nutrients while at the same time decreasing added fats including coconut oil, olive oil, and butter. I occasionally supplement with MCT oil to help increase ketones and keep total calories about the same: 2,250 kcal/day due to the reduction in coconut oil, olive oil, and butter. I estimate I am now eating about 70 grams of carbohydrate per day of which 30 grams is fiber i.e. 40 grams of net carbs per day, 110 grams protein/day, and 170 grams of fat/day which is referred to as a 1:1 ketogenic diet. This is terminology used by neurologists who treat adults and children with epilepsy with ketogenic diets. They often use 4:1 or 3:1 ketogenic diets for epilepsy. The ratio indicates grams of fat divided by the grams of carbohydrate plus protein. For me, for example, 170 grams fat ÷ (70 grams carbohydrate + 110 grams protein) ≈ 1:1. As you can imagine, a 4:1 diet would be more restrictive to emphasize foods high in fat and to avoid foods high in carbohydrates and/or protein.

In January, I achieved a new personal record (PR) in weightlifting in the clean & jerk increasing it from 185 lb. to 195 lb. The snatch remained the same at 155 lb.

In February, I will continue to exercise daily alternating olympic weightlifting and aerobic exercise (swimming, rowing, or cycling at low intensity for ≈ 0.5 – 2 hours). I am using a heart rate (HR) monitor during cycling and rowing with the goal of not exceeding a HR of 124 bpm. This is derived from Phil Maffetone’s formula: 180 – age. The purpose is to exercise aerobically so as to burn mainly fat and to minimize utilizing glucose for muscle energy which can result in hypoglycemia in those with T1DM. It also gives me a day to recover from weightlifting. I will see if this reduces BG reductions during cycling and the need for glucose supplementation during exercise (so far, so good).

My Thoughts About Management of Type 1 Diabetes With A Ketogenic Diet

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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. 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 moderate degrees of hypoglycemia (see blog post #12 for more details). I also think that hypoglycemia unawareness (due to my frequent asymptomatic hypoglycemic episodes) contributes to my lack of symptoms of hypoglycemia. As pointed out in blog post #29, this may not necessarily be a bad thing. Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my insulin doses are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

Happy New Year to all!

Before I get started, just a reminder about the upcoming Metabolic Therapeutics Conference, February 1-4 in Tampa, Florida. I’ll be speaking about The Management of Type 1 Diabetes with a Ketogenic Diet. This is the second annual conference featuring researchers and clinicians with expertise in ketogenic diet therapies, including Dr. Dominic D’Agostino, Dr. Colin Champ, Dr. Thomas Seyfried and many others. Click here to learn more and sign up.

Glycemic Management Results for December 2016

Below are my mean blood glucose (BG) values, insulin doses, and BG frequency distribution for current and previous time periods. I was aiming for less hypoglycemia which I accomplished, 15% vs 19% of BG values were < 61 mg/dl, but I would really prefer this to be less than 10%. For unknown reasons, I experienced a rather sudden increase in BG (32% of BG values were elevated to between 111 and 200 mg/dl) requiring additional insulin beginning on Nov. 21 that came under control by the end of December. And, no, I did not partake in any “holiday” food treats. For me, having the best BG control I can is worth any “sacrifice,” although I don’t view not eating treats as a sacrifice. Note: I immediately address elevated BG with extra doses of rapid-acting (Humalog) insulin and increase my basal insulin (Lantus) if the morning fasting BG is elevated, both of which I had to do this month.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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. As mentioned last month, normal mean BG is in the range 90-95 ± 7-12 mg/dl (mean ± standard deviation (SD)) and coefficient of variation is 8-13% as a frame of reference. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. I hope that adding a continuous glucose monitor (CGM) to my therapeutic regimen will improve my BG control. Monitoring the standard deviation and/or coefficient of variation and finding ways to improve them to the best of one’s ability is desirable. Following a low carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. The ketogenic diet may also provide an alternate/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. And as I mentioned last month, having BG close to normal most of the time also minimizes symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time. I had to take a few days off from weightlifting due to right lateral knee pain (probably due to ileotibial band syndrome which I have had several times before) which resolved spontaneously with rest. This may have contributed to hyperglycemia and the need to increase insulin doses, but probably does not explain it in entirety.

The table below shows the BG variability results for current and previous time periods. In November, I converted time spent (hours) with BG < 61 mg/dl and time spent (hours) with BG > 110 mg/dl to % time by simply dividing each by 24 (hours in a day). I added a column for % time in target range (BG 61-100 mg/dl). I also added additional columns showing the 10th, 25th, 75th, and 90th percentiles of my BG readings and the Interquartile Range which is the difference between the 75th and 25th percentiles. The BG median shown in the previous table is identical to the 50th percentile. Thus, these percentiles show the spread of the BG readings about the median and are measures of BG variability. The other measures of BG variability were defined and explained in blog post #10. Compared to last month, most of the results were improved. I was particularly satisfied with % time with hypoglycemia of 7% (which is an all-time low) coupled with a normal mean BG of 97 mg/dl and % time in target of 65% (which is an all-time high). Overall, satisfactory.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. Similar to what occurred in November, I had to increase my total daily insulin dose from 32 IU/day to 49.5 IU/day over a 16 day period, an increase of 17.5 IU (a 55% increase) due to hyperglycemia for reasons that are unclear to me. Subsequently, I had to decrease the total daily insulin dose back down due to hypoglycemia to 32.5 IU/day over the next 11 days. I have been contacted by several individuals with T1DM who experienced a similar increase in insulin dose at different points in time after starting a ketogenic diet and thought this represented an insulin resistant state caused by the ketogenic diet. I told them that I do not think this is the case and that these increases (and decreases) just represent the usual variability that type 1’s experience. After all, a ketogenic diet is used to treat and reverse insulin resistance. I am aware of “physiologic insulin resistance” in non-diabetics used to describe slightly elevated fasting BG and an attenuated insulin response to a glucose tolerance test in those on a very low carbohydrate ketogenic diet. However, I do not think this would apply to those with T1DM on a ketogenic diet.

My Ketonix breath acetone results since June 1, 2015 are shown below. There has been a gradual reduction in breath ketones. I suspect, but cannot prove, that this is related to an increased carbohydrate content of my meals. I have gradually increased the amount of berries, nuts, and seeds that I eat to help increase diet variety and add nutrients while at the same time decreasing added fats including coconut oil, olive oil, and butter. I occasionally supplement with MCT oil to help increase ketones and keep total calories about the same: 2,150 kcal/day due to the reduction in coconut oil, olive oil, and butter. I estimate I am now eating about 70 grams of carbohydrate per day of which 30 grams is fiber i.e. 40 grams of net carbs per day, 110 grams protein/day, and 170 grams of fat/day which is referred to as a 1:1 ketogenic diet. This is terminology used by neurologists who treat adults and children with epilepsy with ketogenic diets. They often use 4:1 or 3:1 ketogenic diets for epilepsy. The ratio indicates grams of fat to grams of carbohydrate plus protein. For me, for example, 170 grams fat ÷ (70 grams carbohydrate + 110 grams protein) ≈ 1:1. As you can image, a 4:1 diet would be more difficult (but not impossible) to follow long-term as it more severely restricts the quantity of foods that contain carbohydrates and protein.

In December, I achieved a new personal record (PR) in weightlifting in the snatch: increasing it from 150 to 155 lb. My clean & jerk PR is still stuck at 185 lb. since the end of March 2016. Fortunately, I don’t need to make a living from weightlifting, so any PRs are just plain fun.

In January, I will continue exercise daily (weightlifting and aerobic) with about 4 days/week of weightlifting. The aerobic exercise consists of swimming, rowing, or cycling at low intensity for ≈ 0.5 – 2 hours. I am using a heart rate (HR) monitor during cycling and rowing with the goal of not exceeding a HR of 124 bpm. This is derived from Phil Maffetone’s formula: 180 – age. The purpose is to exercise aerobically so as to burn mainly fat and to minimize utilizing glucose for muscle energy which can result in hypoglycemia in those with T1DM. It also gives me a day to recover from weightlifting. I will see if this reduces BG reductions during cycling and the need for glucose supplementation during exercise (so far, so good).

Summary of Results Since Beginning The Ketogenic Diet

In the graph below, I have included all BG results since starting the ketogenic diet on Feb. 8, 2012 (indicated by the blue arrow) as well as some results prior to that for comparison with the one week moving average in black and my BG target range (BG 61-110 mg/dl) indicated in red. When I see the great variation in BG graphically, it is a wonder that I feel and function as well as I do. Again, I hope that the FreeStyle Libre CGM when it becomes available in the United States, will result in additional improvement in my BG control.

In the graph below, I have included all insulin doses since starting the ketogenic diet on Feb. 8, 2012 (indicated by the red arrow) as well as some results prior to that for comparison with the one week moving average in black. Note that there is a lot of variability in the doses needed to control BG over time. With the exception of two periods of time (lasting 2 and 6 weeks respectively) after stopping exercise completely due to back injury, I don’t really understand why I have these recurrent peaks and valleys in insulin doses.

My Thoughts about Management of Type 1 Diabetes with a Ketogenic Diet

My goal of glycemic management in T1DM with a ketogenic diet is to keep BG as close to normal (≈ 90-95 ± 7-12 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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. 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 moderate degrees of hypoglycemia (see blog post #12 for more details). I also think that hypoglycemia unawareness (due to my frequent asymptomatic hypoglycemic episodes) contributes to my lack of symptoms of hypoglycemia. As pointed out in blog post #29, this may not necessarily be a bad thing. Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as my insulin doses are close enough to optimal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….

Before I get started, just a reminder about the upcoming Metabolic Therapeutics Conference, February 1-4 in Tampa, Florida. I’ll be speaking about The Management of Type 1 Diabetes with a Ketogenic Diet. This is the second annual conference featuring researchers and clinicians with expertise in ketogenic diet therapies, including Dr. Dominic D’Agostino, Dr. Colin Champ, Dr. Thomas Seyfried and many others. Click here to learn more and sign up.

In November 2016 I had more low and high blood glucose (BG) values than I would have liked, but we know that perfectly normal BG values are not necessarily achievable with the current technology of subcutaneously injected or pumped insulin analogs and home BG meters even with a ketogenic diet. A continuous glucose monitor (CGM) could improve glycemic control further.

Speaking of CGMs, I have decided to get one as soon as it becomes available in the United States. Americans are eagerly waiting for FDA approval of the Freestyle Libre CGM system (manufactured by Abbott). It is different than any currently CGM on the market, but I think it will serve my needs and active lifestyle well. Thanks to Dr. Troy Stapleton for posting his new CGM on Twitter and direct messaging me about it. The Freestyle Libre CGM system measures interstitial (the fluid below the skin) glucose every minute. Interstitial glucose readings can lag behind BG readings by 5-10 mins which is meaningful if BG is changing rapidly. As a physician, I could get the currently available Freestyle Libre Pro CGM system in the United States. However, my reason for getting the patient, rather than the professional, version is to use the readings to make changes in glycemic management on the fly so to speak. I am particularly interested in being able to treat (with glucose) low interstitial glucose readings that may occur anytime, but especially during exercise, and to treat elevated interstitial glucose readings (due to intense exercise from weightlifting) after exercise with rapid-acting insulin (Humalog). One of the major advantages of this system in my mind is accuracy. The CGMs currently on the market require at least two BG readings/day to be entered into the CGM to keep it calibrated. The Freestyle Libre CGM system does not require any BG readings to be entered into the device. BG may still need to be measured with a home BG meter particularly if symptoms do not correlate with the interstitial glucose readings after the user has determined that the device provides comparable readings to an accurate home BG glucose meter  (I use the FreeStyle Freedom Lite meter also manufactured by Abbott).

Glycemic Management Results for November 2016

My BG results in November were comparable to October with some measures slightly worse and some slightly improved. Overall, satisfactory.

Rather than repeat the results in the tables again in the text, I’ll just comment on them. There are two changes in how I present the data this month. See below.

Below are my mean BG values, insulin doses, and BG frequency distribution for current and previous time periods using the new target ranges mentioned in previous two posts. I was aiming for less hypoglycemia which I accomplished, 19% vs 21% of BG values were < 61 mg/dl, but I would really prefer this to be less than 10%. For unknown reasons, I experienced a rather sudden increase in BG (30% of BG values were elevated to between 111 and 200 mg/dl) requiring additional insulin beginning on Nov. 21 that came under control by the end of the month. Note: I immediately address elevated BG with extra doses of rapid-acting (Humalog) insulin and increase my basal insulin (Lantus) if the morning fasting BG is elevated, both of which I had to do this month.

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes (T1DM) should not expect to have truly normal BG values. They just need to be low enough to prevent long-term complications and not so low as to cause unpleasant hypoglycemic symptoms, 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. As mentioned last month, normal mean BG is in the range 90-95 ± 7-12 mg/dl (mean ± standard deviation (SD)) and coefficient of variation is 8-13% as a frame of reference. The standard deviation and coefficient of variation are measures of BG variability which I believe are important in T1DM. Achieving a normal standard deviation or coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. Monitoring the standard deviation and/or coefficient of variation and finding ways to improve it to the best of one’s ability is desirable. Following a low carbohydrate ketogenic diet is one such method of reducing BG variability, mean BG, insulin doses, and hypoglycemia. The ketogenic diet may also provide an alternate/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. And as I mentioned last month, having BG close to normal most of the time also minimizes symptoms of mild hypoglycemia and potentially the harm from hypoglycemia as well due to lack of activation of the sympathetic nervous system and adrenal gland responses to hypoglycemia i.e. sympathoadrenal-induced fatal cardiac arrhythmia, see here.

Below are my BG readings along with exercise type and time. I managed to increase the number of days of weightlifting which I now enjoy more than aerobic exercise. This is why the mean number of hours of exercise per week increased compared to last month.

The table below shows the BG variability results for current and previous time periods. This month I have converted time spent (hours) with BG < 61 mg/dl and time spent (hours) with BG > 110 mg/dl to % time by simply dividing each by 24 (hours in a day). I also added a column for % time in target range (BG 61-100 mg/dl). I also added two additional columns showing the 10th and 90th percentiles of my BG readings. I changed the labeling of Quintile 1 and Quintile 3 to 25th %tile and 75th %tile (my abbreviation for percentile) to correct the error of using the word Quintile instead of Quartile (my mistake). Also note that Quartile 1 is mathematically identical to 25th percentile as is Quartile 3 and 75th percentile. The BG median shown in the previous table is identical to the 50th percentile. Thus, these percentiles show the spread of the BG readings about the median and are measures of BG variability. The other measures of BG variability were defined and explained in blog post #10. Compared to last month, some of the results were improved while others were not. Overall, satisfactory.

The actual daily insulin doses and daily insulin dose totals are shown in the graphs below. Note I had to increase my total daily insulin dose from 25.5 IU/day to 37.5 IU/day over a twelve day period, an increase of 12 IU (a 47% increase) for reasons that are unclear to me. Similarly, I had to decrease the total daily insulin dose back down to 29 IU/day over the next four days. I have been contacted by several individuals with T1DM who experienced a similar increase in insulin dose at different points in time after starting a ketogenic diet and thought this represented an insulin resistant state caused by the ketogenic diet. I told them that I do not think this is the case and that these increases (and decreases) just represent the usual variability that type 1’s experience. After all, a ketogenic diet is used to treat and reverse insulin resistance. I am aware of “physiologic insulin resistance” in non-diabetics used to describe slightly elevated fasting BG and an attenuated insulin response to a glucose tolerance test in those on a very low carbohydrate ketogenic diet. However, I do not think this would apply to those with T1DM on a ketogenic diet.

My Ketonix breath acetone results since June 1, 2015 are shown below. There has been a gradual reduction in breath ketones. I suspect, but cannot prove, that this is related to an increased carbohydrate content of my meals. I have gradually increased the amount of berries, nuts, and seeds that I eat to help increase diet variety and add nutrients while at the same time decreasing added fats including coconut oil, olive oil, and butter. I recently started to supplement with MCT oil, one tablespoon twice daily with my meals to help increase ketones and keep total calories about the same: 2,500 kcal/day due to the reduction in coconut oil, olive oil, and butter. I estimate I am now eating about 70 grams of carbohydrate per day of which 30 grams is fiber i.e. 40 grams of net carbs per day.

In November, I finally achieved a new personal record (PR) in weightlifting in the snatch: increasing it from 140 to 150 lb. My clean & jerk PR is still stuck at 185 lb. since the end of March 2016. Fortunately, I don’t need to make a living from weightlifting, so any PRs are just plain fun.

In December, I will continue weightlifting and aerobic exercise daily with as many days of weightlifting as I can tolerate i.e. not experiencing fatigue or joint soreness/stiffness. The aerobic exercise consists of swimming, rowing, or cycling at low intensity for ≈ 0.5 – 2 hours. I am using a heart rate (HR) monitor during cycling and rowing with the goal of not exceeding a HR of 124 bpm. This is derived from Phil Maffetone’s formula: 180 – age. See here. The purpose is to exercise aerobically so as to burn mainly fat and to minimize utilizing glucose for muscle energy which can result in hypoglycemia in those with T1DM. It also gives me a day to recover from weightlifting i.e. intense aerobic exercise is fatiguing. I will see if this reduces BG reductions during cycling and the need for glucose supplementation during exercise (typically 6-12 grams of glucose). The three times I cycled at this lower HR in October, I was able to omit glucose supplementation without a large change in BG: a reduction of 24 mg/dl and an increase of 3 mg/dl and 32 mg/dl, respectively. It is too early to say that this is causally related.

My Thoughts about Management of Type 1 Diabetes with a Ketogenic Diet

The goal of glycemic management in T1DM with a ketogenic diet is to keep BG as close to normal (≈ 90-95 ± 7-12 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 (see blog post #9 for more details), daily exercise, frequent BG measurements, and lower insulin-analog doses (Humalog/Lantus) have improved my glycemic control, hypoglycemic reactions, and quality of life. 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 moderate degrees of hypoglycemia (see blog post #12 for more details). I also think that hypoglycemia unawareness (due to my frequent asymptomatic hypoglycemic episodes) contributes to my lack of symptoms of hypoglycemia. As pointed out in blog post #29, this may not necessarily be a bad thing. Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult i.e. challenging, but I enjoy exercise and feel it has other health and lifespan-extending benefits. Hopefully, my BG values and variability as well as lower insulin doses are close enough to normal to avoid any reduction in lifespan, diabetic complications, and harm from hypoglycemia. Only time will tell.

Till next time ….