#36 February 2017 Update on My T1D Management

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%.

post-36-means-table

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.

post-36-exercise-and-blood-glucose

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.

post-36-variability-table

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.

post-36-insulin-doses

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.

post-36-ketonix-graph

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 ….

superfoods for diabetes & nutritional ketosis

This blog post from Marty Kendall of Optimizing Nutrition quantifies my approach to a nutrient dense real-food ketogenic diet for type 1 diabetes.

optimising nutrition

More than carbohydrate counting or the glycemic index, the food insulin index data suggests that our blood glucose and insulin response to food is better predicted by net carbohydrates plus about half the protein we eat.

The chart below show the relationship between carbohydrates  and our insulin response. There is some relationship between carbohydrate and insulin, but it is not that strong, particularly when it comes to high protein foods (e.g. white fish, steak or cheese) or high fibre foods (e.g. All Bran).

food insulin index table - fructose analysis v2 21122015 44912 PM.bmp

Accounting for fibre and protein enables us to more accurately predict the amount of insulin that will be required for a particular food.  This knowledge can be  useful for someone with diabetes and / or a person who is insulin resistant to help them calculate their insulin dosage or to chose foods that will require less insulin.

image02

If your blood glucose levels are typically high you are likely insulin resistant (e.g. …

View original post 1,102 more words

#34 January 2017 Update on My T1D Management

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.

post-34-means-table

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.

post-34-exercise-and-blood-glucose

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.

post-34-variability-table

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.

post-34-insulin-doses

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.

post-34-ketonix-graph

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 ….

#33 December 2016 Update on My T1D Management

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.

post-33-means-table

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.

post-33-exercise-and-blood-glucose

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.

post-33-variability-table

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.

post-33-insulin-doses

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.

post-33-ketonix-graph

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.

post-33-all-blood-glucose-values

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.

post-33-all-insulin-dose-totals

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 ….

#32 November 2016 Update on My T1D Management

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.

post-32-means-table

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.

post-32-exercise-bg-graphs

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.

post-32-variability-table

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.

post-32-insulin-doses-graphs

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.

post-32-ketonix-graph

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 ….

#31 October 2016 Update on My T1D Management

In October 2016 as usual, I had more low and high blood glucose (BG) values than I would have liked. However compared to last month, my results in October were improved.

Below are my BG values using the new target ranges mentioned last month. The mean BG was 87 mg/dl at a lower mean insulin dose of 27.5 IU/day compared to 31.5 IU/day last month. Both the mean basal insulin dose and mean mealtime insulin dose decreased from 24.5 IU/day to 22.8 IU/day and from 7.0 IU/day to 4.6 IU/day, respectively. The percentage of BG values < 61 mg/dl decreased from 25% to 21% whereas the percentage falling in my goal range of 61-110 mg/dl increased from 52% to 61%, and the percentage of BG values > 110 mg/dl decreased from 22% to 18% compared to last month.

post-31-means-table

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 goal BG range at 61-110 mg/dl because values in this range are not likely to lead to harm or complications of T1DM. 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 are important in T1DM. Achieving a normal coefficient of variation in T1DM would be difficult, if not impossible, with current exogenous insulin therapy. Monitoring the 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, and insulin doses. The ketogenic diet may also provide 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 mentioned last month, having BG close to normal most of the time and dipping into the 50s and 60s sometimes also minimizes symptoms of mild hypoglycemia (hypoglycemia unawareness) 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. Although asymptomatic hypoglycemia is not a goal of therapy, it is an expected consequence of near-normal glycemia in those with T1DM on exogenous insulin therapy. My goal is to reduce the frequency of these asymptomatic hypoglycemic episodes from 21% currently to <10%.

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

post-31-bg-exercise-graphs

The table below shows the summary of current and previous BG variability results. Most of the results were improved compared to previous months and years with improvement in the following variability measures: standard deviation = 31, coefficient of variation = 36%, mean daily BG range = 57, mean daily time of hypoglycemia = 3.0 hr/day, interquartile BG range = 40. The measures of BG variability were defined and explained in blog post #10.

post-31-variability-table

The graph below shows that the various measures of BG variation in the table above correlate well with the coefficient of variation. Because the coefficient of variation is easy to calculate (standard deviation ÷ mean X 100 expressed as percent) and compare to normal values, it is the best measure of BG variability for persons with diabetes in my opinion.

post-31-measures-of-variability-correlation-graph

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

post-31-insulin-totals-doses-graphs

In November I will continue weightlifting and aerobic exercise, but hope to increase the frequency of weightlifting as I feel I can now tolerate it more than every other day. The aerobic exercise consists of swimming or cycling at low intensity for ≈0.5-2 hours. I am using a heart rate monitor during cycling with the goal of not exceeding a heart rate of 130 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. I will see if this reduces the number of low BG readings after cycling and/or the need for glucose supplementation prior to cycling (typically 6-12 grams of glucose).

My Thoughts on T1DM Management

The goal of glycemic management in type 1 diabetes with a ketogenic diet is to keep BG as close to normal (≈ 90-95 mg/dl) as is safely possible (i.e. avoiding hypoglycemia). More specifically the purpose is to avoid diabetic complications, a reduction in lifespan, and unpleasant symptoms, 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 blood glucose 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 mild degrees of hypoglycemia (see blog post #12 for more details). Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more challenging, but I enjoy it and feel exercise has other health and lifespan extending benefits. Hopefully, my BG values and insulin doses are close enough to normal to avoid both a reduction in lifespan and diabetic complications. Only time will tell.

I have written two ebooks with Ellen Davis, MS of ketogenic-diet-resource.com that explain how to use a real-food low carbohydrate ketogenic diet to manage type 1 and type 2 diabetes. They also explain how insulin, oral, and other injectable diabetes medications need to be adjusted or discontinued at your physician’s direction after changing to the ketogenic diet. In addition, they explain how the ketogenic diet can be used to support exercise while improving body composition by decreasing fat mass and increasing muscle mass. Recipes, food tables with carb, protein, and fat quantities, and tips for avoiding side-effects are provided to help formulate and sustain a ketogenic diet long-term. Links to relevant scientific literature are included as well.

T1-cover-300

 

T2--book-cover-300

Till next time ….

#30 Hybrid Closed-Loop Insulin Delivery System in Patients With Type 1 Diabetes – A Safety Study

In the October 4, 2016 issue of JAMA, a research letter was published with the results of a safety study of a hybrid closed-loop insulin delivery system in patients with type 1 diabetes (T1D). I have personally been interested in this artificial pancreas since I was diagnosed with T1D in 1998.

The system uses both an insulin pump and a continuous glucose monitor (CGM) that sends its data to a proprietary algorithm to adjust the insulin pump rate (up, down, or off if needed) as well as blood glucose monitoring that is needed to calibrate the CGM.

Patients aged 14 to 75 years with type 1 diabetes for at least 2 years, glycated hemoglobin (HbA1c) less than 10%, and more than 6 months of insulin pump use were recruited from 10 centers (9 in the United States, 1 in Israel) between June 2, 2015, and November 11, 2015. Patients were required to periodically calibrate sensors and enter carbohydrate estimates for meal boluses. Every midnight, multiple parameters were automatically adjusted by the algorithm.

Results

Of the 124 participants (mean age, 37.8 years [SD, 16.5]; men, 44.4%), mean diabetes duration was 21.7 years, mean total daily insulin dose was 47.5 U/d (SD, 22.7), and mean HbA1c was 7.4% (SD, 0.9). Over 12 389 patient-days, no episodes of severe hypoglycemia or ketoacidosis were observed. There were 28 device-related adverse events (Table 1) that were resolved at home. There were 4 serious adverse events (appendicitis, bacterial arthritis, worsening rheumatoid arthritis, Clostridium difficile diarrhea) and 117 adverse events not related to the system, including 7 episodes of severe hyperglycemia due to intercurrent illness or other nonsystem causes.

post-30-table-1-device-related-adverse-events-among-patients-using-hybrid-closed-loop-insulin-systems

The system was in closed-loop mode for a median of 87.2% of the study period (interquartile range, 75.0%- 91.7%). Glycated hemoglobin levels changed from 7.4% (SD, 0.9) at baseline to 6.9% (SD, 0.6) at study end (Table 2). From baseline to the end of the study, daily dose of insulin changed from 47.5 U/d to 50.9 U/d, and weight changed from 76.9 kg to 77.6 kg. The percentage of sensor glucose values within the target range changed from 66.7% at baseline to 72.2% at study end. The percentage of sensor glucose values below and above the target and glycemic variability are also shown in Table 2. Sensor and reference glucose values collected during the hotel stays were in good agreement, with an overall mean absolute relative difference of 10.3% (SD, 9.0).

post-30-table-2-glucose-control-insulin-usage-and-weight-among-patients-using-hybrid-closed-loop-systems

Discussion

To our knowledge, this is the largest outpatient study to date 5,6 and it demonstrated that hybrid closed-loop automated insulin delivery was associated with few serious or device-related adverse events in patients with type 1 diabetes. Limitations include lack of a control group, restriction to relatively healthy and well-controlled patients, the relatively short duration, and an imbalance between the length of the study periods. Differences in HbA1c levels may be attributable to participation in the study. A similar study in children (NCT02660827) is under way. Longer-term registry data and randomized studies are needed to further characterize the safety and efficacy of the hybrid closed-loop system.

The U.S. Food and Drug Administration approved Medtronic’s MiniMed 670G hybrid closed looped system on September 28, 2016. The study above published in JAMA was used for the FDA’s approval process. The glucose target used in the study was not mentioned so I assume it was 120 mg/dL as the Medtronic website states in the comments section that the Auto Mode target will be 120 mg/dL. It is also my understanding that the Auto Mode target cannot be changed by the patient. Thus for those with T1D following a low carbohydrate diet, I suspect this will not produce satisfactory results. Personally, I would not be satisfied with a glucose target of 120 mg/dL or a mean glucose of 150.8 mg/dL (Table 2 above). Use of the device resulted in an improvement in HbA1c from 7.4 to 6.9%, the patients required more insulin 47.5 to 50.9 IU/day, and gained body weight as a result from 76.9 to 77.6 kg. Use of body weight alone is not helpful in understanding whether the weight gain was lean body mass, fat, or some of both. Either way, that dose of insulin (50.9 IU/day) is 61.6% more than my current dose (31.5 IU/day) on a low carb diet. In my opinion, the lower insulin dose which is afforded by a low carb diet has many potential benefits, both short term (less hypoglycemia) and long term (less risk of insulin resistance, dyslipidemia, hypertension, cardiovascular disease, cancer, Alzheimer’s). So it will take time for the system to be tested in real world conditions so that the manufacturer/FDA will allow the patient to set their own glucose target value. However, I will be watching this with interest as I think it does have the potential for improvement in my glycemic control.

#29 September 2016 Update on My T1D Management

In September 2016 since I did so well with glycemic control last month, I decided to raise the bar a bit further. By that I mean, to narrow the blood glucose (BG) range that I am aiming for from 51-120 mg/dl to 61-110 mg/dl. Doing so will increase both the number of hypoglycemic and hyperglycemic BG values. I also reexamined what a normal BG is in non-diabetic healthy individuals. I have been using 83 mg/dl as a normal BG which is found in many different sources. However, that value is usually based on fasting or between meals and does not take into account the excursions due to meals or exercise. By aiming for 83 mg/dl, I have what I consider to be excessive numbers of low BG readings despite the fact that they are either asymptomatic or minimally so. If meal and exercise related BG excursions are taken into account, the “normal” value would definitely be higher. So I searched for studies that measured BG over the entire 24 hours in a day in those without diabetes. I found only one study which I will present below. If anyone finds other such studies please let me know via comment or email. Addendum: A blog follower directed me to another study that measured continuous interstitial glucose in nondiabetic healthy children and adults. For adults >= 45 years of age, the mean interstitial glucose +/- SD was 95 +/- 12.4 mg/dl with a coefficient of variation of 13%. Thanks for that Adam B.

Below are my BG values using the new target ranges mentioned above for September 2016. From the last row for September, the mean BG was 85 mg/dl at a slightly higher insulin dose, 31.5 IU/day compared to 30.4 IU/day last month. The percentage of BG values < 61 mg/dl increased from 15% to 25%.  That’s on average one hypoglycemic value per day and despite the fact that they are asymptomatic or minimally so is more than I am comfortable with.

post-29-bg-table

As presented in blog post #15 exogenous insulin cannot mimic normal insulin secretion, so persons with type 1 diabetes 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 symptoms, brain damage, seizure, injury, coma, or death. What those values are varies from one person to the next and are contextual based on one’s recent level of glycemic control. Aiming for normal 90-95 ± 7-12 mg/dl (mean ± SD) is desirable as long as hypoglycemia is minimized. Following a low carbohydrate ketogenic diet may provide additional brain fuel in the form of ketones to protect the brain when BG does go low. I will also present another study below that shows that hypoglycemic mortality is reduced in rats with recurrent iatrogenic hypoglycemia.

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

post-29-exercise-and-bg-graphs

The table below shows the summary of current and previous BG variability results. Most of the results were improved compared to previous months and years with improvement in the following variability measures: mean daily BG range = 62, mean time of hyperglycemia = 3.8 hr/day, interquartile BG range = 41. The measures of BG variability were defined and explained in blog post #10.

post-29-bg-variability-table

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

post-29-insulin-dose-graphs

The Ketonix breath ketone (acetone) monitor results beginning June 2015 are shown below (see blog post #19 for more details). I have been in continuous nutritional ketosis due to my low carbohydrate ketogenic diet. There is a noticeable gradual decline in the readings. I would guess this is related to either a gradual increase in carbohydrate intake from nuts and seeds or that I am able to utilize the ketones more effectively. I have added MCT oil 2 tbsp./day beginning 9/27/2016 to my diet which may increase the breath acetone values.

post-29-ketonix-graph

The graphs below show the change in BG that results from mealtime rapid-acting insulin. On the x-axis is the Breakfast and Dinner mealtime insulin dose (Humalog) plotted against the change in BG, i.e. Post meal BG minus Pre meal BG on the y-axis. Thus positive values represent an increase in BG and negative values represent a decrease in BG after the meal. Also, note that I removed 14 of 30 Breakfast points and 13 of 30 Dinner points from the graphs where the Post meal BG was not in the range of 61-110 mg/dl. The rationale for this is to eliminate graphing mealtime doses that were “incorrect” so to speak. This way the graph shows both that larger doses of insulin reduce BG more (obvious), but more importantly even when the resulting Post BG was in an acceptable range, that there is a wide variation in the amount of BG reduction for any given dose of insulin. This variation can be due to varying absorption of injected insulin, variation in insulin sensitivity from exercise, or variation in food consumed during the meal from one day to the next. Reducing this variation is an important goal of mine.

post-29-post-pre-bg-graphs

The first study I want to review briefly is titled, Continuous Glucose Profiles in Healthy Subjects under Everyday Life Conditions and after Different Meals.

Continuous interstitial glucose measurement was performed under everyday life conditions (2 days) and after ingestion of four meals with standardized carbohydrate content (50 grams), but with different types of carbohydrates and variable protein and fat content. Twenty-four healthy volunteers (12 female, 12 male, age 27.1 ± 3.6 years) participated in the study. The mean 24-hour interstitial glucose trace under everyday life conditions is shown in Figure 2 [shown below]. The mean 24-hour interstitial glucose concentration was 89.3 ± 6.2 mg/dl (range 79.2–101.3 mg/dl), with a mean glucose concentration of 93.0 ± 7.0 mg/dl at daytime (7 am to 11 pm) and 81.8 ± 6.3 mg/dl during the night (11pm to 7am). The mean 24-hour capillary blood glucose concentration was 90.9 ± 6.8 mg/dl (16 values per 24 hours), and mean blood glucose concentrations at daytime and during the night were 92.7 ± 6.9 mg/dl (14 values per day) and 78.1±7.9 mg/dl (2 values per night).

Thus, a better BG target to aim for is 90.9 ± 6.8 mg/dl rather than 83 mg/dl. By doing so, I should have fewer hypoglycemic values while still having little chance of diabetic complications.

post-29-normal-bg-profile-graph

The second study to review briefly is titled, Severe Hypoglycemia–Induced Lethal Cardiac Arrhythmias Are Mediated by Sympathoadrenal Activation. The abstract and two figures from the paper are shown below.

For people with insulin-treated diabetes, severe hypoglycemia can be lethal, though potential mechanisms involved are poorly understood. To investigate how severe hypoglycemia can be fatal, hyperinsulinemic, severe hypoglycemic (10–15 mg/dL) clamps were performed in Sprague-Dawley rats with simultaneous electrocardiogram monitoring. With goals of reducing hypoglycemia-induced mortality, the hypotheses tested were that: 1) antecedent glycemic control impacts mortality associated with severe hypoglycemia; 2) with limitation of hypokalemia, potassium supplementation could limit hypoglycemia-associated deaths; 3) with prevention of central neuroglycopenia, brain glucose infusion could prevent hypoglycemia-associated arrhythmias and deaths; and 4) with limitation of sympathoadrenal activation, adrenergic blockers could prevent hypoglycemia-induced arrhythmic deaths. Severe hypoglycemia–induced mortality was noted to be worsened by diabetes, but recurrent antecedent hypoglycemia markedly improved the ability to survive an episode of severe hypoglycemia. Potassium supplementation tended to reduce mortality. Severe hypoglycemia caused numerous cardiac arrhythmias including premature ventricular contractions, tachycardia, and high-degree heart block. Intracerebroventricular glucose infusion reduced severe hypoglycemia–induced arrhythmias and overall mortality. β-Adrenergic blockade markedly reduced cardiac arrhythmias and completely abrogated deaths due to severe hypoglycemia. Under conditions studied, sudden deaths caused by insulin-induced severe hypoglycemia were mediated by lethal cardiac arrhythmias triggered by brain neuroglycopenia and the marked sympathoadrenal response. Diabetes 62:3570–3581, 2013

post-29-hypoglycemic-mortality-study

As discussed in this paper, hypoglycemia is both maladaptive and adaptive.

Hypoglycemia attenuates sympathoadrenal and symptomatic responses to the same level of subsequent hypoglycemia and thus causes hypoglycemia-associated autonomic failure (HAAF) in diabetes… On the other hand, HAAF appears to be adaptive in that it reduces the most devastating effect of severe hypoglycemia—death.

If blood ketones are sufficiently high during nutritional ketosis to prevent neuroglycopenia during hypoglycemia, then a ketogenic diet ± MCT oil supplementation ± exogenous ketone supplementation might prevent death from hypoglycemia in persons taking insulin for type 1 diabetes by preventing neuroglycopenia. Second, those with type 1 diabetes who are seeking close to normal glycemic control will likely experience multiple hypoglycemic episodes despite their efforts to avoid them. This study suggests that these recurrent hypoglycemic episodes may actually blunt the sympathoadrenal response and thus reduce the likelihood of death from cardiac arrhythmia. Thus, not having the sympathoadrenal-mediated symptoms during hypoglycemia whether that is due to either hypoglycemia unawareness or to brain utilization of ketones may actually reduce the risk of death. Just to be clear, I am not suggesting that it is okay to have hypoglycemia. Rather, I am saying that hypoglycemia does occur in type 1 diabetes despite one’s best efforts to avoid it and nutritional ketosis from a ketogenic diet may reduce the likelihood of hypoglycemia–induced lethal cardiac arrhythmias. Hopefully, this will be studied in humans in the near future.

In October, I will continue weightlifting and aerobic exercise on alternate days. I have added back two additional exercises: deadlifts and jerks from the rack. My olympic weightlifting takes about 2 hours to complete including warmup, cool down, and stretching to maintain mobility. The aerobic exercise consists of swimming or cycling at low intensity for ≈ 0.5 – 2 hours. The goal is to exercise consistently to maintain insulin sensitivity while avoiding injury and overtraining.

The goal of glycemic management in type 1 diabetes is to keep BG as close to normal (≈ 90 mg/dl) as is safely possible (i.e. avoiding hypoglycemia) to avoid both diabetic complications, a reduction in lifespan, and injury and death from hypoglycemia. For me, a nutrient-dense real-food low carbohydrate ketogenic diet (see blog post #9 for more details) combined with insulin analogs (Humalog/Lantus) have been the best tools so far in accomplishing this goal. I also feel, but cannot prove, that this eating plan and the resulting nutritional ketosis reduces the symptoms of hypoglycemia and protects the brain from the consequences of mild degrees of hypoglycemia (see blog post #12 for more details). Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult, but I both enjoy it and feel exercise has other health and lifespan extending benefits. Hopefully, my BG values and insulin doses are close enough to normal to avoid both a reduction in lifespan and diabetic complications. Only time will tell.

Till next time ….

#28 August 2016 Update on My T1D Management

I am pleased to announce the 2nd Annual Conference on Nutritional Ketosis and Metabolic Therapeutics to be held in Tampa, Florida, February 1-4, 2017. I would like to thank the organizers, Angela Poff, PhD and Dominic D’Agostino, PhD, for inviting me to speak on the “Management of Type 1 Diabetes with a Ketogenic Diet.” I think anyone interested in ketogenic diets would enjoy this conference. You can see some of the talks from the inaugural event at the Epigenix Foundation YouTube channel. You can register for the event here.

In August 2016, I achieved a personal best in glycemic control. Although glucose management in diabetes is subject to many factors that are difficult to quantify, I attribute this month’s results to my most recent exercise schedule. Starting the second week of August, I changed to an alternating schedule of weightlifting with swimming or cycling. This facilitated recovery from each activity and the daily exercise hopefully stabilized my insulin sensitivity and improved glycemic control. I hope this continues and results in some improvement in the weights I am able to lift. Currently, I’m at 135 lb. snatch and 175 lb. clean and jerk which is just short of my personal bests of 140 lb. and 185 lb., respectively. There has been no significant change in my low carb healthy fat ketogenic lifestyle.

The summary table of current and previous mean blood glucose (BG) and insulin doses is shown below. Compared to July 2016, my mean BG decreased from 101 to 95 mg/dl in part as a result of an increase in mean total daily insulin dose from 28.1 to 30.4 IU/day due to an increase in basal insulin (from a mean of 21.2 to 21.8 IU/day Lantus) and an increase in rapid-acting insulin (from a mean of 6.9 to 8.5 IU/day Humalog). I had 3 of 130 (2%) BG readings < 51 mg/dl, but all were without symptoms due to either nutritional ketosis or hypoglycemia unawareness (see blog post #12 for more details). I had 102 of 130 (79%) BG readings between 51 and 120 mg/dl, 24 of 130 (18%) between 121 and 200 mg/dl, and 1 of 130 (1%) > 200 mg/dl.

Post 28 Means Table

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

Post 28 Blood Glucose and Exercise

The table below shows the summary of current and previous BG variability results. Most of the results were improved compared to previous months and years with improvement in the following variability measures: standard deviation = 32, coefficient of variation = 34%, mean daily BG range = 66, mean time of hyperglycemia = 3.7 hr/day, mean time of hypoglycemia = 0.1 hr/day, interquartile BG range = 47. The measures of BG variability were defined and explained in blog post #10.

Post 28 Variability Table

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

Post 28 Insulin Doses

The Ketonix breath ketone (acetone) monitor results beginning June 2015 are shown below (see blog post #19 for more details). I have been in continuous nutritional ketosis due to my low carbohydrate ketogenic diet. There is a noticeable gradual decline in the readings. I would guess this is related to a gradual increase in carbohydrate intake from nuts and seeds.

Post 28 Ketonix Breath Ketones

The graphs below show the change in BG that results from mealtime rapid-acting insulin. On the x-axis is the Breakfast and Dinner mealtime insulin dose (Humalog) plotted against the change in BG, i.e. Post meal BG minus Pre meal BG on the y-axis. Thus positive values represent an increase in BG and negative values represent a decrease in BG after the meal. Also, note that I removed 3 of 31 Breakfast points and 3 of 31 Dinner points from the graphs where the Post meal BG was not in the range of 51-120 mg/dl. The rationale for this is to eliminate graphing mealtime doses that were “incorrect” so to speak. This way the graph shows both that larger doses of insulin reduce BG more (obvious), but more importantly even when the resulting Post BG was in an acceptable range, that there is a wide variation in the amount of BG reduction for any given dose of insulin. This variation can be due to varying absorption of injected insulin, variation in insulin sensitivity from exercise, or variation in food consumed during the meal from one day to the next. Reducing this variation is an important goal of mine.

Post 28 Breakfast &amp; Dinner Post BG - Pre BG

I required quite a few doses of rapid-acting insulin (Humalog) to correct hyperglycemia this month. The resulting change in BG is shown in the graph below. Negative values represent a decrease in BG. Note that I removed 2 of 15 correction doses from the graphs where the Post meal BG was not in the range of 51-120 mg/dl. The rationale for this is to eliminate graphing correction doses that were “incorrect” so to speak. Again, the main feature is variability and unpredictability of the BG response to insulin injections. In contrast to the mealtime insulin doses, this may be an over interpretation. To make this statement, I would have to recheck the BG about 3 hr. after the correction dose. This occurred the minority of the time. Instead in most instances, I wait until my next “usual” time to check the BG. Thus, other factors can affect the subsequent BG result other than the correction dose of Humalog.

Post 28 Humalog Correction Doses

The graph below shows the change in BG due to weightlifting. On the y-axis, positive values represent an increase in BG due to weightlifting. There were thirteen positive values representing an increase in BG due to weightlifting, but the degree of increase declined through the month (red linear regression line). The main feature is that intense resistance exercise stimulates catabolic hormones (epinephrine, cortisol, glucagon) to release nutrients into the blood stream and to stimulate muscle contractions. In a person with T1DM who cannot make insulin to correct the rise in BG, this results in hyperglycemia as shown in the graph.

Post 28 Post BG - Pre BG due to weightlifting

Since I did more swimming this month I decided to graph the change in BG due to swimming. On the y-axis, positive values represent an increase in BG whereas negative values represent a decrease in BG due to swimming. There were four negative values representing a decrease and five positive values representing an increase in BG due to swimming. As I have mentioned before, changes in BG with exercise are not very predictable, i.e. sometimes up, sometimes down. It really keeps you on your toes so to speak. The red linear regression line indicates a general increase in BG with swimming during the month, but the changes in BG were rather modest.

Post 28 Post BG - Pre BG due to swimming

In September, I will continue weightlifting and aerobic exercise on alternate days. Thus I will continue weightlifting to 3.5 days/week and aerobic exercise to 3.5 days/week. The olympic weightlifting consists of only 4 exercises (snatch, clean and jerk, snatch overhead squat, front squat) which takes about 2 hours to complete including warmup, cool down, and stretching to maintain mobility. The aerobic exercise consists of swimming or cycling at low intensity for 0.5 – 2 hours. The goal is to exercise consistently to maintain insulin sensitivity while avoiding injury and overtraining.

The goal of glycemic management in type 1 diabetes is to keep BG as close to normal (83 mg/dl) as is safely possible (i.e. avoiding hypoglycemia) to avoid both diabetic complications and a reduction in lifespan. For me, a nutrient-dense whole food low carbohydrate ketogenic diet (see blog post #9 for more details) combined with insulin analogs (Humalog/Lantus) have been the best tools so far in accomplishing this goal. I also feel, but cannot prove, that this eating plan and the resulting nutritional ketosis reduces the symptoms of hypoglycemia and protects the brain from the consequences of mild degrees of hypoglycemia (see blog post #12 for more details). Exercise with its resulting varying insulin sensitivity and hormonal changes actually makes glycemic management more difficult, but I both enjoy it and feel exercise has other health and lifespan extending benefits. Hopefully, my BG values and insulin doses are close enough to normal to avoid both a reduction in lifespan and diabetic complications. Only time will tell.

Till next time ….

#27 July 2016 Update on My T1D Management

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

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

Post 27 Means Table

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

Post 27 Blood Glucose and Exercise

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

Post 27 Variability Table

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

Post 27 Insulin Doses

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

Post 27 Ketonix Breath Ketones

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

Post 27 Breakfast Dinner BG changes

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

Post 27 BG change due to weightlifting

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

Post 27 Humalog Correction Doses

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

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

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

Till next time ….