This is a monthly update on my glycemic management of type 1 diabetes (T1DM) using Humalog and Lantus insulin injections with resistance exercise and a ketogenic whole-food diet as described in my book, The Ketogenic Diet for Type 1 Diabetes also available on Amazon in print. My other book, Conquer Type 2 Diabetes with a Ketogenic Diet, is also available on Amazon in print. I would appreciate anyone who has read and benefited from either of these books to leave a review on Amazon. The number and ratings of the reviews are used by Amazon to order the search results when people are looking for books on diabetes.
I have made several changes over the past three months to further improve the glycemic control of my T1DM. These include:
- I returned to two meals per day on 8/8/2018, but now eating breakfast (8 AM) and late lunch (3 PM) instead of breakfast and dinner. This will allow me to administer Humalog at 8 AM and 3 PM and Lantus at 6 PM separately rather than Humalog and Lantus together at 6 PM as I had been doing for many years. Turns out my basal Lantus dose was too high and my dinner-time Humalog dose was too low (many days I was not even taking Humalog at dinner-time). I check my blood glucose (BG) five times a day at 8:00 AM (fasting i.e. before breakfast) and 11:00 AM, at noon I exercise, another BG check and lunch at 3 PM, another BG check at 6 PM and take my dose of Lantus, then check BG at 10 PM (bedtime).
- I returned to weighing my food on a kitchen scale last month to more accurately balance the Humalog dose with food. The last time I did this was about 10 years ago when I was carbohydrate counting. I did it for two years with very unsatisfactory results. IMO carbohydrate counting does not work for T1DM (or for T2DM for that matter) primarily because eating a lot a carbs in those with diabetes does not work.
- Last month, I increased my dose of metformin to the maximum of 2,500 mg/day, 1,500 mg with breakfast and 1,000 mg with lunch. I have been tolerating this maximal dose without any side effects. I am convinced that even though I am relatively insulin sensitive, the metformin helps control post-meal BG by suppressing liver glucose production in response to meals and may be increasing muscle glucose uptake as well. These are the known mechanisms of metformin in helping to control BG in diabetes. I believe metformin is helping me because on the several occasions when I forgot to take the dose my post-meal BG was significantly elevated (by 30 – 40 mg/dl) compared to the previous days when I took the metformin. It makes sense that metformin would help T1DM because as I reviewed in other articles on my website lowcarbdiabetesdoctor.com, exogenous insulin is at a relatively low concentration around the pancreatic alpha-cells compared to normal and thus glucagon secretion is chronically elevated and particularly elevated after meals since amino acids (from the protein in the meal) directly stimulate alpha-cell glucagon secretion. Glucagon in turn stimulates liver glucose production (and ketone production). Less liver glucose production by taking metformin in turn means either lower BG or since my BG is low already, means lower insulin doses. I think lower insulin doses while BG is controlled is beneficial in terms of prevention of insulin resistance (and therefore “double diabetes”), cardiovascular disease, cancer, and Alzheimer’s dementia. These chronic conditions constitute the top causes of death amongst Americans. See the section below about euglycemic diabetic ketoacidosis where exogenous insulin doses can be too low!
- Last month, all of the above resulted in a reduction in total daily insulin dose from 24.5 IU/day on 8/8/2018 to 16 IU/day on 9/30/2018 as well as a reduction in body weight from 163.4 to 150.6 lb. (over a 10 week period). I am sure the reduction in body weight contributed greatly to the reduction in insulin dose. However, insulin dose is usually expressed as IU/kg body weight and when expressed this way it is a reflection of insulin sensitivity. In general the lower the dose, the more insulin sensitive (assuming BG control is the same) the person is. Expressed this way, my total daily insulin dose decreased from 0.33 IU/kg BW/day on 8/8/2018 to 0.23 IU/kg BW/day on 9/30/2018. Thus, my insulin sensitivity improved due to the weight reduction and the increase in metformin dose from 2,000 mg/day to 2,500 mg/day. This is the lowest dose of insulin I have taken since my diagnosis in 1998. Fortunately, my insulin doses remained just as low in October, on average 15.7 IU/day, and my weight declined slightly more as well to 147.3 lb. Thus, the total daily insulin dose based on body weight was 0.24 IU/kg/day which is almost one-fourth the amount I was taking prior to starting my low carb ketogenic diet.
- The last change I made last month was to decrease the volume of vegetables I was eating. This was due to some GI disturbances after meals. I was really eating more than I needed in terms of getting my micronutrients and fiber. I am glad to report that the GI disturbances resolved completely in October.
Glycemic Management Results for October 2018
My October glycemic results were about the same in terms of mean BG (96 mg/dl) and standard deviation (30 mg/dl) compared to September. Of course, I was hoping for more improvement (a reduction in standard deviation), but I did not achieve that. I did reach my desired BG goal of about 70% of time spent with a BG value between 61 and 110 mg/dl. I had a reduced frequency of asymptomatic hypoglycemia this month compared to last month. In October, 8.4% of my BG meter readings were less than 61 mg/dl, 61.3% were between 61 and 110 mg/dl, 30.3% were between 111 and 200 mg/dl, and none were in excess of 200 mg/dl. Preventing hypoglycemia is my top priority now so this reduction is asymptomatic hypoglycemia was encouraging.
The graph below shows my actual BG readings and the total daily insulin doses of Humalog and Lantus insulin and the total of both insulin doses.
The graph below shows the BG readings and the Humalog doses given.
I had more fluctuations in insulin doses this month compared to prior months. Hopefully this will smooth out in November.
The graph below shows the % Time spent in different ranges of BG on each day of October.
The graph below shows the % Time my BG was low, in target, or high and the mean BG value in those intervals for the month of October.
The graph below shows the % of meter BG readings in three different ranges at each of the five times of day that I measure it for October.
New Diet Regimen beginning October 2018
The table below shows my new diet menu.
Note: the MCT oil is only to be used if my body weight falls below 66 kg or 145 lb. I haven’t needed to use it yet.
From the table above you can see I eat different breakfast menus on Sunday Tuesday Thursday Saturday (beef and egg) compared to Monday Wednesday Friday (salmon). The weight of food and macronutrients are almost identical. Pictures of the meals are shown below. I realize I am not a professional food photographer. LOL.
Below is lunch at 3 PM everyday.
The macronutrient counts are as follows:
Note that I am consuming 2.1 grams of protein/kg body weight/day. This is more protein than many who follow a ketogenic diet might consume. I am doing this due my age and and athletic goals as I desire to hold on to as much lean muscle mass as I can as I age. Aging has been shown to create some resistance to dietary protein in promoting skeletal muscle synthesis as well as resistance to the muscle building effects of resistance exercise. Stuart M Phillips, PhD in the Department of Kinesiology, McMaster University, Hamilton, Canada, based on his meta-analysis of multiple studies recommends a dietary protein intake of 1.62 grams protein/kg/day. However the 95% confidence interval is 1.03 to 2.20 grams protein/kg/day, so I decided to consume protein at the higher end of his recommendation since I have no contraindications to doing so. The paper is here for your reference. At this level of protein intake, my blood ketones last month on two occasions were 0.5 and 0.6 mM.
You may wonder if eating the same menu over and over each day is difficult. For me it is not. I realize not everyone would be satisfied with the monotony. However, I did pick foods that I really enjoy and secondly, for me anyway, the lack of hunger produced by a ketogenic diet eliminates all cravings for other foods. If the above diet will result in the type of BG control that I am seeking, then the lack of variety will be worth it. Additionally, I can change the menu in small ways from time to time as long as I do so infrequently.
The graph below is a pictorial version of the above macronutrient table.
The graph below shows the % of the RDA (Recommended Daily Allowances) of vitamins provided by my diet. This was to confirm that I am getting all the micronutrients in adequate amounts. So as not to make this post too long, I will skip for now the meaning of RDA. Turns out that the confidence one should place on the RDA amounts is not very high.
The graph below shows the % of the RDA (Recommended Daily Allowances) of minerals provided by my diet.
I would like to give credit to cronometer.com as an easy to use application to enter foods and determine both the macronutrient and micronutrient components of a menu.
Side Bar Regarding Euglycemic Diabetic Ketoacidosis
I have written on this blog in a prior post about nutritional ketosis as apposed to diabetic ketoacidosis (DKA). I think nutritional ketosis is a desirable state in general, but that the ketone levels do not need to be particularly elevated and in fact probably should not be particularly elevated, e.g. > 4 mM. I recently heard a talk by Jake Kushner, MD (a pediatric endocrinologist) at the Low Carb Houston conference where he said that persons with T1DM using a ketogenic diet to help manage their BG should be aware that nutritional ketosis may in rare cases increase the likelihood of euglycemic diabetic ketoacidosis (EDKA). DKA and EKDA are both pathological and potentially life-threatening states where the liver is overproducing ketones due to a high glucagon to insulin ratio in the blood, but in contrast to DKA, in EDKA the BG is not particularly elevated (generally less than 200 mg/dl). The fact that the BG is not particularly elevated makes the person with T1DM not be on the lookout for DKA. This phenomenon of EDKA has become more prominent recently due to some persons with T1DM being prescribed an SGLT2 inhibitor drug (which include the following: canagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (Jardiance), empagliflozin/linagliptin (Glyxambi), empagliflozin/metformin (Synjardy), dapagliflozin/metformin (Xigduo XR)) off label to improve BG control and subsequently developed EDKA. SGLT2 inhibitors are FDA approved for T2DM and more commonly used for T2DM. The number of cases of EDKA has also increased in those with T2DM. Thus, this problem is not limited to just T1DM.
Dr. Kushner explained that nutritional ketosis has some physiological similarities to the effect of SGLT2 inhibitors. One is that SGLT2 inhibitors lead to chronically elevated glucagon levels and an elevated glucagon to insulin ratio. This elevated glucagon to insulin ratio occurs in those with T1DM (even not taking an SGLT2 inhibitor) because exogenous insulin does not adequately suppress alpha-cell glucagon production and I believe that nutritional ketosis and the resulting lower exogenous insulin doses probably magnifies this effect (although I don’t think it has been actually measured). So first, in my opinion, SGLT2 inhibitors should not be used in T1DM especially if a low carb ketogenic diet is being consumed. The second condition that can lead to an elevated glucagon to insulin ratio and the potential risk for EDKA in persons with T1DM is restriction of food intake either voluntarily (intentional fasting) or involuntarily due to an illness like gastroenteritis. The reduction in food intake requires a further (beyond what the low carb diet requires) reduction in exogenous insulin doses to avoid hypoglycemia. However, because as mentioned earlier exogenous insulin at very low doses does not adequately suppress alpha-cell glucagon production, the liver receives a signal (a high glucagon to insulin ratio) to overproduce ketones. This would not occur normally in a non-diabetic person who intentionally fasts or does not eat due to illness. So the take home message is that very low (or large reductions in) exogenous insulin doses in persons with T1DM should be a waving red flag. The blood ketone levels should be monitored along with BG and exogenous insulin doses need to be increased to keep blood ketones below, say 4 mM, even if that requires eating a significant amount of dietary carbohydrates. Obviously, illnesses can and do occur and cannot necessarily be avoided. However, voluntary fasting or significant reductions in caloric intake for the purpose of body fat loss, or other potential benefits (e.g. autophagy) can be moderated or avoided in those with T1DM. The benefits of fasting for autophagy and improvements in lifespan or health-span has only been studied in microorganisms and small animals, not in humans. Thus, implementing fasting for these purposes given the potential risks in those with T1DM is unwarranted in my opinion. As far as body fat loss is concerned, achieving a normal amount of body fat is important, but it must be achieved gradually with a modest caloric deficit (e.g. 100 – 200 kcal/day) to be safe in those with T1DM.
My Goals For November 2018 and Beyond
I am going to raise the bar further in terms of my glycemic management. I am not, by any means, sure that I will be able to achieve these lofty goals, but without goals, there is no direction to move toward. These are my goals:
- Achieve near-normal BG values including mean BG of 96 mg/dl with a standard deviation as close to 12 mg/dl as possible.
- Adjust my target BG range up from 61 – 110 mg/dl to 71 – 120 mg/dl and spend 80% of the day in this new higher range, 71 – 120 mg/dl. Honestly, with the elevation in BG that results from olympic weightlifting, this will be difficult to achieve. I do not feel the temporary elevation in BG that results from exercise is harmful. The elevation in BG is a normal response to exercise. The part that is not normal is that without exogenous insulin, the BG would remain elevated. This is why I eat lunch and take insulin right after I finish exercising. The main purpose of increasing the target BG range is to encourage me to avoid hypoglycemia. However, this elevation in BG after olympic weightlifting increases both the mean BG and the standard deviation. Thus, normalizing both of these parameters may not be compatible with olympic weightlifting.
- Eliminate hypoglycemia or make it a rare event. I my case, my odds of developing long-term diabetic complications due to hyperglycemia are quite small, but I think my risk of having adverse effects of hypoglycemia are significantly higher. I want to eliminate that risk. This is my highest priority.
How Will I Achieve These Goals
In addition to the changes made in the past two months enumerated above, I am going make smaller adjustments in insulin doses by using 0.25 IU increments or decrements on my insulin syringes. This is because my total insulin doses are smaller than in the past and thus I need to have finer adjustments to the doses so the % change remains small. I have become aware that this applies to my basal insulin, Lantus, dose as well. I have noticed that changes in the Lantus dose have significant BG implications the following morning. I had been operating under the assumption that because it was “long-acting” it would take larger adjustments and require several days to have an effect. This is not the case. So any changes in my Lantus dose will be smaller than I have used in the past.
I hope next month I will have some improvements to report.