Learn how to control your blood sugar to avoid the many life-threatening complications of diabetes with a low carb diet and lifestyle changes from a physician with type 1 diabetes who has achieved near-normal blood sugars with less insulin. My name is Keith Runyan, MD. I am an allopathic physician who has had type 1 diabetes since 1998. Over the years since my diagnosis, I have read extensively to acquire a deeper understanding of type 1 diabetes and how to improve my blood sugar control with diet and lifestyle changes. Each person with type 1 diabetes has their own challenges with controlling this condition. In this article, I will discuss the most common problems in managing type 1 diabetes that are encountered and how they can be overcome. I hope you will be able to take this information to your physician and together as a team, you can improve your blood sugar control to the point that you can either prevent or improve any long-term diabetic complications. This article is intended for persons with type 1 diabetes, the parents of children with type 1 diabetes, or anyone who wants a better understanding of the challenges that persons with type 1 diabetes are faced with every hour of every day for the rest of their lives.
Type 1 diabetes (T1DM) is an autoimmune condition caused by unknown environmental factors in persons who are genetically susceptible. The fact that the incidence of T1DM has been increasing over the past 50 years by 3-5% per year is good evidence that environmental factors play a big part in causing this condition. The incidence of T1DM varies greatly with geographic location. Children living in Finland, for example, are 100 times more likely to develop T1DM than those living in China. Migrants also acquire a similar incidence of T1DM as the children in the country that they move to. Suspected environmental factors include viral infections, components of cow's milk including bovine insulin and casein, and gluten- and non-gluten containing cereals. The most common viruses felt to be initiators of autoimmune responses include herpes viruses, mumps, rubella, and retroviruses. For reasons that are unknown, the body recognizes proteins in the dietary or viral components as foreign invaders and mounts an immune attack against them. The structure of the environmental agents are similar enough to human insulin and/or the human beta-cells in the pancreas that they are attacked and destroyed in the process. The immune system has a memory such that even if the viral infection that initiated the attack lasted just a week or so, the immune system continues to destroy the beta-cells until they are essentially all gone within 3 years of diagnosis. That said, as many as 15% of older T1DM patients may retain some beta-cell function for 10 years after diagnosis. Immune cells secrete autoantibodies to insulin, GAD65 (Glutamic Acid Decarboxylase), ICA512 (called also IA-2) or ZnT8 (Zinc Transporter 8), and precedes the onset of elevated blood glucose by several years. Routine childhood vaccinations have not been linked to the development of T1DM, and two studies showed a possible protective effect of the measles-mumps-rubella vaccine here.
Even though the above suspected initiating environmental agents are based on epidemiological studies which are a weaker type of scientific evidence, I have chosen to eliminate dairy from my diet. Many dairy foods are an acceptable part of a ketogenic diet including butter, cheese, yogurt, whipping cream, and sour cream. However, persons with T1DM are at risk for other autoimmune diseases including autoimmune thyroid disease, celiac disease, autoimmune gastritis, pernicious anemia, Addison's disease and vitiligo. Autoimmune thyroid disease is the most prevalent endocrinopathy among diabetic patients. Thus, eliminating dairy in addition to all grains (due to their highly refined carbohydrate content as well as potential for initiating autoimmune disease) is a simple step I can take to reduce my risk of other acquiring other autoimmune diseases.
The symptoms of T1DM are notable when about half of the beta-cells have been destroyed. The younger the age at the time of diagnosis, the greater the degree of beta-cell destruction and the more likely the person will present with diabetic ketoacidosis (DKA). The initial symptoms of diabetes are caused by both insulin deficiency and elevated blood glucose (hyperglycemia) and include frequent urination, increased thirst, generalized fatigue, and unintentional weight loss despite increased food intake.
The long-term complications of diabetes are many but the major ones that lead to disability and death include nerve damage called diabetic neuropathy, eye damage called diabetic retinopathy, and kidney damage called diabetic nephropathy. Although these complications do not occur in all of those with diabetes, there is a direct correlation between the long-term glycemic control and the development of these complications. The better the glycemic control, the less likely one is to develop these long-term complications. Because type 2 diabetes (T2DM) is now so prevalent, diabetes accounts for the majority of cases of blindness, the majority of cases of end-stage kidney failure which then must be treated with dialysis or kidney transplantation, and the majority of cases of toe, foot, and leg amputations. Diabetic retinopathy and nephropathy are referred to as microvascular complications and toe, foot, and leg amputations result from both microvascular and macrovascular complications of diabetes. Both elevated blood glucose (BG) and elevated insulin levels participate in these pathologic conditions. In T2DM, insulin levels are elevated in response to insulin resistance. In T1DM, insulin levels are elevated from both a high-carbohydrate diet and from the fact that injecting exogenous insulin is not physiological and therefore does not have quite the same effects on key organs as occurs normally. The other important category of long-term complications of diabetes is called macrovascular disease. This also results from both elevated blood glucose and elevated insulin levels. Macrovascular disease results from inflammation of the interior of artery walls (called the endothelium) and causes deposition of cholesterol containing plagues in the artery walls. The deposition of cholesterol is the body's attempt to repair the damage of inflammation. This plaque results in narrowing of the lumen of the vessel and over time, a reduction in the amount of blood that can move through the artery, starving the tissues downstream of nutrients and oxygen. In addition, the plaques formed in macrovascular disease can spontaneously rupture causing clots to form that can completely obstruct the blood vessel. This is what causes most heart attacks and strokes. Because macrovascular disease can occur anywhere in the body, virtually every organ and part of the body is at risk for damage. The combination of macrovascular disease in the legs and feet with sensory diabetic neuropathy is what leads to diabetic foot ulcers and eventually toe, foot, and leg amputations. All of these complications lead to a reduced life span and quality of life. The good news is that all of these diabetic complications are preventable and most are reversible. You might ask why I make this last statement because I can't quote any studies that show a low carb ketogenic diet can prevent or reverse diabetic complications. Well, we do know that more and more studies are coming out showing that a low carb ketogenic diet does result in improved glycemic control here and here . The second paper published in the journal Pediatrics, titled Management of Type 1 Diabetes With a Very Low–Carbohydrate Diet, here did show that more than 300 motivated children and adults did achieve normal HbA1c and BG values with no increase in the incidence of hypoglycemia. It is true that this was not the most rigorous type of study: a randomized controlled trial, but rather was a survey of subjects, their medical records, and their physicians, who follow a very low-carbohydrate diet from the TypeOneGrit Facebook Group. I happened to be one of the study subjects. Finally, we know from The Diabetes Control and Complications Trial (DCCT) published in 1993 here that improving glycemic control in T1DM did reduce the incidence and progression of diabetic complications. However in contrast to the study mentioned above, Management of Type 1 Diabetes With a Very Low–Carbohydrate Diet, the DCCT subjects made no change to their diet, but simply increased their insulin doses to reduce their HbA1c from on average 9% to 7%. This did significantly reduce their diabetic complications, but also resulted in a three-fold increase in severe hypoglycemia. So by extrapolation from these studies and from anecdotal reports from physicians like Dr. Richard Bernstein who was able to reverse his own kidney, heart, nerve, and eye disease with the very low carb diet, I am confident in saying that the very low carb diet (which is also ketogenic) can prevent, slow or reverse progression of, and at least for some of the diabetic complications can reverse long-term diabetic complications. The complications that I would expect to not be reversible are end-stage conditions like end-stage (stage 5) or advanced chronic kidney disease (stage 4), end-stage cardiomyopathy from atherosclerotic heart disease, and blindness from diabetic retinopathy. The conditions that I believe are reversible include sensory peripheral neuropathy (numbness of toes and feet), milder stages of chronic kidney disease (stages 1-3) due to diabetic nephropathy, early stages of diabetic retinopathy before there is significant vision loss, as well as atherosclerotic vascular disease before there is end-organ damage (infarcted heart muscle from a heart attack, for example). That is not to say that a low carb ketogenic diet will not be beneficial after developing more advanced disease, I am just saying that once end-stage organ damage occurs, one should not expect the low carb diet to reverse that damage. It has been documented that a low carb ketogenic diet reduces inflammation which is part of the initiating process that leads to atherosclerotic vascular disease here and here . This would likely not only prevent vascular disease, but also prevent worsening of existing vascular disease, in my opinion.
Exogenous insulin means insulin coming from outside the body. It is the insulin that those of us with T1DM must inject to control our blood glucose (BG) and in fact to be able to live. Although many people do not trust the pharmaceutical industry and their medications, I can say without any hesitation that I am alive today because of their efforts. Endogenous insulin means the insulin coming from inside the normal body. It is endogenous insulin that is severely deficient or nonexistent in persons with T1DM. As mentioned above, this is due to the autoimmune destruction of the beta-cells in the pancreas. Since the beta-cells are the only cells in the body that can make insulin, their destruction results in the loss of the ability to make insulin altogether.
However, in order to understand how exogenous insulin does not reproduce the same physiologic effects of endogenous insulin, we have to have some understanding of the location of the beta-cells in the body and how that location influences other hormones that also regulate BG.
The beta-cells are located in the islets of Langerhans which contain other peptide hormone producing cells. About 70% of the islet cells are beta-cells which produce both insulin and amylin. Therefore, persons with T1DM do not produce either insulin or amylin. About 20% of the islet cells are alpha-cells which produce glucagon. About 10% of the islet cells are delta-cells which produce somatostatin (which can inhibit glucagon secretion). About 5% of the islet cells are PP cells (also called gamma cells or F cells) which produce pancreatic polypeptide. About 1% of the islet cells are epsilon-cells which produce ghrelin (a hormone that signals the sensation of hunger in the brain).
The physiologic effects insulin, amylin, and glucagon on glucose metabolism are shown in Table 1 below. Insulin is an anabolic hormone that promotes tissue building and energy utilization, whereas glucagon is a catabolic hormone that breaks down hepatic (liver) glycogen to produce glucose and stimulates new glucose production (gluconeogenesis) in the liver. Amylin inhibits glucagon secretion by the alpha-cells. Amylin plays a smaller role compared to insulin but its loss in T1DM does contribute to increased glucagon secretion by alpha-cells. Once the functions of the these hormones are understood, one can predict what happens to those with T1DM. In T1DM, the lack of insulin stimulates hepatic (liver) glucose production (via increased glucagon) as well as through its own lack of direct suppression of liver glucose production. However to understand why exogenous insulin does not correct this to the degree that occurs in non-diabetics, you need to know that it is the close proximity of the alpha-cells and beta-cells in the pancreatic islet that makes exogenous insulin much less effective in suppressing alpha-cell glucagon secretion and thus much less effective in suppressing hepatic (liver) glucose production. When exogenous insulin is injected into the subcutaneous fat, it results in a similar low concentration of insulin throughout the entire body. However normally in persons without diabetes, the alpha-cells are exposed to much higher concentrations of insulin, up to 100 times as high. These higher concentrations of insulin are needed to properly suppress glucagon. These higher concentrations are never achieved with exogenous insulin. Similarly, the liver receives blood directly from the pancreas via the portal vein. The insulin concentrations in the portal vein especially after meals can be three to four times higher than can possibly occur in a person with T1DM by injecting a meal-time exogenous insulin bolus. Thus, after a meal when the liver should not be producing glucose and in fact should be storing glucose in the form of glycogen, it can still be making glucose under the stimulation of (or lack of suppression of) glucagon. A low carbohydrate diet helps to reduce post-meal hyperglycemia due to the greatly reduced glucose load of the low carb diet, but one must still consume adequate amounts of dietary protein to sustain life and muscle mass. The dietary protein you eat is broken down into amino acids in the intestine and absorbed into the bloodstream. These post-meal amino acids reach the pancreatic islet cells and stimulate the alpha-cells to secrete glucagon. In non-diabetic persons, amino acids also stimulate insulin secretion and thus a protein meal does not result in either hypoglycemia or hyperglycemia due to the appropriate secretion of both insulin and glucagon. However in T1DM, amino acids will only stimulate the alpha-cells to produce glucagon since there are no beta-cells to make insulin. Thus in T1DM, a protein meal will result in hyperglycemia unless exogenous insulin is available.
This arrangement of the islet cells also explains why hypoglycemia is such a problem for those with T1DM. The normal response to hypoglycemia is a reduction in beta-cell insulin secretion which in turn stimulates the alpha-cells to secrete glucagon. Both the reduction in insulin secretion and increase in glucagon secretion, stimulates liver glucose production which corrects hypoglycemia. In T1DM once exogenous insulin has been injected, the insulin is not under physiologic control. It will diffuse out of the injected site regardless of the current BG level. If too much was injected compared to current requirements, there is no way to reduce the insulin concentration around the alpha-cells. Thus when hypoglycemia occurs, the alpha-cells have no stimulus to secrete more glucagon and therefore the liver has no stimulus to produce more glucose. The only way for the BG to increase in T1DM is for the sympathetic nervous system and adrenal glands to respond to the hypoglycemia by making epinephrine, norepinephrine, and acetylcholine which both stimulate the liver to make glucose and result in the typical symptoms of hypoglycemia (sweating, anxiety, hunger, and many more) which hopefully will signal the person with T1DM to consume one or more glucose tablets to correct the BG.
Thus for those with T1DM, exogenous insulin is necessary for life and without it or not enough of it, diabetic ketoacidosis and death are the result. Exogenous insulin injected in the subcutaneous fat results in many of insulin's normal functions and when combined with several other lifestyle changes and behaviors can result in a near-normal BG profile. However, exogenous insulin is not and never will be equivalent to endogenous insulin due to the above reviewed loss of the normal feedback mechanisms between the current BG level, insulin and glucagon and the response of the cells in the islets of Langerhans and the liver which all work together to maintain normal BG under all conditions of fasting and feeding.
For more information on exogenous insulin see here.
Treating type 1 diabetes (T1DM) requires insulin therapy. In fact, insulin is life-saving and without it death occurs somewhere between a few days and a couple of years depending on how quickly the loss of insulin occurred and how much residual beta-cell function remains. You can learn more about insulin here.
I developed T1DM (actually LADA) at the age of 38 in 1998. For the first 14 years after my diagnosis of T1DM, I followed my usual balanced diet. I would describe it as a "healthy" version of the Standard American Diet (SAD). Breakfast consisted of meat or egg with bagel or potato, fruit or orange juice, and coffee. Starting in 2001, I avoided lunch most days in order to avoid hypoglycemia due to having to take lunch-time rapid-acting insulin. Dinner consisted of meat, chicken, or fish, cooked vegetables (starchy and non-starchy) or salad, a refined starch like rice or pasta, and often some dessert like chocolate or sorbet. I rarely ate at restaurants, never ate fast food, rarely ate processed snack foods like potato chips, etc. None of the quantities were particularly large and I was lean, but the number of refined carbs in these meals (over 100 grams of carbohydrate per meal) put me on the proverbial blood sugar rollercoaster.
In the graph below, you can see my blood glucose (BG) meter readings during 27 days in April 2007. At this time, I was working full-time as a nephrologist in private practice. I was measuring my BG on average 3 times per day (which is too infrequent): a fasting, a pre-dinner, and post-dinner BG. My average BG was 123 mg/dl and standard deviation was 54 mg/dl. Standard deviation is a good measure of BG variability. My BG values ranged between 50 and 350 mg/dl that month (the rollercoaster effect). My HbA1c was 6.7% and I took on average 24.9 IU/day of rapid-acting insulin (Humalog) and 32.3 IU/day of long-acting insulin (Lantus), for a total of 57.3 IU/day. I weighed 153 lb. so my total daily insulin dose based on my body weight was 0.82 IU/kg/day. Now is this good or not so good? Well at the time I thought the HbA1c was good, because it was in the recommended range for those with diabetes: 6.5-7%. However, I was not convinced I could avoid all the long-term complications with this level of glycemic control. However, what you can't see in the graph was that I was having hypoglycemic episodes, most often after meals, but they could and did occur at anytime. I estimate they occurred 2-5 times per week. These hypoglycemic episodes were very uncomfortable, sometimes scary, sometimes embarrassing, and overall, I hated them.
Thus, trying to follow a "normal" diet which unfortunately is what most patients are instructed to do is the most common problem persons with T1DM will encounter. It is simply not possible to have well-controlled BG eating a "normal" standard American diet. The best solution, in my opinion, is to follow a whole-food low carbohydrate ketogenic diet. I do believe that other dietary approaches can improve glycemic control especially ones that eliminate processed foods and focus on whole unprocessed foods. However, the low carbohydrate approach will also result in the lowest insulin requirement. The lower insulin dose has the beneficial side-effect of reducing the likelihood of gaining excess body fat or providing the ability to lose excess body fat as well as reducing the likelihood of hypoglycemia. In addition, lower insulin doses will reduce the likelihood of long-term diabetic complications.
On Feb. 8, 2012, I started using a whole-food low carb ketogenic diet for T1DM. I gradually reduced my dietary carb intake over the next two weeks to about 30 grams/day to allow time to adjust my insulin doses. You can read more about why I chose a low carb ketogenic diet here. Because dietary carbohydrates all end-up being converted to a simple sugar: primarily glucose, but also fructose and galactose, the more carbs you eat, the greater the rise in blood glucose (BG) after a meal. In non-diabetics, the beta-cells in the pancreas detect the rise in BG and secrete insulin which over the next couple of hours moves the BG into the liver and muscles (to make glycogen) or into fat cells (to make fat) and stimulates the oxidation (burning) of glucose as an energy source. However, the person with T1DM must inject or pump exogenous (meaning from outside the body) insulin in the exact correct amount to dispose of the BG and return it to normal levels. The catch is finding the exact correct amount. This task is exceedingly difficult and the more carbs eaten in a meal and the larger the insulin dose taken, the more extreme the potential imbalance becomes. This is the cause of the blood sugar rollercoaster. Fortunately, it can be avoided or greatly improved by simply avoiding eating most dietary carbohydrates. As it turns out, the majority of dietary carbohydrates and sugar in the Standard American Diet comes in the form of processed foods. They are often snack foods and are low in nutrients. So by eliminating most dietary carbohydrates, we are eliminating low-nutrient junk food. No big loss there!
What we are keeping by following a low carb ketogenic diet, is nutritious whole unprocessed food that is naturally low in carbohydrates and is composed of protein and healthy fat. here This is actually all our bodies need in the first place. In essence, we are eliminating junk food that makes T1DM difficult to manage and replacing it with healthy nutritious food that makes T1DM much easier to manage. It really is a win win decision.
In the graph below, you can see my BG meter readings during 30 days in July 2018 and the rapid-acting insulin (Humalog) and long-acting insulin (Lantus) dose totals given. In contrast to 2007, my average BG was 89 mg/dl and standard deviation was 28 mg/dl. The BG values ranged between 47 and 175 mg/dl that month (much reduced rollercoaster effect). My HbA1c was 5.4% and I took on average 5.8 IU/day of rapid-acting insulin (Humalog) and 25.1 IU/day of long-acting insulin (Lantus), for a total of 30.9 IU/day. I weighed 165 lb. so my total daily insulin dose based on my body weight was 0.41 IU/kg/day. This is half of what I was taking in 2007, but with much improved BG control. Better yet since starting the low carb ketogenic diet, I have experienced on average 2-3 hypoglycemic episodes per year! No that was not a typo. Even with a BG in the upper 40s, 50s, and 60s, I rarely experience symptoms. This will be discussed in detail in an article coming soon on hypoglycemia. Of course, I am trying my best to avoid any BG < 70 mg/dl, but I'm not perfectly successful. My current level of BG control has not and likely will not result in any long-term complications. What I am most concerned about and attentive to is avoiding hypoglycemia. Hypoglycemia is a danger that must be taken seriously even when one is lacking symptoms. This is discussed in more detail in the article on hypoglycemia.
Since my diagnosis of type 1 diabetes (T1DM), I have been searching for ways to improve my glycemic control. I have not tried everything and you might be surprised that I have not tried either an insulin pump or a continuous glucose monitor. I had plans to try the Libre Freestyle CGM when it became available in the US. However at least at this point, I feel I am doing well enough without it. However, there are several things that I have found to be helpful that I will share with you now.
I live a regimented lifestyle. This does require discipline and a strong desire to succeed because making changes in lifestyle are not easy. However, I can assure you that once you make the changes and see the positive results, you will be glad that you did and motivated to continue doing it.
Both books are available as a PDF ebook and as a print book from Amazon. Note: Clicking on the links above will take you to the website of Ellen Davis, MS, my coauthor. Her website is ketogenic-diet-resource.com.
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