Type 2 Diabetes, a Dietary Disease #329: My FBGs have been transformed, Part 1

I believe a combination of recent “tweaks” to my self-treatment of Type 2 Diabetes has resulted in a blood sugar control “breakthrough.” It may be too soon to say definitively that I have found “the secret” for me, but I think I have. Below are the variables that have changed in recent months.

1) I am now adhering with a high level of compliance to the following 5 guidelines that Andreas Eenfeldt (www.thedietdoctor.com) mentioned in a video I watched in January:  I now a) follow strictly a low carb diet, b) eat only when hungry, c) sleep 7-8 hours a night, d) weigh myself daily, and e) practice intermittent fasting. The two IF methods Dr. Eenfeldt “prescribes” are 5:2 and 16:8. I chose 16:8, seven days a week! I skip breakfast because I’m not hungry at breakfast (see #326). I also sometimes skip lunch, or eat a very light one (one or two hard boiled eggs). As a result of the IF, I think I am in a mild form of nutritional ketosis for more hours every day.

2) For the last 10-12 years, as my only oral anti-diabetes medication, I have been taking 500mg of Metformin once a day. (Before that, I had titrated off a sulfonylurea (Glyburide) from 5mg to 2½ to 0 after starting the Bernstein Diet. Before that, after starting Atkins Induction in September 2002, to avoid hypos, I quickly had to stop taking Avandia, which I had just started, and then had to cut my Glyburide from 20mg to 10 to 5 and my Metformin from 2000mg to 1000 to 500).

I provide this history to explain why I had been reluctant to increase my oral anti-diabetes meds. It was pride, and the fact that no one had suggested that I increase my Metformin or add a new oral anti-diabetes med, until last year. (And, if they had, I’m not sure I would have agreed to either.) The conventional wisdom is that type 2 diabetes is a condition that is “progressive.” I am not saying here that I agree. However, my A1c was creeping up (at one point to 6.5%), and it was becoming increasingly difficult for me to get fasting readings below 100mg/dl. In fact, it had been a few months since I had seen even one below 100. As a result, my resolve not to increase the Met or add a new med, and my pride, were both slipping. After all, my health (the risk of all the microvascular and macrovascular complications) was at stake.

So, I decided that the first step for me was more vigilant self-management. After all, type 2 diabetes is a dietary disease. (Here’s where I do a little shameless self-promotion: Read my blog at www.thenutritiondebate.com where the theme, starting with #306, has evolved to “Type 2 Diabetes, a Dietary Disease.”) That’s why I began the steps described in 1) above, and they had an effect. But that still left the question: If my disease was in fact progressing (not a case entirely of my “compliance” slipping), should I consider increasing my medication from just 500mg of Metformin once a day or adding another class of meds? I pondered this question for months.

For years I have attended classes offered by a Certified Diabetes Educator, both to support her as well as try to persuade her to subscribe to and teach a Low Carb Way of Eating for diabetics. Last year she suggested I try a SGLT2 inhibitor. SLGT2s block the re-absorption of glucose in the kidney, increase glucose excretion, and thus lower blood glucose levels. I read all the latest research and decided I was not ready to go there. So, last December, I asked my doctor to increase my Metformin to 1000mg once a day, and he said, “okay.”

Then in January I attended a conference on Metabolic Therapeutics and discovered that a sub-set of attendees, all of whom were very healthy athletes/body builders, were taking supplemental ketones to help lose weight and stay in ketosis. Some of them, including the PhD researcher who was the conference organizer, were also maxed out on Metformin, taking 2000mg/day, to increase their insulin sensitivity and suppress gluconeogenesis, thus minimizing body fat by promoting breakdown and burning of fat cells and maximizing muscle synthesis. This was an eye-opener for me. Of course, Metformin is a wonder drug. It’s mechanism of action is still not completely understood, but as I wrote about here, in this recent JAMA article, it has been seriously advocated for everyone. And, unlike the SLGT2s, is has been around for over 50 years, is demonstrably safe, and really cheap. So, after the conference, with supplies on hand, in February I decided to increase my Metformin dose to 1500mg/day.

In the weeks following implementation of that decision, my fasting blood sugars slowly began to transition. And by the second half of March, after a long hiatus, I was beginning to get fasting readings below 100mg/dl again (mostly in the 90s). What happened next, however, was quite remarkable. See Part 2 of this story next week.