Sunday, May 29, 2016

Type 2 Diabetes, a Dietary Disease #330: My FBGs have been transformed, Part 2

In #329 here, I related two major changes in self-management of my 30-year Type 2 Diabetes that marked the beginning of a transition – a transformation really, in my blood sugar control. Like many Type 2s who treat their disease as a “dietary disease” (as I do), worsening blood sugar control is hard to attribute. There is always the question: is it a “compliance” issue with the Low Carb Way of Eating (WOE) or, as is the conventional wisdom, is it a “natural progression” of worsening Insulin Resistance (IR), especially if carb restriction is not the main means of BS control.  Whichever the case, the Type 2 needs to be both vigilant for changes in control and flexible. I was prepared to change my regimen, first by improved compliance, and if necessary, as a last resort, my medications. After all, my health is at stake, and control of blood sugar levels, starting with a low fasting blood sugar, is critical.
So, In January I started Andreas Eenfeldt’s 5-part program that I described in #329, and at my April appointment, my doctor agreed to increase my prescription for Metformin to 1500mg/day. I chose that level because I had read somewhere, sometime in the past (then quickly buried the memory) that 1500mg/day is where Metformin really begins to work. (So, “Why,” I’m asking myself now, “have neither I nor any of the doctors I have seen for the past 10 years ever suggested that I increase my dose from 500mg?” For myself, I have already answered that question in #329: it was pride from having given up virtually all my oral antidiabetic meds, and not wanting again to be “drug dependent.” I cannot answer, however, for the doctors. Perhaps it is because they thought that I wanted to manage my type 2 diabetes. Or perhaps they just don’t know much about type 2 meds.
Or perhaps – and this is what I suspect is the most likely reason – all the doctors I have seen have considered my type 2 diabetes already “well controlled.” After all, my A1c’s were always below the level of concern of the American Diabetes Association guidelines for clinical care. And as for my current doctor, I love him, but except for my insisting on it, he would not even have me testing my blood sugars once a day, much less twice. He’s only interested now in my A1c and wouldn’t even order a fasting glucose if I didn’t ask for it. And when I first went to see him (after he “inherited” me from my previous doctor who had died), he suggested I only come to see him once a year. I was, in his mind, “well controlled” and thus “healthy” and just needed an annual checkup!
3) The 3rd “tweak” in my routine (for #1 and #2 see #329) was to add 6 grams of MCT oil (in gel form) to my daily supplements, as a prophylactic and therapeutic treatment for insulin resistance (IR) in regions of the brain. The brain uses about 20% of the glucose the body makes. Alzheimer’s Disease (AD), like type 2 diabetes, develops over many years, before its symptoms become apparent. The brain simply can’t get the glucose it needs due to the Insulin Resistance. Alzheimer’s has thus been described as Type 3 Diabetes. MCT oil, which is 100% Medium Chain Triglycerides extracted from coconut oil and palm kernel oil, go directly to the liver which converts them to ketone bodies. Ketones are an alternate fuel for the brain, and the brain loves them. I wrote about AD and Supplemental Ketones in The Nutrition Debate #322 here and in #323, #324 and #325.
So, what’s all the hullabaloo about? What’s the breakthrough? The answer: My fasting blood sugars have been TRANSFORMED. They are now ALL below 100mg/dl. WELL below 100. Two weekly AVERAGES in a row of 79mg/dl, range 68 to 92. This transformation began in mid-March, with increasingly regular FBGs in the 90s. By mid-April it was in full swing: Now virtually all my FBGs are in the 70s and 80s, with only an occasional outlier.
And I’ve not been “perfect.” I have even had a little French bread, with butter, at one restaurant meal. And 3 thin French bread slices slathered with rillette at another, both with no discernible effect on my fasting blood sugar the next morning! Previously, any transgression as “egregious” as this would definitely have shown up 12 hours later in my FBG (and for a few days after!) THIS IS VERY LIBERATING.

In addition, the impact of starting the day with a FBG in the “normal” range will surely have a lowering effect on my next A1c. And the lower blood sugars mean a lower circulating insulin level, which means more breakdown and burning of body fat, as long as I don’t overeat fat. After all, for most people, losing weight is as powerful, or more powerful, a motivator as blood sugar control. But when you’re not hungry (because your body is chugging along on its own fat), you really don’t have a good excuse to overeat…not that I ever needed one!

Sunday, May 22, 2016

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 ( 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 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.

Sunday, May 15, 2016

Type 2 Diabetes, a Dietary Disease #328, “…the most sustainable diet ever!”

I am so sick and tired of hearing the public health and medical professions declare that eating Low Carb (LC), or heaven forbid, Very Low Carb, is “not sustainable” over the long haul; that most people don’t have the will power to restrict their diet to primarily foods that are comprised of protein and fat. Well, I doubt these PhDs and MDs were themselves ever obese or, if they were, had tried LC. But now that the “science” behind the diet/heart hypothesis has been debunked, and dietary cholesterol is no longer verboten, the reasons not to try it are gone.
Let’s face it: The reason people eat is because they are hungry. More accurately, the reason people eat is because their bodies are hungry. The brain, specifically, is the nerve center for messages from the blood and digestive system that tells you to eat. It wants you to think about, look for and eat food. It’s a primordial thing.
And why is the body hungry? Because it needs to maintain a constant flow of energy to keep everything running and in balance. This condition is called “homeostasis.” The body works relentlessly to also maintain your set point weight. These are very powerful forces. And they are autonomous, which means they work automatically without your conscious input. In fact, as you know, they fight your conscious efforts to lose weight. And they have a built-in evolutionary bias to add weight, for unforeseen events (an unproductive hunt, a poor harvest, or winter).
So, when you think it’s all about your “will power,” you are deluding yourself. You have an overly optimistic bias toward your ability to not eat. It’s not about your conscious will. Hunger is driven by forces beyond your control. It’s driven by your biology, which is more powerful than your conscious you. But, once you understand how your biology works, you can work with it. You can “defeat” the message that drives you to eat when you have plenty of fat stores hanging on your body. And you know you do. And you want to get rid of that extra fat, right?
Of course, you can stay with the restricted calorie, balanced diet and see how it works for you. But, you know in your heart of hearts that that regimen doesn’t work. And if you want to figure out how to get your body to naturally burn its own fat, stay with me. I am not selling snake oil or anything else; just a dietary idea that works.
How would you feel about a diet that works without hunger? That’s right, the hunger is gone. There will no longer be physiological signals and messages telling you to put something in your mouth. Why, because your body is satisfied with the available food source: your body fat. How did this condition come to pass?
“Just one word…Insulin” (apologies to “The Graduate”). Insulin is both the glucose-transporter hormone and the fat storage hormone. When you eat carbohydrates, they all break down to simple sugars – glucose primarily – and are “escorted” in your blood by insulin secreted for the purpose. If you’re pre-diabetic or a type 2, you have a degree of insulin resistance (from eating too many carbs for too many years), so your blood glucose and your blood insulin stay elevated. If you eat carbs at every meal (even a small, calorie restricted meal), they (glucose and insulin) are at a continuously “high” level. Result: You don’t lose weight, and you’re still hungry!!! Why?
Insulin is also the fat storage hormone. That means, it regulates when to make fat (when you eat too many carbs or too much fat), and when to burn fat…to maintain homeostasis. And your brain reasons that if you have a high level of insulin circulating in your blood, you must have glucose availability (from carbs, mostly) for energy to maintain homeostasis. It doesn’t recognize, unfortunately, that your glucose metabolism is disregulated by insulin resistance (your Pre-Diabetes or Type 2 Diabetes). It just looks at your elevated blood insulin level.
 Your body (not you) then “reasons” that it doesn’t need your body fat for energy, and so it blocks its breakdown. Your body would be very happy to burn your body fat for energy, but your elevated blood insulin level is blocking the signal. You simply can’t lose weight if your blood glucose and blood insulin remain high. Your body won’t let you. You have to lower your circulating blood glucose and blood insulin levels. How? By not eating carbohydrates.
When you abstain from eating carbs for a few days, your body’s blood glucose and blood insulin will decrease and unblock the path to burning body fat for energy, making free fatty acids and ketones. Your body will be happy and you will have been launched on “…the most sustainable diet ever” because THE HUNGER IS GONE!

Sunday, May 8, 2016

Type 2 Diabetes, a Dietary Disease #327: “Just by changing what I ate…”

Doctors treat Type 2 Diabetes by focusing on its salient symptom: high blood sugar. What they tell you is to “eat right, exercise and lose weight,” but then they treat you with oral antidiabetic medications.  But that’s why you went to the doctor, right? For him or her to “treat” your pre-diabetes or type 2 diabetes; to take care of you; to write a script to make you “better” (or at least to manage your condition)? That’s their job, right?
But high blood sugar is only a symptom!!! So is being overweight or obese. They are not the cause of Type 2 Diabetes; they are only associated with it. But, the doctor tells you to lose weight and take the pills anyway. And when you don’t lose weight and your high blood sugars persist, your type 2 diabetes inevitably progresses.
Did you ever wonder why doctors don’t treat the cause of Type 2 Diabetes? They know that the cause of Type 2 Diabetes is Insulin resistance (IR). Why don’t they treat that? Or tell you how you became IR? Well, I’ll tell you.
First you probably have a genetic predisposition. Some of your genes have come to “express” an intolerance for carbohydrates. How? By eating too many of them for too long! (The government has told you to since 1977.) Type 2 Diabetes (IR) takes many years to develop but, for some people (the genetically predisposed), it inexorably leads to Insulin Resistance. And Insulin Resistance means that you are now to some greater or lessor degree intolerant of carbs.
The mechanism is, when you overload your digestion/absorption system with glucose, which is the breakdown product of all carbohydrates, insulin, the hormone responsible for transporting those glucose molecules to your cells, is likewise in overload mode, and the level of insulin in your blood rises. This results in a slight resistance to its uptake, and that resistance, over time (years of overeating carbs at every meal), creates a vicious cycle.
Besides developing Insulin Resistance, what happens when you eat too many carbs at every meal and your blood insulin levels are in a constantly elevated state? Well, insulin, besides being the glucose-transporter hormone, is also the fat-storage hormone. See, the brain (where all these thing are regulated in a place called the hypothalamus), thinks that if you have an elevated blood insulin, you have a ready source of glucose (carbs) for energy (e.g., ripe fruits and vegetables), so it doesn’t have to use its precious fat stores (around your waist). So, it “starves” you and sends you a hunger message to go out and pick more fruit. It can conserve your body fat.
That’s the other function of insulin: fat synthesis and storage. It enables your body to make fat and store it for when you really need it (famine, winter). It still thinks you live in the Stone Age. So long as you have an elevated blood insulin, from constantly eating carbohydrates (combined with insulin resistance), and glucose availability either from food-by-mouth or some stored in your liver (glycogen from the carbs you ate yesterday), it won’t switch over to fat-burning mode. And you’ll be hungry.
But let’s face it. Your doctor isn’t going to tell you this. He or she would have to admit that the advice you’ve been getting for the last forty or fisty years to eat 55% to 60% carbs has been all wrong. My doctor did, however, inadvertently. He thought that being obese was a cause of Type 2 Diabetes, and he knew my blood sugars were out of control even though I was loaded up with antidiabetic meds. More than anything, he wanted me to lose weight.
Then, one Sunday morning in July 2002, on the cover of the New York Times Magazine, my doctor saw a big, sizzling rib-eye steak with a pat of butter on top. He read the article, “What If It’s All Been a Big Fat Lie,” tried the diet himself, lost 17 pounds in a month, and said to me, “Have I got a diet for you…” The first day on it I had a hypoglycemic episode (low blood sugar) and the next day another. In less than a week he took me off one antidiabetic med and had twice reduced the other two by half. Later I totally eliminated one of those and today take just metformin.
And I did all of that JUST BY CHANGING WHAT I ATE…”  PS: I also lost 170 pounds.

Sunday, May 1, 2016

Type 2 Diabetes, a Dietary Disease #326: Are you hungry in the morning?

Seriously. Your mileage may vary (YMMV), but I’m not hungry in the morning. . I don’t know if that’s an adaptation my hormones have made since I began eating Very Low Carb (VLC) in 2002. Or if it’s evidence that I’m in ketosis after an overnight fast (with only a little stored glycogen in the liver from VLC, and taking Metformin ER to suppress unwanted gluconeogenesis). Either way, I’m not hungry.

So, I don’t eat breakfast anymore. That’s a big change for me. Ever since I began VLC on Atkins INDUCTION (20g/d) for 9 months in 2002, losing 60 lbs), I have eaten a breakfast of just eggs, bacon and coffee. A few years later, after gaining back a little weight and reading Dr. Richard K. Bernstein’s “Diabetes Diet,” I lost 110 more on his 30g of CHO per day (6-12-12) WOE (Way of Eating).

Since then, however, some of my 170 lb weight loss has crept back, and eating VLC doesn’t seem to be enough by itself. My metabolism adjusts and refuses to move my “set point.” So, in January I added an additional weapon to my arsenal: Intermittent Fasting (IF). It’s a “fad,” you say? Well, yes, but it is grounded in ancestral/evolutionary precepts, and it is good science. It’s only in modern times that 3 meals a day is the norm. And even today, many Europeans eat a very light breakfast. Americans are the exception to the rule, and look where it got us
My new approach employs 5 simple rules that Andreas Eenfeldt, “The Diet Doctor,” described in this video (2/2): 1) Follow strictly a low carb diet, 2) Eat only when hungry, 3) Sleep 7-8 hours a night, 4) weigh yourself daily, and 5) 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. I sometimes even skip lunch. I’m honestly not hungry.

I’m doing this to lose weight, to break the plateau and reset my “set point,” and it’s working. After losing 20 pounds by just eating strictly VLC (addressing the “compliance issue”), I stalled. That’s when I started IF (skipping breakfast) and “eating only when hungry.” I quickly (in 5 weeks) lost another 10 pounds. Then I stalled again. Hmmm, I wondered. Did my metabolism do another adjustment, or did I sub-consciously sabotage myself by eating when I wasn’t hungry, or even eating too much fat, instead of letting my body break down stored fat?

The answer, Eenfeldt says, is to mix it up a little. Instead of an 18 hour fast, go to a 23½ hour fast, from supper one day to supper the next. Just taking water and maybe 70-80 calories in supplements. (I take 2g fish oil and 6g of MCT oil a day. When I started this IF regimen, I also added a 2nd multivitamin, just for insurance. I don’t care if I piss away some of it. I take 8 oz water and my morning supplements at the “breakfast” table with my wife, and others, including Metformin ER, at supper. Anyway, mixing it up seems to be working. I’m losing weight again.

I am now totally off coffee at breakfast. I know it’s a good antioxidant, but I’ve never liked it black or bulletproof, and I am now abstaining from all sweeteners at breakfast, artificial or otherwise. Before, I used pure stevia powder (w/o maltodextrin added as a bulking agent), but I do not want to stimulate an insulin response from the sweetener, even if it is calorie-free. My object is to lower my serum insulin, not just my serum glucose. It is insulin levels that 1) contributes to insulin resistance and 2) blocks body-fat breakdown (lipolysis) for energy.

We used to think of insulin primarily as the glucose transporter hormone that it is, but it is much more than that. Insulin is also the body’s fat storage hormone. And, if you have Insulin Resistance (pre-diabetes or type 2 diabetes) and you want to lose weight and keep it off, you have to severely restrict dietary carbohydrates to lower serum insulin. When the level of insulin in your blood drops (since it isn’t needed as a glucose-transporter), it signals the body (your brain actually) to break down stored fat (triglycerides) into free fatty acids and ketones for energy. Now that you understand the physiology, you know how to “eat right,” lose weight, and be healthy.