Retrospective #335: Gerald Reaven’s Unified Hypothesis, Part 2

Yesterday’s column was heavily cribbed, with attribution, from a 2016 post by Dr. Tim Noakes on South African Marika Sboros’s excellent blog FOODMED.NET. Today I’m going to continue with an almost verbatim extract. It is so well written, and so profound in its implications, I don’t want to botch it with “editing”! Props, Dr. Tim!

We left off with Dr. Noakes explaining how endocrinologist and Stanford professor Dr. Gerald Reaven presented at the 1988 ADA annual Banting lecture a “unified hypothesis of chronic disease,” called Syndrome X by Reaven but which thereafter became known as Reaven’s Syndrome. These days it is called “Metabolic Syndrome.”

Noakes continues, “To determine whether nutritional factors contribute to the development of the metabolic syndrome, beginning in the 1980s, Reaven completed a number of RCTs of the effects of low-carbohydrate diets in patients with this condition. Without exception his studies showed that removing carbohydrates from the diet uniformly improved all measures of health in those with insulin resistance and metabolic syndrome.”

“So besides establishing the fundamental role of insulin resistance in these chronic diseases, Reaven also discovered the optimum treatment – carbohydrate restriction. By any measures, Reaven should be a shoe-in for the Nobel Prize in Medicine.  But perhaps not.  For he failed subsequently to emphasize the curative effects of low-carbohydrate diets in insulin resistance.”

“Why [did Reaven fail to emphasize the curative effects of low-carb diets in insulin resistance],” Noakes asks?

“I suspect that during his daily work at Stanford Medical School, Reaven was in close contact with some of the more important cardiologists in the USA and perhaps in the world. They would not have taken kindly to their colleague’s suggestion that, to prevent heart attacks, cardiologists should be prescribing high fat diets instead of the low fat diet dictated, then as now, by the American Heart Association.” (emphases added by me)

“Had he chosen that route, Reaven’s colleagues would have excommunicated him, his research funding would have dried up, and his career would have been over, exactly as happened to Dr John Yudkin in England for his (correct) suggestion in the 1970s that sugar, not saturated fat, causes heart disease.”

“So, it seems to me that Reaven kept quiet, choosing rather to continue researching insulin resistance without paying much attention to how a low-carbohydrate, high-fat diet might – simply, effectively and at low cost – prevent and reverse all the medical disguises through which insulin resistance reveals itself.”

Thus, Reaven’s unified hypothesis of chronic disease: “One disease, one cause, many symptoms:”

“Reaven’s problem is not unlike that faced by Darwin and Galileo whose findings estranged each from religious orthodoxy.  For Reaven’s unifying hypothesis of chronic disease must offend not just his colleagues in cardiology.  For his hypothesis strikes at the very heart (pun intended) of the pharmacological model that we practice in modern medicine.” (Statins, do ya think?)

“For if obesity, diabetes, heart disease, NAFLD and high blood pressure (and perhaps also cancer and dementia) are in fact all symptoms of the same underlying condition, insulin resistance, then our current model of medical management must be wrong, requiring as it does, specific but different pharmacological treatments for each separate condition, overseen by different hierarchies of medical specialists.”

“BUT WHAT IF THE CORNERSTONE FOR THE TREATMENT OF ALL THESE CONDITIONS IS A LOW-CARBOHYDRATE DIET – the very diet that has now been vilified by my profession for the past 50 years?  That must be an extremely frightening thought for very, very many.  How does one come to terms with the possibility that, by following medical orthodoxy, one may have harmed very many patients?”

Thank you, Dr. Tim Noakes, for the courage to speak out. Note: Dr. Gerald Reaven died in 2019, but Dr. Tim Noakes and Marika Sboros (FOODMED.COM) still speak out. Check out Dr. Noakes’s “Part 4” just published.

Retrospective #334: A Unifying Hypothesis of Chronic Disease: Part 1

I don’t remember how, but in early 2016, I landed on South African blogger Marika Sboros’s site, FOODMED.NET. I loved it and signed up for regular delivery. The blog’s subtitle is “Let food be your medicine,” so you can see my affinity. The first post I read, in her “Managing Your Blood Sugar” series, was titled “NOAKES: IT'S THE FATTY LIVER DISEASE, STUPID' PART 2,” tagged “LCHF.” Marika explains that LCHF in her lexicon means “Low Carb Healthy Fats.”

The author of this particular post was world-renowned scientist and University of Cape Town Professor Emeritus Dr. Tim Noakes. Noakes introduces his subject with a discussion of the misunderstood term “risk factors,” frequently used in epidemiology and “observational” or “associational” studies. He delves briefly into “hazard ratios” (HRs), relative and absolute risk, and related subjects to show how data is commonly manipulated and misused.

“This is intellectually absurd,” Noakes says. “How can everything be a risk factor for everything else?” he asks. He answers, “The answer can be found in the ignored work of Dr. Gerald Reaven, Emeritus Professor of Medicine at Stanford University.” “Reaven has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance.” (As I rewrite this in 2020 for the Retrospective Series, I note that Gerald Reaven died in 2019.)

Reaven’s interest in insulin resistance was piqued by the distinction between Type 1 and Type 2 diabetes. Type 1 is characterized by the (almost) total absence of endogenous insulin; Type 2, insulin resistant diabetes, by “abnormally high amounts [of insulin] because the target cells on which the insulin normally acts are resistant to its action; hence the condition of insulin resistance or carbohydrate intolerance. Persons with insulin resistance have blood insulin concentrations that are elevated most of the time, a condition known as hyperinsulinemia.” (my emphases).

Noakes says, “Reaven’s great contribution has been to show this persistent hyperinsulinemia in insulin resistance, whether or not associated with t2dm, produces a collection of grave secondary consequences.”

Noakes then says, “But Reaven’s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinemia are the necessary biological precursors definitely for four and perhaps for all six of the most prevalent chronic conditions of our day: 1) Obesity; 2) Arterial disease (local: heart attack or stroke; disseminated: T2DM; 3) High blood pressure; 4) Non-Alcoholic Fatty Live Disease (NAFLD); Cancer; and Dementia (Alzheimer’s Disease, also known as Type 3 Diabetes).”

Reaven gave the keynote Banting lecture at the 1988 American Diabetes Association annual meeting. His talk explained the underlying factor for a constellation of abnormalities: glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension.  Reaven named it “Syndrome X”; it was also given the moniker Reaven’s syndrome. Today it is simply called Metabolic Syndrome.

“The key finding from Reaven’s work,” Noakes says, “is that these conditions are not separate – they are different expressions of the same underlying condition. Thus, a patient should not be labeled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).”

“Instead,” Noakes continues, “the patient should be diagnosed with the underlying condition – insulin resistance – with the realization that the high blood pressure, the obesity, the diabetes, the NAFLD, or the heart attack or the stroke are simply markers, symptoms if you will, of the basic condition.”

“And that basic condition,” Noakes concludes, “is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day. “

Thus, we have it: Reaven’s unifying hypothesis of chronic disease: “One disease, one cause, many symptoms.” Tomorrow’s post will offer insight into the profound implications of this fundamental advance in medical science.

Aside: This column was based on Noakes’s 2016 “Part 2” in a Series. By sheer coincidence, a link to “Part 4,” recently published by Tim Noakes, appeared on Twitter on January 13, 2020. It is a long encomium to the late Gerald Reaven.

Retrospective #333: NAFLD, Fructose and PUFAs

A friend recently asked me to look over a list of supplements suggested as “interventions” for a diagnosis of NAFLD (Non-alcoholic fatty liver disease). So, she sent me a link from Life Extension (LE), a supplement seller recommended by her doctor. Can you believe that? Doctors are now shilling for supplement sellers!

Life Extension’s “suggestions” include eight (8) “supplements,” all but one of which – a drug, metformin – they sell. All “have been shown to boost liver health and help manage NAFLD,” and “prevent progression to the more deadly NASH, which is a precursor of liver failure.” Pretty scary stuff! “Which of these supplements should I buy,” she asked? Then, at the bottom of the page, I saw that the tab on the link my friend sent was pg. 2. I clicked on pg. 1.

“Roughly one-third of the American population suffers from nonalcoholic fatty liver disease or NAFLD. NAFLD can go undetected for years and may eventually progress to inflammation and scarring of the liver (cirrhosis) and, in some cases, full-blown liver failure.” More scary stuff. “A formerly rare condition, its rapid emergence has been linked to skyrocketing rates of metabolic syndrome and diabesity, the term many experts use for co-occurring diabetes and obesity.”

My friend is not obese, but her IR and abnormal lipid profile puts her squarely in the Metabolic Syndrome box.

“While POOR DIETARY CHOICES are often to blame, cutting-edge research suggests that hidden genetic factors may also play a role, and some people do not metabolize polyunsaturated fats properly, resulting in fatty deposits in the liver.”

Life Extension’s “fix,” of course, is supplements: They offer to sell you a passel of supplements. That’s their business.

“As mainstream medicine continues to struggle in the search for drugs to manage this widespread condition, emerging scientific evidence has shed light on effective natural interventions that may halt or even reverse its progress.”

But wait, these “interventions” are just surrogates for drugs, THE BEST “TREATMENT” FOR A CONDITION CAUSED BY POOR DIETARY CHOICES, INCLUDING POLYUNSATURATED FATS, IS GOOD DIETARY CHOICES AND HEALTHY FATS.

And, Life Extension has identified the likely causes of NAFLD: poor dietary choices and polyunsaturated fats.

What are those “poor dietary choices”? Life Extension hones in on the main one, a simple sugar, fructose. Fructose is half of every cane (i.e. table sugar) molecule, and, being toxic in big slugs, fructose goes directly to the liver to be detoxified. If the liver is already full of stored carbs (glycogen), via de novo lipogenesis, the liver makes new fat molecules IN THE LIVER from the fructose. And, ipso facto, there you have the beginnings of NAFLD.

“Of course, what we eat is as important as the calories it contains. One of the major bad actors in today’s world is fructose, found in high quantities in high-fructose corn syrup. Fructose promotes formation of new fat molecules in the liver, blocks breakdown of existing fats, stimulates free radical production, and promotes insulin resistance. Increasing numbers of studies are linking increased fructose consumption with NAFLD, and even with its deadlier consequence, NASH. Patients with NAFLD consume 2-3 times as much fructose as do control patients, even corrected for body weight.”

Okay, LE focuses on HFCS, which is 55% fructose, but remember, table (cane) sugar is 50% fructose, which is just as bad!

The other dietary choice Life Extension cites as a probable cause of NAFLD is “polyunsaturated fats,” or PUFAs, the highly processed vegetable oils, soybean and corn oil being the most prevalent. These are unnatural food oils that did not exist before technology developed to extract them. I have written about the harm of PUFAs many times, but Life Extension’s citation was refreshing because these liquid fats are still recommended by the Dietary Guidelines.

A small amount of PUFAs are “essential,” i.e., the body can’t make them. However, the ratio of the “essential” fatty acids (n6s and n3s) is important because they compete to be taken up by the cells. Historically this ratio has been 2:1 but with the proliferation of “industrial” food oils over the last century, and the USDA’s advocacy of them (and Cargill’s and ADM’s production and marketing of them), the ratio for most Americans is now 20:1 to 30:1.

You can’t fix this ratio by just supplementing with fish oil (n3s). You need to cut bac on fried foods, commercial baked goods and bottled salad dressings. Replace PUFAs with monounsaturated fat (olive oil) and healthy saturated fats from coconut oil and butter, lamb, beef, pork, chicken and full-fat dairy and wild-caught fish. All Real Foods!

Retrospective #332: Are you an un-diagnosed Type 2?

I recently talked for an hour or so to a friend who knows that I know a lot about Type 2 Diabetes. He sought me out to ask me what he should do. I asked him, “What is your situation?” Here’s what he told me:

His fasting blood sugars (FBG), he said, are consistently running in the 140s. That’s 140mg/dl. I told him that was “out of control.” I asked him what his postprandials were. He said he didn’t know “postprandial,” so I said rephrased it: your blood sugar 1 or 2 hours after starting a meal. He said he didn’t know. He didn’t do postprandials.

I then asked him what his latest A1c was. He replied 6.9. That’s 6.9%, but he said it was almost 2 years ago. I asked him if his doctor had told him that he was diabetic. He said “No,” and I said, “Well, you are!” The American College of Endocrinologists defines Type 2 Diabetes as an A1c of ≥6.5%. The American Diabetes Association advocates ≤7.0%, but definitions are a big part of the problem. Some clinicians today regard an A1c of ≥5.7% as full-blown Type 2 diabetes.

I asked my friend if he was currently taking any medications to control his blood sugar. He said, “Yes.” He was taking a two 500 mg tablets of Metformin twice a day, plus glyburide (micronase, a sulfonylurea). He didn’t remember how much, and I don’t remember how often he takes it, because this set me off on a rant.

I said, “You are already maxed out on Metformin” at 2000 mg/day, and you are taking a sulfonylurea (SU), a class of medications that pumps the pancreas to produce insulin to “cover” the carbs you are eating, AND IT’S NOT ENOUGH!” SUs ARE A DRUG THAT, WHILE STILL PRESCRIBED BY UNKNOWING PHYSICIANS (BECAUSE ITS CHEAP AND “EFFECTIVE”) BEAT UP AND WEAR OUT THE BETA CELLS IN THE PANCREAS THAT MAKE YOUR INSULIN, AND THEY EVENTUALLY STOP WORKING!!! RESULT: YOU WILL SOON BE INJECTING BOTH LONG ACTING (BASAL) AND MEALTIME (BOLUS) INSULIN TO CONTROL YOUR BLOOD SUGAR. And YOU haven’t even been told YOU’RE DIABETIC!!!!!!

He said, “What should I do?” I didn’t hesitate to tell him. I said, “You’ve got to change what you eat! I mean seriously change what you eat.” “What do you have for breakfast,” I asked? “Oatmeal,” he said, “with milk and a little sugar.” “Switch to eggs,” I said, “any way (fried, scrambled, poached, even hard boiled).” “How many”, he asked? “One, two or three; add a strip of bacon if you like,” I said, “but no juice, no cereal, no yogurt, bread or jelly. Only heavy cream and a little stevia in your coffee, if you must.” I told him he wouldn’t be hungry. He wouldn’t need a mid-morning snack. (When he told me he ate an apple in mid-morning because he was “starving.” I just rolled my eyes in horror.)

I also told my friend that he had to get off the SU no matter what he ate. The effect could be that his A1c will go up unless he replaced the SU with a drug that acts in a different way, sparing the pancreas, or changed what he ate. There are now several newer (but expensive) drugs, both oral and injectable, that are effective. Many clinicians would even argue reasonably that a temporary course of exogenous (injected) insulin would perhaps be the best course of treatment in his case to get his blood sugar under “good control.” BUT I WOULD ARGUE THE BEST COURSE OF TREATMENT, AND THE ONLY ONE THAT ADDRESSES THE CAUSE OF TYPE 2 DIABETES (INSULIN RESISTANCE), IS TO BASICALLY CHANGE WHAT YOU EAT.

My own experience supports this course of action. In 2002 I weighed 375 pounds and I was maxed out on Metformin and a sulfonylurea and starting a DPP-4 inhibitor (Avandia). I was, like my friend, clearly on my way to injecting insulin. My doctor wanted me to lose weight, of course, so he “prescribed” a radical change of diet, a Very Low Carb: just 20g of carbs a day. The surprising result (for both of us) was that on the very 1^st day of strict compliance I got a hypo (a low blood sugar). The doc ordered me to stop the Avandia. The next day, I had another hypo, and he told me to cut the Metformin and the glyburide (the SU) in half. A few days later I had to cut both the Met and the SU in half again. Still later, when I returned to strictly eating VLC, just 30g of carbs a day, for a year, I cut out the glyburide altogether.

After a few years or eating this very different way, I had lost 170 pounds, my blood pressure dropped to 110/70 (on fewer meds), my HDL-C more than doubled and my triglycerides dropped by 2/3rds. And I saved a ton of money on medication. And I was much, much healthier!!! And all I did was change what I ate, starting with breakfast.

Retrospective #331: Dear Max: Don’t Eat Oatmeal for breakfast!

(Note: This is a Universal Fill-in Form. Just change the name of the person and the carb food as appropriate.)

I know you’re busy, Max, but…your health is at stake, so pay attention: You’re Pre-Diabetic, and in all likelihood, you’re will become a full-blown Type 2, unless you change what you eat. TYPE 2 DIABETES IS A DIETARY DISEASE.

Doctors treat Type 2 Diabetes by treating the symptom: high blood sugar. They give you vapid advice (lip service, really) to undertake “lifestyle changes,” like “eat less and exercise more,” to lose weight! Then, they treat your symptom (high blood sugar) with meds. They follow up by monitoring your blood sugars at intervals to see that they are “well controlled,” by very poor Diabetic Association standards, and, when they are not, they will add medications.

Their response, to treat you with more meds (too little, too late, and all wrong!), will only result in wearing out your pancreas, the organ that makes insulin in your body. And when your pancreas doesn’t work anymore, you will have to inject insulin. And you will probably die from one of the macrovascular or microvascular complications of the disease.

Doctors should advise you to “treat” the cause of Type 2 Diabetes: Insulin Resistance (IR). But the dietary advice you will probably get from a medical doctor is likely to be just plain wrong. If you follow it, you do so at your own risk. For example, eating a “balanced” diet contains much too high a level of carbs and will result in your diabetes worsening.

They will also treat your disease to much too lax a standard. They will regard your blood sugar as “well controlled” at a level where it is doing you harm, and your diabetes is worsening. Eating carbs raises blood sugars. To repeat, if you don’t change what you eat, your Type 2 Diabetes will progress, with increased risk for all the attendant complications.

Insulin Resistance means that insulin receptors in your cells are refusing to open to take up the glucose that is being transported by insulin in your blood. Glucose is a fuel that your body makes from digesting carbs. Result: your blood sugar rises. Solution: eat fewer – many fewer, carbs. There is no (zero) nutritional requirement for carbs? And your IR means you are becoming, or have become, Carbohydrate Intolerant. Insulin Resistance = Carbohydrate Intolerance.

Your body needs some glucose (but NOT carbs).  Some glucose – a very small amount – is so essential to the body that the body has multiple ways to make glucose from protein and fat. And your body does need both protein and fat, and that is what you have to eat if you want to treat the cause of your Pre-Diabetes. Repeat: Eat mostly protein and fat.

Hunger is the principal (but not the only) biological driver of eating. It is both intrinsic and autonomic. Your conscious will pales by comparison. You are a slave to your hunger – especially if you are carb dependent. If you eat carbs at every meal, and in-between meals at snacks, your body will become dependent on them, thinking that since carbs are readily available, you can depend on them as an easy and quick source of energy. Of course, in today’s world, carbs are abundant year-round, and ubiquitous. They are a quick and easy and cheap source of energy today, 24/7/365.

Physiologically, when your body becomes dependent on carbs, your body blocks access to an alternate and totally complete source of fuel that everyone has: stored body fat. Your body can’t access your dense stored energy source because, in the Insulin Resistant person, an elevated insulin, accompanying the glucose still circulating in your blood, prevents energy from body fat from contributing to the body’s steady energy requirement (homeostasis). As a Pre-Diabetic, because of your Insulin Resistance, both your blood glucose and your blood insulin are continuously elevated.

Translation: soon after the carbs you last ate are digested, your body tells you that you are hungry again! It tells you to eat more. SOLUTION: After an overnight fast, just eat protein and fat for breakfast. “No” carbs. That means: no juice, no cereal, no yogurt, or bread or jelly. You will feel full. After a few days, your body adjusts and you will never be hungry again at breakfast or in mid-morning. If you continue with protein and fat for lunch (no carbs), you will not eat again until cocktail time. And if you eat a small supper of mostly protein and fat, with a serving of low-carb veggies, you will not have to eat again until breakfast. Within days your fasting blood sugars will drop back into the “normal” range, and after a few months your A1c’s will too. And your doctor will be happy because you lost weight.

Retrospective #330: My FBGs have been transformed, Part 2

In Retrospective #329, I related how, in 2016, two major changes in self-management of my then 30-year Type 2 Diabetes marked the beginning of a transition in my blood sugar control. Like many Type 2s who treat Type 2 Diabetes 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 eating Very Low Carb or, as is the conventional wisdom, is it a “natural progression” of worsening Insulin Resistance (IR), especially if carbohydrate restriction is not the main means of control.  Whichever, Type 2s need to be both vigilant for changes in control and flexible. I was prepared to change my regimen, first by improved compliance, and then, if necessary, as a last resort, increase my meds. 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, that 1500mg/day is where Metformin really begins to work. I hadn’t previously considered increasing Metformin because of pride. Pride from having given up virtually all my oral antidiabetic meds, and not wanting again to be “drug dependent.” As for my doctor not suggesting it, I can only speculate it is because he thought that I wanted to manage my Type 2 diabetes. Or maybe he just didn’t know that much about Metformin.

In retrospect, though, I think the most likely reason he didn’t increase it is that all the doctors and nurses I have seen have considered my Type 2 diabetes already “very well controlled.” After all, my A1c’s have always been low to mid 5s, well below the level of concern of the American Diabetes Association guidelines. 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. Now, he’s only interested in my A1c. And when I first went to see him (he “inherited” me from my previous doctor), he suggested I only come to see him once a year. Because I was “very well controlled,” I just needed an annual checkup!

3) The 3^rd “tweak” in my regimen (for tweaks #1 and #2 see Retrospective #329) was to add 6 grams of MCT oil (in gel form) to my daily supplements, as a PROPHYLACTIC TREATMENT for insulin resistance (IR) of the brain (Cognitive Impairment). The brain uses about 20% of the body’s glucose supply. Alzheimer’s Disease (AD), like Type 2 diabetes, develops over many years, well before its symptoms become apparent. The brain simply can’t get the glucose it needs due to its Insulin Resistance. Alzheimer’s has thus been described as Type 3 Diabetes. MCT oil, which is 100% Medium Chain Triglycerides (MCTs) extracted from coconut oil and palm kernel oil, goes directly to the liver which converts it to ketones. KETONES ARE AN ALTERNATE FUEL FOR THE BRAIN, and the brain LOVES them. I wrote about AD and Supplemental Ketones in Retrospective #322 and again 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 a “perfect” VLC eater. I have even had a little French bread, with butter, at one restaurant meal. And 3 French bread slices slathered with rillette at another, both with no discernible effect on my fasting blood sugar the next morning! Previously, any transgressions as egregious as these would definitely have shown up 12 hours later in my Fasting Blood Glucose (and for a few days later too!) THIS IS VERY LIBERATING.

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

Retrospective #329: My FBGs have been transformed, Part 1

In early 2016 I believed a couple “tweaks” to my self-treatment of Type 2 Diabetes resulted in a blood sugar control “break through.” When originally written, it was too soon to say I had found “the secret.” Here’s what I wrote then:

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 [2016]:  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, keto lunch (e.g., 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, while eating Very Low Carb (VLC), I have been taking 500mg of Metformin once a day as my only oral anti-diabetes medication. (Before that, to avoid hypos, my doctor stopped my Avandia, which I had just started, and had titrated me off a sulfonylurea (Glyburide) from 20mg to 10 to 5mg and then later from 5mg to 2½ to 0. He also had cut my Metformin from 2000mg to 1000 to 500. These changes all occurred during “week 1” of VLC.

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 ever suggested that I needed more Metformin or that I add another anti-diabetes med, until last year – and if they had, I’m not sure I would have agreed. But the conventional medical wisdom is that Type 2 diabetes is a “progressive” disease. That’s what drives the medical corollary to increase medications. And, my A1c had been creeping up, and it was becoming increasingly difficult for me to get fasting readings below 100mg/dl. Was I having “compliance issues” with my VLC diet or was the disease actually progressing? This question was unanswered, so adding a new medicine was an existential question, and it was a matter of pride for me. But my health (the risk of all the microvascular and macrovascular complications) was at stake. This is the crossroads: – more medication or better compliance with diet – that every Type 2 or “Pre-diabetic” faces every day, or on every doctor’s visit, for a lifetime.

I decided that for me the first step for was more vigilant self-management of my diet. After all, TYPE 2 DIABETES IS A DIETARY DISEASE. That’s why I began the steps described in 1) above.  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.

Scene 2: For years I have attended classes offered by a Certified Diabetes Educator (CDE), both to support her as well as try to persuade her to subscribe to and teach a Low Carb Way of Eating for diabetics. So far, I’ve failed! Last year she suggested I try the new SGLT2 inhibitors. 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 instead, last December, I asked my doctor to increase my Metformin to 500mg TWICE a day, and he said, “okay.”

Scene 3: In January I attended a conference on Metabolic Therapeutics and learned 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 conference organizer and a major presenter, were also maxed out on Metformin, which increases insulin sensitivity and suppresses gluconeogenesis to minimize body fat by promoting breakdown and burning of body fat for energy. This was an eye-opener for me. Metformin is a wonder drug for many reasons. It’s mechanism of action is not completely understood, but in a recent JAMA article, it was seriously advocated for everyone. And, unlike the SLGT2s, is has been around for well over 50 years, is demonstrably safe, and really cheap. So, after the conference, in February I decided to ask my doctor 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 (2016), after a long hiatus, I was routinely getting fasting readings (FBG) below 100mg/dl again, mostly in the 90s. What happened next, however, was quite remarkable. See Part 2 of this story tomorrow.