Type 2 Diabetes, a Dietary Disease #352: If you’re a Type 2, DON’T READ THIS.

Metformin* is designed for cheaters, like me! By that I mean Metformin is designed to work, or works best, with a “load” or “carbohydrate challenge.” That is my hypothesis, which recently came to mind after a “test” or “experiment,” as a friend jokingly refers to it, in which I consumed a large quantity of carbs in a short time.

I have to admit my judgment was impaired. We’d been indulging all afternoon with friends, and I’d had more than a little red wine. Then, after a light supper that my wife prepared, she “raided” the freezer, and while her back was turned, I snuck a taste of her ice cream. And then – she is so noble – to be sure that I ate no more, she finished the container. Later, when I snuck back to the kitchen, opened the freezer and discovered this, I found a new pint of Talenti Gelato (Hazel Nut Chocolate Chip) and ate half of it, about 50g of carbs.

And if that wasn’t bad enough, the next day was Sunday, my weekly comeuppance day. It’s the day my Excel program averages the previous week’s seven Fasting Blood Glucoses and records my week’s weight loss. But, lo and behold my FBG was only 98, up from 91mg/dl the day before. And the weekly average was 96, up from 94 the week before. Thus, my hypothesis: Metformin works best with a carbohydrate challenge.

So, if Metformin is so effective at improving glucose uptake when presented with a big carb load, like a 50g slug, what incentive is there to not indulge now and then? I mean, we all do it from time to time, right?

Well, I didn’t test my blood sugar post gelato, but considering it’s been more than 30 years since I first developed Insulin Resistance (IR), I can only imagine the rise that my blood sugar and blood insulin levels took in the immediate aftermath of that slug of sugar. It had to be precipitous, taking me well into the over 140mg/dl zone where damage is done to my organs. And it certainly took me out of a mild state of ketosis.

My weight the next morning was only a pound more than the day before, but how long, I wondered, would it be before the new glycogen stores were used up and my water weight dropped again. And how long would it be before my blood insulin level dropped, the bloat was gone, and I had that lean, high-energy feeling again.

Was it worth it? Probably not. But was it avoidable? For some, the answer apparently is “yes,”, or so I’m told by readers who profess not to be tempted. But then they may be people to whom temptation is not often presented – people who either live alone or with someone who is also attempting to eat Very Low Carb. In these households there IS no ice cream in the freezer. I am also definitely tempted by visual stimuli, or a lack of will to resist a visual stimulus. Or maybe it’s just a case of “arrested development” from a dysfunctional adolescence. Who knows? We are all, as we non-compliant folks rationalize, different. Indeed.

*  My current Metformin regimen (recently up from 500mg/d), is 1500mg/d, divided between AM and PM. That’s the only anti-diabetic medication that I have taken since I started to eat Very Low Carb (…most of the time, lol) in 2002. I am experimenting (there I go again) with the larger dose since recently reading that Metformin is really effective only at higher doses. I wish I could find that reference to link to.

I had also observed at a Metabolic Therapeutics conference that I attended earlier this year that a large cohort of normoglycemic men, specifically fitness experts and body builders, were taking maximum doses of metformin (2000mg/day) to enhance glucose uptake and suppress gluconeogenesis. They want to facilitate ketogenesis to break down body fat, enabling them to reduce stored body fat and, by rigorous exercise, to build muscle. Metformin has several known mechanisms of action and, in general, is very well tolerated. 

Type 2 Diabetes, a Dietary Disease #351: Am I a Type 2 Diabetic?

Note: If you are asking this question for yourself, look at “How Diabetic Do You Want to Be?” Part 1 (#344) and Part 2 (#345) But read on if you are interested in a short essay on the subject “Am I a Type 2 Diabetic?” The answer depends on whom you ask.

First, you need some “history.” I was diagnosed a Type 2 in 1986, before the A1c test was developed and the glucose test standard was fasting blood glucoses on two consecutive office visits of ≥140mg/dl. That changed to ≥126mg/dl in 1997, and the ADA adopted the hemoglobin A1c test to replace the FBG in 2002.

In 1986 my doctor started me out on the only anti-diabetic oral medication available in the U.S. at the time, a sulfonylurea (SU) called Micronase (generic name: Glyburide). No doubt he advised me to lose weight (I was obese), but instead I gained. I do not recall if he gave me any dietary advice, but if he did, it no doubt would have followed the ADA’s Standard of Practice and the Dietary Guidelines for Americans, first issued in 1980.

When Metformin (in use in Europe since the mid ‘50s) was permitted in the U.S. in 1995, my doctor started me on that too. When in a few years I was maxed out on both, he then started me on a 3^rd class of oral drugs, the TZDs. I was then at my heaviest weight, and in yet another effort to get me to lose, my doctor suggested I try a Very Low Carb diet he had read about in The New York Times. It was Atkins Induction (20g of carbs a day) as described by award-winning science writer Gary Taubes in the Magazine cover story, “What If It’s All Been a Big Fat Lie?” It created quite a stir. I tried it and, over time, lost altogether 170 pounds.

On strict Atkins Induction, from the first day, to prevent hypoglycemia (low blood sugars) I had to give up first the Avandia (the TZD), then cut the other two meds in half, and then cut them in half again. A while later, I gave up the SU (glyburide) altogether and continued the 500mg Metformin once a day for the next 14 years.

In addition, in no time at all my lipids (cholesterol) improved dramatically. My HDL average more than doubled (39 to 81), my triglyceride average plummeted by 2/3rds (from 137 to 49), and even my LDL came down! And with all the weight lost my blood pressure improved substantially (on the same meds). All these changes were from diet alone, no exercise.

So, am I a Type 2 Diabetic? A clinician who looked at my fasting blood glucose today (90mg/dl) would say, “Consistent with the absence of diabetes.” Yet, 30 years ago I was diagnosed a Type 2. Was it a mistake? Am I still a Type 2 Diabetic? Or, has my Type 2 Diabetes been “cured” because my “symptom” has gone away.

A clinician who looked at my hemoglobin A1c would see 5.7% and say, “Consistent with an increased risk for diabetes (prediabetes).” They would have no basis to conclude otherwise. They’d say, “We’ll continue to monitor that” (until it gets worse), and then maybe they’d write a script for a minimum dose of Metformin.

An endocrinologist would order a 2-hr Oral Glucose Tolerance Test (OGTT) in a hospital outpatient setting. It would reveal the underlying Impaired Glucose Tolerance (IGT). Result: Definitely, a Type 2 Diabetic.

The truth: Starting probably 40 years ago, I gradually developed Insulin Resistance. I became Carbohydrate Intolerant. Insulin receptors on the surface of muscle, that are supposed to “open the door” to allow glucose to be taken up, started to gradually fail. My pancreas made more insulin. With overuse, its capacity to make beta cells began to wear out. That loss of function is not going to change. It’s not reversible, but my Type 2 Diabetes is treatable, by making my insulin receptors work better. The only treatment that works for that underlying metabolic dysfunction (Insulin Resistance) is a low carbohydrate diet. This treatment works!

It’s not as hard as you might think. After a few days, you lose your sense of hunger because your body has started to break down fat for energy. It’s good energy. You feel alert. Pumped, actually. You don’t get sleepy after lunch. Your energy level is constant and your blood sugar pretty flat – no peaks and crashes – and you feel lean. You’re ready to hunt. 

Type 2 Diabetes, a Dietary Disease #350: My latest lipid panel (cholesterol test)

I realize that no one (besides me, and my doctor) is interested in my latest cholesterol test, but…I think they can be used to impart a wider message – a lesson really – on the effect that diet can have on the health markers the medical establishment considers important. Doctors don’t really know much about nutrition, and if they follow the Standards of Practice and the “Dietary Guidelines”, well…you’d be well advised not to follow that dietary advice. Doctors do like a good lipid panel though, so what dietary advice produces that?

My doctor scribbled “good” next to my latest lipid panel. From my perspective, it was better than good; it was stellar! Total Cholesterol: 184, HDL Cholesterol: 91; Cholesterol/HDL ratio: 2.0; LDL Cholesterol (calculated): 84; and Triglycerides: 46. To these, I always add the TG/HDL ratio, considered by some clinicians today to be "...the strongest predictor of a heart attack." Mine is 46/91 or 0.5, nothing less than outstanding! 

In response, some (like my wife) will say, “Well, it’s genetic, and you’ve always had a ‘low cholesterol’” (i.e. Total Cholesterol). That is the value that most people (and their doctors) remember. It’s not true, in my case (as I’ll point out later), but, apart from that, why is it that most doctors only treat a high Total Cholesterol?

The answer is because most people who eat a Standard American Diet will have a borderline HDL (40mg/dl for men and 50mg/dl for women). They will also probably have borderline Triglycerides (near 150mg/dl). That leaves only LDL (and Total Cholesterol), and guess what? While doctors don’t have a handy drug to treat borderline HDL and triglycerides, they sure do have drugs to lower LDL, and thus Total Cholesterol: STATINS.

So, if your “cholesterol” isn’t so good, your doctor will likely prescribe a statin for you. If you take it, and tolerate it without harsh side effects, be assured: statins WILL lower your LDL cholesterol and your Total Cholesterol. The Friedewald equation explains it: TC = LDL + HDL + TG/5. Lower your LDL and you will lower your TC! You are now in good standing with your doctor, ‘cause there’s not much more they can do for you.

But what about ...the strongest predictor of a heart attack, the TG/HDL ratio? Only diet can transform TG and HDL, and fix them good! I eat a Very Low Carb diet and practice Intermittent Fasting. I do it to keep my blood sugar low and stable, to keep my serum insulin low as well, and thus burn body fat to lose weight.

I originally went on a Very Low Carb diet (20g/day)  just to lose weight. We – both my doctor and I – were  surprised to see that it had an immediate and very dramatic effect on my long-standing Type 2 Diabetes. To avoid hypoglycemic events (“hypos”), I had to immediately (the very 1^st day and throughout the 1st week) stop taking the oral diabetes medications I had been prescribed over many years. I had been maxed out on 2 classes of oral meds and was starting a 3^rd.  Afterwards, I was left with only a small dose of Metformin which I continued for 14 years.

But the other effect that neither my doctor nor I expected was that, over time, my HDL Cholesterol more than doubled (from 39 to 81mg/dl average) and my triglycerides dropped by 2/3s from 137 to 49mg/dl average. And this remarkable change continues to this day (15 years later), as my most recent lipid panel (HDL = 91 and TG = 46) demonstrates. Of course, as I lost weight my blood pressure improved (on the same meds) from 140/90 to 110/70. The most recent was 120/75 (I regained 35 of the 170 pounds initially lost.) And my inflammation marker, the hsCRP, a reliable “risk factor” for a constellation of morbid outcomes, is now almost always <1.0.

So, what difference does diet make? I attribute all of these changes to diet, a Very Low Carb diet. My Type 2 diabetes is in remission, my lipids (cholesterol) are “good” or “stellar,” depending on whose interpretation, my blood pressure is well controlled, and my chronic systemic inflammation is indiscernible. Even my LDL is excellent (84mg/dl vs. <130mg/dl reference range, or “<100mg/dl for patients with CHD or diabetes.” And I did it all without a statin. You can too, but you have to be willing to treat yourself, and change your diet.

Type 2 Diabetes, a Dietary Disease #349: Yoga for Diabetes

I woke up the other day during the last minute of a “Yoga for Diabetes” TV program, so I missed it. Dang! Fascinated by the idea, though, I decide to Google it. I found a gazillion sites, with videos. Whoda thunk it?

No offense (intended), folks, but this idea made me laugh. It reminded me of the time in the 1970s when, after 5 years of working for one of the best solar architects in the country, I opened my own architectural practice specializing in active and passive solar energy design. Unfortunately for me, so did everyone else in my practice area. Everyone wants to be on the bandwagon, without regard to whether they are qualified.

Yoga is no doubt a useful activity for meditation, stress reduction, and even stretching. I hesitate to call it exercise, but if you are old or unfit, it may be good fitness training for you. I’m not knocking it, but to suggest that yoga has real benefit for “treating” or even “curing” Type 2 Diabetes as many of the TV sites do, well, give me a break! Type 2 Diabetes is a Dietary Disease, and the only effective treatment is a low carb diet.

But if that isn’t enough, you could add Metformin. It will increase your Insulin Sensitivity (i.e, reduce your Insulin Resistance), and suppress unwanted glucose production in the liver (gluconeogenesis). But a low carb diet alone, with fasting, will result in weight loss and a reduction in A1c such that, for many people diagnosed with Pre-Diabetes or even long-term Type 2 (like mine), your disease will go into remission.

You will not be cured (you will always be Carbohydrate Intolerant), but nobody will know it – not even your doctor – if you don’t tell him or her. That’s because doctors are trained to treat symptoms, and you won’t have any symptoms detectable by any lab test (s)he will likely administer. So, from your doctor’s perspective, you will be “cured.” If there is nothing for him or her to treat (because you are treating yourself with a low carb diet and intermittent fasting), what other conclusion could be reached?

It’s that simple folks. Don’t waste your time looking for a miracle cure, or trying to re-invent the wheel. And don’t think you can cheat Mother Nature. Your body is a very complex biological organism and is much smarter than even you! You can’t fool it. And even though you might talk yourself into thinking it will only cost you a little to cheat, kachung, the “cheat” will register in your blood glucose. Every carb will wind up “under the curve” and have to be absorbed eventually. If not burned for energy, these extra carbs will end up as fat, via a process called de novo lipogenesis, another good reason to take Metformin. Didja know that?

In basic science, the funding continues to flow from government sources (NIH, etc), for an understanding of what causes Insulin Resistance (IR), Type 2’s underlying metabolic dysfunction. It is the first in a galaxy of related metabolic disorders and the one that appears to cause, first, Impaired Glucose Tolerance (IGT), and then Impaired Fasting Glucose (IFG), the two blood measurements that characterize incipient diabetes.

They are reflected, respectively, in the blood tests used by clinicians to diagnose Type 2: Fasting Blood Glucose (FBG) originally, and today the hemoglobin A1c test. The latter is a better test because, like Impaired Glucose Tolerance, it incorporates postprandial (after meal) excursions and thus catches the rise and fall of your blood sugar after eating. The Oral Glucose Tolerance Test (OGTT), usually administered over 2 hours in an outpatient hospital setting, is the gold standard, but it’s more expensive.

In applied science (pharmacology) the search continues for a miracle drug – TO TREAT THE SYMPTOM: AN ELEVATED BLOOD SUGAR. What did you expect? That’s how Big Pharma got big. It’s their raison d’être. And that’s because they can’t patent the cure for the cause; because IR is caused by Carbohydrate Intolerance!

But you can treat the cause. YOU CAN EAT LOW CARB. It will put your Type 2 Diabetes into full remission.

Type 2 Diabetes, a Dietary Disease #348: Nervous Eating

In an earlier column (#342), I asked, “Is cheating okay?” I answered “no,” with an explanation. I stipulated:

“So long as I remain in a state of mild ketosis (remember: without hunger), IF I EAT, it is for another reason, and there are many: a) the sight or smell or food, b) the thought of food, c) rationalizations (an open bag or box in the pantry), d) social pressures (when a dinner guest, food is offered), e) unsolicited food (bread at the restaurant table, hors d’hoeuvres at a party), e) thoughts of deprivation (everyone else is eating dessert at the pot luck), and habit, such as eating two or three meals a day. To all these things I have – in fact, I need, only one reply: I ask myself, “Am I hungry?” The answer, of course, is “no,” and that is almost always sufficient.”

It occurred to me afterwards, however, that the most common “other” occasion for my non-hunger driven eating is “nervous eating”: eating (alone mostly) and for no good reason! How could I have overlooked this!

I have managed somehow to mostly stick to the plan. It has gotten easier and easier, because so long as I eat mostly foods that are protein and fat, I’m never hungry. Day after day, week after week!

In the morning I have cream in my coffee. That’s it. Enough to take pleasure from it, and swallow a few pills.

For lunch, I have a small meal, a snack really. Just a can of kippered herring in brine, or 2 hard boiled eggs with some homemade mayo. Sometimes, I eat a can of sardines in EVOO. Why do I eat lunch? (I’m still not hungry, and therefore I’m breaking Rule #2 in #326, “Eat only when hungry”). My rationale? Habit? Boredom? A break from morning activity? Who knows… but it’s a small meal, and it’s all protein and fat, I rationalize.

Then, for supper, my wife prepares a small plate of protein/fat and a low-carb vegetable. Last night it was two small New Zealand grass-fed lamb chops and cauliflower pureed with cream cheese and pecorino Romano. Delicious! I wanted more, but not because I was hungry; it was that good! My supper was accompanied by a 2^nd red wine spritzer, to wash down my evening pills. The first one preceded supper – a happy hour of sorts.

And then as we settled in to watch Jeopardy, I got “restless.” I say “restless” because it was an urge of sorts. I was tempted to eat, but not because I was hungry. I was in a “fed” state; my stomach was not the source. Yet I wanted something else? Was it an emotional need? Hey, I’m not of a mind for the couch – too much there to explore, and way too dangerous (LOL). But if my need was not alimentary, then the gastrointestinal tract was not the road to fulfillment. If the need lay elsewhere, I reasoned, I would need an alternate way to satisfy it.

I recall that when I addressed this issue 4 years ago in #63, “Impulse Control and Metacognition,” I relied on a substitution approach, using an alternate thought (to the urge to eat) to replace and distract me from temptation. This usually worked, but it was indirect. It replaced one thought (the “temptation”) with another, such as becoming engrossed in a book. The approach advocated in #326, #342 and reprised above and again here is, “To all these things [temptations or urges] I have – in fact, I need, only one response: I ask myself directly, ‘Am I hungry?’ The answer, of course, is ‘no,’ and that is almost always sufficient.” It really is. It completely eliminates the emotional or “nervous need” to eat. It is entirely rational, and it’s working for me.

I have been helped in this direct approach by insights I’ve obtained from Daniel Kahneman’s brilliant book, “Thinking Fast and Slow.” It is premised on his concept of System 1 (fast) thinking which operates automatically, intuitively, involuntary, and effortlessly, and System 2 (slow) thinking, which requires slowing down, deliberating, solving problems, reasoning, computing, focusing, concentrating, considering other data, and not jumping to quick conclusions. Nervous eating is System 1. Not eating when not hungry is System 2.  

Of course, slow thinking is made easier if you are “keto adapted.” When you are mildly ketogenic, with low serum insulin, and low and stable blood sugar, your body is breaking down stored body fat for energy. Your metabolism is “pumped;” it’s in a happy balance, called “homeostasis.” It’s “the normal state of man.”

Type 2 Diabetes, a Dietary Disease #347: Lowering glucose in T2D is largely useless, unless…

If my last post (#346 here) left you, dear reader, in a quandary, that was not my purpose. Nor do I think it was Dr. Jason Fung’s intention. The title of his blog post, “Futility of Blood Sugar Lowering in T2D,” was an accurate reflection of this premise: lowering blood glucose by using medications that cause weight gain (such as insulin and sulfonylureas), is demonstrably harmful to the patient. So, lowering blood glucose by that method, as is still the standard of practice, is worse than useless; it is malpractice. There, I said it (if he didn’t).

To see that conclusively, you have only to read #346, or Dr. Fung’s blog, or acquaint yourself with the cardiovascular outcomes of the UKPDS and ACCORD studies. On the other hand, Metformin does suppress unwanted hepatic (liver) glucose production and improve insulin sensitivity/glucose uptake, and thus lower blood glucose, without weight gain. Dr. Fung concludes his blog, however, with the lamentation: “Yet, here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars.” However, his implication goes further.

Dr. Fung’s point was that lowering blood glucose alone, as practiced today by most clinicians, though well-intentioned, has negative consequences and is insufficient; it must instead be in conjunction with lowering blood insulin levels. “It only makes sense to reduce BOTH glucotoxicity and insulin toxicity,” he says here in an earlier blog post. “Drugs such as SGLT2 Inhibitors do this, but diet is obviously the best way. Low Carb diets. Intermittent Fasting.” For the mechanism of action, see here or read Dr. Fung’s book, “The Obesity Code.”

Why is an elevated blood insulin (from the ingestion of carbs) considered “toxic”? Because it is the impetus for a constellation of metabolic disorders, starting with Insulin Resistance, that have come to be known as Metabolic Syndrome. They have all been precipitated by the changed dietary practices of the last century, during which we have seen the introduction and proliferation of highly processed carbohydrate “foods” and vegetable oils.

These two developments have been abetted by an officialdom who, in a misguided effort to protect our arteries from foods containing saturated fat and cholesterol, has encouraged us, since 1977, to avoid them and instead eat more highly processed carbs and vegetable oils. The Dietary Guidelines for Americans were first published in 1980 and have changed little since. Recently they dropped the limitation on total fats, and are struggling with the guideline on dietary cholesterol, but they have doubled down on replacing saturated fat with vegetable oils. And the Nutrition Facts panel on processed foods is still based on 60% carbohydrate, 30% fat and 10% protein.

The effect of these guidelines has been an accelerated introduction of manufactured food products to conform to them and a mass movement in the culture to adopt them. The outcome, as we develop the markers of metabolic disease – obesity, hypertension, type 2 diabetes, hypercholesterolemia, dyslipidemia, and NAFLD – is a growing body of evidence that this nationwide dietary experiment has, tragically, gone awry (see chart).

All of these chronic metabolic disorders are related, and all of them can be traced back to a chronic elevated blood insulin, i.e. Insulin Resistance (IR). They are caused by what we eat. Carbohydrates start the process by signaling the pancreas to secrete insulin. Insulin is required to transport the glucose (digested carbs) and to open the door to the cells that take up the glucose for energy. While more and more insulin is circulating, trying to “open the door,” it signals our other source of energy, stored body fat, that they are not needed. They are in fact blocked from use. So, while the glucose and insulin circulate, we do not burn body fat for energy. And any glucose from overeating that is not needed for immediate energy is converted by the liver to more body fat.

An elevated insulin starts it: insulin resistance, obesity, hypertension, type 2 diabetes, hypercholesterolemia, ED and NAFLD all follow. So, as Jason Fung says, “It only makes sense to reduce BOTH glucotoxicity and insulin toxicity,” and “diet is obviously the best way” to do it. “Low Carb diets. Intermittent Fasting.”

Type 2 Diabetes, a Dietary Disease #346: “Glucose lowering in T2D is largely useless”

Okay, I’m a big fan – a devotee you might say – of Jason Fung, MD, a Canadian nephrologist, blogger, and author. His very good book, “The Obesity Code” (2016), appears to be targeted to medical professionals but is equally comprehensible to the lay reader. He is also a frequent blogger, and his recent, “Futility of Blood Sugar Lowering in T2D,” like a previous one, “Obesity is Protective,” is getting attention. It certainly got mine (#341).

All reasonably well-informed students of diabetes – including clinicians who treat diabetics, endocrinologists, diabetologists, as well as Certified Diabetes Educators (CDEs) and Registered Dieticians (RDs), are familiar with the large, long-term UK studies, the DCCT and the UKPDS, and the US follow-up, the ACCORD study. What Fung did in his recent blog post was succinctly summarize the findings of those studies and posit, in conclusion, “…that blood glucose lowering in type 2 diabetes is largely useless.” That’s a pretty stunning conclusion.

His logic, however, is impeccable. “The DCCT study…had already established the paradigm of tight blood sugar control in Type 1, but whether this held true for Type 2 remained to be seen,” he said. In UKPDS33, he went on, a large cohort of “newly diagnosed T2D patients who failed a 3 month lifestyle therapy trial were enrolled into an intensive group of sulfonylureas or insulin vs. conventional control.”

“The drugs certainly were successful in lowering blood sugars” [to 7.0% vs. 7.9% in the diet group], he said, “but there was a price too. Weight gain was far worse on the drug group….” But over the 10 years of the study, they found no “benefits for the end points that everybody was interested in – cardiovascular disease. Despite reducing blood sugars, CV disease showed no benefits,” he averred. “Since the majority of deaths are due to CV disease, the primary goal of therapy was reduction in deaths and CV disease, not microvascular disease.”

In a sub-study called UKPDS34, overweight patients with T2D were randomized to either metformin or diet control alone. “Once again, over the space of over 10 years, the average blood sugar was lowered by metformin to 7.4% compared to an average A1c of 8% in the conventional group,” he said, but, “In contrast to the previous study, intensive control with metformin showed a substantial improvement in clinically important outcomes – there was a 36% decrease in death (all cause mortality) as well as a 39% decrease in risk of heart attack.”

“Metformin performed far better than the insulin/SU group despite the fact that average blood sugar control was worse,” Dr. Fung concluded (emphasis his). “What’s the major difference between the two medication groups,” he asked? “Insulin! Insulin and sulfonylureas (SU) increase insulin levels. Metformin does not.”

Refrain, all together now: “Because it does not raise insulin, and insulin drives obesity, metformin does not cause weight gain.”

Troubled by the failure of the original UHPDS study to show a benefit from reducing high blood sugar in Type 2s, the U.S. National Institutes of Health (NIH) undertook “an ambitious large trial called the ACCORD study (Action to Control Cardiac Risk in Diabetes).” Two groups with an average A1c of 7.5% were randomly assigned, the 1^st to “standard therapy,” the 2^nd to “intensive drug therapy,” “…with the goal of seeing whether this intervention would reduce disease.” They were successful in lowering their A1c to 6.5%.

But that was not the primary end point. They “wanted to know whether this made any difference. It sure did,” Dr. Fung says. “When the trial results broke, there was a media firestorm. Why? Because the intensive treatment was killing people! The risk of death increased by a horrifying 21% in the intensively treated group,” he wrote. Then, with 17 months before the scheduled end of the trial, “the safety committee looked at the available data and forced the premature end of the [ACCORD] trial.”

Was the study design flawed because there was no specification of which medications to use to intensify treatment, and the drug Avandia, which was very popular at the time, was included? I took Avandia briefly before I began to eat VLC. Avandia now carries a black label warning that it may cause heart attacks, angina, and heart failure. “Yet, here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars,” Dr. Fung concludes.

(Read Part 2 next week to see what Dr. Fung suggests be done about it.)