Type 2 Diabetes, a Dietary Disease #360: Ten years ago, I had a relapse (Part 5)

As readers following this series know, I decided to write it after I stumbled on an old misfiled Excel folder detailing my early “carb counting” days from 14 years ago. After regaining 12 pounds of 60 that I had lost on Atkins Induction in 2002, in 2006 I rededicated myself to Dr. Richard K. Bernstein’s 6-12-12 plan for diabetics. Fifty weeks later, with strict adherence and record keeping, I had lost another 96 pounds. When added to the previous 48 (60 – 12), my loss then totaled 144. I would eventually go on to lose a total of 170 pounds.

In the beginning I still ate a lot, but I did not limit calories, fat or protein. Just carbs. I had a much larger body to feed then and therefore a lot more organism (and psyche) to satisfy. A person who is used to eating, and receives gratification from eating a lot, needs to acclimate him/herself to this new lifestyle. You need to make a gradual adjustment to smaller meals. And you need to shift gratification from a feeling of being full to a feeling of liking that “lean” feeling and seeing the weight loss as recorded every day and every week.

What surprised me (and amazingly my doctor as well), was how, from Day 1 on strict Atkins Induction, the very low number of carb grams had an immediate effect on my blood sugar readings and on my medications. On Day 1 I had a hypoglycemic episode, and several more that first week. My doctor immediately dropped the 3^rd oral anti-diabetic med he had recently started me on and then in successive days that first week, recognizing that I was overmedicated, cut the other two meds, on which I was maxed out, in half twice. In just one week, before weight loss was even noted, I had reduced my diabetes medications by 90% (8/9^ths).

When I started on Bernstein in October 2006, I was still on 5mg Micronase (glyburide, a sulphonylurea or SU) and 500mg of Metformin. I only kept a record of estimated carb grams, and took 4 took blood sugar readings a day: Fasting, 2 hr postprandial, late afternoon (before Happy Hour) and 2 hours after supper. I would later add protein, fat, and calories to my records. Still later I added saturated fat, cholesterol, sodium, fiber and simple sugars (mono and disaccharides, added and naturally occurring). Total sugars were always VERY low.

I kept records in 4-week tables. My goal was simply 30 grams of carbohydrate a day, ala Bernstein’s program.My first 4-week average carb count was 33 grams a day, range 16 to 59, but those were outliers. Most were 20s and 30s. The interesting thing about this month was my blood tests. The fasting average the first week was 139mg/dl. It dropped in weeks 2, 3 and 4 to 107, 104 and 104. But the really interesting result was my late afternoon blood glucose readings. The first week’s average was 85mg/dl. The second week’s was 78, but by the 3^rd and 4^th weeks it had dropped to 59 and 56, with 6 out of 7 readings in the last 2 weeks in the 40s.

On only 5mg of a SU, while eating VERY LOW CARB, I WAS OVERMEDICATED! So, in the next 4-week period I stopped the SU for 2 weeks and then added it back at a reduced dose of 2½mg. My late afternoon averages were now 95 and 114mg/dl for the weeks without an SU, and 57 and 81 for the weeks at the reduced dose. My carb gram average for this 4 week period was 31, down from 33, and very close to my goal of 30.

Not bad, considering this period included Thanksgiving… and Christmas was coming. Oh, by the way, I also lost weight during these successive 4-week periods: 10 pounds the 1^st, 14 the 2^nd, only 1 the 3^rd (including a 150 carb binge on Christmas Eve and on Christmas Day another 94g carb binge). These and a few more seasonal indulgences bumped the December carb gram average up to 51 grams a day. And my weekly fasting sugar averages increased as well in December (105, 109, 111 & 112), but my late afternoon weekly averages held sort of steady (72, 77, 83 & 95) and my evening 2-hr postprandial averages were fine (87, 87, 83 & 95).

In January, I got back to eating according to plan, and my carb gram average dropped to 32 grams a day. Increasingly, however, my late afternoon readings were again dropping below normal (70-100mg/dl), with weekly averages going from 85 to 71 to 67 to 68. So, in the next 4-week period, my average daily carbs dropped to 23! I took no glyburide in week 3, and starting in week 4 I split the tiny pill in half and took just 1.25mg/day. My late afternoon blood glucose average went from 72 to 77 to 95 and back to 87mg/dl.

On March 17, 2007 (end of week 23 on Bernstein 6-12-12), I stopped the sulphonylurea altogether. SU’s are bad news. They effectively lower your blood sugars but at a very big price. They beat up and deplete the pancreas of beta cells and impair its ability to make insulin. Eventually you must inject insulin as your body loses its ability to produce it. 

Type 2 Diabetes, a Dietary Disease #359: Ten years ago, I had a relapse (Part 4)

In Parts 1, 2 and 3 of this series (#356, #357 and #358), I described how I lost 170 pounds on Very Low Carb diets. I related how it all began after my doctor read “What if It's All Been a Big Fat Lie?,” a 2002 NYT Sunday Magazine cover story. He tried the diet to lose weight. After losing 17 pounds, my doctor suggested I try it, also to lose weight. Unfortunately, my doctor soon regained all his lost weight when he went back to eating “normally.” He would afterwards ask me, “What do you eat?” and “How do you do it?” I said, “It’s no secret.”

He also said though, “It might even help your diabetes.” He was sure right about that. Of course, neither of us knew at the time how much it would help my diabetes, but I you’ve read Parts 1, 2 and 3, you know what happened: my Type 2 Diabetes went into total remission. He would probably say that I was “cured,” because I no longer had any symptoms discoverable by the routine lab tests. I am, however, still a Type 2 diabetic because I have Insulin Resistance. I am Carbohydrate Intolerant. That still leaves the questions, “What do you eat?” and “How do you do it?” That’s what Parts 4 and 5 are about.

Ten years ago this past summer, after several years of maintaining my weight at about 315 pounds, I relapsed. I regained 12 of the 60 pounds I had lost on Atkins Induction. That’s when, in October 2006, I started on the Bernstein program for diabetics. I built an Excel table (Fig.1) to keep track of the carbs I ate.

But Bernstein also requires that you limit protein, since some amino acids (digested protein) are glucogenic (can be made into glucose by the liver). So, after a few months on Bernstein, I built a new table (Fig.2) to add protein, and then fat, calories, blood sugars (4 times a day) and weight. I used an online program to get the numbers for everything I ate. It took about a half hour a day at the start, then a little less with practice.

I weighed myself daily, but only noted the change weekly. In the beginning, while I was learning the effect that different foods had on my blood sugar, I took a morning fasting blood sugar (FBG) and a 2 hour post prandial. I also took one in late afternoon (usually my daily low reading) and another 2 hours after supper. Now, since I know about carbs, I only weigh-in daily and take a FBG in the morning to get a weekly average.

I kept a detailed food log for a few years, until I learned what I could eat and what I couldn’t. It was also a good way to show me the price I paid when I ate something I knew was taboo. It had another effect too. Besides the shame and guilt I felt, and the disappointment with myself for the “lack of discipline,” it always ruined my averages. If you’re completely honest with yourself, and record everything, the numbers don’t lie. That was probably more devastating than the guilt! You’ve got to be totally honest with yourself. You have to record everything you eat and drink. No rationalizing. No forgetting! And then, you have to face the truth.

After a while, you won’t need to keep records. You figure out what works. You learn, and then you know that eating certain foods will not spike your blood sugar. And others will. You know that eating fat and limited protein with nil carbs, will not leave you hungry. You will also be able to fast easily because YOU WILL NOT BE HUNGRY. When lunchtime rolls around, you will ask yourself, “Am I hungry?” and if the answer is “no,” it will be easy to skip that meal, or eat a smaller meal, without hunger. And, you will lose your “sweet tooth.”

None of this is to say that you will not want to eat something for reasons other than real need (hunger). For example, the sight of food is a tremendous stimulus for me. It has been my downfall more times that I can count. Nervous eating, bored eating, habit (mealtimes), social events, social convention, (fellow workers and family members) all present challenges. But, need is the only biological imperative, and real hunger is what drives that need. And if you are in a state of mild ketosis, described as “ketoadapted” (Google it!), your body is content with burning body fat for fuel. So, my new mantra is to ask myself, “Am I hungry?” If the answer is “no,” I try not to eat. But, if I succumb for whatever reason, I eat a small meal of just protein and fat.

Type 2 Diabetes, a Dietary Disease #358: Ten years ago, I had a relapse (Part 3)

When I told my wife that I was writing a series about my weight loss journey since I started Bernstein 10 years ago this fall, she asked me if that was the year we were in Puerta Vallarta in September. I checked and it was. What a memory she has! My recollection was a little different…

As I related in “Ten years ago, I had a relapse (Part 2),” I recalled that my motivation was that I had regained 12 pounds (20%) of the 60 pounds I had lost on Atkins Induction (20g a day of carbs) back in 2002-03. That was true, but my wife reminded me of a conversation I had had with a Canadian MD I met in Mexico who told me that I was “IN DENIAL.” What a service that doctor did for me that day!

I came home with renewed resolve to do something about that 12 pound weight gain. Having just read Richard K. Bernstein’s “Diabetes Diet,” I bought and read his Diabetes Solution  and decided to go for it: eat just 30g of carbs a day. For medications, I was still 5mg Glyburide and 500mg of Metformin a day.

Beginning in October 2006, I started counting carbs and taking blood sugar readings again (see Fig.1  ). By November ( Fig.2), I had cut back the Glyburide from 5mg to 2½. In late January (Fig.3), I started a 4-week drug trial to reduce it further from 2.5mg to 1.25. And in late February (Fig.4), I started limiting proteins, since so many of their component amino acids are glucogenic, i.e., are made into glucose by the liver.

Then, on March 17,^, 2007, I stopped taking Glyburide altogether. By April I was eating just 90g of protein a day (see #357 for how I chose this amount). In May, I reduced protein further to 80g/d. I also reduced my fat intake from 110 to 100 to 90g/day. By September 23, 2007 (Fig.5), 50 weeks after starting Bernstein, I had lost 96 pounds, going from 327 to 231. Added to the 48 net (60-12) that I had lost on Atkins Induction, my total weight loss from 375 pounds to 231 on both Very Low Carb diets, was 144 pounds…with more to come.

Remember too (or if you didn’t, read #356 here), starting with the first week on Atkins Induction back in 2002, I had stopped taking all of my oral anti-diabetic medications except 500mg Metformin and 5mg Glyburide.  Now I was only on 500mg of Metformin, which I was to continue for the next 14 years.

With all the weight loss, my blood pressure also improved significantly, on the same pill “cocktail.” It went from 130/90 to 110/70 at my lowest weight (late 2008). Currently it’s 120/75. And my lowest A1c was 5.4%.

Now, returning back to late 2003, after a year of monthly office visits while monitoring my 60 pound weight loss and maintenance while on Atkins Induction, my doctor suggested we change to quarterly visits. My Total Cholesterol and LDL-C hadn’t changed much. They were both “borderline” by NCEP Guidelines for a “healthy” person. But, based on my still “morbidly obese” status, and Type 2 diabetes, my doctor declared that I was still at “high risk” for cardiovascular disease, so he put me on a statin. He started me on Lipitor, and quickly raised it to the max. My LDL-C (and Total Cholesterol) responded as expected. They plummeted.

But, prior to my starting statins, on both Atkins Induction and Bernstein, my HDL-D and triglycerides both improved a little. Before starting Atkins, my average HDL-C had been just 39mg/dl and my TGs 143mg/dl. Now, my HDL was 51 average (range 43 to 60) and my triglycerides 84 average (range 36 to 157). As I continued from mid-2004 to mid 2007 on both Bernstein and a generic statin, Simvastatin, my TC and LDL-C were very, very low (TC: 116 & LDL-C: 48, average of 12); however, since starting on Bernstein, my HDL-C soared and TGs crashed. My HDL-C average was now 84mg/dl and my TGs averaged 49mg/dl.

Given the death-from-all-cause benefit of a high HDL-C and low triglycerides, and my total weight loss (by this point 170 pounds), on first, Atkins Induction, and then Bernstein, in December 2008 my doctor (on his own!) took me off statins. I have been statin-free now for 8 years. And while my weight has inched up a little, my latest lipid panel was Total Cholesterol 184, HDL-C 91, LDL-C 84 and triglycerides 46. How’s them apples?

Type 2 Diabetes, a Dietary Disease #357: Ten years ago…I had a relapse (Part 2).

As I started to tell you in #356 here, ten years ago this past summer, I had a relapse. I regained 12 of the 60 pounds I had lost over a nine month period 4 years earlier. I had lost focus. So, I decided that it was time to get serious again and rededicate myself to the principles and practice of the Very Low Carb Way of Eating.

That summer of 2006, 10 years ago, I also read Dr. Richard K. Bernstein’s book, “The Diabetes Diet.” So, with my renewed resolve, I decided to switch to Bernstein’s Diet Plan for Diabetics. Dr. Bernstein has been a Type 1 Diabetic for most of his 70-odd years and was an engineer before he became an MD, like his wife. She had a big blood sugar testing machine in her office, so he used it to develop a strict regimen for “eating to the meter.” After all, he reasoned (as an engineer), if carbs make your blood sugar rise, the best treatment for regulating your blood sugar would be to restrict carbs. That makes sense doesn’t it? It’s just common sense!

Bernstein’s credo is that “everyone deserves a normal A1c.” His is in the 4s. Being a Type 1, he achieves this by injecting insulin, both 24-hour and at mealtimes, on a 30g-of-carbs-a-day plan. He calls it 6-12-12: 6 grams at breakfast (lower due to what he calls the “Dawn Phenomenon”), 12g at lunch and 12g at supper. No snacks. These principles are all well documented in the latest edition of his book, “The Diabetes Solution.”

Another difference from Atkins Induction is that Bernstein limits protein. When digested, protein breaks down into amino acids, from which some are made into glucose by the liver and thus raise your blood sugar. So, to limit this unwanted glucose production (called gluconeogenesis), protein needs to be limited. But how much protein should a person eat? In 2006 I studied the question carefully and discovered that opinions vary widely, but the “correct” way is to use a number based on an estimate of ideal, or lean body weight.

Lean Body Weight is the optimal weight for a person, and it is your lean body that needs protein. In 1998 the HHS/NIH adopted the Body Mass Index (BMI) Chart used by WHO, the World Health Organization. Your doctor is required to use this chart to “evaluate” your weight. It is a really gross metric that takes no account of gender, body type, or your cultural environment. It is also a pie-in-the-sky number for almost everyone who will read this post, i.e. people living in a part of the world where food is abundant and where processed food has replaced real food in our lives. Thus, according to the BMI, most of us are now overweight or obese. Nevertheless, your BMI “normal” weight is what you should use to calculate the amount of protein to eat.

The middle of the “normal” range in the BMI chart for a 5’-11” person (me) is 150 pounds. I still weighed 300 pounds in 2006, so that sounded totally ridiculous to me, so, by “mistake,” I chose instead a “goal” weight of 180 pounds for my calculation. And since I was pretty sedentary and did no exercises, I used 0.5 grams of protein per pound (1.1g/kg) of my goal body weight. So, 180 x 0.5 = 90 grams of protein a day. Honestly, though, the grams per pound is also a variable where opinions vary widely, so the number you settle on is up to you. That’s how I started. Note: I was soon to reduce my protein budget further, but not the carbs…yet.

For fat, I followed Bernstein’s dictum: Eat enough to be satisfied. I didn’t avoid saturated fat or cholesterol. I was convinced by Taubes, and others by this point, that the 1977 “Dietary Goals for the United States” and The Dietary Guidelines from 1980 on, every five years thereafter, were a failed Public Health experiment and were in fact the cause of our obesity and diabetes epidemic. And they certainly weren’t the right diet for anyone who was diabetic, pre-diabetic, or had even a touch of Insulin Resistance. It just didn’t make sense.

So, for breakfast, I usually ate 2 fried eggs and 2 strips of bacon, with coffee and whole cream. That’s all. No juice. No bread. No jelly. No fruit and No cereal. Period! No exceptions. I found this small meal very satiating. I wasn’t hungry later in the morning or even at lunch time. I ate something though – out of habit – but it was usually a couple of hard boiled eggs, or later a can of sardines in olive oil or kippered herring in brine. Yum.

Type 2 Diabetes, a Dietary Disease #356: Ten Years Ago, I Had a Relapse…

Ten years ago this past summer, I had a relapse. I regained 12 pounds of the 60 I had lost over a 9 month period 4 years earlier. All I can remember from that misspent summer (I was 65 then) was that I regularly raided the freezer after supper or before bedtime to have a big dish of ice cream. That was all it took.

Four years earlier, my doctor had just read “What If It's All Been a Big Fat Lie?,” the July 7, 2002, Sunday Magazine cover story in The New York Times. For years my doctor had been trying, unsuccessfully, to get me to lose weight. And since the diet described in the Times’ story went against the medical establishment’s “Standard of Practice,” my doctor was reluctant to recommend it. He had a little paunch, though, so he decided to try it on himself first…and he lost 17 pounds.

A little later when my doctor suggested that I try this diet – Atkins Induction (20g of carbohydrate a day) – I decided to give it a shot. I weighed 375 pounds in 2002, and I didn’t think I was going to be healthy or even live that much longer. I was then taking a cocktail of drugs for hypertension (high blood pressure). In addition, I had been diagnosed a Type 2 Diabetic 16 years before, and had probably begun to develop Insulin Resistance a decade before that. Insulin Resistant meant I had become, in stages, Carbohydrate Intolerant .

I was taking maximum doses of two classes of oral antidiabetic medications and starting on a third. When the 3^rd class of meds would eventually fail to control my blood sugar, I would “graduate” to insulin. That is the standard treatment for Type 2s; it is the “Standard of Practice” when “diet and exercise” fail. And diet and exercise inevitably do fail because the one-size-fits-all diet that doctors prescribe, again according to the “Standard of Practice,” is the USDA’s Dietary Guidelines for Americans, a low-fat, high-carb diet!

So, starting on a strict “Very Low Carb” regimen had an immediate effect on my health: I had a “hypo” the very first day. After eating a candy bar and waiting for “the sweats” to subside, I called my doctor. He told me to stop taking the 3^rd oral that I had recently begun. But then, the next day I had another hypo. This time he told me to cut the dose of the other 2 meds in half, and before the week was out I had to cut them both in half again. I hadn’t noticed any weight loss, but in just one week I had eliminated almost all my T2 meds.

I did start to lose weight of course. Remember, that was why my doctor had started my on a Very Low Carb diet.  He was almost as surprised as I was at the “unexpected” effectiveness of the Very Low Carb diet in treating my Type 2 Diabetes. My blood sugar was stable and in control. And over the course of 9 months, I lost the 60 pounds, 1½ pounds a week. And then I retired from work and the weight loss stopped. I didn’t gain any back; I just stopped losing. I don’t recall my state of mind, but I must have kept eating Lower Carb because for three years, until the summer of ‘06, I kept the 60 pounds off, and my blood sugar was stable.

Along the way, with time on my hands (being retired) and being “a little OC” (lol), to be sure that I adhered to the basics of Low Carbohydrate eating, in March 2004 I decided to keep a record of how many carbs I ate. To do this I constructed an Excel table (see this template) to record for a week everything I ate every day and to estimate the carb content only. To do this I used carb counting guides and free on-line services.

The concept was 1) to learn more about carbs and 2) to be accountable to myself – to fully “fess up,” to me alone, everything I put in my mouth. My estimate of food quantities and carb content was crude and approximate. It was just a way to keep daily carb counts, but it had the added benefit of keeping me honest.

As I recently discovered when I found a misfiled folder in my directory, I kept these charts on and off from March 2004 until mid-2006, when I went off on that ice cream bender. Fortunately, by that time, I was well connected with an online community that showed me the way forward and provided much needed help and support. See next week’s post to learn how I was soon to lose another 100 pounds in just 50 weeks.

Type 2 Diabetes, a Dietary Disease #355, Before and After

It strikes me as odd that the axiom, “A picture is worth a thousand words,” is barely a hundred years old. It is not surprising, though, that it is attributed to a newspaper editor. As hackneyed as it is, it is nevertheless true, as these pictures, taken before and after a few years of Low Carb eating, testify.

Equally persuasive are line charts, with values, as these two, which show respectively my HDL-C and triglycerides over the last 35 years, the last 14 of which were driven by my Low Carb Way of Eating.

Lest any doubt remain, this next chart shows that my Total Cholesterol averages has been stable, contrary to the perennial declamations of naysayers of the conventional medical persuasion.

Type 2 Diabetes, a Dietary Disease #354: Macro and Keto Ratios

While exploring the Very Low Carb world over the years, I have been interested in the workings of both Macronutrient Ratios and Ketogenic Ratios. I started with the study of Macronutrient Ratios soon after I realized that “counting carbs” was not enough. I added protein and then fat (and total calories) and adjusted them over the years to where I have now settled on 75% fat, 20% protein and 5% carbs, on only 1,200 calories a day. This calculates to a ketogenic ratio of about 2.0. More on these values later.

Of course these Macronutrient ratios account for only ingested food – food and drink that I put in my mouth. But since I strive to eat so few carbs, when I am not eating too many carbs or too much fat (and protein), I am able to add to the calorie burn – what my body requires to maintain energy balance and an active metabolism – by burning body fat. I know that I have access to these fat calories because my serum insulin levels remain fairly low because there is a correspondingly low level of glucose circulating from both carbohydrate and protein restriction. I know that my body is not shutting down – or even slowing my metabolism to compensate for the low calorie intake by mouth – because I feel “pumped” all the time.

This additional fat burning would imply that my actual Macronutrient Ratios are higher than 75/20/5. It also would imply a higher Ketogenic Ratio, since only fat is being added to the equation, almost all in the numerator.

So, let’s do the numbers. If my daily food intake is 1,200 calories, and the Macronutrient Ratios are 75% fat, 20% protein and 5% carbs, my intake is composed of 100g of fat (900kcal), 60g of protein (240kcal) and 15g of carbs (60kcal). But if my metabolism stays up, that is, is not slowed down by the lower food intake – because the low carb intake allows my body access to its fat stores – then my actual fat contribution, at the cellular level where the nutrients are absorbed, is going to be much higher. How much higher, you ask?

That depends on my metabolic rate. How many calories does my body burn?  That would be the sum of my resting metabolism plus activity level, when not slowed down by either calorie restriction or from blocked access to fat stores.

Let’s say, for argument’s sake, that my metabolism chugs along at 2,550kcal/hr. If I am only taking in (by mouth) 100g of fat, 60g of protein and 15g of carbs, it is theoretically getting a contribution from body fat of 2,550 – 1,200 = 1,350kcals, or another 150g of body fat (1,350kcal/9kcal/g = 150g). That substantially changes the Macronutrient Ratio at the cellular level, where the body is actually fed. Check out this chart:

Nutrition & Metabolism	kcal	fat(g)	pro(g)	carb(g)	k/g ratio
Intake orally (food my mouth)	1200	100	60	15	2.0
Intake at the cellular level	2550	250	60	15	3.5

The formula for ketogenic ratio is derived from the work of Wilder and Winter (1922):

K/G ratio = (0.9*FAT+0.46*PRO)/(0.1*FAT+0.54*PRO+1*CHO.)

N.B.: Ideally, I am only burning extra body fat – and sparing protein. My body will use the carbs that I ate, which are going to be oxidized first, when it needs to make glucose for those cells that do not have mitochondria and therefore lack the ability to make ATP. Plus, amino acids from digested protein, not taken up in circulation, will become glucose via gluconeogenesis in the liver. And, the liver can also make glucose from the glycerol backbones of catabolized triglycerides when body fat is broken down and burned.

Type 2 Diabetes, a Dietary Disease #353: Advice for a friend who is “pre-diabetic”

“Just remembered, I didn’t answer your ‘other news’ question,” I emailed her back. Then, I continued:

“As you now realize, having just lost over 20 pounds, you are in a metabolic balancing act 1) to control your genetic predisposition to be Insulin Resistant (by managing what you eat -- i.e. eating fewer carbs -- to control both your blood sugar and blood insulin), 2) to maintain your weight loss (i.e., to not lose more and not gain), and 3) to do this without hunger. If you are successful, you will secure the reversal of the continuum you were on that was leading you to progressively worsening blood sugar control – even with medication – and eventually to full-blown Type 2 Diabetes Mellitus.

“You learned that you could reverse your ‘pre-diabetes’ by managing your diet. You learned to do that because you “ate to the meter,” testing your blood sugar before and after eating suspect foods. Because you acted in time, your ‘pre-diabetes’ had not progressed to where you’d seriously damaged your pancreas and developed non-reversible Insulin Resistance (IR). If you continue to eat the way you have learned for the rest of your life, you should be alright. You really have no other choice, unless you’re willing to accept progressive worsening of your IR and, despite medical therapy (more pills and eventually injected insulin), developing the inevitable complications. Your way allows you to cheat much more than someone like me who learned much too late. Your genetic predisposition -- to become a T2 -- has been checked. Congratulations!

“With respect to your ‘hunger,’ there is of course the possibility that this may be something other than your body telling you that you need energy from eating something. But if it is actually hunger, here's what I think: N.B., your body and mine are in different metabolic states, so what I am telling you now is my understanding of how the body’s mechanisms work for someone in your current ‘state.’ My body is never hungry so long as I abstain from eating more than a minimum number of carbs. My body is always being fueled by fat, in my case both dietary and body fat. Both are triglycerides and break down to fatty acids. I eat plenty of fat, and I have plenty of stored fat on my body. So, my metabolism is always running in high gear. I am pumped. And my blood sugars are stable. I can even cheat because by always keeping my blood sugar and blood insulin levels ‘low,’ and by taking 750mg of metformin twice a day, my insulin sensitivity has improved. That means when I cheat, the sugar in my blood is taken up and my FBG returns to ‘my normal’ (90s) more easily. 

“In your case, you want to stop losing weight (and maintain your weight loss), and continue to remain insulin sensitive, and avoid hunger (a sign of a restricted calorie diet and/or a roller coaster blood sugar. In other words, instead of letting your body use either your body fat or ingested fat for energy (thus maintaining a high energy level, i.e. always feeling pumped like me, and keeping a stable blood sugar), you need to use only dietary fat, that is, fat that you ear. If you instead eat carbs with every meal (together with fat and protein), your blood sugar will fluctuate, even if it returns to "your normal" (low 100s) one or two hours after eating. Your metabolism is being fed both dietary carbs and dietary fat for energy. So, your blood insulin level never goes down. And because your body won’t (and you don’t want it to) burn body fat, you get signals from your body that you are hungry. It tells you to eat something because (as you intend) the path to letting your body break down its own fat for energy is blocked by the constantly elevated blood insulin level.

“Your solution: Skip carbs altogether for one or two meals a day. Try limiting them only to supper, say, or breakfast if you must have that "chocolate cocktail" you seem to enjoy. Eat mostly fat and protein for energy, and just eat carbs from time to time, on special occasions, like making deadline, not every day at every meal!

“I don't always listen to my own advice,” I told my friend, “but I have found this little piece really works well for me: When I feel the urge to eat something, I ask myself, "Am I hungry?" Invariably the answer for me is ‘no.’ Sometimes I eat anyway, but more and more often I am deciding not to. Learning how to do this is about changing habits, and giving up comfort foods. It is also about an emotional/psychological/need. In my case, when I answer ‘no,’ I find an alternative to eating. Reading or writing (or a happy hour spritzer or two) works for me. I would think this would work for you too. As I turn to something else, the ‘need’ goes away.”

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.)

Type 2 Diabetes, a Dietary Disease #345: How Diabetic Do You Want to Be? (Part 2)

That sounds like a stupid question, I know. Nobody wants to be diabetic. But once you’ve been diagnosed as Pre-Diabetic or Type 2, you have, for life, for better or worse, to one degree or another, a condition called Insulin Resistance (IR)). For all intents and purposes, that means you are to some degree Carbohydrate Intolerant. You got this way by 1) having a genetic predisposition and 2) eating a diet too high in carbohydrates for too long.

Don’t blame yourself entirely. By 1961 the AMA had come out against saturated fat and dietary cholesterol and in 1977, the Senate Select (McGovern) Committee issued their Dietary Goals of the United States, recommending we all eat a low-fat, high-carbohydrate diet. Both the medical and public health establishments were tragically misguided in these recommendations, and they were soon ably abetted by Agribusiness and Big Pharma.

So, if you’ve been diagnosed either Pre-Diabetic or Diabetic (Type 2), as I ask rhetorically in #344, using the hemoglobin A1c, today’s marker for blood sugar control, “How Diabetic Do You Want to Be?”

Is an A1c of <7.0% (or <8.0% if you are elderly) the target that you and your doctor are comfortable with?

Or, is <6.5% your target, to avoid being officially diagnosed a type 2 (by current medical standards)?

Or, is <5.7% your target, so you can comfort yourself with the phrase, “consistent with the absence of diabetes”?

Or, is an A1c in the “low 5s” your target? It has been for me for half of the 30 years that I have been a diagnosed Type 2. My doctor isn’t worried, though. He, like most and the ADA, considers under 7.0% “well controlled.”

Or, is an A1c ≤5.0% your target? I know several long-term type 2s who manage their disease this way; this is the true “optimal” or normal A1c. They do this with a combination of a strict Low Carb diet and insulin injections.

So, to be an informed consumer/patient, you need to be armed with some facts. The following is filched from one of, if not the best, on-line sites for Pre-diabetics, Type 2s and Type 1s: Jenny Ruhl’s “Blood Sugar 101.”

“Risk Quantified For Non-Diabetic A1cs and Heart Attack Risk

The Atherosclerosis Risk in Communities study tracked 11,092 black or white adults who did not have a history of diabetes or cardiovascular disease for 15 years. It found no association between fasting blood sugar and risk of heart disease, but A1c was a different story. The table below summarizes the correlation of baseline A1c with the risk of developing cardiovascular disease. [CVD]

Multivariate-Adjusted Hazard Ratio [with my translation, for the statistically challenged].

5%:                    0.96 (0.74-1.24) [If you have an A1c of 5.0%, your chance of developing CVD is just                           below “even.”
5% to < 5.5%:  1.00 (reference) [In this range, your CVD risk is THE SAME AS ANYONE ELSE!]

5.5% to < 6%:  1.23 (1.07-1.41) [In this range, you are almost 25% more likely than if your A1c is                               5% to <5.5%.]
6% to < 6.5%:  1.78 (1.48-2.15) [In this range you are more than 75% more likely (range almost 1½                           to >2 times)].
≥6.5%:              1.95 (1.53-2.48) [If your A1c is ≥6.5%, you are almost twice as likely to develop                                   cardiovascular disease, and the range of risk is from more than 1½ times to almost                               2½ times.

Glycated Hemoglobin, Diabetes, and Cardiovascular Risk in Nondiabetic Adults. Elizabeth Selvin et al.NEJM Volume 362:800-811. March 4, 2010 Number 9.

Keep in mind that because these subjects were probably diagnosed as "non-diabetic" using a fasting glucose test many of those with the higher A1cs probably were diabetic at the study outset based on post-meal values. If you are recently diagnosed with diabetes and have no signs of heart disease, your risk/A1c ratio should be similar if not identical to those shown here.”

So remember, if your doctor is like mine (or any MD, DO, RD or CDE who follows the ADA Standard of Care), (s)he is going to consider anything under 7.0% (or maybe 6.5%) to be “good control,” or worse, “optimal,” so you are pretty much on your own if you choose to strive to attain an A1c lower than 6.5%, or <6.0% or even <5.5%.