The Nutrition Debate #88: “Reversal of Type 2 Diabetes”

This column is about an open access article published online in Diabetologia 09 June 2011. I found it in my search for answers to questions I raised in #86, “Beta Cell Function and Insulin Sensitivity,” here. Unfortunately, I will not learn the answers from my new endo since he fired me as reported here in #87, “Optimal Blood Lipid Levels.” The Diabetologia article is “Reversal of type 2 diabetes: normalization of beta cell function in association with decreased pancreas and liver triacylglycerol.” The authors, E. L Lim, K. G Holingsworth, B. S. Aribisala, M. J. Chen, J. C. Mathers and R. Taylor, all of whom are associated with institutes at Newcastle University in the UK, begin their abstract thus:

“Aims/hypothesis Type 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.”

The plot thickens, however, with an exposition of this theme in the “Introduction,” from which I delete only footnotes:

“Type 2 diabetes has long been regarded as a chronic progressive condition, capable of amelioration but not cure. A steady rise in plasma glucose occurs irrespective of the degree of control or type of treatment. Beta cell function declines linearly with time, and after 10 years more than 50% of individuals require insulin therapy. The underlying changes in beta cell function have been well described, and beta-cell mass decreases steadily during the course of type 2 diabetes. Overall, there is strong evidence that type 2 diabetes is inexorably progressive, with a high likelihood of insulin therapy being eventually required to maintain glycaemic control.

However, type 2 diabetes is clearly reversible following bariatric surgery. The normalization of plasma glucose concentration follows within days of surgery, long before major weight loss has occurred, and it has become widely assumed that the protective effects of gastrointestinal surgery are mediated by altered secretion of incretin hormones. Improved control of blood glucose in type 2 diabetes by moderate energy restriction has been demonstrated by others. We have hypothesized that the profound effect of a sudden negative energy balance on the metabolism could explain the post-bariatric surgery effect and, specifically, that the decrease in the intracellular fatty acid concentrations in the liver would lead to a lower export of lipoprotein triacylglycerol [i.e., TG or triglycerides] to the pancreas, with the release of beta cells from the chronic inhibitory effects of excess fatty acid exposure.

This study was designed to test the hypothesis that acute negative energy balance alone reverses type 2 diabetes by normalizing both the beta cell function and insulin sensitivity. We examined the restoration of first-phase and total insulin response as well as hepatic and peripheral insulin sensitivity. Additionally, to examine the mechanistic basis of observed outcomes, we quantified the changes in fat content in the pancreas and liver.”

This last paragraph is particularly notable for the word “alone,” and even more so when you consider the study participants’ diet. It was basically 2.1 MJ/day (510 kcal/day for non-Brits) of Optifast, which is a “liquid diet formula” manufactured by Nestlé Nutrition. This was supplemented with “three portions of non-starchy vegetables” such that total energy intake was about 2.5 MJ (600kcal)/day. The authors aver that “Nestlé UK provided the Optifast on request but had no other input into the research.” The authors declare “no duality of interest.” And I believe them.

Another reason why this is notable is that the formulation of Optifast used in this study was 46.4% carbohydrate, 32.5% protein and 20.1% fat. And that was before the 3 servings (0.4 MJ or +/-90 calories) of vegetables, essentially all carbs, was added. So the results of this study are all the more striking since the participants during the 8 week duration of the program ate a high carb, high protein, low fat mostly liquid diet. Type 2s take note. The paradox is about to get starker.

Eleven people with type 2 diabetes (aver. age 49.5, BMI 33.6) were studied before and after 1, 4, and 8 weeks. An age-, sex-, and weight-matched group of eight non-diabetic participants was studied also. Key metrics were taken using state-of-art measurement techniques (e.g. magnetic resonance imaging) and study practices. All the protocols for exclusion, ethics, etc. were followed. The results (selected only to omit arcane statistics):  “After 1 week of restricted energy intake, fasting plasma glucose normalized in the diabetic group from 9.2 to 5.9mmol/l (166 to 106mg/dl US). Insulin suppression of hepatic glucose output improved from 43% to 74% vs. 68% for the control group. Hepatic triacylglycerol (TG) content fell from 12.8% in the diabetic group to 2.9% by week 8; The first-phase insulin response increased during the study period…and approached control values; Maximal insulin response became supernormal at 8 weeks vs. controls; pancreatic triacylglycerol decreased from 8.0% to 6.2%, compared to 6.0% in the control group.

Conclusions/interpretation Normalization of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone (emphasis mine). This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.”

The implications of this are still reverberating in my brain. This paper is pretty “brainy” and certainly way above my pay grade, but I wonder why many others who are qualified to discuss it aren’t.  Could it be a “duality of interest”? Or maybe our clinicians are too busy figuring out the latest medical reimbursement rules and insurance regulations. Who knows!!!

The Nutrition Debate #87: Optimal Blood Lipid Levels

Be warned! This is a very hot topic, particularly if you are as intemperate as I can be (am?). I recently refused the recommendation of an endocrinologist given to me over the phone by his nurse, saying to her “the doctor really should be ashamed of himself” for suggesting I “try” a certain statin drug. The next morning the doctor called me at 7:30 AM, saying I had hung up on his nurse. Not true, she hung up on me after I made that comment.

Apparently she hadn’t told him what I’d said, leaving it to me to tell him directly. It definitely added fuel to the fire. He then calmly told me that the LDL value in my Lipid Panel was high and that both the ADA and the AHA guided that my LDL should be below 100mg/dl. I told him that I didn’t care what the ADA and the AHA guidelines said. I then went into a bit of a harangue about Ancel Keys, and suggested the doctor really should “go back to school.” That did it. He declared, “You need to find a new doctor. I’m not going to treat you.” And then he hung up. Two hang-ups in a row! But I don’t blame him. I was rude – really rude. Maybe even hostile? Perhaps a “little” angry? But I think mostly just disappointed.

But I don’t apologize for what I said. I had high hopes that I would find an endo who was enlightened. I haven’t seen any endo in over 20 years, seeing only an internist/cardiologist 3 or 4 times yearly, and I wanted to establish a relationship with an endo in the community near our winter home. I failed, and it was my fault. Of course, I could have accepted the prescription he offered and then refused to fill it. Then the doctor could simply have written in my chart that, like all the other old people (his PA told me) who “don’t care about their health,” I was just “non-compliant.” She told me that when I asked her why other patients didn’t follow her recommendation to eat Low Carb. She eats about 60 carbohydrate grams a day. I eat about 15, for glucose control. I am a 26-year-long Type 2 diabetic who is carb intolerant.

Anyway, in reaching my latest level of self-assurance (expressed as arrogance or ignorance or both, depending on your perspective) about the optimal blood lipid levels, I had a fresh recollection of Chapter 41, “Blood Lipids,” in “Perfect Health Diet” (Scribner, 2012), the new book by Paul and Shou-Ching Jaminet (both PHDs). It’s a very good book, even if I recommend it only for “background” for most Type 2s. They do get “into the weeds” a bit, but explain everything very well, and I really like their approach to healing – finding the root causes rather than treating the symptoms.

Chapter 41 has the following sub-sections: “Optimal HDL Levels,” “How to Raise HDL Levels,” “The Immune Functions of LDL,” “Optimal Blood Lipid Levels,” and “Troubleshooting Blood Lipids.” I will discuss only the section “Optimal Blood Lipid Levels” in this missive and then relate it to my own test results from the lipid panel performed by my “new” (and now former) endo. For the other sections of this chapter and the rest of the book, you should buy the book. I regard it as an essential reference and a must for any nutrition “library.”

“The ideal serum lipid profile – the one that produces the best health and minimizes mortality – looks like this:” (pg 366)

·         Total Cholesterol level between 200 and 260 milligrams per deciliter

·         LDL Cholesterol level above 100 milligrams per deciliter

·         HDL Cholesterol level above 60 milligrams per deciliter

·         Triglyceride level around50 to 60 milligrams per deciliter

How did my profile compare to the Jaminet’s ideal? Here is the endo’s lab report for my serum lipid profile:

·         Total Cholesterol level = 245

·         LDL Cholesterol level = 176

·         HDL Cholesterol level = 58

·         Triglyceride level = 54

Okay, I missed the HDL target by 2. But, this was the lowest HDL I have had in over 4 years (12/08 = 57) and the average of my last 15 HDLs going back to July 2007 is 75. But, in all other respects my scores appear to fit the Jaminet’s ideal.

My LDL (176) was high – the highest it has ever been (since 1992, when my lab reports first starting calculating LDLs). And my Total Cholesterol, at 245, was the highest ever, and my Total Cholesterols go back almost 40 years to 1974. So, I am intrigued and will look forward with some anticipation to my next “home” doctor’s appointment on 4/22/13.

I am comforted somewhat, however, by the knowledge that my TG/HDL ratio = 0.93, which is <1.0 and therefore “ideal.” In my column #27, a 2008 paper published in Clinics and available though PubMed (2008 August 63(4) 427-432) here, the conclusion is that this ratio is “…the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.” I would like to have known, though, what my hs C-Reactive Protein score was. Oh, well.

© Dan Brown 2/9/13

The Nutrition Debate #86: Beta Cell Function and Insulin Sensitivity

 I recently visited (as a new patient) an endocrinologist in Florida. My purpose was to find out what was going on with my glucose metabolism. Specifically, I was interested in knowing my % Beta cell function and my % Insulin Sensitivity (and its reciprocal, Insulin Resistance, or IR). I had read about a test that determines those values and wanted to be tested. The HOMA Assessment determines these values by formula. There is also a more sophisticated model that Oxford University developed called the HOMA2 that employs a “calculator.”

I haven’t been seen by an endo in more than 20 years (the last time to measure my testosterone, as I recall). Five years before that I consulted an old-timer who had me visit the out-patient department of a local hospital for a 4-hour glucose tolerance test. That test just confirmed the diagnosis that had been made a few years earlier that I was a Type 2 diabetic. That endo also upped my prescription for a sulfonylurea, the only oral diabetes med permitted in the U.S. at the time. Eventually I was maxed out at 20mg of glyburide (the sulfonylurea).

It would be another 10 years (in 1995) before my current doctor added metformin, which by then was finally allowed in the U. S. It had been in use in Europe for some time. But before long I was maxed out on that drug too and was then started on a TZD (Avandia). That is when my doctor suggested I try the Atkins Induction diet to lose weight. He had just read the Gary Taubes cover story, “What If is All Been a Big Fat Lie?” in the NYT Magazine on July 7, 2002. Within a few days on Atkins Induction, I was having frequent hypos. I called my doctor, and he told me to drop the Avandia. When the hypos continued, he cut the sulfonylurea and the metformin dosages in half, and then soon afterwards, in half again.

I lost 60 pounds on Atkins Induction but, after a few years of stable weight, I gained back 12. I then decided to try the Bernstein diet for diabetics. I lost 100 pounds in the next 50 weeks and eventually another 22 for a total loss of 170 pounds. Along the way, I weaned myself off the final 5mg of Micronase (the brand-name of the sulfonylurea), by halving it to 2½ and then halving it again (cutting the 2½ mg pill in half). I still take 500mg metformin once a day. But, all told, I figured I had been on a sulfonylurea, which pushes the pancreas to secrete more insulin in response to a glucose challenge, for the better part of 20 years. Remembering Dr. Ralph DeFronzo’s Banting Lecture at the 2008 ADA Convention in San Francisco, I figured I had lost 80% of my Beta cell function by the time I was diagnosed in 1986. He also said, at the end of the introduction to the full paper published in the ADA magazine “Diabetes,” and available here, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function” (emphasis added).

Given my history on sulfonylureas and Dr. DeFronzo’s prognostications, the implications for my Beta cell function were not promising. So, my visit to the endo in Florida was for the specific purpose of testing my % Beta cell function and % (Insulin) Sensitivity. I was surprised with the test results: Beta Cell function = 68.2%; Sensitivity = 94.6%; and IR = 1.1 (1.057). I don’t have a follow-up visit scheduled with the endo for another 10 weeks, so I decided to do a little homework on my own. I would also like to put these results “out there” for comment by others. Has anyone out there ever had a HOMA assessment done? The endo’s nurse said she had been working with this doctor for about 10 years, and he had never ordered the test before. She knew, she said, because she’s the one who places the orders for tests.

The doctor said the test was mostly used in research, and he would have to look up the formula to apply it. Okay, but, I wondered, if not commonly used in clinical practice, does the test have clinical value? What can be learned from it? My first read is that I am not in as bad a shape as I thought I was. True, I have been eating VLC “on and off” for over 10 years, and now “totally on” for the last four and a half months. My last HbA1C was 5.7, down from recent low 6s. I expect the one from blood taken last week will be 5.6 or even 5.5. And I have been eating a very restricted ketogenic diet, recently under 1000 calories a day (without hunger), which is the direct consequence of being ketoadapted and in ketosis virtually all the time. My body is in balance and happy with my dietary intake, my supplements, and with the fatty acids, glycerol and ketone bodies it is making every day from the body fat it is breaking down for energy.

But I have not been satisfied with my fasting blood glucose readings these last 4 months. I no longer have weekly averages around 90. I have to work hard to get them under 100, and they should never be higher than 95. My daily FBG readings should never be above 100. I am very careful to eat VLC and to never eat too much protein.

So, what does my HOMA assessment test reveal? If my Type 2 diabetes is in “clinical remission,” is it attributable solely to my VLC diet? If my diet has “reversed” my Type 2 diabetes, has it also “normalized” my Beta Cell function and improved my insulin sensitivity? If Beta Cells can regenerate themselves, can they do this over and over, year after year?

I hope to learn the answers to these questions from my new endo in my follow-up appointment. I can hardly wait.

© Dan Brown 2/2/13

The Nutrition Debate #85: My Goal Weight and the BMI Table

Like many who are overweight, obese or morbidly obese (what a dreadful term!), I have spent a lot of time over the years thinking – dreaming really, about my goal weight. I think this may be especially true of those of us who have finally found a way to lose weight without hunger and now see the pounds dropping off easily. And they are fat pounds, because we have become “fat burners,” through ketosis, enabling us to burn fat for energy by severely restricting our carbohydrate intake. We are always wondering, How far can I go? How far do I really want to go? How thin could I be?

The “experts” tell us not to be too ambitious – to set modest goals, because they know how common it is to fail. They say that even a 10% (or less) weight loss will make a big difference in our health markers, especially for Cardiovascular Disease (CVD). But we can dream, can’t we? We can imagine ourselves as much thinner (if we are more than 10% “overweight,” as many of us now are). As I was seeing two pounds of fat dissolve a week for about a year (about 5 years ago), I imagined that I could be just 187 pounds – half my starting weight of 375 pounds. At my low point I had lost 170 pounds (45% of me), and was just 17 pounds shy of my goal when, on a 3-week vacation, I stopped losing.

Today, after regaining 70 pounds over the last four years, I am starting to lose again. As of this posting I have re-lost 30 pounds (60%) of the 50 I am targeting towards my new goal of 225 pounds. That will represent a loss of 150 pounds (40%) from the start. That weight, 225 lbs, is my new goal weight – the one I will strive to maintain for the rest of my life.

But what do all these numbers mean? My wife told me I would look like a scarecrow if I had lost all 187 pounds. A neighbor who saw me on the street when I was near my low of 205 said, “Are you okay? Are you well?” Funny! Maybe I wouldn’t recognize myself, had I gotten there. Who knows? I certainly would have been a different man – just half the man I used to be, my wife used to joke. And at 225 I will still be clinically classified as obese. But I’ll be happy, for a time.

Goal weight is a very subjective thing. It is purely personal. My present goal is to lose 50 pounds in two stages. I started at 275 and want to get to 225. The first stage, which I started last September, was to lose 25 pounds by year’s end, then 25 more before my next doctor’s appointment in late-April. So the first part required that I persevere through the Thanksgiving and Christmas holidays. I reached the first goal, on January 3rd, a few days late.

The second 25 pounds has to be lost while we are at our winter home in Florida, and includes a week-long vacation in Aruba. I’ve never lost weight, or even been able to maintain my weight, in Florida or on vacation, when we eat out (and drink) every night. But the trip to Aruba is now history – and I made history. I went there at 250 and came home at 250! Now, the challenge is to lose 25 pounds in the next 13 weeks. That’s very doable; just 2 pounds a week. I’ve done it before, many times. The question is: Will I do it in Florida? Will I make history again? I’ll let you know – end of April.

Ideal weight is a total other thing. It is also very subjective, if a bit more impersonal.  What I call my body type (“big boned”) might actually just be my body image from having lived a lifetime looking at it. Why else would there be just one clinical standard in the U.S. (since 1998) for judging weight? It is universal and requires only height and weight and is, in my subjective opinion, totally unrealistic. I am referring, of course, to the Body Mass Index (BMI) table, linked here. In it a person (male or female of any “body type” who is now 5’-11” tall should weigh between 136 and 172 to be considered “normal “weight. The average “normal weight for a person my height would be 150 pounds. That’s ridiculous. It’s skeletal, a mere scarecrow. My father told me he weighed 150 in the Great Depression, and again when he was diagnosed with TB in 1950. After a nine-month stay in hospital put a little flesh on his bones, he weighed 175!

So, my goal weight of 225 pounds is still much higher than my ideal weight. It is in fact 75 pounds higher. It is higher even than the BMI scale range (179 to 208) allows for me to be considered “overweight.” In fact, 225 pounds is still considered “obese” for a 5’ – 11” person. The “obese” range is 215 to 279. But that’s okay. It’s my goal weight.

Lean Body Weight is another term that is sometimes used by athletes (and thin people) with only a small amount of body fat. To me it is a foreign concept, an exotic species.  It is achievable, no doubt, and the most desirable weight to be, if you have the physique ,the genetic predisposition and a history of eating right and staying “trim.” It is also a very useful weight to use when deciding how much protein to eat to avoid unwanted gluconeogenesis if you are a Type 2 diabetic and are working to achieve optimal glucose control and weight loss through diet. But that’s another story.

© Dan Brown 1/26/13

The Nutrition Debate #84: Carbohydrate Intolerance – the new ‘buzz’ words

Authors Jeff Volek and Stephen Phinney use the phrase “carbohydrate intolerance” seven times in their introduction to “The Art and Science of Low Carbohydrate Living.”  They’re telling us something. They’re want to replace the medical term Impaired Glucose Tolerance (IGT) with “carbohydrate intolerance” to make it more “accessible,” and I approve.

IGT involves hormones, enzymes and cell receptors, and unless you’re a molecular biologist, these terms make the eyes glaze over. Besides, the biological actions that occur within the body are autonomic, whereas we eat food consciously, for the most part. And we don’t eat glucose. We eat carbs. Our digestive system breaks down  all carbs, including all simple sugars and all complex carbohydrates (starches), into single molecules, most of them glucose.

So, “carbohydrate intolerance” is an excellent way to describe some people’s metabolic response to eating ALL carbs. I am stressing all carbs because of the popularity of distinguishing between simple sugars (mono and disaccharides) from complex carbs, or polysaccharides (starches).  And to differentiate “natural sugars” (as in fruits) from “added” sugars. Sure, they contain some small amounts of indigestible fiber, but they’re all the same, folks! They’re all glucose.

It is true that the common simple disaccharide sugar, sucrose, breaks down to 50% glucose and 50% fructose, and fructose is metabolized differently than glucose. (It is diverted to the liver where it is detoxified and turned into fat.) But all complex carbohydrates (the starches) break down and are absorbed into the blood as glucose. All glucose will raise blood sugar by the same total amount, and some complex carbohydrates will raise blood sugar more and more quickly that sucrose, e.g. a slice of bread vs. a hard candy or watermelon, or even popcorn.

Another extreme example of misinformation about nutrition is a statement I read recently in a magazine: “The complex carbohydrates in apples give your body a longer, more even energy boost compared to high-sugar snacks.” That is false. Utter nonsense. There are no complex carbohydrates in an apple. An apple is 86% water, 3% (indigestible) fiber and 11% simple sugars (67% fructose/33%glucose). An apple is, in fact, just a delicious “high-sugar, high-fructose snack.”

So I applaud the initiative of Volek and Phinney to create a user-friendly “buzz word” to describe the condition that affects a large and rapidly growing “cohort” of the population – those of us who have eaten a “Western Diet” and have succumbed (perhaps due to  genetic predisposition) to one of the most common diseases of Western Civilization, Metabolic Syndrome. See the Nutrition Debate #9 here for the indications. But here I want to focus on understanding that we are, many of us, carbohydrate intolerant. We must accept that and learn what we can do about it.

We are the obese. Okay, a more user-friendly term: we are the overweight. This applies to all of us from a little overweight to the morbidly obese. Our mechanism of fat synthesis and metabolism is a little or a lot broken. We are also the hypertensive. Our blood pressures rise as we gain weight (and drop when we lose it). We are also the ones with “high cholesterol,” often misdiagnosed as high Total Cholesterol and high LDL lipoproteins (which can be manipulated easily with a statin); instead, we have a more difficult-to-treat form of dyslipidemia characterized by low HLD lipoproteins and high triglycerides. See the Nutrition Debate #25, #27, #67, #68 and #72 for what to do about that.

The first step is to recognize ourselves – to know that we are members of this “cohort” that has an association with being obese or overweight, and has high blood sugar, high blood pressure and “high cholesterol.” And that having all these indications puts us at much higher risk of death or another “morbid” outcome. Are you motivated yet? Will you reject the failed treatment protocols of taking more pills and being constantly hectored to lose weight? Remember the old aphorism: “The definition of insanity is doing the same thing over and over again and expecting different results.”

A reasoned approach, on the other hand, would be a different diet. If you are a Type 2 or even prediabetic, and you and your doctor know that carbohydrates raise your blood sugar unnaturally, then why in heaven’s name would your doctor advise you to eat carbohydrates? YOU ARE CARBOHYDRATE INTOLERANT! Accept it, and then do something about it!  

You’re in good company. Many kinds of intolerances are now recognized as detrimental to health: Fructose intolerance, FODMAPs, salicylates, gluten, casein, etc. The consequences, short and long term, vary, but in general individuals who recognize, accept, and deal with intolerances report greatly improved health and day to day quality of life.

Sorry for all my “shouting.” Learn what carbohydrate foods are. Then, try a Low Carbohydrate diet. For this, you’re on your own; I can’t do everything for you. Just kidding. Start with one of my favorites at The Nutrition Debate #19 here.

© Dan Brown 1/19/13

The Nutrition Debate #83: “The 8-Hour Diet,” based on “brand new science”

On the Today Show on January 2^nd author David Zinczenco told host Matt Lauer that his new book, “The 8-Hour Diet,” described a way to lose weight based on “brand new science.”  My wife told me about this segment of the morning TV show, and so I searched the archives and played it back. I also found an excerpt from the book on NBCNews.com here.

When I asked my wife how it worked, she was a little vague, saying something about stomach shrinking… When I saw the re-play, I understood why. The author, with Lauer as critic and foil, showed lots of goodies: yoghurt, berries, orange juice and bran muffin for breakfast, a big salad, two slices of pizza, cup of soup plus potato chips or French fries for lunch, and a big rib eye steak with potatoes, veggies and a piece of chocolate cake for dinner. Lots and lots of comfort foods and no counting of anything: calories, carbs, protein or fat. This diet didn’t look like a diet at all! And it had eye appeal as well. Zinczenco described the diet as “lean protein, good fats, and complex carbs” – the current, politically-correct composition.

The only limiting factor was that all the food for any particular day had to be consumed within an 8-hour window: 9 to 5, 10 to 6, or even 11 to 7. The particular example given was 10:30 for breakfast, 12:30 for lunch, and 6:30 for dinner. The day starts with coffee or tea (black?) but no breakfast before work, the “breakfast” being eaten at a mid-morning break, and lunch and dinner at conventional times. Instead of the conventional breakfast at home, the author suggested a brief (under 10 minute) period of strenuous exercise to “turbocharge” (jump start) your metabolism and “get rid of the calories stored in your liver.” Translation: burn the stored carbohydrates, in the form of glycogen, in your muscles and liver – a pretty good idea actually.

The other “indulgence” the author offered is that you could do this 8-hour diet for only (“even just”) 3 days a week to lose as much as 5 pounds a week and 20 pounds in 6 weeks.  He tried it himself, he said, and lost 7 pounds in 10 days. He called this 3-day-a-week practice “intermittent fasting.” Known as IF, this is a common weight-loss practice. I did it recently for two days (after my weight drifted above “target”) and lost 7 pounds in two days while eating only a VLC breakfast (no-lunch or dinner and no snacks) for two days. It was mostly water loss but my body needed to get energy from somewhere so it burned fat (and muscle) to maintain my energy balance. This is not a good thing to do as a rule, but okay if you need a quick momentum shift.

David Mendoza, a well-known, low-carb Type 2 diabetic author, recently offered a similar “weight-loss tip.” He said that whenever his weight drifted above “target” (he describes his current weight as “low-normal,” which is truly enviable, if not skeletal), he skips dinner that day. He said he has only had to do that 9 times in the last 6 months).

So, I have to say this diet has obvious appeal for a “healthy” person with “normal” metabolism, which excludes anyone with any of the indications of Metabolic Syndrome (see #9 here). It is clever merchandizing to sell a book on the Today Show to an audience of women who aren’t the least bit interested in the mechanism or counting  – only in the eye-appeal of all their favorite foods and the comfort of not having to deny themselves anything except eating for 16 hours a day for three days a week. Zinczenco points out that that’s not so tough either, since most people already fast between dinner and breakfast. To stress this point he noted the word breakfast is composed of “break” and “fast.” He also spoke disparagingly of the practice many have today of “grazing all day long,” including sometimes after dinner. For three days a week, at least, that is a “no-no.” And if you’re still eating carbs, I like the idea of a brief strenuous exercise routine early in the morning to burn them up.

But what’s the real physiological mechanism of the 8-Hour Diet?  It works on the principle of the fed state and the fasting state, hardly a brand-new science. It is the basis of the hard scrabble existence of mankind on this earth from the beginning of the Paleolithic Era. You hunt, you eat, you rest while you digest, and then you burn stored fat while you hunt again when your hormones tell you that you need to eat again. Your body regulates this “harmonic ensemble” to maintain homeostasis, quoting ‘certain conclusion’ #2 from Gary Taubes’s “Good Calories-Bad Calories” (see The Nutrition Debate #5 here).And this cycle continued throughout life and for 500 generations, until the advent of the Neolithic Era 10,000 years ago. Agriculture introduced cultivated grains, grain storage, domesticated animals, and more-permanent human settlements.

The fed state echoes the time in the Paleo Era when, after eating, food is digested and absorbed. This is known as the glucogenic state since all carbohydrates and about half the protein we eat eventually becomes glucose, the latter through a process called gluconeogenesis. The fasting state begins when the glucose energy from the last meal has left the stomach and small intestine (where most of it is absorbed into the blood stream), and hormones switch the body to a ketogenic state. In a ketogenic state our bodies break down body fat (triglycerides) for energy. This state is also called ketosis because when the triglycerides are broken down to fatty acids and glycerol, they produce ketone bodies as a byproduct. Dr. Richard Veech of the National Institutes of Health says, “…ketosis is a normal physiologic state. I would argue it is the normal state of man.”

This natural state of ketosis occurs today every day between dinner and breakfast when we fast (>12 hours, if we don’t ‘snack’ after dinner). The 8-Hour Diet being promoted in this book just extends the nightly fast from 12 to 18 hours, 3 days a week.

© Dan Brown 1/12/13

The Nutrition Debate #82: A New Dietary Paradigm?

A new dietary paradigm is emerging for a Way of Eating that could avoid, mitigate or ameliorate the devastating impact of Metabolic Syndrome and the Diseases of Civilization with which it is strongly associated. These outcomes affect about half the population that may be genetically predisposed and therefore susceptible. The new paradigm arises from what biologists are learning of the benefits, in terms of longevity and health, associated with Calorie Restriction (CR).

This blog does not, however, advocate for Calorie Restriction per se. It is instead advocating a restricted-calorie Very Low Carbohydrate Ketogenic diet. It closely resembles the concept of “nutritional ketosis,” a phrase that was, I believe, first used by Jeff Volek and Stephen Phinney in their book, “The Art and Science of Low Carbohydrate Living.” It was later further popularized by Jimmy Moore (of “Livin’ La Vida Low-Carb” fame), who recently lost over 50 pounds in 5 months on their program. “Nutritional Ketosis” refers to a low level of ketosis in which the body is “keto adapted” so that it burns ketone bodies instead of glucose as its primary energy source. A low millimolar concentration of ketone bodies can be measured in the blood. To me, the two best aspects of being in mild ketosis are: 1) you have lots of energy and 2) you’re not hungry, so long as you have a supply of body fat to ‘burn’ for energy (and you continue to eschew carbs!).

To quote Dr. Richard L. Veech of the National Institutes of Health: “Doctors are scared of ketosis. They’re always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man.” This ketosis falls far short, however, of the level of ketone concentration that is required for the anticonvulsive “ketogenic diet” used to treat juvenile epileptics. That “ketogenic diet” is a very high fat diet in use since the 1920s as an effective treatment for childhood epilepsy. It’s still used at places like Johns Hopkins for treatment of drug-resistant forms of childhood epilepsy. It is effective in about 50% of cases. The level of ketosis that I am advocating is much less extreme.

I have inferred and constructed my interpretation of this new dietary paradigm from “The Neuroprotective Properties of Calorie Restriction, The Ketogenic Diet and Ketone Bodies” (see Sect #3 of the full manuscript). I first referred to that manuscript here in The Nutrition Debate #79, “Calorie Restriction and Longevity.” In that column I spoke of the benefits of Calorie Restriction in animal models. In #81, “Calorie Restriction in Humans” here, I describe the concept of “altered pathways of nutrient disposal,” introduced by other authors that I cite, as they affect glucose metabolism. I also discuss some health concerns of CR in humans. But the authors, after discussing the neuroprotective properties of CR, then discuss the ketogenic diet (Sect. 4) and ketone bodies (Sect. 5). This is how and where I came to this new paradigm.

The “ketogenic diet” is also associated with multiple benefits. In the author’s words (Sect. 4), “the neuroprotective effects of the ketogenic diet are not limited to epilepsy;” “The antiepileptic effects of the ketogenic diet have been associated with improvements in cognitive function”; “Similarly, oral intake of a ketogenic medium-chain triglyceride diet improved cognitive function in patients with Alzheimer’s disease.” “Neuroprotective” is how they describe the effect that the ketogenic diet has in reducing the incidence of diseases like Parkinson’s, Alzheimer’s and Huntington’s.

 And here’s the key or “link” to the new paradigm: the authors assert in this paper that the “underlying mechanisms” of the ketogenic diet are “similar to those activated by calorie restriction” (emphasis mine). But does this mean that you have to eat a diet that is so very high in fat as to be anticonvulsive (+/-90% fat content)? Happily, it does not. That’s why, I think, the title and the text of this manuscript includes section (#5) on ketone bodies. What are ketone bodies? They are byproducts of catabolism, i.e., the breakdown of fat molecules (triglycerides). “During conditions of reduced glucose availability, energy is derived from the conversion of fats to ketone bodies,” they explain. Reduced glucose availability!

“Following a day of fasting or exposure to the ketogenic diet, ketone bodies reach low millimolar concentrations in the blood” (my emphasis). “Fasting and the ketogenic diet increase the permeability of the blood-brain barrier to ketones,” so that “ketone bodies cross the blood-brain barrier.” Ketone bodies are good – in fact, they are the ideal – brain food.

The conclusion (Sect. 6) of the article begins: “Calorie restriction and the ketogenic diet share two characteristics: reduced carbohydrate intake and a compensatory rise in ketone bodies.” A further conclusion: “An expanding body of evidence indicates that ketone bodies are indeed neuroprotective, and that the underlying mechanisms are similar to those associated with calorie restriction – specifically at the mitochondrial level.” That is their conclusion, not mine!

Come to think of it though, this “new dietary paradigm” is exactly what I have been advocating consistently throughout this blog. For a quick look at a list of past subjects, open “The Nutrition Debate Index of Columns” in the upper right corner of the blog. It’s listed first under “Favorite Links and Videos.” It’s all there for you in the archives. Check it out.

 

© Dan Brown 1/5/13