The Nutrition Debate #284: The A TO Z Weight Loss Study: a Randomized Trial

A dear reader – and I mean that sincerely because I wouldn’t write this blog except for my readers – was disappointed (upset, actually) that I said, “…if you are insulin resistant, as almost all fat people are…” Okay, “fat people” is an inflammatory phrase, and I have never used it before, but that is not what upset Valerie. It was an assumption, and a slight exaggeration that I made, that did the trick. She concluded: “I wish your ‘nutrition debate’ weren’t so one-sided.”

Valerie’s frustration (and upset) is a result of my writing about two overlapping and related but different phenomena: the co-incident epidemics of diabetes and obesity that have come together in the last 35 years. It all began with the publication of the Dietary Guidelines for Americans in 1980, the U.S. government’s attempt to tell us as a population what to eat. That followed the 1977 Dietary Goals for Americans produced by a Select Committee of Congress: the McGovern Commission.

This combination of type 2 diabetes and obesity is so prevalent today that the word “diabesity” has been coined. However, as Valerie points out, not all “fat people” have Insulin Resistance (IR), a requisite condition for progression from a normal glucose metabolism to Impaired Glucose Tolerance (IGT), Impaired Fasting Glucose (IGT), and then to a frank diagnosis of Type 2 Diabetes Mellitus (T2DM). That is the Natural History of Type 2 Diabetes. Apparently Valerie is not Insulin Resistant or therefore by definition a type 2 diabetic (FBG at diagnosis ≥126mg/dL) or pre-diabetic (FBG from 100 to 125mg/dL).

So, I give Valerie her point that, “…there are plenty of slim people with insulin resistance and plenty of fat people without insulin resistance…” I will resist getting into a “pissing contest” over percentages. I will concede that apparently Valerie is one of them. But I will contest the assertion Valerie makes that “fat people without insulin resistance” did not benefit from the “A to Z diet trial.” She states erroneously that “low-carb diets don’t help [them], if you remember the A to Z diet trial.”

The A to Z diet trial, not to be confused with a statin trial by a very similar name, was a “Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic [emphasis mine], premenopausal women.” Note: this trial EXCLUDED (type 2) diabetics, which by definition means that the participants did not have IR. It was a “Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors…,”published in JAMA in July 2007. The following are excerpts from the ABSTRACT:

“MAIN OUTCOME MEASURES: Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.”

“RESULTS: Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets. Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.”

“CONCLUSIONS: In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight at 12 months than women assigned to follow the Zone diet, and had experienced comparable or more favorable metabolic effects than those assigned to the Zone, Ornish, or LEARN diets…”

So, just to be perfectly clear, non-diabetic, premenopausal overweight and obese women who ate the diet with the lowest carbohydrate intake lost the most weight and had the best improvement in related risk factors (including “lipid profile (low-density lipoprotein, high-density lipoprotein, and non-high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.”)

In other words, the low-carb diet DID help “fat people without insulin resistance,” and by a large margin. After 12 months, the Atkins cohort actually lost 3 times as much weight at the Zone cohort and twice as much as the average Ornish and LEARN dieter and had “comparable or more favorable metabolic effects” than those on the Zone, Ornish, or LEARN diets.

I’m sorry to have to come down so hard on this point, but it must be made clear to all my dear readers that low-carb diets do work (for the vast majority of people, if I have to hedge). If you haven’t given it an honest try, you really should.

The Nutrition Debate #283: TC/HDL, TG/HDL and Triglycerides

The Nutrition Debate #281 dealt with HDL cholesterol (HDL-C) and triglycerides (TG), and The Nutrition Debate #282 took a look at Total Cholesterol (TC), LDL cholesterol (LDL-C) and statin therapy. Now, I will tie them all together and discuss ratios and some recent thinking about dysfunctional HDL and using triglycerides alone to “predict” CVD risk.

You may have seen the Total Cholesterol to HDL-C ratio (expressed as TC/HDL) on the lipid panel in a typical lab report. The standard reference range (goal or target) is <5.0. There are no units because both components of the ratio have the same units (in U.S. measure, of mg/dL). So, If your TC is 200mg/dL, the limit under which the clinician wants your TC to be, and your HDL is 40mg/dL, the level above which your doctor wants to see your HDL, then your ratio would be 200/40 = 5.0. You’re living on the edge, the doctor will tell you.

Now, since most people’s TC is about 200 or a little higher, and most people who eat a Standard American or “Western” diet will have an HDL hovering around 40, much of the population is at risk of Cardio Vascular Disease (CVD), according to this standard. So, what’s a doctor to do? Prescribe a statin, of course! Because a statin, by lowering your LDL cholesterol will lower your Total Cholesterol. Remember the Friedewald formula: TC = HDL + LDL + TG/5. (Also, see The Nutrition Debate #25, “Understanding Your Lipid Panel” for an example of a “good” and a “bad” cholesterol panel.

However, since LDL is not assayed in the typical inexpensive lipid panel lab test, in reality the formula is “transposed” to calculate LDL from the other values which are inexpensively assayed. So, LDL is now calculated as LDL = TC – HDL – TG/5. However, as the math wizards among you will readily grasp, in the original form, TC = HDL + LDL +TG/5, your TC could be over 200 if any of the components (LDL, HDL or TG/5) was high since TC is the sum of these factors. So, TC is really a pretty worthless number. Nevertheless, when you take a statin, TC will get lower – much lower – as statins will lower your LDL.

And as a consequence, if your TC goes lower and your HDL stays the same, your ratio will go lower. For example, a TC of 120 with an HDL of 40 produces a ratio of 3.0. (120/40 = 3.0). Voilà! Your risk of CVD is now much lower than if your ratio is 5.0, like most people eating a Western diet. If you believe this, I have a bridge to sell you. (The Brooklyn Bridge, for those unfamiliar with the old joke.) But what’s a person to do if taking a pill is not the panacea it’s all trumped up to be?

Epidemiological evidence suggests that “…the strongest predictor of a heart attack” is another ratio: the ratio of your serum triglycerides to your HDL cholesterol, expressed as TG/HDL. I wrote about this several years ago in The Nutrition Debate #27 here. In #27 I said, “Using this new gold standard, a TG/HDL ≤ 1.0 is considered ideal, a ratio of ≤2.0 is good, a ratio of 4.0 is considered high.” Figure #6 tracks my personal TC/HDL and TG/HDL ratios from 1980 to the present.

The CONCLUSION in the reference cited in #27 above was: “Elevation in the ratio of TG to HDL-c was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.” The full text of the Clinics paper can be seen here at Pub Med Central, the U. S. National Library of Medicine, National Institutes of Health. Note that both my TC/HDL and TG/HDL ratios were “borderline bad” until I started eating Very Low Carb in 2002. They trended down (except when I went “off diet” in the summers of 2003 and 2006), and dropped sharply to “low risk” when I started Bernstein. Note also that my TG/HDL ratios have been “ideal” (≤1.0) since 11/07, over 7 years and 23 lab reports ago.

Now, the latest thinking – this is cutting edge “science” folks – is that triglycerides alone may be the most reliable risk factor for CVD. The thinking here is that TG, although much more variable than HDL (and TC and LDL), rules out the possibility that high HDL, viewed as generally a very good thing, can also be elevated but “dysfunctional” due to infection, inflammation, diabetes, etc. My editor cited this recent piece in the Public Library of Science (PLOS) to support the new notion. And this piece from PubMed delves into the subject of dysfunctional HDL-C. So, I plotted another graph charting just triglycerides.

 A cursory glance tells the reader that my TGs averaged about 150 (once again: “borderline”) until I started Atkins Induction in September 2002. Then in the summer of 2003 I went “off diet” and my TGs skyrocketed. I returned to “the program” until the summer of 2006 when I started raiding the freezer at bedtime and gained back 12 pounds from the sugar/fat (ice cream). And when I started on Bernstein in September 2006, they fell again. But when I started to supplement with fish oil, and then to eat a can of sardines for lunch almost every day, they plummeted to 21 and have averaged about 50 ever since.

I used to think it was Very Low Carb (Atkins Induction and Bernstein 6-12-12) that caused my triglycerides to be so very low. Now that I’ve charted them and researched the milestone dates, I am convinced it is the fish oil supplementation and the sardines that are the reason. And quite possibly the reason for my high HDLs as well. As I show in Figure #3 in The Nutrition Debate #281 here, there is a very strong inverse correlation between low triglycerides and high HDL cholesterol.

Have you checked your ratios?   Do you know your trig level? 

The Nutrition Debate #282: Total Cholesterol, LDL-C and Statin Therapy

In The Nutrition Debate #281 I documented the phenomenal transformation of my triglycerides (TG) and HDL cholesterol (HDL-C) over the last 35 years, since I began keeping lab reports from my doctor’s visits. Okay, mock me, but this slightly obsessive behavior does have redeeming value: it gives an objective picture of changes brought about by my diet. The transformation started in 2002 when, on my internist/cardiologist doctor’s advice, I began to eat Very Low Carb to lose weight. He said, as we went down the hall to schedule my next appointment, “It might even help your [type 2] diabetes.”

He was “right as rain,” of course. Besides eventually losing 170 pounds, I was able to stop taking almost all of my oral diabetes meds, and my fasting blood sugars were consistently under 100 without meds, something I hadn’t seen in the previous 16 years of leaving my diabetes management to my doctor/meds.  My A1c’s dropped to the mid 5s, my blood pressure improved from 130/90 to 110/70 on the same meds, and my CRP, an inflammation marker, went from “high” to “low” risk of CVD. Finally, my lipid (Cholesterol) panel dramatically improved, specifically HDL-C and TGs. (See #281.)

Figure #4, in highly compressed format, shows a composite history of my HDL-C and TG values over this 35-year odyssey.

About a year after starting Very Low Carb (Atkins Induction), my doctor started me on a high dose statin. It was warranted, he said, by the guidelines. I was both a long-time type 2 (since 1986) and I was, according to the scoring method he used, at “high” risk for cardiovascular disease (CVD). And I was still morbidly obese, although 60 pounds lighter by Atkins Induction.

 As Figure #5 shows, the statin “worked” in the sense that it lowered both my Total Cholesterol (TC) and LDL Cholesterol (LDL-C) dramatically. Note that before starting on a statin, my TC and LDL-C were “borderline” and “slightly high” respectively. Thirty-two TCs averaged 195 and twenty-eight LDLs averaged 131. These were both “typical” for people who have been eating the Standard American or “Western” Diet for a long time. But for diagnosed type 2s who were at high risk of CVD for reasons, including obesity, an LDL target <100 was recommended. For type 2s with diagnosed CVD (I was not), the goal was <70.

During the five years (12/03 – 10/08) that I took various statin drugs, my TC averaged 125 and my LDL averaged 58 (average of 20 lab tests). You might fairly conclude that the statin “worked” perhaps too well. In the meantime, as a consequence of my dietary changes alone, I had lost 170 pounds, my blood pressure had dropped to below goal, my HDL had more than doubled and my triglycerides had dropped by more than two-thirds (see #281). (On the Bernstein 6-12-12 diet, a Very Low Carb diet program to which I had transitioned in September 2006, I had lost another 100 pounds in just under a year.)

So, after all my risk factors had improved so dramatically, and all had stabilized, after 10 more months on low-dose simvastatin, my DOCTOR suggested that I discontinue taking a statin altogether. Again, see the Nutrition Debate #9, “Metabolic Syndrome,” and The Nutrition Debate #25, “Understanding Your Lipid Panel,” to understand the rationale.

After stopping the statin, my TC increased to 214 and my LDL increased to 125 (average of 19 tests), versus 195 and 131 before.  But while both are still “borderline” by the old standard, neither is of any concern to my doctor. Nor should they be, because of my greatly improved HDL-C and triglycerides. Remember, TC = HDL + LDL + TG/5. PS: PLEASE read the Nutrition Debate #9, “Metabolic Syndrome,” and The Nutrition Debate #25, “Understanding Your Lipid Panel,” to understand why. Also, stay tuned for the next column which will delve into TC/HDL and TG/HDL ratios as predictors of CVD.

We will also describe some recent scientific studies and hypotheses regarding using triglycerides alone to track and monitor CVD risk…all of which brings me back to Figure #4 in this post (above) and to Figure #3 in The Nutrition Debate #281. If you are persuaded by these data and would like to lower your triglycerides (and raise your HDL-C, since they are, as I have shown, inversely related), then I hope you will consider cutting your carbs along with supplementing with fish oil (at least 2g/day but not more than 3g/day), and of course eating a can of those delicious sardines in olive oil for lunch every day.

What’s your favorite brand of sardine?  How do you get fish into your diet?

The Nutrition Debate #281: HDL-C and Triglycerides

“A picture is worth a thousand words,” the saying goes. Well, I have three “pictures” that I think will get your attention. They are graphs of my 70+ lab tests for HDL cholesterol and serum triglycerides between 1980 and the present. They are by definition n=1, dismissed therefore as “anecdotal.” In the whole, however, for the early years (Fig. #1) they are illustrative of the human condition for people eating the Standard American or “Western” Diet. In the middle years (Fig. #2) and later years (Fig. #3) they reflect the changes that can – and did occur in my case – with a change in diet.

Figure #1 below shows my HDL-C as the almost perfectly flat blue line from 1980 through September 2002, all the while eating the Standard American Diet. The first 11 tests (from 1980 until 12/01) are all in the high 30s and low 40s (range 37 to 42; average 39), which is “low,” i.e. just below “normal” range for 40 for men (50 for women).

Do you know what your HDL cholesterol lab test values are? You should. They and your triglycerides are more important than your Total Cholesterol (TC) and LDL-C scores. The reason your doctor tracks your Total Cholesterol is that he can affect TC and LDL by writing a script to lower them. He can put you a statin. My doctor put me on a statin in December 2003.

The upper line, in red, tracks 17 triglycerides (TG) over the same period. They are more variable (TGs usually vary from 20 to 23 percent, and can range as much as 40% (fasting vs. non-fasting). Note that they are not “high” (>200), but they hover around the “borderline” level of >150. The average is 143 (range 107 to 187). Neither of these tests would get your average doctor too exercised. He would say he’s going to “watch” them (what else can he do), and to “continue taking the statin.”

Figure #2 shows HDL-C after I started on Atkins Induction (20g of carbs a day!) and followed it faithfully for nine months, then a sort of Atkins Maintenance for the next three years. I then went “off plan” in the summer of 2006, and to get back on track, I did the Bernstein 6-12-12 plan for diabetics (30g of carbs a day) for a year (9/06 to 9/07). Note that during this 5-year period my HDL-C crept slowly up from 43 to 60. The “curve” was still straight with most values in the high 40s and low 50s (average 51 vs. 39 on the SAD). TGs were lower (average 84, range 36 to 157 with one aberrant (222). Your average doctor would be pleased with these HDL-C and triglyceride lab tests, and he would advise “keep taking the statin”

Figure #3 is the most interesting by far because it is in every respect “aberrant” to the clinician. In fact, it’s paradoxical.

Note that the blue and red lines are inverted. The HDL-C in virtually every case is greater than the triglycerides! The average of 25 HDL-Cs is 75 (range 52 to 98). The average of 25 TGs is 49 (range 21 to 65). Note also that there is definitely an inverse relationship between HDL-C and TG: when HDLs are high, the corresponding TG is low. Examples of the most extreme inverse relationships are HDL: 86/TG: 21; HDL: 98/TG: 29; HDL: 92/TG: 32; HDL: 90/TG: 34. My doctors (and others) want to know how I did it. My answer was originally that I didn’t know but that I attributed it to eating a Very Low Carb Ketogenic Diet (VLCKD). As the last chart shows, that was only a small, perhaps not significant, part of the story.

My editor made the observation that the can of sardines in olive oil probably made a big difference.  So, when I finally decided to chart my HDL-C and triglycerides I noticed that the really big change (the inversion of HDL-C and TGs) began long after I had been eating Very Low Carb. It began while I was in the middle of Bernstein, still taking a statin, and starting to take fish oil supplements (April 2007) and then eating a can of sardines for lunch (July 2007). I found the dates by searching my posts on the Bernstein Forum, a good place to hang out, btw, if you’re diabetic.

I started taking 2 grams of fish oil supplements a day (each 1 gram capsule containing 300mg of EPA and 200mg of DHA). I posted on the Bernstein site that “I had read on the Mayo Clinic website, on a drugs and supplement tab, that ‘There is strong scientific evidence from human trials that omega-3 fatty acids from fish and fish oil supplements (EPA + DHA) significantly reduce blood triglyceride levels.’  It goes on to say, ‘Benefits appear to be dose-dependent, with effects at doses as low as 2 grams of omega-3 fatty acids per day. Higher doses have greater effects, and 4 grams per day can lower triglyceride levels by 25-40%.’ It continues, ‘Effects appear to be additive with...statin drugs…’”

In 2007 I was still taking a statin. I had now lost 170 pounds, my bp and bs were in control, and my type 2 diabetes was in remission. Then, when my doctor observed how my HDLs had skyrocketed and my triglycerides had plummeted, he concluded that I was no longer at “high” risk of CVD. In October 2008, without any “coaching” from me, my doctor took me off statin drugs.

In the next column I’ll tell you about my history of Total Cholesterol and LDL-C (before, during and after statins). Then, in the next, about my TC/HDL and TG/HDL ratios and an interesting hypothesis about triglycerides and dysfunctional HDL. 

The Nutrition Debate #280: Putting Fat Loss on Autopilot

I would have “Putting Fat Loss on Autopilot” in quotes in this title if I could remember where I copped it from. I wrote it down some time ago thinking it would make a good subject to write about, and promptly lost the reference. Oh well. I don’t need a citation because I know how to put fat loss on autopilot. And when I follow “my prescription,” it works splendidly. Of course, the operative word is “when.” But that’s tangential to the main theme; I’ll come back to it later.

The key to losing body fat “on autopilot” is to learn to fly in a space without turbulence, that is, in a place without cross-winds wracking the air frame – where you can just sit back and let your body “fly the plane.” This requires that you get to a place where there is less resistance, few disturbances and “traffic.” Your attention will be required at take-off, but once you are up to speed and “on course,” and have reached a certain comfort level, you can safely put fat loss on autopilot.

The first thing you need to do is go to school. You need to become a good pilot before you can learn to use autopilot. This is actually more difficult than going to flight school, I think, because besides learning how to “fly right,” you first have to unlearn all the things we, and virtually all the doctors who are alive today, have been taught about nutrition. In principle, that shouldn’t be too difficult for us or them because they’ll be the first to tell you they didn’t learn diddly squat about nutrition in medical school.  However, like most professionals today, medical doctors are required to get “CEUs”” to maintain their licenses, so the best we can hope for is that they spent their convention time on the golf course.

For your own part, if a lifetime of empirical evidence – your own knowledge acquired from observation or experiments – leads you to the conclusion that eating a low-fat, high-carb diet is the way to lose your body fat and keep it off, without cravings and hunger, then you can take that turbulent journey – hands on the stick all the way – and have a bumpy ride.

On the other hand, a very-low-carb “eating pattern,” is like having a tail wind all the way. It’s a little rough getting up to speed and altitude – and here it requires your full attention, knowledge and skills – but once you’re on the right flight path, it is pretty much “smooth sailing.” You will experience very little turbulence. No hunger. No cravings. Just effortless, fuel-efficient flying at cruising altitude while you burn body fat for energy. Your body wants to cruise along. It seeks metabolic homeostasis. Eat low carb, and your body will fly the plane. You can sit back and relax; you will be on autopilot.

Take-offs are the hardest part, people tell me. It wasn’t for me, but everyone’s different. In my experience it takes only a few days – maybe 3 or 4 – for the stomach rumblings to go away, after which you won’t “feel hungry” any more, if you eat strictly Very Low Carb. I salted my meals to remain hydrated. Some people drink a cup of bouillon in late afternoon to avoid dehydration/headaches. And if you’re taking meds for diabetes, you’ll need to carefully monitor your blood sugars and stay in touch with your doctor as your BS will go dramatically lower (especially if you are taking a sulfonylurea like glyburide).

I stayed on Atkins Induction (20 grams of carb a day) for 9 months and Iost 60 pounds. I then moderated my carb intake a little, but didn’t gain any weight back for several years until I started cheating (late night bowls of ice cream).

At first I kept a log of everything I ate. I just estimated grams of carbs for everything I ate. I tracked nothing else. I just wanted to raise my awareness about carbs, and my knowledge of what foods contained carbs and how many. Later I used a web-based resource to track calories, fat and protein (as well as carbs), and I began to study macronutrient ratios and reduced gram counts for each macro (fat, carbs and protein). Eventually, after I felt well enough educated about that to make good food choices, I stopped keeping a daily log. Now, I take a fasting BG every day, weigh myself regularly, and see my doctor 3 times a year (at my insistence). He would see me just once a year, but I want the blood tests.

How can you “go to school” to acquire the knowledge and skills required to “fly right”? Well, there are now dozens of good books and hundreds of bloggers to help you. If you decide to try it, of course I hope you’ll hang out here. It’s not the lounge of a 747, but it’s almost as safe. And in writing 280 columns like this one over 4½ years I have covered just about everything of interest to me relating to “fat loss on autopilot.” Obviously, I think this is the right way to fly for weight loss, glucose metabolism, metabolic syndrome, lipid health and mediation of chronic systemic inflammation. I have also addressed the macro and microvascular complications of type 2 diabetes (all of which I have avoided), including CVD, various cancers, dementia (including Alzheimer’s), and peripheral neuropathy, retinopathy, and nephropathy (end-stage kidney disease).

And each week I discover bloggers who knock my socks off. The skies are full of helpful resources, and most of them are knowledgeable pilots flying above the clouds where the air is clear and the winds are favorable. Try it. Come fly with us.

What are your favorite low carb resources - bloggers, books, videos?

The Nutrition Debate #279: My fasting blood glucose is 85mg/dl

My Fasting Blood Glucose (FBG) was 85mg/dl (4.22mmol/l) this morning. That’s not “normal” for me. I have a “broken glucose metabolism.” It has been broken for more than half my life. I am Carbohydrate Intolerant. I was diagnosed a type 2 diabetic over 28 years ago (1986) and was probably diabetic for a few years before. I was certainly “pre-diabetic,” with Impaired Glucose Tolerance (IGT) and then Impaired Fasting Glucose (IFG) for years. That’s how my type 2 diabetes was spotted. On my first office visit, an observant GP saw that I was obese and ordered a fasting plasma glucose test. Voilà.

In those days the threshold for a diagnosis of type 2 diabetes was two consecutive lab tests of 140mg/dl or more. (Today it’s 126mg/dl and an A1c test.) That doctor, whom I only saw once (I moved), and whose name I don’t even remember, did the usual thing in those days: he prescribed a sulfonylurea, micronase (generic: glyburide), and undoubtedly advised me to lose weigh by “eating less and exercising more.” The “medically advised” diet in those days hewed to the newly formulated Dietary Guidelines for Americans, first promulgated in 1980 and updated every 5 years afterward. Unbelievably, it still does.

Of course, as everybody knows, it’s virtually impossible to lose weight and keep it off on a calorie-restricted, balanced diet. Your body “craves” more. It doesn’t want you to “starve.” So it’s constantly signaling that you’re “hungry.” I put all these words in quotes because they have become part of the lexicon of dieting by this failed meme. You know it. I know it. You would think that individual medical practitioners would (actually do?) know it, but the profession today is more a business that is governed (for most docs) by the “bottom line” and the “standards of practice” they must follow in order to be paid for the medical codes they submit. Too bad for us that the government has intervened in the patient-doctor relationship.

So, how did my blood sugar get to be 85mg/dl this morning?  Briefly, on the restricted-calorie, balanced diet my weight (300 in 1986) continued to rise until I weighed 375 pounds in 2002. And my oral anti-diabetic medications increased as well until I was maxed out on two drug classes and starting a third. Before long, I would become an insulin-dependent type 2, if I didn’t change my Way of Eating (WOE). Newer drugs were not yet available.

Then, one day in 2002, on a regular office visit, my doctor said to me, “Have I got a diet for you!” A few months earlier he had read the Sunday Magazine cover story in the New York Times: Gary Taubes’ “What It It's All Been a Big Fat Lie.” He tried the diet himself, lost 17 pounds, liked his blood lipids, and decided to “prescribe” the diet for me. I was ready. I was really motivated and willing to try something different. The diet was Atkins Induction, and I lost 60 pounds in the next 9 months – and then I retired. That was a major “lifestyle change,” but I managed to retain my new VLC “eating pattern.” 

But even before I lost this weight – upon starting Atkins Induction, actually – I started to get hypos, which are dangerously low blood sugars. I called the doctor, and he immediately told me to stop taking the 3rd med. The next day, when the hypos continued, he told me to cut the other two classes of meds in half. The next day he ordered me to cut them again. Eventually, I titrated off the sulfonylurea altogether and today just take a small dose of Metformin with supper. Over time, I saw my A1c’s drop to the mid 5s, my HDL-Cs double (from 39 to 84), my triglycerides drop 2/3rds from 137 to 49 average, and my hs-CRPs (an inflammation marker) drop from “high risk” to “normal risk” to “low risk” of cardiovascular disease. 

I kept the 60 pounds off for several years and then, over the summer of 2006, I regained 12. (It could have been those late-night freezer raids.) I recommitted to a Very Low Carb WOE and switched to “Bernstein” – Richard K. Bernstein’sDiabetes Solution “6-12-12 program” for diabetics. I lost 100 pounds in 50 weeks. Altogether I lost 170 pounds.

Along the way, until I learned (from my meter) what I could eat and what I couldn’t, my total calories on Atkins dropped (as my weight dropped) from over 2,000/day to 1,700 to 1,550 to 1,470, and eventually to 1,200 calories/day (375/375/450). My carbs of course have always been VERY LOW (from 8% down to 5% today). My diet is mostly moderate protein (25 to 20%) and high (70 to 75%) “good” fat: saturated and monounsaturated. I try to completely avoid polyunsaturated fats (PUFAs). PUFAs are vegetable and seed oils, like soybean, corn, sunflower and Canola oil. 

I eat 2-3 small meals a day, with no snacks at the moment. I’m trying to lose some of the pounds that have crept back on. If I were snacking, it would only be before supper, with sliced radishes with salt and ghee and diet tonic (vodka optional). I am not ever hungry. I have great energy levels and (at age 73) nohealth complaints. And when I eat like this for just a few days, my FBG drops from the low 100s to the 80s and 90s once again. What’s your Fasting Blood Glucose?

The Nutrition Debate #278: Skipping Breakfast

The Nutrition Debate #278: Skipping Breakfast

“Skipping breakfast doesn't cause weight gain. Bye bye, conventional wisdom,” tweeted Stephan Guyenet, PhD, obesity researcher, neuroscientist (“reward” theory expert) and blogger at Whole Health Source.  To support his tweet @whsource, Stephan attached this link to a randomized controlled trial published online in November 2014 in the Journal of Nutritional Science, a Cambridge University Press, UK, peer-reviewed journal. But his was not my takeaway.

In scientific fashion, this “study” has a hypothesis and a study design. The abstract begins, “Eating breakfast may reduce appetite, body weight and CVD risk factors, but the breakfast type that produces the greatest health benefits remains unclear. We compared the effects of consuming a high-fibre breakfast, a non-fibre breakfast, or no-breakfast control on body weight, CVD risk factors and appetite.” If I’m not being clear, we need an “unclear” condition in order to clear it up!

The study RESULT is seen in the title: “Skipping breakfast leads to weight loss but also elevated cholesterol compared with consuming daily breakfasts of oat porridge or frosted cornflakes in overweight individuals: a randomized controlled trial.” 

Unusually, this paper has no CONCLUSIONS section, but the last paragraph of DISCUSSION begins, “In summary, the present study shows that in overweight individuals, skipping breakfast daily for 4 weeks leads to a reduction in body weight, but this is accompanied by an increase in total cholesterol concentrations compared with consuming either a frosted cornflakes or oat porridge breakfast.” Note: Everybody knows that elevated total cholesterol concentrations are bad, right?           

Then – and this is where I start to get even more skeptical (cynical?) – the “summary” continues: “There were no differences in changes in body weight or total cholesterol concentrations between the groups consuming the frosted cornflakes no-fibre breakfast or the group that consumed the high-fibre oat porridge breakfast. These findings suggest that although skipping breakfast may be the more effective strategy to achieve weight loss than eating breakfast, there are associated detrimental effects on total cholesterol concentrations” (emphases added). To be clear, this publication is in the UK, and the “fibre” spelling, is for the Brits, who eat a lot of “oat porridge.” We call it “oatmeal” in the U.S.

Let’s cut to the chase. If you didn’t notice my emphases, “The present study was funded by the Quaker Oats Center of Excellence, PepsiCo R&D Nutrition.” The Quaker Oats division of PepsiCo makes the high-fibre oat porridge used. Their competitor, Kellogg’s, is the world’s second-largest snack company (after Pepsico) and makes the “no-fibre cornflakes.”

The lead author, Allan Geliebter (A.G.), is an MD, PhD, Professor of Psychology and Senior Researcher at the New York Obesity Nutrition Research Center, St. Luke’s-Roosevelt HC, Institute of Human Nutrition, Columbia U. College of Physicians and Surgeons, and in the Department of Psychiatry at the Columbia University MC. “A.G. was responsible for the study conception and design, and supervised acquisition of the data and edited the manuscript.” And,“A.G. received funding from Quaker Oats Center for Excellence, Pepsico R&D Nutrition for the design, conduct and analysis of the study and for the preparation of the manuscript.” Also: “The funder contributed [they’re nottalking money here] to the study design and editing of the manuscript.” And this: “We thank Yi Fang of Pepsico for his helpful comments on the manuscript.”

To be CLEAR, there was no attempt on the part of the authors, their peer reviewers or their helpful funders to conceal the purpose of funding this study. “The aim,” the ABSTRACT concludes, “of the present study was to investigate the effects of consuming a high-fibre oat porridge, an isocaloric non-fibre cornflakes breakfast, and a no-breakfast water control daily for 4 weeks on body-weight changes, subjective appetite and CVD risk factors in overweight but otherwise healthy individuals.” 

Stepping back for a minute from the obvious “editorial bias,” several queer things struck me about this study when I first read it. For one, why wouldn’t any serious, unbiased scientist, who didn’t have an axe to grind or a funder to satisfy, and was genuinely interested in a breakfast type that “reduces appetite, body weight and CVD risk factors,” i.e., “produces the greatest health benefits,” include an isocaloric breakfast like bacon and eggs? Well, I guess that too is pretty CLEAR now.

For another, according to the Study Design section, the “data were collected in 1998 and 1999.” Why, then, is this old NYC study being dredged up and republicized in the UK in 2014? My answer is speculation: Perhaps it didn’t pass peer-review muster the first time, or perhaps Quaker Oats/Pepsico was just trying to get some more mileage out of their previously funded research with some new marketing in the U.K. To be CLEAR, Quaker Oats/Pepsico is a world-wide cereal marketer, and this study was just a hack job designed, in the way drug trials are designed, to show superiority of one breakfast cereal over another. Nobody intended the outcome to advocate not eating breakfast. That wouldn’t be good for business. 

Personally, I was unaware of the widespread “conventional wisdom” that skipping breakfast causes weight gain. I eat a good breakfast of bacon and eggs and H&H in my coffee almost every day. It can carry me all day if I want it to, but I usually eat a can of sardines in olive oil for lunch. If I were going to skip a meal – because I wasn’t hungry or I was trying to lose weight, I’d skip lunch. My wife makes breakfast, and she says she married me for better or worse, but not for lunch.

The Nutrition Debate #277: What is hunger?

“I’m hungry…all the time,” the overweight and obese person frequently says when trying to lose weight on a restricted- calorie, low-fat (high-carb) diet. But is this really hunger? “Hunger,” Wikipedia says, “is a condition in which a person, for a sustained period, is unable to eat sufficient food to meet basic nutritional needs.” It precedes this definition with, “In politics, humanitarian aid and social science…” Wiki is talking, of course, about the condition preceding starvation, which is often a precursor of death. Fat people are not “starving.” They may be malnourished, but they are not actually starving.

So the “hunger” a fat person experiences is different from that which a starving person experiences. A person who, for a sustained period, is unable to eat sufficient (or any) food will, for a few days, experience stomach rumblings (“pangs”), but then those pangs will go away. As the body adjusts to a lack of ingested food, it transitions to another source of “food” for energy: body fat and muscle.  After the available fat and muscle have been consumed, the body enters into a period of “wasting” in which the organs begin to fail. But if you are overweight or obese, you want your body to consume body fat.

In that sense, fat people have a biological advantage. Their bodies can run for a long time on “stored energy,” providing that energy comes from stored body fat. But before they get to use it, they will feel “hungry” for a few days. Why? Because their gut hormones (ghrelin, et al.) are sending the brain a signal to seek food. It’s part of a normal fed/fasted cycle. The stomach is empty and the ingested ingredients have been almost completely absorbed from the small intestine into the blood stream for distribution. It’s time to seek more nourishment (and yet conserve stored energy).

The glucose component of these nutrients (the “sugar” that carbs break down into) requires insulin to transport it in the blood, and such elevated insulin levels tell the liver that stored fat is not needed (and in fact is blocked from breaking down by the elevated serum insulin). So, if you eat things that break down to glucose, your body will tell you it needs more glucose (carbs to break down) because your body fat is locked up. Ergo, YOU Will Feel Hungry (for more carbs).

On the other hand, if you cut back carbs, especially processed, highly refined carbs, and sugar-sweetened beverages (SSBs), the “sugar” in your blood will not be elevated and neither will your insulin. In that case, knowing that “sugar” (carbs → glucose) is unavailable, the liver will release your stored fat (“triglycerides”) to break down to smaller free fatty acid (FFA) molecules that pass into the bloodstream. Your energy will flow as well, if not better, than if you had eaten carbs. Whereas, if you are Insulin Resistant, as almost all fat people are, eating carbs will cause your blood sugar to spike and then crash, leaving you tired and hungry. But when burning body fat, you energy level will be high and your blood sugar low and flat.

When you are in this steady state of ketosis (fat-burning) – a condition your body, especially the brain, really likes – you can go for days, weeks and months with high energy levels and stable blood glucose all day long. When I strictly followed the Bernstein program (designed for diabetics) some years ago, I lost 100 pounds in 50 weeks. Before that, in the first 9 months on Atkins Induction, I lost 60 pounds. Altogether, over several years, I lost a total of 170 pounds, without hunger.

Of course, it was hard for me to give up so many of my favorite foods – foods that I had eaten for a lifetime. But it wasn’t because I needed to eat them to stave off hunger. I liked them. They were available and convenient. And they were often prepared, take-out, packaged, drive-up, processed and sweetened, and when I ate them, I was hungry all the time.

Once I figured out how to lose weight without hunger, and get control of my blood sugar and type 2 diabetes – and I learned that by eating a certain way all my health markers would dramatically improve – it was a “no-brainer.” All I had to do was develop new habits about what I could eat and what I should (try to) avoid. A good way to do that is to get into the habit of eating the same thing for breakfast almost every day. For me that’s eggs and bacon and coffee with a little H&H and stevia powder. For lunch (if I eat it), I usually eat a can of Brisling sardines packed in olive oil. And that’s all folks.

For dinner (we call it supper), we usually have a protein portion and a serving of vegetables either roasted in olive oil or tossed in butter. At the moment I’m on a fresh campaign to lose some of the pounds I have added back over the years (about 1/3 of the total lost). I’m doing that by reducing my eggs at breakfast from 3 to 2, eliminating lunch about half the time (I’m never hungry), no snacks before supper (radishes with salt and ghee) and never eating anything after supper.

I’ve been doing this for a week now. I’ve lost 6 pounds, and my fasting blood sugars are steady and under 100mg/dl again.

The Nutrition Debate #276: “Why do I eat…even when I’m not hungry?”

“Why do I eat, even when I’m not hungry?” This is a nagging question. It really sticks in my craw. And this is one of the questions that arises in the HBO Documentary series, “The Weight of the Nation,” that I reviewed (as “disappointing,” for the most part) in my last blog post (#275 here). It is in a segment of the series (Part 4: “Challenges”) that dips briefly into science. The answer is hinted at by a guy in a lab jacket: “Evolution happens slowly; DNA changes slowly.” The scientist is Rudolph Leibel, MD, Co-Director, at the New York Obesity Research Center, Columbia University Medical Center.

I have asked this question many times. I think all of us who overeat (or are prone to overeating) have asked it countless times. In the beginning of Part 1, “Consequences,” an obese man says, “You try [to eat less]…and you lose hope.” Another says, “I know I should eat the right things. I’m gonna try.” But then in Part 2, “Choices,” despair returns: Another obese man says, “What can I do? I love good food. I love cheeseburgers. Sure, I know what to do; I just can’t do it.”

A commenter in #268, “Help With Cravings,” – an intelligent, informed, serious student of the science of overeating – says to me, “So you do not experience cravings? If you do not have them, you are lucky. I have had periods without cravings, and periods with cravings. They are a non-rational desire for something, or an insatiable appetite, even on NO carb. This suggests that there is some unknown biological cause, but nobody knows the cause of cravings.” My reply included the idea, suggested by among others the Jaminets in “The Perfect Health Diet,” that we may eat UNTIL our body is satisfied that it has all the essential nutrients it needs (including EFAs and amino acids). Hence, we eat more nutritionally poor foods (carbs) to the point of obesity.” This specialized craving hypothesis has a certain appeal to me, but it’s only part of a complex answer. As Francis Collins, Director, National Institutes of Health, says in Part 2, “It’s a challenge for sure!”

I agree with the statement about the “unknown biological cause,” especially in the context of the brain and nervous system being part of the control/signaling mechanism. And that includes the concept that the gut is home to the Enteric Nervous System, a largely independent entity “in which 95% of the body’s serotonin is made.” This discovery was made by Michael D. Gershon, MD, and described in his brainy memoir, “The Second Brain: Your Gut Has a Mind of Its Own.” And perhaps the microbiome (the micro-organisms that are your intestinal co-residents) is involved as well.

For me, the bottom line is to acknowledge that my body is in charge of my well being. That’s hard for me to admit; I do not lack for hubris. But in my own “conscious” self-interest, that is the conclusion that I must come to if I am to figure out how “I” can help “it” (my body) maintain homeostasis. Think about all the “insults” I throw at “it” every day (eating choices and other behaviors that I do or do not do, like physical activity) that challenge my whole-body condition. If “evolution happens slowly,” and “DNA changes slowly,” my body must suffer somewhat from these unremitting “insults”.

But without knowing this “unknown biological cause” [of craving] – what I will call our “biological imperative,” I attempted a few years ago (2010) to address the subject of why I eat, even when I’m not hungry, in a long-running thread (200 posts, 4000 hits) I started at Dr. Bernstein's Diabetes Forum (registration required), called, “Impulse Control and Metacognition.” The idea was to be “conscious” of the “cue,” an impulse to eat when I’m not hungry, and to deal with it by another means, e.g. by distraction (absorbing reading, compelling TV, writing a column, yard work, fishing, etc.).

Right at the start, the Global Moderator commented, “Isn’t it likely the problem is actually physiological rather than psychological?” (Georgette is always so gentle with me; this is a really “safe” place to be if you are interested in getting answers from very knowledgeable people about diabetes and related health issues.) Anyway, I replied (this is more than 4½ years ago): “I am not pursuing this aspect of it, however, because I know of nothing I can do to manage or control the hormone(s) in question. It is, after all, an autonomic function of homeostasis, the body's self-regulatory system.”

So, while science continues to advance, and I am a little wiser today than I was then, I still hold that 99.99% of our body’s activity is autonomic and totally out of my “conscious” control. All I can do is “listen” to it carefully and do what I think is the “right thing,” to minimize the “insults.” In my case, since I have a broken glucose metabolism – I have Insulin Resistance and fewer operative beta cells in my pancreas – I am carbohydrate intolerant. So, to achieve the best health that I can, I watch my carbohydrate intake very carefully, and to a lesser extent, my protein intake. And I also use my glucose meter for daily feedback, and I use my triennial doctor’s visits for blood tests (glucose, HbA1c, CBC, lipid panel, hs-CRP, etc.). I figure that if I take care of my body, my body will take care of me. After all, it’s 99.99% of me. It’s simple self-interest.