Saturday, June 29, 2013

The Nutrition Debate #121: “Behavior Change is Incredibly Difficult.”

That’s a conclusion of Jason Vassy’s piece in “Personalized Medicine” that came up recently on a Medscape alert. He was referring to the outcome of two recent trials that examined whether genotype information was helpful in motivating health behavior changes in a population that was genetically susceptible to Type 2 diabetes. It was “hoped” that knowledge of one’s genetic susceptibility might be a “clinically useful tool” in targeting “primary prevention strategies before the onset of certain diseases.” Sadly, he concluded that “At present, however, genetic testing for T2D risk likely does not improve preventive health behaviors in today’s diabetogenic environment.” Quelle surprise!

If you are interested in genetic testing for Type 2 diabetes susceptibility, however, there were some tidbits to glean from this article, to wit: “At least 65 genetic loci contribute to T2D risk. Of these, rs790316 in the TCF7L2 gene is associated with the greatest risk: each copy of the T allele carries an odds ratio for T2D of 1.39. The effect sizes of most other T2D loci are generally much smaller (odds ratios typically ranging from 1.05 to 1.15).” This is, of course, all “Greek” to me, but it is worth noting that some people argue that you should ignore almost any study with an odds ratio under 2.

Vassy hastens to point out, though, that “This (greater susceptibility to T2D risk) contrasts with the much larger effect-sizes of family history: T2D in one or both parents multiplies one’s risk by up to two- and six-fold, respectively.” He does not point out, though, that the association with family history goes far beyond genetics or ethnicity; it includes diet, economics, cultural practices, and many other environmental factors generally too complex to reliably isolate in even large epidemiological studies. Alas, he finally concludes, “Genotype risk scores that combine multiple T2D-associated loci significantly predict the future risk of T2D, but they may not improve traditional T2D prediction models consisting of routine risk factors such as family history, BMI, and fasting glucose.”

Behavior change, however, was the hoped-for outcome of these two studies and this author’s commentary. They were all disappointed but, I suspect, not surprised. The medical establishment has come to expect failure. Vassy expresses that outcome succinctly: “These results will not surprise clinicians, whose efforts at counseling patients for weight loss and improvement in diet and exercise habits often fail.” The implication is it’s the patient’s fault. The patient is deemed “non-compliant” with the “prescription” because, they say empathetically “behavior change is incredibly difficult.”

It never seems to occur to the practitioner that that expected outcome failed to materialize because it was a failed protocol – the wrong prescription to treat the cause of the syndrome (see #9, "Metabolic Syndrome," here for the indications), of which obesity is merely a symptom, not the cause. A large percentage of the world’s peoples are apparently genetically predisposed and therefore susceptible to this scourge. It is the outcome of eating a Westernized diet. We become fat not because we eat too much fat and cholesterol (and are too sedentary), but because we (who are susceptible) eat too many sugars and processed carbohydrates. Our metabolism becomes deranged (“disregulated”) – in other words “broken.” We make and store fat as a consequence of eating sugars, processed carbs and fat. The body uses the sugars and processed carbs for energy and stores the fat for the inevitable famine that it is designed to expect and be prepared for. The trouble is the famine never comes. We live in a world with an overabundance of relatively cheap carbohydrates in the form of manufactured and processed foods. This is in contrast to the animal-based dietary of protein and fat, plus seasonal whole foods (including unprocessed carbohydrates) our ancestors ate. Instead, we now graze on processed carbohydrates all day long as though we lived in a veritable corn-utopia©, which, in fact, we do.

Our body is an exquisitely designed system that works flawlessly until or unless we mess with it. Even then, it works against even our best efforts to subvert its protective mechanisms. It will until it “breaks” or unless we learn how to work with it. If we eat Low Carb or Very Low Carb, and just two or three small meals a day of moderate protein/high fat over an 8 or 10 hour period, and then fast for 16 or 14 hours, we will be living much the way our ancestors did. The outcomes of this Way of Eating are weight loss for most, high energy levels, improved health markers (even before weight loss), well being, and longevity.
This “prescription” doesn’t occur to our health care providers. Their “hopes” are still pinned on weight loss, and their protocol is still a balanced diet, with less saturated fat and dietary cholesterol, and more exercise. That this bias is assumed and built into the two studies and the commentary of Vassy’s piece is self-evident: “Overall, participants did not change their dietary fat intake or exercise habits over the study period, although most already had ‘good’ habits at baseline.” Then, “However, receiving a higher genetic risk estimate for obesity was associated with greater fat intake and lower exercise scores…” Thus, these changes in diet and energy expenditure, the universally prescribed standard lifestyle modification program, did not work to reduce T2D risk. Behavior change is incredibly difficult, when it is the wrong lifestyle modification. The right one, VLC, is simple. Outcome: Weight loss and improved health, without hunger.

Wednesday, June 26, 2013

The Nutrition Debate #120: Nutrigenomics – an emerging new science

When I showed my step-daughter this Wikipedia piece on Nutrigenomics recently, she was curious. She had just earned her master’s in Forensic Biology at UConn, where she has worked in the Medical Center’s research labs for 20 years (after getting her Bachelor’s in Biology there), and she had never heard of it. This subject is ‘cutting edge’ and certainly not ‘mainstream,’ yet. But I think it’s time has come because we are now entering an age where the juncture of technologies will enable its rapid development. It is an exciting concept, and I will try to describe it to you here, briefly.

Cribbing almost entirely from various entries in Wikipedia, “In modern molecular biology and genetics, the genome is the entirety of an organism's hereditary information.”  “The study of the global properties of genomes of related organisms is usually referred to as genomics, which distinguishes it from genetics which generally studies the properties of single genes or groups of genes.” “Nutrigenomics,” then, “is the study of the effects of foods and food constituents on gene expression.” “By doing so, nutrigenomics aims to develop rational means to optimize nutrition with respect to the subject's genotype, which in the case of humans is the “genetic make-up,” colloquially speaking, of an individual.

As an individual then, I could look at this from a purely personal perspective.  I was diagnosed a Type 2 diabetic 27 years ago. I probably “presented” with all the symptoms of Metabolic Syndrome some 35 years ago – half a lifetime. But now this cohort includes roughly half of the human race who are overweight or obese and have all the indications of Metabolic Syndrome: central obesity, hypertension, dyslipidemia, and dysfunctional glucose regulation (pre-diabetes or “frank” Type 2 diabetes). This is the cohort of the earth’s population that now eats a Western diet.

“It is hoped that by building up knowledge in this area, nutrigenomics will promote an increased understanding of how nutrition influences metabolic pathways and homeostatic control, which will then be used to prevent the development of chronic diet related diseases such as obesity and type two diabetes. Part of the approach of nutrigenomics involves finding markers of the early phase of diet related diseases; this is the phase at which intervention with nutrition can return the patient to health. As nutrigenomics seeks to understand the effect of different genetic predispositions in the development of such diseases, once a marker has been found and measured in an individual, the extent to which they are susceptible to the development of that disease will be quantified, and personalized dietary recommendation(s) can be given for that person.”

The prospect that, as this new science develops, “personalized dietary recommendation(s) can be given for that person” is appealing. It would be nice to have some scientific proof that if one changed one’s diet it “would return the patient to health.” It would be nice to know the particulars of the gene and protein expression, and the metabolite production and genetic sequencing, that half of the human race has that gives it a “genetic predisposition in the development of such diseases” and is therefore “susceptible to the development of that disease” (obesity and/or type two diabetes). Such “personalized dietary recommendations” could then be given to half the world’s population who have this genotype that predisposes them and makes them susceptible to such diseases as obesity and type two diabetes.” 

Wait a minute! Am I missing something? Am I being dense? We already have the “markers” – okay, they’re admittedly crude markers compared to a DNA microarray, but they are the indications of Metabolic Syndrome: 1) central “truncal” obesity with associated hypertension, 2) dyslipidemia, particularly low HDL and elevated triglycerides, 3) and a broken glucose metabolism. Your waist-hip ratio can tell you almost everything you need to know.  And we already know what “intervention with nutrition can return the patient to health”: a low-carb, high-fat diet. This is my “prescription,” and I aver it would work for half the human race, if they would just try it.

If I sound frustrated, it is only that I know that science needs to prove the self-evident truth by the scientific process: In science you start with a hypothesis, demonstrate it, test it, test it again to attempt to disprove it, obtain grant money from an unbiased source to pay salaries, and then patent your discovery and get rich. That’s how science works today.

But I digress. Nutrigenomics has a laudatory goal. It will be helpful for the more specialized and increasingly common disorders related to diet, such as Celiac disease,  the inflammatory bowel diseases (autoimmune conditions such as Crohn’s and various forms of colitis, including ulcerative colitis), and Irritable Bowel Syndrome which can be caused or exacerbated by fiber and food intolerances (FODMAP, fructose, gluten and casein, for example). To find “markers” in the early phase of such “chronic diet related diseases” would be a boon for the sufferers. That will be especially true if in this phase “intervention with nutrition (could) return the patient to health.” These sufferers will anxiously await developments in this new science. Of course, when fully developed the symptoms of these diseases are manifest, and the sufferers already know what they have to do to avoid them. Just as some of us Type 2s have learned.
If you want to help advance the cause of science (and for just $99 fund some research), you could participate in a small way through an ongoing “study”: 23andme. From a saliva sample, they will analyze your DNA and send you a report.

Saturday, June 22, 2013

The Nutrition Debate #119: “Lifestyle Intervention is Great Therapy.”

Ralph A DeFronzo, MD, Director of the Diabetes Division at the University of Texas Health Science Center, made this comment at the May 2013 American Association of Clinical Endocrinologists (AACE) meeting. His presentation in the “Diabetes Update – 2013” session got my attention since Dr. DeFronzo is a favorite of mine for his Banting award lecture at the 2008 ADA convention. That full paper was published in the ADA’s Diabetes. In it he said “By the time that the diagnosis of diabetes is made, the patient has lost over 80% of his/her β-cell function, and it is essential that the physician intervene aggressively with therapies known to correct known pathophysiological disturbances in β-cell function.”

So, I eagerly read a digest of his recent remarks in "Diabetes in Control." The paragraph that “set me off” was this: “There’s no doubt – then you look at diabetes prevention – if you can get people to lose weight and exercise on a regular basis, lifestyle intervention is great therapy,” he stated. “The issue is not whether diet and exercise works. It works. The issue is can you get people to do it on a long-term basis. I think it’s time to face reality. The reality is, it doesn’t work long term.”

Obviously, I was expecting a lot more than I got, but I shouldn’t have. He is just a physician, albeit a leading one. He is a pill peddler; when pills fail or something better comes along, i.e., an injection, he’ll push that. He is a prescriber. Whatever big pharma comes up with to treat the “pre-diabetic” or diabetic patient, he’ll prescribe. That’s the modus operendi of the MD.

There is also the legitimate question of what can a physician do to get his patient to lose weight if there is no magic pill to “pop.” If he and you view him as being in charge of your health, therein lies the problem. He’s in charge of your healthcare; you are in charge of your health. You have it in your power to lose weight, and you can do it with the right dietary.

I also cannot deny that moving the goal posts for diagnosis of pre-diabetes and diabetes to new markers (like lowering FBG thresholds and adding the A1c’s to the diagnostician’s quiver, of which DeFronzo has been a leading proponent, are steps in the right direction. I applaud these changes. It’s just that they’re shooting at the wrong target. The target for weight loss is dietary. And the bull’s eye is a Low Carb diet. But, what do you expect a doctor to do? What do they know about nutrition? Nothing! Ask them. They usually are the first to acknowledge that they just follow “practice guidelines.” And it isn’t getting any better. This NIH article, “The Status of Nutrition Education in Medical Schools,” concludes the range is 2 to 70 hours! 2!!

So, if “lifestyle intervention is great therapy,” but “it doesn’t work long term,” what’s the problem? If one pill doesn’t work to lower blood pressure, what would my doctor do? He’d prescribe another one! Why don’t doctors do this for weight loss? My doctor did. He “prescribed” Atkins Induction after reading Gary Taubes’s “What If It’s All Been a Big Fat Lie?”, the July 7, 2002 New York Times Sunday Magazine cover story. He tried it and lost 17 pounds in a month. Unfortunately, he didn’t stick with it long term. He regained all that weight and more when he went back to his old ways of eating.

But it worked for me. And it still works for me. And it could work for you too, if you don’t listen to everyone who tells you it doesn’t work long term. What they mean is that people don’t stick to it. Because it does work, I’m telling you, it does, if you try it and like it and stick to it, as I do.

Part of the problem is that “Lifestyle Intervention” is intentionally vague. It could be defended as being “inclusive” but is more likely intentionally undefined to avoid controversy and going against the prevailing dogma. It is convenient as a phrase as it includes the idea of exercise. Exercise is good, I suppose, but I don’t do any formal or regular exercise. I am active, working in my garden in New York and kayaking in the winter in Florida, but I do no formal exercise. It is said to increase insulin sensitivity, but I would bet that lowering serum insulin, by eating Very Low Carb, is more effective at raising insulin sensitivity, and doesn’t involve sweating. Besides, my “exercise” is all outdoors. You should see my Vitamin D levels!

Because Lifestyle Intervention is so vague, it is left to everyone to interpret in the way they chose, along with the meaning of the word moderation. We think of moderation as the way we prefer to approach the way we eat or exercise. And a healthy lifestyle is thought to include the restricted calorie, low-fat “balanced diet,” which is still the standard therapy for weight loss. And don’t forget low-salt and low-sugar. No mention of protein, but everybody knows, don’t they, that eating too much protein is bad for you.  

That this “standard therapy” doesn’t work is what Dr. DeFronzo is talking about. He’s primarily an academician, but he’s right. Many patients don’t stay on a low-carb diet long term, and the minute they leave the diet, it ceases to work because they are still carbohydrate intolerant. That some don’t stick with it is irrelevant for you and your long term health. “It works,” remember. See the quote in paragraph two above. And I know plenty of diabetics and a few non-diabetics who’ve eaten low carb for over 10 years.  They tend to be on the quiet side, unlike me.
Do you know anyone who has eaten low carb for a year, or five or ten years, or more?

Wednesday, June 19, 2013

The Nutrition Debate #118: “Nobody Weights 375 Pounds”

I don’t know how to punctuate this quote, because it was said to me as a rejoinder in conversation as I was rattling on about my “discovery” that I weighed so much – but it was said with a slightly upturned lip and a wry smile that I interpreted as something between disbelief and admiration. Regardless, it was true. I weighed 375 pounds when I undertook a Very Low Carb diet to lose weight (not to treat my worsening type 2 diabetes of 16 years) at the suggestion of my doctor, an internist and cardiologist. After he had tried it himself, he suggested I go on the Atkins diet, specifically Atkins Induction.

Admittedly, I came to that appointment with my doctor in August 2002 motivated to lose weight. For about a year his nursing staff had been unable to weigh me. The office scale only went up to 350 pounds. So, a day or two before my scheduled appointment, on my way to work I stopped by the Fulton Fish Market in NYC. I asked permission, took off my jacket, emptied my pockets, and stepped onto a wholesaler’s certified platform scale. I was stunned. The shock was genuine. I thought I might be 360 pounds or so, but the scale told the story. I could no longer be “in denial.”

Then, as I walked into my doctor’s office the next day, my doctor saw me and said, “Have I got a diet for you!” So, I was motivated – to lose weight. It never occurred to me, or to my doctor at first, that this would be beneficial to my blood sugar metabolism or my lipid health; but, as we left his office to schedule my next appointment, he put his hand on my shoulder and said, “Dan, this might be good for your diabetes too.” Boy, was that an understatement!

Regular readers here have heard this story before, so I will be brief: Immediately upon starting Atkins Induction, having virtually eliminated carbohydrates from my diet, I started getting hypoglycemic episodes every afternoon. I ate a candy bar and called the doctor (in that order). He told me to eliminate first one and then to cut back on the other two oral antidiabetic meds he had prescribed progressively more of over time. I dutifully followed “doctor’s orders.” After eliminating the Avandia, I quickly reduced the Metformin and the Micronase from “maxed out” to half and then one-quarter the original dose. Later, when I switched to the Bernstein diet for diabetics, I titrated completely off the Micronase.

Interestingly, as I stayed on this Very Low Carb diet, my blood lipids (cholesterol panel) also improved very dramatically. My HDL cholesterol more than doubled from average 39 to average 84. And my triglycerides were reduced by two-thirds from about 150 to 50, where they have remained for many years now. In addition, as I lost well over 150 pounds (about 170 at one point), my blood pressure came down from 130/90 to 110/70 on the same meds. I subsequently regained some of the weight (I’m currently 232 and dropping again), and my blood pressure is stable at 120/80.  Other markers like C-Reactive Protein also dramatically improved and my A1c’s are now mid-5s and my fasting blood glucose (FBG) usually 80s and 90s.

So, is my Type 2 diabetes cured? I would say no! I have and will always have a broken, damaged, deranged, disregulated glucose metabolism. I have insulin resistance “in spades.” There’s no denying that. I could weigh 375 pounds again. But, so long as I continue to eat Very Low Carb, my type 2 diabetes is and will remain in remission, undetected and virtually undetectable to any clinician or laboratory test routinely administered in an office visit by an unsuspecting practitioner. Typically, because I am still overweight (technically obese; my BMI is 32), a doctor would advise me to eat a restricted-calorie, low-fat, “balanced” diet, and exercise regularly.

THAT would be a prescription for disaster. I would immediately return to out of control blood glucose, again becoming progressively dependent on anti-diabetic oral medications, eventually becoming an insulin-dependent type 2 diabetic. In addition, my lipids, which are now stellar, would return to borderline or worse. Then, my doctor would be aggressively pushing me to start on statins, with all their dubious benefits and consequences. The low-fat diet he would recommend is by definition high carbohydrate (50% to 60% by calorie). The Nutrition Facts panel on processed food packaging is proof of it. It is based on 60% carbohydrate or 1,200 calories on a 2,000 calorie a day diet. Check it out, if you don’t believe me.

But best of all, I think, is the certainty that eating Very Low Carb, which unavoidably means eating high fat, is a very good way to lose weight. That is why my cardiologist doctor, who tried it himself, recommended it to me. It worked as a weight loss diet for him and for me. It just happens that I was also a type 2 diabetic, and it drove that condition into total, complete remission, so long as I continue to eat Very Low Carb. There’s no going back, in case you were wondering…

VLC will do the same for you if you are prediabetic, defined as having two successive fasting blood glucoses between 100 and 125 or an A1c between 5.8 and 6.5 (or 7.0 for general physicians and internists. Endocrinologists are more aggressive.) But if you don’t know what your blood sugars are and you are just overweight, particularly if your waist hip ratio is above .9 (male) or .85 (female) at any weight level, eating VLC will “regularize” your blood sugar, making it more stable; And eating Very Low Carb (and therefore high fat) will improve your blood lipids, especially HDL and triglycerides. So, why not try it?

Saturday, June 15, 2013

The Nutrition Debate #117: “Sugar, Salt and Fat”—the new “Bad Boy” Linkup

Have you noticed lately that “sugar, salt and fat,” or “fat, salt and sugar” (in any order) are the new trio of “bad boys” of the dietary Dictocrats? Maybe this linkage has been around longer, and I’ve just been unconsciously suppressing the message, especially the “deadly duo” of salt and “solid” (saturated) fat. The salt myth was exploded by Gary Taubes in his 1998 Science piece here, but fat has been demonized for half a century, starting with Ancel Keys association of saturated fat and dietary cholesterol with heart disease in his infamous “Diet/Heart Hypothesis.” See The Nutrition Debate #3 here.

Mary Enig (see #23 here) has been trumpeting the dangers of artificial trans fats since the McGovern Select Committee hearings (1977). In that, of course, she was “spot on,” and the government finally acknowledged in 2003. But, not without wrongly linking the danger of artificial trans fats (made from corn and other vegetable oils) to saturated fats from animals. They also conveniently ignored the natural trans fat (conjugated linoleic acid or CLA) that is found in animal fats and is very good for our health. Chemically these two fats are very different. Natural: very good. Artificial: very bad. Just avoid them!

Further differentiation among fats has occurred more recently: our government has declared that SOLID FATS (lumping together both the naturally occurring saturated fats and the artificial trans fats) are “bad,” but VEGETABLE OILS, which are processed from seeds and grains, are “good.” Given the extreme heat and hexane bath required to make it edible, it is impossible to consider vegetable oil as “good” – or even “real food.”  And try to ignore that the United States Department of Agriculture is the federal agency responsible for both promoting corn and soy, the mainstays of the U. S. agricultural and food manufacturing industries, and protecting the public health, in that order. It’s pretty scary, if you think about it.

Anyway, sugar has now been added to this nefarious grouping and with good cause –sugar is indeed a “bad boy.” Note, however, that sugar is not identified as a carbohydrate. It is, in fact, a simple carbohydrate. By definition, a sugar is either a monosaccharide or a disaccharide. There are three monosaccharides: glucose, fructose and galactose. Glucose is the most common and the most useful. It is easily used for energy. The body “prefers” to burn glucose and to conserve fat in storage for the coming famine. Don’t we all know this? If we become “sugar  burners” by grazing on carbs all day, we (our body, through the action of insulin) will not burn any of our stored body fat. As long as there’s sugar aplenty, it will pile more fat on to prepare for the “lean times” ahead. Winter is always coming, and foods become richer in sugar in the autumn. That’s the way the body is built! And that’s the way plants mature. It’s nature!

Fructose, in large amounts, is a “bad boy.” A chronic toxin, it isn’t burned like glucose. It is shunted to the liver to be detoxified. If the liver can’t handle the load, it converts it to fat by lipogenesis and we get NAFLD – nonalcoholic fatty liver disease. In 2008, 75% of all chronic liver disease was NAFLD (see here). How do you overload the liver with fructose? Drink sugary beverages, including fruit drinks. Sucrose, the common table (cane) sugar, is 50% fructose. Beet sugar is also 50% fructose. The sweetener used in American soft drinks, high fructose corn syrup (HFCS), which is cheaper to make than cane sugar, is 55% fructose, a prescription for NAFLD. And it’s not just beverages. See “Fructose in Foods” (The Nutrition Debate # 97 here) and then check your pantry against For my more biologically informed readers (nurses, CDEs, etc.), this PubMed abstract has great epidemiological statistics, including the prevalence of NAFLD among males.

So what’s wrong with the new triumvirate the government has created? If you believe that salt and solid fats are bad for you, then I suppose nothing. The government has invested billions in vilifying salt and fat; lumping sugar (sorry) together with salt and fat condemns it by association. The problem is that salt and solid fats are not bad for you, but excessive simple sugars are. And if you’re a type 2 diabetic, as I have been for 27 years, then anything that will become glucose in the blood (simple or complex carbohydrate or even protein) has to be eaten in limited quantities. But that’s my problem. For most of us, it’s enough to just eat reasonable amounts, and be aware of the effect they have on your overall health and wellbeing.

Again, from my perspective, I hew to the injunction first articulated for me by Kurt Harris, MD, in his Archevore Diet: avoid as much as possible the “NADs (Neolithic Agents of Disease): wheat, excess fructose and excess linoleic acids.” The latter are “the grain and seed derived oils (cooking oils): Eat or fry with ghee, pastured butter, animal fats, or coconut oil. Avoid temperate plant oils like corn, soy, canola, flax, walnut, etc. Go easy on the nuts, especially soy and peanuts.” For me, this generally translates to a different triumvirate: Wheat, corn and soy. And legumes, except young green beans. Harris adds:

Eat “whole foods from animals. Favor grass-fed ruminants like beef and lamb for your red meat. Animal fats are an excellent dietary fuel and come with lots of fat soluble vitamins. It can work very well to simply replace your sugar and wheat calories with animal fats. If you are not diabetic, you can eat more starch and less animal fat. A low carb diet can rely more on ruminant fat and pastured butter.”

And I add salt to most things I eat. An argument in favor of this practice is made by Michael Eades, MD, here, and Volek and Phinney in their excellent book, “The Art and Science of Low Carbohydrate Eating.” See the Nutrition Debate #74 here.
My bottom line: By all means, avoid sugar, but not salt and saturated fat. Both are good and necessary for your health.

Wednesday, June 12, 2013

The Nutrition Debate #116: “A Modifiable Risk Factor”

Letters to the Editor in the online edition of my Lancet subscription are usually interesting, and the 11 May 2013 letters were no exception. One on the subject of “Statins and Exercise Prescription” contained the comment: “Physical inactivity should be considered as a modifiable risk factor. Improving of population health should not simply be made the work of drug companies.” The authors of the article agreed. They replied: “…we concur with the eloquently stated and obvious truth that has been ignored by health-care professionals for many years: ‘improving of population health should not simply be made the work of drug companies.’” And I say, would that this were said of obesity and T2 diabetes as well!

Obesity is also “a modifiable risk factor,” and “improving of population health” – both through weight loss and the concomitant remission of type 2 diabetes – is achievable through modifying the macronutrient composition of the diet. It stands to reason, doesn’t it, that if carbohydrates increase the amount of glucose in the blood, particularly among the population that has become carbohydrate intolerant by reason of insulin resistance, then reducing the number of carbs in the diet will reduce the concentration of glucose in the blood? I mean, who doesn’t get this? And for our government to ignore this “obvious truth,” with what amounts to a “one size fits all” prescription in its Dietary Guidelines for Americans, amounts to gross negligence and medical malpractice on a humongous scale.

I say “concomitant” because remission of type 2 diabetes is a “phenomenon that naturally accompanies or follows” adoption of a Very Low Carb diet. That’s what happened to me. Eleven years ago my doctor, who had been trying to get me to lose weight for years, read about the Atkins Diet (Induction Phase) in a cover story in the New York Times Sunday magazine. The article, “What If It’s All Been a Big Fat Lie,” was written by the acclaimed science writer Gary Taubes. What attracted my doctor to the story, though, was the photo of the ribeye steak on the cover. As a cardiologist, he hewed to the company line to avoid saturated fats, but the visual image got his salivary juices started. So, he decided to try the diet himself. He lost 17 pounds in a month and decided to suggest it to me…to lose weight, not to treat my type 2 diabetes!

He did suggest, as an afterthought as we walked down the hall of his office to make an appointment for another visit in a month (to monitor me closely), that the low-carb diet “might be good for your diabetes too.” In retrospect, I have to say, how clueless could he be?!!!!! Anyway, he didn’t have to wait a month to see how the dramatic reduction in carbohydrates affected my diabetes; within a day, I was getting hypos. A hypo (hypoglycemia) is a dangerously low blood glucose condition which if not treated can lead to coma and death. When I felt the sweating, tingling and loss of mental acuity, I got up from my desk and went to the building lobby and bought and ate a Chunky candy bar at the newsstand. A bit of an overreaction, I admit, but this was my first ever hypo, and I was scared.

The next thing I did was call my doctor. I had never done that before either. He told me to immediately drop one of the oral anti-diabetic medications he had prescribed for me (Avandia). I did, but the next day the situation repeated itself. I bought and ate a Reese’s Peanut Butter Cup, as I recall, and called my doctor again. This time he said to cut by half the other two oral anti-diabetic meds I was on (at maximum dosage actually: 2000mg metformin and 20mg micronase, a sulfonylurea). I did, but the next day, or a few days later, I was still getting hypos (and eating Reese’s Cups), and I called him again. This time he told me to cut the dosage of both meds by half again.

Over the years (I have been doing this now for 11 years), as I adhered strictly to a Very Low Carb diet, I lost 170 pounds and  dropped the remaining 5mg micronase to 2½ and then to 1¼ (cutting the pill in half), and then went off it completely. I still take 500 metformin with supper, though, just to be sure no unwanted glucose in made in the liver.

Along the way, my blood pressure improved from 130/90 to 110/70 on the same meds. And my blood lipids dramatically improved. My triglycerides dropped from about 150 to about 50 and my HDL (good) cholesterol more than doubled from about 40 to about 80. My total cholesterol remained pretty constant (at about 215) while by LDL increased slightly (to about 130). But because of my very good triglycerides and HDL, my doctor advised me “your cholesterol results…are good” and “currently conform to (NCEP-3) guidelines.” I would say so! I would say most of his patients would love to have my lipid profile! And my fasting blood glucoses: average mid-80s. You would never know I was diagnosed diabetic 27 years ago.
So, obesity is “a modifiable risk factor” and the concomitant benefits of losing weight on a Very Low Carb diet are 1) remission of type 2 diabetes, 2) improved lipid profiles and 2) improved blood pressure. Indeed, “Improving of population health should not simply be made the work of drug companies.” We concur. This eloquently stated and obvious truth has been ignored by health-care professionals for many years. But, just as the obvious truth that eating fewer carbs will lower serum glucose levels in the insulin resistant patient, it is also a very effective way to lose weight in the patient whose glucose metabolism is normal. The weight loss occurs regardless. The blood lipid and blood pressure benefits will follow, even where blood glucose regulation is not required…”improving… population health” concomitantly. No Rx required!

Saturday, June 8, 2013

The Nutrition Debate #115: “My Doctor Never Told Me…”

Sound familiar? In a recent class conducted by a Certified Diabetes Educator, I heard the phrase “My doctor never told me…” a few times from newly diagnosed type 2 diabetics. It’s been years since I was diagnosed, but I sensed palpable anger among some of my classmates. They are still in shock and looking for help. They are trying to cope with how to live with this disease for the rest of their lives. And as I see it they are in denial about the how they came to be in this place, and they are trying to transfer responsibility of how it came about to others. But it’s not as simple as laying it off on your doctor.

I know this from my personal experience. I was diagnosed a type 2 at age 44 in 1986 by an observant physician who looked at some clinical signs (my weight, my fasting blood glucose, and my blood pressure), and decided to treat me for type 2 diabetes and hypertension. I don’t have the lab report from that doctor’s visit, or even remember his name, but this guy was ahead of the curve, and I am grateful for his treatment. He started me on oral medications for my incipient diabetes and frank hypertension. I was lucky. My doctor acted, proactively, on the clinical signs; he did not wait for my fasting blood sugar to be 140, the threshold for a type 2 diagnosis then (vs. 126 today). Neither do I recall what, if anything, he told me at the time about my weight, or my high blood pressure and elevated blood sugar. Whatever it was, I chose to ignore it. I just filled the prescriptions and took the pills as directed. A little later I had a physical at a local hospital wellness center and my weight was 300 pounds, my fasting blood sugar (with meds) was 108, and my blood pressure was still 174/124 (with meds).

Five years later I was living in a different city and had a different doctor. At my first visit to him (on my 50th birthday), I weighed 310 pounds (not much gain in 5 years), my BP was 130/112 (improved but still much too high), and my fasting blood sugar was 135 (out of control). He upped my diabetes meds, added a blood pressure med, and made an appointment for me to see his Registered Dietitian. For the next 11 years his treatments for blood pressure and blood sugar had some salutary effects. In 2002, my blood pressure was 140/90 and my fasting blood sugar was 81, but my weight had ballooned to 375 pounds. All his efforts over the years to get me to lose weight were fruitless. His dietitian, of course, had advocated eating a restricted calorie “balanced diet,” with regular exercise. What would you expect?! And that’s still the drill today.

Anyway, I can’t berate either of the doctors. They treated my hypertension and my type 2 diabetes. Both of them acted proactively and aggressively. What I’m saying is they did what they could. The fact that they did not know how to treat me for my obesity is not their fault. Besides, losing weight was not something they could do for me. That was my responsibility. I had to do it. But they, or at least the one I had been seeing from 1991 until 2012 (when he died), had been telling me to lose weight from the get-go, and he had done all he knew how to do and in his power, to get me to do it. He did tell me.

So, this is not a case of “My doctor never told me…” This is a case of my doctor didn’t know what to tell me. He didn’t know how, or he’d forgotten how, my physiology worked when my glucose metabolism was broken by insulin resistance. He didn’t understand that I am carbohydrate intolerant. He didn’t even know, but suspected and actually remarked that, if I lost weight by eating Very Low Carb (on the Atkins Induction diet that he suggested), that “it might even help your diabetes.” He just wanted me to try Atkins to lose weight. He never gave up on me. He had my diabetes “under control” (he thought, with progressively increasing amounts of oral antidiabetic medications), and he just wanted me to lose weight.

Well, little did he know (literally) how right he was. Of course, eating Very Low Carb did make it easy to lose weight, and it dramatically reduced, instantaneously, the need for oral antidiabetic medications. And, as I adapted to this Way of Eating, my HDL doubled, my triglycerides dropped by two-thirds, and after I Iost a lot of weight, my blood pressure dropped from 140/90 to at one point 110/70 and is now stable at 120/80 on the same meds. How did all this happen? Answer: I took responsibility for my own weight loss. My doctor suggested the diet, even if for the “wrong” reason, but after I started it, he just sat back and watched…and smiled every time he saw me. He never had to cajole or badger me again to lose weight.

Occasionally he would ask me, “How do you do it?” And I would just smile and answer, “It’s easy, doc! You just stop eating carbs. After a few days, you never feel hungry again.” And that’s the truth. You switch from being a “sugar burner,” with constant cravings for sweets and snacks, to being a “fat burner,” who lives off the fat you eat and the fat you’ve stored. Your body is “happy.” If you are not eating carbs, you need to eat some protein and fat at every meal. Allowing at least 14 hours between supper and breakfast will make for some serious fat burning in a “fasting state.” Your body will naturally switch to fat burning when the evening meal is fully digested and while you sleep. More details on how I eat here: #59:
Your doctor is not likely to tell you this (or approve, if you tell him). He isn’t trained in nutrition, and his advice would likely be wrong anyway. But the bottom line for both you and your doctor is results. If you adopt a Very Low Carb WOE, your results will tell that you’re doing it right. He may ask you how you did it, but he is more likely to say to you, “just keep on doing what you’re doing.” As mine did. “Just keep on doing what you’re doing,” he said. We both couldn’t be happier.

Wednesday, June 5, 2013

The Nutrition Debate #114: My Insulin-dependent Type 2 Pharmacist

When I was first diagnosed a type 2 diabetic in 1986, my doctor gave me a prescription for an oral anti-diabetic drug (Micronase, a sulfonylurea) and another for a meter and test strips. I asked the pharmacist, a friend, for his advice on which meter to buy. As we were looking over my choices, to my utter amazement he mentioned to me in passing that he was also a type 2 diabetic – in fact, an insulin-dependent type 2 diabetic.

In retrospect, I’m not sure what was so shocking to me: Dick wasn’t especially fat. He was overweight but not more than “normal” for someone of our age and generation. We were both in our mid-40s. Maybe what shocked me was that his disease had ‘progressed’ as far as it had; was ‘this’(becoming insulin-dependent) an omen of what was to come for me? Maybe that was Dick’s message to me. If so, it was a friendly warning, and it worked. I never forgot it.

After buying my meter and start-up supplies from Dick, I went into a mail order program for ongoing drugs and supplies and never had occasion to discuss the disease we shared again. Years later, Dick retired and moved to Florida. In 2010, I read in the local paper that, “after a long illness,” my former pharmacist and friend had died at age 72 (my age today). I don’t know this for a fact, but in all likelihood, Dick died of one of the complications of the disease we shared, type 2 diabetes mellitus.

I recall and tell this story because that is how I got into writing about type 2 diabetes. I was initially stunned that this disease had advanced in my friend to the point where he was insulin dependent. And today, knowing what I know and what I think he should have known (as I see it today), I am flabbergasted that Dick allowed his disease to progress to the point that he was insulin-dependent, and then to where he likely became a victim of one of its tentacles: the myriad causes of morbidity and all-cause mortality that are associated with “controlled” diabetes – “controlled,” that is, as defined by the medical establishment and our government. His loss was such a waste, and so unnecessary. With Dick, it was personal for me, but this is a tragedy of immense proportions being repeated all over the world today, and it doesn’t need to be

So, a few weeks after learning of his death, I was talking informally with the publisher of a local weekly newspaper who “knew” me, and I him, by reputation only. He knew me because he had read many letters-to-the-editor that I had written to another then-defunct weekly. He knew that I knew how to write, and he invited me to write “on any subject” for his fledgling newspaper. Thinking of my friend Dick, the insulin-dependent type 2 diabetic pharmacist who never should have allowed his diabetes to progress to that point, I said that I wanted to write about diabetes. I wanted to educate people so that they did not have to blindly follow the prescription for “control” that leads to more and more maxed-out anti-diabetic medications (up to 3 types, usually) – and then to becoming insulin-dependent – all the while allowing blood glucose levels, that are dangerously high on average, to course through the veins doing untold damage, until it is too late

There is an alternative. We know it today. To be fair, “low-carb” and Atkins were “out-of-favor” in 1986 when Dick was already insulin-dependent. But today, we (many practitioners and patients) know that “progression” is not the natural or necessary or inevitable course of type 2 diabetes, IF WE TAKE CORRECTIVE ACTION. Unless you have an enlightened physician, or you are willing to “go it alone,” that is an unlikely scenario. But, if you decide to take charge of your own health, and avail yourself of all the resources (on-line especially, but there are many good books as well), you can beat this thing. You can put your type 2 diabetes in remission. And along the way, you will lose a lot of weight easily and greatly improve other health markers such as blood lipids (cholesterol) and high blood pressure, as you lose weight.

As my regular readers know, eleven years ago I was maxed out on two anti-diabetic medications and starting a third and had A1c’s in the 8s. I was also, at 375 pounds, morbidly obese (BMI=52), had borderline cholesterol, and was taking 3 BP meds and was still poorly controlled. Today, my A1c is 5.6, I weight 235 (BMI=33), I’ve doubled my HDLs and cut my TGs by 2/3rds, and my BP has dropped from 130/90 to 120/80 on the same meds. And I feel great. I am healthier today at 72 than I was when I retired 10 years ago. THE SIMPLE REASON: I changed from eating a “balanced diet” to a “Very Low Carb” diet.

The key to a healthy body is what you put into it. Whole foods are good, in fact essential, to transforming our health. If you are a little overweight, with marginal cholesterol, or mildly elevated blood pressure (symptoms of Metabolic Syndrome), you may well be pre-diabetic, or even an undiagnosed full-blown type 2. Ignore carbohydrate intolerance at your peril. You can live and eventually, but prematurely, die a diabetes related death, as Dick did, if you continue to eat a “balanced” diet, or you can wake up and do something about it. I did.
Do you track your blood sugar levels as a pre-diabetic or diabetic? Have you experimented with reducing the carbs in your diet?

Saturday, June 1, 2013

The Nutrition Debate #113: What are We, Chopped Liver?

I have adopted this blog title from the Jewish mother-in-law who asks, “What Am I, Chopped Liver?” If you are unfamiliar with the question, the Ask the Rabbi website opines, “As far as I know, the origins of the phrase are not Yiddish; I believe the phrase was originally coined in America. Being that chopped liver was always considered a side dish and not a main course, the phrase is used to express hurt and amazement when a person feels he has been overlooked and treated just like a ‘side dish.’”

I have appropriated the phrase for my purposes at The Nutrition Debate to make the point that WE, THE TYPE 2 DIABETIC PATIENT, are left out of the discussion, and the treatment plan, by the medical community. We are treated like a “side dish.” And it’s our own fault. We have left our health care to “the professionals.” After all, they’re the experts. They went to school to become our health care professionals. They go to annual conventions to get continuing education from doctors paid by the pharmaceutical industry to tout their newest products (and play a round or two of golf). They get visits at the office from pretty young things who give them free samples of BIG PHARMA’s latest FDA-approved drugs. Get the picture?

We are also impressed with how, when they speak, they speak with such authority on every subject related to our health. If you’re lucky, that is. Some doctors play it very close to the vest. They say very little. They’ve got so little time. But, as far as I’m concerned, the big problem is that they’ve got the wrong message, at least with respect to diet. But they’re got their backs covered. The USDA, representing BIG AGRIBUSINESS, tells them it is okay for us to eat 50% to 60% of our diet in the form of highly processed carbohydrates and sugars. And NOT to eat dietary cholesterol and fat, at least not saturated (solid) fats. Well, they’ve got it exactly backwards, haven’t they? It’s the liquid fats (oils) such as corn oil and soy bean oil – the damaged, oxidized Omega-6 industrial oils - that are killing us. See the USDA/BIG AGRIBUSINESS connection?

My latest favorite quote, discovered on Beth Mazur’s blog, Weight Maven, is from Wendell Berry:

“People are fed by the FOOD industry, which pays no attention to HEALTH…and are treated by the HEALTH industry, which pays no attention to FOOD.”

The disconnect here really resonates with me. I’ve re-read it many times, but only today did I see a syntactical thread that makes these opposites the same: Both clauses use the passive voice. They both use a form of the helper verb “to be” (“are”) with a past participle (”fed” and “treated”). The passive rather than active voice is used where the emphasis is meant to be placed on the subject. The recipient of the action (“People”), rather than the “agent” (performer) of the action, is the subject of the sentence. Wikipedia has a good explanation of the use of the passive vs. the active voice in English.

“The principal criticism against the passive voice is its potential for evasion of responsibility. This is because a passive clause may omit the agent even where it is important… However, the passive can also be used to emphasize the agent, and it may be better for that role than the active voice, because the end of a clause is the ideal place to put something you wish to emphasize, or a long noun phrase, as in the examples given in the previous section.”


“Don't you see? The patient was murdered by his own doctor!” (Wikipedia’s emphasis)


Don’t you love it? You can’t make this stuff up, folks. That’s really the Wikipedia example for good use of the passive voice.

So, putting these two things – dichotomy and passive voice – you get both the mutual exclusivity and contradiction required for dichotomy with the emphasis on the agent of the action in UPPERCASE at the end of each long phrase. It takes good writing skills to make memorable quotes, and Berry has them. Thanks, Beth, for bringing him to my attention.

I’m afraid the “fix” for the problem that Berry points out so eloquently is out of reach. The relationship between the FOOD and HEALTH industries, and the central and terribly misguided role of government in both, is beyond redemption.

The only “fix” that I see that will affect our personal health and wellbeing is to extricate ourselves from the passive voice. We can do that by not “being fed” and not “being treated.” We can take the active role. We can feed and treat ourselves. When we reverse these positions, we no longer are beholden to the FOOD and HEALTH industries to tell us what to eat and how to take care of ourselves.  We will no longer be “a person (who) feels he has been overlooked and treated just like a ‘side dish.’” We will no longer be “chopped liver.”

Liver as a food, on the other hand, is a highly recommended food. It is a staple of the Perfect Health Diet, as are other organ meats. Chicken liver, beef liver, or original goose liver (pate or chopped) are all perfect foods to be enjoyed once a week.

Does anybody have a favorite liver recipe that they would like to share? Comments are open.