Saturday, March 29, 2014

The Nutrition Debate #196: The Diagnostic Power of A1c vs. Fasting Glucose

There have been scads of scientific papers published on this subject. I promise not to cite any of them in this piece. Instead, I will offer the example of two people’s A1c’s and fasting glucoses to illustrate the wisdom of using A1c rather than fasting glucose in diagnosing incipient or “incident T2DM.”

Until a few years ago the ADA official criterion for diagnosing T2DM was 2 consecutive fasting glucose tests (on separate office visits) of 126mg/dl. At the time of the introduction of the 126 value, the ADA also guided physicians that a fasting value of 100-125mg/dl was to be considered “pre-diabetic.” A “normal” fasting glucose was then 70-100mg/dl.

The A1c became increasingly the diagnostic tool of choice in 2009, although the fasting glucose test, while seriously flawed, particularly for middle aged women, is still widely used. But first, what is the A1c test? Officially, the hg A1c (hemoglobin A1c), is a measurement (percent) of the glucose on the surface of red blood cells that are continuously circulating in your body. Since red blood cells live about 2 to 3 months before they die and your bone marrow replaces them, the test is then a measurement of the level of glucose circulating in your body 24/7 during that time period. It’s like wearing a “monitor.”

The idea is that the A1c test will thus captures the postprandial spikes (called “excursions”) that your blood sugar takes after eating. Everyone’s blood sugar surges after eating. As food digests, to the extent that there are carbohydrates in the food, they will break down to glucose and will be transported, by insulin secreted in the pancreas for the purpose, to the cells. That is how your body gets the (sugar) “energy” from food to, and hopefully into, your cells. In people with a “normal” metabolic process, the sugar moves from the blood into the cell and, after a couple of hours, when all the carbs have been digested, then circulated and “taken up,” the level of glucose (and insulin) in the blood returns to where it began.

However, in people whose metabolism has developed a specific “dysregulation” called “insulin resistance,” the surface of the destination cell resists the up-take of insulin (and the glucose it’s transporting), and the level of both insulin and glucose in the blood remains “elevated” (and you get hungry and tired and lack energy, literally. So, these people, who are developing insulin resistance, will have a higher A1c, corresponding to the higher blood glucose and insulin that is circulating for hours/days and the worst (and increasingly common) case, continuously, so long as you regularly eat carbs.

So, insulin resistance is the mechanism that starts T2DM. I describe the “history” of T2DM here. It leads to your pancreas making more insulin to overcome the resistance, eventually wearing out the beta cells where it is made. The longer and the more your insulin resistance persists, the more your pancreas’ ability to make insulin will be lost, forever.

Now, the two examples I promised you: Person #1 is the email correspondent referred to in The Nutrition Debate #195. He was diagnosed a type 2 diabetic about 9 months ago (he doesn’t say “how” exactly: A1c, or fasting glucose, or both); in response, he changed his diet (“just stopped eating bread, potatoes, pasta and ice cream”). Now, I’m thinking, that’s not an “extreme” or “very low carb” diet. The result: nine months later he had “lost 20 pounds” and his “A1c (was) totally normal (5.7) and fasting glucose (was) at 100-105 over 3 blood works.” To be clear, he is still a type 2 diabetic. He still has insulin resistance, and probably a slightly damaged pancreas, but he has learned how to control his blood glucose, and thus his diabetes, through a moderately low carbohydrate diet. His A1c, at 5.7%, is “borderline.” You could say (this is something of a “conceit”) that his diabetes is “in remission,” but it will be so only so long as he stays “moderately low carb.

Person #2 (lab tests read to me over the phone): fasting glucose 100; A1c test = 5.0mg/dl. (Interestingly, the range on this lab test, performed by the VA, was 70 to 110mg/dl. vs.70-100 on Quest, and other labs. Hmmmm… Is this the “new normal” to reflect not what is “normal” but the trend toward a higher population average as we lemmings follow our government’s dietary advice? But I digress.) Note: this “patient” has the same blood glucose value (+/-100mg/dl), but a “normal” A1c (for a 70yo male) of 5.0mg/dl. This person eats a typical American “balanced diet,” between 40 and 60% carbohydrate, and is not diabetic or even pre-diabetic, whereas the other person definitely is, even though their fasting glucoses are the same.

Thus, the A1c test is what differentiates #1 (controlled diabetic) from #2 (non-diabetic). And #1 has learned to control his diabetes through diet alone. That’s what keeps his A1c in the clinically “non-diabetic” range, so long as he stays moderately low carb. I hope this is instructive, for all the “pre-diabetics” and “newly diagnosed type 2s” out there. Watch what you eat!

Wednesday, March 26, 2014

The Nutrition Debate #195: “I did it myself, with no help from doctor”

The other day I had an email exchange with someone I’ve never met. It began like this:
“I was diagnosed with Type 2 Diabetes 9 months ago. Dr gave me 3 months to see what a diet might do before putting me on meds. Just stopped eating bread, potatoes, pasta, and ice cream. Been 9 months, lost 20 pounds, A1C totally normal (5.7) and fasting glucose at 100-105 over 3 blood works.”
I said: “Good story. And your ‘diet’ doesn't sound too restrictive. That's good. One thing I'd like to know is WHO told you to try ‘low carb.’ Was it someone specific (e.g. your doctor), or was it just what you've been hearing and reading increasingly in the media these days. Your answer is important to me.”
He replied: “I did it myself with no help from Doctor. Just made sense since I was a big white carb eater and knew that was a big sugar source.”
There, you see. I’m not that crazy fanatic that you all think I am. And youdon’t have to be one either. Here’s this regular guy, with a regular work and family life, who saw what had happened to him (he was “diagnosed”), he saw what he was doing (he was a “big white carb eater”), and he saw where it was leading (being put on meds by his doctor).
So, he decided to DO something about it. He “just stopped eating bread, potatoes, pasta and ice cream” for 9 months and lost 20 pounds! And his A1c’s returned to “normal” (clinically “non-diabetic” on the ADA scale), and his fasting blood glucose just barely inched into the low end of the pre-diabetic scale “over 3 (successive) blood works.” That, as I said, is a “good story.” It could be yours too, if you did the same.
Notice, though, that his doctor didn’t give him orders to eat low carb. He just gave him 3 months to get his act together before putting me on meds.” I think this is typical. In fact, I think that’s the ADA protocol: Try “lifestyle changes” (diet and exercise) first, and then start a regimen of meds. The problem is thatthe ADA medical protocol doesn’t advocate the right dietary changes.Surprised? No. Doctors aren’t trained in nutrition. But the ADA’s newNutritional Guidelines” (#155, #156#157)prepared by an enlightened group of the ADA’s RDs and CDEs, however, no longer prescribe a “one size fits all” approach.  So, your doctor is now free to sanctionand even advocate, low carb lifestyleif she wants to.
In my opinion, though, It’s immaterial. What your doctor wants to see areresults. Good labs: A1c’s and fasting blood glucose, and other markers, like weight, waistline and BMI. And blood pressure. She is probably also testingyour cholesterol, and if she is paying attention to more than total cholesterol and LDL, she will note improvements in HDL and triglycerides, as well as inflammation markers like hsCRP. She will also likely test kidney and thyroid function annually.
So, how complicated is this? To quote my correspondent: “(It) just made sense since I was a big white carb eater and knew that was a big sugar source.” What did he have to do to turn his health around? He Just stopped eating bread, potatoes, pasta, and ice cream.” In nine months he lost 20 pounds, just doing this (I take him at his word). But whatever, the important thing is, he said“I did it myself with no help from Doctor.” I would argue, though, that the doctordid help. He made an explicit threat: “Dr gave me 3 months to see what a diet might do before putting me on meds.
That kind of motivation (coercion?) works for many people: the kind of people who want to have control over their own lives, who don’t see themselves as victims, who don’t want to be dependent on others or other things. I rememberthinking when I was in my early 40s that I would never be someone who had to take medications or supplements every day for the rest of my life. LOL. Such is life. We are invincible, until we are no longer invincible. But as long as I can, I want to be able to say, as my email friend” (and new reader) said, “I did it myself…” I say, props to you!
Note to regular readers: With this post (#195) I will begin to post shorterentries to my blog, still twice a week. They will generally be 800 to 850 wordsin length instead of the 900 to 1,000 words they have been for the last couple of years. I am not getting tired of writing; I just want to try this out to see if myon-line readership increases. It will also conform my column to a more typicallength for print publication, as a newspaper publisher once told me. It’s just an experiment.

Saturday, March 22, 2014

The Nutrition Debate #194: Live Fermented Foods

Okay, I’m not an “expert” on this class of foods, but I find the subject interesting and increasingly in the news. Besides, if the purpose of The Nutrition Debate is to inform the reader, and if along the way the writer learns a little, that’s good too. We are open to new ideas, and new foods, in our unending pursuit of healthy eating and “the truth.” We hope you are too.

Generally, we have an idea of what fermented foods are. There are hundreds of varieties, made by traditional methods for thousands of pre-refrigeration years. The Wikipedia listing for “fermented foods” has hundreds of pages of every kind of fermented food imaginable from cultures all over the world. American readers will be familiar with some: yoghurt, sauerkraut, salami and other sausages, wine, beer, cheese, sour-dough bread, soy sauce, salsa, kefir, natto and my current favorite kim chi, a spicy Korean cabbage side dish.

The process also varies considerably and oft times involves lacto fermentation with salt (in brine); however, today many of the foods mentioned above are made by modern methods that do not involve fermentation. In which case, a listed food made from pasteurized products is not “live.” Pasteurization kills the pro-biotic friendly bacteria that live fermented foods contain. To get the benefits of live fermented foods, you must look for the words “live” or “contains live cultured products.”

So why do we want “pro-biotic friendly bacteria” in our gut? Mark Sisson, of Mark’s Daily Apple and Primal Blueprint (PB) fame, offers a good primer in his “Definitive Guide to Fermented Foods” here. Even though his Primal diet (similar to Paleo) excludes Neolithic foods like dairy, grains and soy, he explains that with “proper fermentation,” such foods become tolerable. His list of “tolerable” (for those who do not follow a strict Primal Blueprint) includes “aged raw-milk cheese” (for the vitamin K-2), real, long-fermented, sour dough bread, and traditionally fermented soy sauce or natto (also for the K-2).

Sisson says that fermentation can render previously inedible or even dangerous foods edible and somewhat nutritious. “The lectins, gluten, and phytates in grains, for example, can be greatly reduced by fermentation,” he says.  Again, he’s not advocating these foods; he simple wants to explain how fermentation makes these foods “tolerable for PBers.”

Another resource I checked out is, the site of a high-profile osteopathic physician (DO) and web entrepreneur. The following excerpt from an interview with a British neurologist, in Dr. Mercola’s words, tells the story “at-a-glance.”

“The importance of your gut flora and its influence on your health cannot be overstated. It's truly profound. Your gut literally serves as your second brain, and even produces more of the neurotransmitter serotonin—known to have a beneficial influence on your mood—than your brain does. Your gut is also home to countless bacteria, both good and bad. These bacteria outnumber the cells in your body by at least 10 to one, and maintaining the ideal balance of good and bad bacteria forms the foundation for good health—physical, mental and emotional.”

But my favorite recent piece on “live fermented foods” related to another subject of interest to me: Chronic Systemic Inflammation (The Nutrition Debate # 187 here). It was written by Dr. Art Ayers, whose blog Cooling Inflammation was a major resource for #187. The piece is titled, “Gut Flora Risk and Repair.” I suggest you stop reading this column and click here now. It is the best information that I have found on the subject.

My interest in gut health was probably piqued by my editor, whose husband has severe gluten sensitivity. They participated in the gut biota testing program offered by the American Gut Project. (  But I also recall that, when I visited the emergency room a few years ago for some reason, the “attending” MD “prescribed” a probiotic to counter the antibiotic he wrote a script for, and I took notice. Previously, although I had heard of them, I had no idea that they should be taken seriously. I do now. Again, please stop reading this now and click on a link in the paragraph above and read that piece by Dr. Ayers. You will gain a new perspective that you will take with you for a lifetime.

Anyway, as kim chi is my favorite live fermented food for now, I’m lucky that I can buy 2 homemade types from a local Korean green grocer in a town near my hometown. Curiously, there is none offered in the large farmers’ market in Ft. Pierce that I visit every week in winter, but I found some in the Publix supermarkets that are ubiquitous in Florida. They’re in the refrigerated case near the fresh vegetables (think horseradish). I haven’t found any “live” sauerkraut though; it is all pasteurized, as I suspect all the yoghurt is in the dairy case. I wonder if they have any raw milk cheeses.

The regulatory environment is improving in some places, however, thanks to the efforts of organizations like the Weston A. Price Foundation. Raw milk can now be sold in New York. And the vendor next to my eggs/organ meat vendor (who also sells grass-fed, grass finished meat) is hopeful that Florida will soon allow it too. And the organic, free-range chicken vendor is hopeful too. I wonder why there are no live fermented food vendors. Maybe veggies are just too inexpensive, or maybe they take too long to ferment, or maybe they are just so easy to make yourself that everyone is making their own at home! (If you’d like to try it, check out Cultures for Health, a commercial website. My editor says the sour cream is really very good). And she has found live kraut, pickles, and other veggies at Whole Foods and several natural food stores in Florida.
But, if you’re fermenting in warm weather, it’s a little tricky, and the food can go past the tasty stage really fast. When you make or buy fermented foods, you need to refrigerate it to slow the process down so you can eat it while it’s still at its best.

Wednesday, March 19, 2014

The Nutrition Debate #193: “We never changed our mind,” he said.

A recent story in the Los Angeles Times headlined, “High-protein diets: Bad for the middle-aged, good for the elderly.” The last sentence of the piece concludes, “But over 20 years of research linking heavy protein consumption to diseases of aging, eventually to higher IGF-1 levels, he said, ‘we never changed our mind’: Americans’ protein-packed diets ‘are hurting them in a major way.’” This “research” is just another example of “sort-of-science,” an aphorism I attribute to Gary Taubes, and adroitly used in his recent New York Times op-ed described in more detail in The Nutrition Debate #192.

The reporter, Melissa Healy, and the journal Cell Metabolism, where the “research” originally appeared, are also complicit in this “sort-of-science.” Quoting from The Nutrition Debate #192 (and the Taubes’ op-ed):

“The scientific method requires that a hypothesis be rigorously tested, with a skeptical bias, and then ‘the proof’ replicated. Such clinical trials to ‘prove’ that dietary fat caused heart disease, were necessary, scientists acknowledged, but could not be undertaken, for reasons he gives. ‘Since then,’ Taubes wrote, ‘advice to restrict fat and avoid saturated fat has been based on supposition about what would have happened had such trials been done, not on the trials themselves.’

Taubes continues, ‘Nutritionists have adjusted to this reality by accepting a lower standard of evidence on what they’ll believe to be true. One lesson of science, though, is that if the best you can do isn’t good enough to establish reliable knowledge, first acknowledge it – relentless honesty about what can and cannot be extrapolated from data is another core principle of science – and then do more, or do something else. We have a field of sort-of-science in which hypotheses are treated as facts because they’re too hard or expensive to test.’ (Emphasis mine.)

The problem with this “research,” in general is that it is from a “large-population study” (“20 years of research”) and the findings are all “supposition about what would have happened” if a randomized controlled trial of the subject population had been done. The evidence of this is clear to the discerning reader, as I will illustrate shortly. Quoting from #192 again:

This “research is of the kind called “observational studies,” wherein what the researchers do is “observe populations for decades, document what people eat and what illnesses beset them, and then assume that the associations they observe between diet and disease are indeed causal,” to quote Taubes again from his NYT op-ed. Taubes continues: “– that if people who eat copious vegetables, for instance, live longer than those who don’t, it’s the vegetables that cause the effect of a longer life. And maybe they do, but there’s no way to know without experimental trials to test the hypothesis.”

The associations that emerge from these studies used to be known as “hypothesis generating data,’ based on the fact that an association tells us only that two things changed together in time, not that one caused the other. So associations generate hypotheses of causality that then have to be tested. But this hypothesis-generating caveat has been dropped over the years as researchers studying nutrition have decided that this is the best that they can do,” Taubes concludes kindly.

I would not be so kind. I would conclude, cynically, that the “scientists” (and the reporters, et. al.) have another agenda: in this case, to push a plant-based diet. In the LATimes piece it is patently transparent: “But the source of the protein mattered a great deal: for those whose sources of protein were heavily plant-based, nuts and legumes – the increased risk of dying of cancer declined and the increased risk of all-cause mortality disappeared altogether.”

The reporter, in case you wondered about her objectivity, further extends the “associations” of the researcher’s “sort-of-science,” piling on with this “observation”: “The findings of Longo’s team are in line with mounting research on the hazards of heavy consumption of red meats and the protective effects of plant-based nutrients.” Could she be a vegan?

To illustrate the language of “supposition,” here are some “key words” from this piece: “appears to be,” “more likely,” “less likely,” “coaxed the researchers,” “clues outside the lab,” “linked to” “tended to,” “are in line with,” “comparable to,” “promoted,” “common to,” and the granddaddy of them all, “associated with.” The “links” are to dire comparisons and outcomes: “the effect of smoking cigarettes,” “rapid cancerous growth, “increased risk of death,” and “all-cause mortality.”

So, where does all this agenda-based science lead us? To confusion, for the uninitiated, which is most of the health news- consuming public. Advocacy science is not science at all. Studies of hypothesis-generating data produce more hypotheses, as they should, Taubes says. But the public suffers, asking the perennial question, “Whom am I to believe?” For me, when I browse the science news and journal articles, and digests of so-called science designed for the medical profession, I take all such observational studies with a heavy dose of salt (which I like anyway). Increasingly, I tend to not even bother reading them. I might skim an abstract here and there, but, in doing it, I’m acquiring better and better speed-reading skills.

I myself, obviously, am also an advocate, and I too have a bias. I have to wonder how Gary Taubes maintains his objectivity, given that he also admits to a bias. He concludes in his NYT op-ed that “most of us are surely eating too much of something (My vote is sugars and refined grains; we all have our biases).” But I suspect that he is being a bit disingenuous, (or well edited by the NYT). Somehow he manages to have it both ways at the end of his piece: “Making inroads against obesity and diabetes on a population level requires that we know how to treat and prevent it on an individual level.” That’s his pitch to individual readers, guided by hubris and his own just-stated bias? Then to scientists he says, “We’re going to have to stop believing we know the answer, and challenge ourselves to come up with trials that do a better job of testing our beliefs.” In other words, leaving your mind open, rather than “never changing” it. I’m doing my best to keep an open mind.

Saturday, March 15, 2014

The Nutrition Debate #192: Climate Change and The Nutrition Debate

It is ironic, and at the same time amusing to me, that many in the climate change community, who fashion themselves as “sophisticated, fact-based practitioners of science,” would deny dissent from skeptics yet embrace the alternative view of nutritional science espoused here at The Nutrition Debate. The quote above is from a recent on-line opinion piece in SFGate by Debra J. Saunders. The San Francisco Journal on-line article is titled, “Climate Change Consensus, no dissent allowed.”

Saunders quotes CNN’s Brian Shelter that “some stories don’t have two sides.” There’s no need to present climate-change dissenters, he argued, because “between 95 percent and 97 percent of scientists agree that climate change is happening, now, and it’s damaging the planet, and that it’s man-made.” She also reminds us that, “Last year the Los Angeles Times revealed it won’t print letters that deny a human cause to global warming.” Well, I guess that finally settles that argument.

The SFGate piece continues, “A 2013 British study of peer-reviewed papers found that of the 33 percent of papers that took a position on global warming, 97 percent endorsed the “consensus” position. A Google search on “global warming consensus” produced 15,700,000 hits, no doubt 97 percent in agreement with the “happy conceit.” This is what is known as “scientific consensus.” Everybody piles on to the “accepted” wisdom, and that constitutes “scientific proof.”

A commenter noted that One Hundred Authors Against Einstein, a book published in 1931, said the Theory of Relativity is wrong. When asked to comment, Einstein replied that to defeat relativity one did not need the word of 100 scientists, just one fact. Another commenter recalled Nicolaus Copernicus who in 1543 published Revolutions of the Celestial Orbs, a treatise that put forth his revolutionary idea that the Sun was at the center of the universe and that the Earth – rotating on an axis – orbited around the Sun once a year.” We all know what happened to him and his revolutionary ideas.

In September 2012, Peter Attia, MD, announced the launch of the Nutrition Science Initiative. Co-founded with acclaimed science journalist Gary Taubes, Attia described the venture as a “journey to find the truth.” He quotes 19th century physicist John Tyndall, referring to scientists who follow evolution as a guide, “They have but one desire – to know the truth. They have but one fear – to believe a lie.” His piece is also an encomium to the physicist Richard Feynman who said, “It doesn’t matter how beautiful your theory is, it doesn’t matter how smart you are. If it doesn’t agree with experiment, it’s wrong.”

More recently (Feb ’14), Taubes wrote yet another New York Times op-ed, “Why Nutrition Is So Confusing.”  He asks, is the failure of our New Year’s resolution to lose weight “a failure of willpower or of technique?” “The health of the nation,” he says, “may depend on which is the correct answer.” There are two “conflicting observations” at play here, he notes: “We know how to eat healthy and maintain a healthy weight,” or “something about the conventional thinking is simply wrong.”

Since 1960, he says, 600,000 articles (and tens of thousands of diet books) have been published. “It would be nice to think that this deluge of research has brought clarity to the issue. The trend data argue otherwise. If we understand these disorders [i.e., obesity and type 2 diabetes] so well, why have we failed so miserably to prevent them?”

The unfortunate reality, Taubes says, is that, “Type 2 diabetes is caused or exacerbated by obesity, and obesity is a complex, intractable disorder. The more we learn, the more we need to know,” and the research to date is “the noise generated by a dysfunctional research establishment.” (This is Taubes’s not-so-subtle pitch for support for his “baby,” the Nutrition Science Initiative, linked to above, that he and Dr. Attia started in 2012.

The rest of the piece in the NYT is an explanation of how long-term clinical trials, especially the gold standard, randomized controlled trials, are prohibitively expensive and exceedingly difficult. He jibes that “no pharmaceutical company stands to benefit” and further laments “prospective sources of funding are limited…”particularly when we insist the answers are already known,” which brings me back to the climate change dissent point wherein I began…and to the search for truth.

The scientific method requires that a hypothesis be rigorously tested, with a skeptical bias, and then “the proof” replicated. Such clinical trials to “prove” that dietary fat caused heart disease, were necessary, scientists acknowledged, but could not be undertaken, for reasons he gives. “Since then,” Taubes wrote, “advice to restrict fat and avoid saturated fat has been based on supposition about what would have happened had such trials been done, not on the trials themselves.”

Taubes continues, “Nutritionists have adjusted to this reality by accepting a lower standard of evidence on what they’ll believe to be true.” “One lesson of science, though, is that if the best you can do isn’t good enough to establish reliable knowledge, first acknowledge it – relentless honesty about what can and cannot be extrapolated from data is another core principle of science – and then do more, or do something else. We have a field of sort-of-science in which hypotheses are treated as facts because they’re too hard or expensive to test” (emphases added by me). Wow! I love that.
But Taubes isn’t ambiguous about what his personal bias is (He says, “My vote is sugars and refined grains; we all have our biases.”)  I admit to the same bias, and will continue to test my beliefs in my ever vigilant search for the truth. Stay tuned.

Wednesday, March 12, 2014

The Nutrition Debate #191: Insulin-Dependent Type 2s

Okay, this is going to be an opinion piece. I admit to bias, but I will strive to present the subject in a factual way. That being said, I am not a doctor, and I have no formal medical/scientific training. I am a type 2 diabetic with almost 28 years of personal experience, all of which gives me certain bona fides (and contributes to my bias). In fact, the revelation that my pharmacist was an insulin-dependent type 2 diabetic, and had died prematurely some years ago, was the impetus for me to start writing “The Nutrition Debate.” I view his death as a tragedy and totally unnecessary.

First, a little background about insulin and diabetes. There are basically two types of diabetes: Type 1 and Type 2. Type 1 is an autoimmune disease. The onset usually occurs in childhood, permanently destroying the body’s ability to make insulin, a key hormone produced by the pancreas. Until the discovery of man-made insulin in 1922, most Type 1s didn’t live long. The only medical treatment was a strict medical “ketogenic diet” in which the patient’s food intake was 90%+ fat.

Type 2 diabetes, formerly called “adult onset diabetes” but now found in children (scary read here), is a disorder of metabolic disregulation resulting from insulin-resistance at the cellular level. The pancreas thus overworks to produce insulin. It is diagnosed by testing blood glucose since one of insulin’s key duties is the transport of glucose, the molecules that originate in food as complex carbohydrates and simple sugars. If the cells are resistant to insulin, glucose can’t get into the cells and the level of glucose in the blood rises. Hence, the diagnosis of type 2 diabetes is made with an elevated fasting blood glucose or an elevated A1c test (a 3-month “average” of circulating glucose as measured on red blood cells).

Type 2 diabetes is often suspected in overweight and obese individuals. Why? Because insulin stores fat.  When we consume carbohydrates, the body chooses wisely to use the exogenous “sugars” of foods (that all convert to glucose) that we catch or gather (or buy) as its primary energy source. It conserves energy in the form of body fat for use when those foods are not available – think winter and very early spring. So, when we eat foods that include carbs, we will burn sugar for energy and not body fat. It’s a brilliant design, anthropologically thinking, since fat is a very good storage vehicle. It is more than twice as dense in energy value (9 calories per gram vs. 4 calories for either protein or “sugar”).

When a doctor determines a patient is a type 2 diabetic, the conventional medical treatment is to 1) council weight loss via diet and exercise (lifestyle changes), and 2) prescribe an oral medication to help. If the patient is not successful in losing weight, which is, after all, an effect – not a cause – of type 2 diabetes, the doctor adds another oral med and then maybe a 3rd to the “cocktail.” More recently, injectable medications (GLP-1s) are sometimes prescribed. Traditionally, though, insulin injection has been reserved by most patients and their doctors as a “last resort” due to stigma.

Many (this suggests it is 26%) patients who are treated using the conventional treatment standards for blood glucose control, which are much too lax, will eventually progress to becoming insulin-dependent type 2s. Conventional treatment standards don’t call for the dramatic diet changes that can stop the progression of the disease.  The medical community acknowledges this. They consider type 2 diabetes a progressive disease, with a decrease of 10 years in the expected lifespan for T2 adults and 15 years for T2 children, compared to non-diabetics. See this link to a paper in the journal of the ADA.

Alternatively, some doctors today (and others, for many years, like Richard K. Bernstein) have developed a protocol to prescribe insulin as a first treatment upon diagnosis of type 2 diabetes. The thinking is that 1) it will spare the pancreas from further destruction of the beta cells that create insulin, and 2) it will result in much, much better glucose control.

Normalized glucose control is essential to reduce the complications of long-term elevated blood glucose levels: peripheral neuropathy (nerve and microvascular damage), commonly resulting in gangrene and amputations of limbs; retinopathy (damage to the blood vessels of the retina, resulting in blindness); and nephropathy, resulting in end-stage kidney disease.

Insulin therapy for type 2 diabetics usually begins with a regimen called “basal” insulin, injected once or twice a day. To this is added “meal time” insulin in which you, the patient, estimate the amount of carbohydrate you will eat at a meal and then inject an appropriate dose 20 minutes or so before sitting down to each meal. Some people now wear an “insulin pump” in which a needle, embedded under the skin, injects an amount that you determine by making an adjustment on the pump.

Dr. Bernstein, who is a type 1 diabetic himself, says that everyone is entitled to “normal blood sugar.” His own A1c’s are in the 4s, which is truly remarkable, but he has studied this subject, in the very real sense of the word, for half a century. He “eats to the meter,” because he has to, as a type 1; his body makes no insulin - he must inject it! And he manages his type 1 very well by eating small numbers of carbohydrates and consequently only needing to inject small amounts of insulin.

If you are a type 2, what does this suggest for you? If your pancreas still makes insulin, couldn’t you do the same? Eat small amounts of carbohydrates and only need to use small amounts of your body’s precious supply of insulin? And by avoiding glucose spikes, protecting your beta cells from further destruction.  I say you can. Eat fewer carbohydrates. Reduce your body’s reliance on your weakened pancreas to avoid the comorbid complications of heart attack, stroke and Alzheimer’s. Preserve and protect your feet, your vision, and your kidneys. Reclaim your life expectancy.

Saturday, March 8, 2014

The Nutrition Debate #190: “Can (sic) I ask you a personal question?”

I had walked up to the bar at the jazz club to get a refill of my glass of red wine, and a “young” woman (in her 40s), sitting at a nearby table with her mother and her mothers friend, struck up a conversation with me. I engaged the brazen hussy, gave her my “business” card (The Nutrition Debate) and began almost immediately to proselytize about my Very Low Carb lifestyle. She indulged me, with indifference bordering on insouciance, and then said, “Can I ask you a personal question?”

Two thoughts crossed my mind immediately: How much had she had to drink? And why am I feeling on the defensive? Anyway, I said “sure.” It could be interesting, and I (as my regular readers here know) do not guard my health and medical information. I am not only willing, I am anxious to share the “good” news (and the bad, if it should be) about how changes in what I eat over the last 12 years have transformed my health.

I wont repeat all the statistics here; I will just say (for new readers) that I have been a type 2 diabetic for 28 years, and 12 years ago I weighed 375 pounds. After changing what I ate from the Standard American Diet (“balanced” and very high in carbs), I lost 170 pounds, my blood glucose went from “uncontrolled” on 3 oral meds to well-controlled (“non-diabetic”) on a minimum dose of Metformin. My blood lipids (cholesterol panel) also improved very dramatically, my blood pressure improved (on the same meds) and my inflammation markers also dramatically improved. So, I was ready. Ask away!

To my surprise, she asked, “How can you drink on your diet?” Relieved, I went into a boring explanation of how many carbs are in 2 glasses of wine (my “limit”), how much ethyl alcohol, etc. It must have sounded like a rationalization, but she was satisfied. Once again, however, like so many other questions I have fielded over the years, the question and my answer lingered on with my answer improving each time I revisited the subject. Final answer: I am not an ascetic; I am a hedonist. I do not eat (or drink) to survive; I eat and drink for pleasure. Bottom line: I had better like what I eat (and drink) or 1) I wont like doing it and 2) I wont be able to do it indefinitely as a “lifestyle change,” which is needed if I am to succeed long term.

Okay, I said it: I like to eat. But this is not just about my former licentious and libidinous lifestyle. I had to give them up to save my health, and my marriage. (I got married about the same time.) But, as I said, I am not an ascetic, so I had to find an “alternate” lifestyle with equal or greater gustatory rewards. This is not about volitional eating. This is about a driving force that controls the urge to “consume food just for pleasure” and not to “maintain energy homeostasis.” This is called “hedonistic hunger.” Im not making this up, folks. Check out this piece in the Journal of Clinical Endocrinal Metabolism.

The title, “Hedonic eating is associated with increased peripheral levels of ghrelin and the endocannabinoid 2-arachidonoyl-glycerol in healthy humans: a pilot study,” tells the story: the hunger hormone (ghrelin) and opioid receptors in the brain regulate eating behavior based on palatability. As I said, its not volition or will power. So, the “trick” to sidestep cravings is to transition from a high-carb dietary engineered by processed food manufacturers for maximum palatability, to an equally hedonistic lifestyle based on energy homeostasis. Eat for pleasure, but just enough to be healthy. The key is to avoid feeling hungry. Cravings, as we know them, are signals from the brain (and ghrelin from the stomach) telling us to eat low energy density foods (carbohydrates) with high palatability. They are, frankly, sometimes almost impossible to resist.

But, if you eat a breakfast that enables you to go all day long without feeling hungry, because your blood glucose has been stable all day long, you will not have cravings. The body will regulate energy homeostasis using different mechanisms. You body is “happy” to burn body fat for energy if you dont feed yourself carbs. It is designed to work that way. We didnt evolve eating “three squares” a day. We ate “catch as catch can” and sometimes went days working off stored energy from a previous feast. It is completely natural.

This PubMed Abstract comes to a thought-provoking conclusion: “The present preliminary findings suggest that when motivation to eat is generated by the availability of highly palatable food and not by food deprivation, a peripheral activation of two endogenous rewarding chemical signals is observed. Future research should confirm and extend our results to better understand the phenomenon of hedonic eating, which influences food intake and, ultimately, body mass.”

Ive been working on this “future research” for years, long before this paper was published. I always ate for pleasure, for sure; that is, I was hooked on carbs. I craved carbs; now, I still eat for pleasure, but I am not craven. I eat foods that satiate (fat and protein), and so I am not hungry between meals. I will often skip lunch, like today when we plan to eat dinner around 5PM. I will even have a glass or two of wine occasionally, for pleasure, for sure.
Its not a perfect solution. The body has other mechanisms that drive us to eat (besides pleasure and short-term energy depletion). One of them is the hormonal stimulation that comes from seeing or smelling food. I call it “opportunistic” eating, and it is definitely a driving force to which I am especially susceptible. Like the other driving forces, I suspect it is a genetic thing, and I am “blessed” with this survival gene. The 2 glasses of red wine, though, is purely hedonistic.

Wednesday, March 5, 2014

The Nutrition Debate #189: The Proposed New F.D.A Nutrition Labels

My feed to Jimmy Moore’s Livin’ La Vida Low-Carb blog recently brought me this piece about the proposed new F.D.A Food labels to be announced by first lady Michelle Obama at a White House press conference later that day. It looked interesting, so I Googled and found the New York Times’ same-day coverage here. There are four major changes in the draft proposal.

1) The calorie count per serving will be displayed much more prominently. That’s a good thing, generally, but as Jimmy points out, total calories is about as useful as total cholesterol is in a blood test, which is “not very” or “not at all” for many. With cholesterol, the component parts (LDL, HDL and triglycerides) matter more than the total. So it is with total calories. A high calorie count is not bad if it is made up of the “right” (“good”) kind of fat. But here, the government hasn’t got it right yet, so it’s not going to make any sense to press this point with the powers-that-be yet.

2) “Added sugar” (from external sources not naturally found in the food) will be listed separately. This is a very good first step, and it may have the effect of having food manufacturers lower the amount of added sugar (as it has with trans fats) in processed foods. It will certainly make everyone more aware of how many foods have added sugars in them, and how much. But, after flour and water, sugar, in some form, is always the 3rd ingredient in a loaf of bread. Would the new labels consider this an “added sugar” or an essential ingredient in the basic recipe for bread? This topic is starting to get mainstream attention. People are looking for the sugar and finding it in astonishing quantities. Check out this story on NPR.

Of course, this change will not address the fact that a) a 12oz glass of Minute Maid orange juice has just as much “natural” sugar (36g) as a 12oz. regular Coke has “added” sugar (39g), and they are both equally “bad.” The ADA says that the juice is worth it because of the minerals and fiber, but hyperglycemia affects mineral balance in the body (of rats); or b) that virtually every other carbohydrate you eat will be quickly broken down by digestive enzymes to “simple sugars,” and they will have the same effect on your blood glucose level as either “natural sugars” or “added sugars.” So, what difference, at this point, does it make? Oops…My politics are showing. Check out this link to sugar in beverages at

Anyway, I think it is time to take advantage of the present and growing level of awareness about the amount of sugar we eat and capture the moment in these new food label changes. It’s been about 20 years since the last major changes (except for the trans fat change, enacted in 2002, that took effect in 2006).

3) Serving sizes will increase. This is a very good thing, for the food categories covered. The New York Times piece, however, says it will affect only “17% of the approximately 150 categories of packaged food,” according to the F.D.A. commissioner Dr. Margaret Hamburg. Well have to see what will change and what will not. Everyone agrees the present serving sizes are a joke and a charade, so this change is also long overdue. Examples given to the press included a) a serving size of ice cream will increase from ½ cup to 1 cup. That means those pint containers are meant for 2 people, folks. Don’t forget to share! Also, a muffin serving size will change from 2oz to 4oz, and a 20oz beverage will be just one serving. Two straws, anybody?

4) “Calories from fat” will be deleted. That’s a good thing. It singled out fat unfairly. It stigmatized fat and by contrast favored carbohydrates, which includes sugars. Now, with the seeming shift from vilifying all fats to vilifying “added sugars,” the F.D.A is continuing to “turn the Titanic,” first addressed by me in this column in 2011. In as many years, the F.D.A has also transitioned from the “food pyramid” to a “pyramid” of streamers (wedges) to “My Plate.” They (the government) still hasn’t got it right, but they are 1) trying to figure it out and 2) trying to figure out how to tell us (the consumers of food) and the food manufacturers, the public health establishment and the medical community, how and where they got it all wrong.

Regrettably, they still lump dietary cholesterol and saturated (good) fat and artificial trans (bad)fats together on the label and do not require that monounsaturated and polyunsaturated fats be listed on the label. They frequently are, but they, unlike cholesterol, saturated fat, and trans fat are not required. And regrettably, they do not require that quantities (e.g added sugar) be listed in measures with which Americans are familiar, i.e., teaspoons instead of grams. Did you know, for example, that a 12 oz Coke or 12oz glass of orange juice has the equivalent of 10 or 9 teaspoons of sugar in it, respectively?

And finally, although this is just a label change, I lament that this proposal is still based on the same old macronutrient proportions that have also long been outdated even on the government websites: 60% carbohydrates, 30% fat and 10% protein.  That’s 300 grams (1,200 calories) of carbohydrate a day, 50 grams (200 calories) of protein, and 67 grams (600 calories) of fat. If we are going to eat a healthier diet, isn’t that where the changes should begin? And, let’s face it, if we didn’t ever eat another packaged and processed food that had a food label on it, wouldn’t we already be healthier?
What do you think of the proposed food label changes? As Jimmy Moore says in his blog header, the “proposed food label changes need to focus on what really matters.” IMHO, there’s not much chance of that, but this isn’t a bad change. Maybe public comment will even make it better. Or maybe industry influence will make it worse. It’ll be interesting to see which.

Saturday, March 1, 2014

The Nutrition Debate #188: “Older Patients with T2DM and Comorbidities…”

A recent Diabetes in headline got my attention. Diabetes in Control is a weekly digest of articles primarily for physicians who treat patients with type 2 diabetes. The headline was, “Older Patients with T2DM and Comorbidities Dont Feel Heard.The lede was, “Most adults with T2DM have at least one comorbid condition, and almost half of them have three or more.” The most commonly reported chronic comorbid conditions were hypertension, arthritis, retinopathy, hypercholesterolemia (high cholesterol), coronary artery disease, and neuropathy. All patients in the study were ≥ 60 years old, white, highly-educated and had good glucose control.

The source for the story was this piece in Clinical Diabetes. The protocol for the study was that all the patients had been diagnosed withT2DM at least one year previous and also diagnosed with one or more additional chronic conditions. According to the Control article, diabetes is now the 7th leading cause of death in the United States but its management and complications account for 23% of current health care expenditures. So, whats all the fuss about? Wheres the disconnect?

First, this is progress. The study was making an important point. I can tell you from recent personal experiences how difficult it is for a “new” patient to sometimes get the attention and cooperation of a physician when, in their professional opinion, the “proper care” differs from “my opinion.” Some physicians dont take the time to look at the record (as in, history of lab reports and clinical examinations) to see what “my preferences” for a treatment protocol are.

This is, to a certain degree, understandable. I am just a layman with no professional training and no professional liability for malpractice, sanctions from medical practice boards, or loss of reimbursement from Medicare and supplemental insurance for not following professional practice standards and guidelines. But, Im spoiled. My doctor (now deceased) in New York, who treated me for over 20 years, set me on the course of eating Very Low Carb and oversaw the complete transformation of my progressively worsening T2DM from “out-of-control on 3 oral meds” to “in-remission” on a minimum dose of  just one (Metformin). He has my everlasting gratitude. My “new” doctor in New York is also great. He has reviewed my “history” and tells me to just keep on “doing what I’m doing.  Bottom line: The physician and the patient have to determine the risks and benefits of following treatment guidelines. But not every doctor is willing to do that. The Control piece said:

Many participants also felt that their preferences for care were not taken into account by their provider. Participants also reported feeling that their care was not addressed to their individual needs and medical history, and desired more tailored treatment regimens specific to their needs. Generally speaking, patients want to have more interaction with their providers so that they can discuss the difficulties they are experiencing and vocalize their preference for treatment.”

The Control piece concludes, “Effective patient-provider communications and shared decision-making have been shown to not only improve patient satisfaction, but also increase adherence to treatment plans and improve health outcomes.”

Setting aside the “empathy” and “older age” aspects of these criticisms (I personally have not felt either in my interactions), I note how “their [the patients] preferences were not being listened to,” is a recurring theme. My first reaction, to be unbiased, was, “Why should the physician listen to me and “my preference” for a treatment protocol? Then, two things came to mind. I am dead set about not taking a statin (again). I did 5 or 6 years ago (before I knew better), but my doctor discontinued it all by himself. Today, however, even with the new AHA/ACC guidelines (see #180 and #181 here and here), I am still considered (by most doctors) a candidate for a statin. Personally, I consider my latest lipid test lab results to be stellar: TC = 207, HDL = 90, LDL = 110, TC/HDL ratio = 2.3 and triglycerides = 34. And my Trig/HDL ratio (0.38), a powerful statistical indicator of cardiovascular risk, is also stellar. And, when they were last tested, my LDL particles were Pattern A (large, buoyant and fluffy). Many doctors would not prescribe a statin with these “labs,” but some would, and the new AHA/ACC guidelines dictate that I should take one. But “my preference” is a definite “no.”

Then theres the question of diet. What should I eat? Should I follow what has worked for me for the last 11 years, resulting in my losing and keeping off (currently) 130 pounds? Should I eat what my doctor, and the government, and the practice specialty guidelines tell me to eat? Once again, “my preference” tells me that I know more about what diet I should eat than my doctor does. My n = 1 experience, aided by frequent testing with a blood glucose meter before and after meals for years, has taught me what to eat. What experience (or training!) does my doctor have to dictate what I should eat? Well…

As reported in this Medscape Physician Lifestyle Report 2014, 68% of overweight or obese doctors eat a Typical American, AHA, or Mediterranean style diet. Just 14 percent eat a “Weight Loss (calorie restricted or otherwise) Diet,” 11% various other diets and only 5% a “Paleo” style diet. Atkins or Very Low Carb or Ketogenic diets were not even mentioned. So, why should I follow my overweight doctors advice when he doesn’t know how to lose weight and improve his own health?!!!