Retrospective #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 the A1c rather than the fasting blood glucose in diagnosing incipient or “incident T2DM” (see The Nutrition Debate #182).

Until a few years ago the ADA criterion for diagnosing T2DM (Type 2 diabetes) was 2 consecutive fasting blood glucose tests (on separate office visits) of ≥126mg/dl. The ADA also guided 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 increasingly became the diagnostic tool of choice in 2009, although the fasting glucose test, while seriously flawed, is still widely used. So, what is the A1c test? Technically, the A1c (glycated hemoglobin A1c), is a percentage measurement of the glucose on the surface of red blood cells. Since red blood cells live about 2 to 3 months (before they die and bone marrow replaces them), the test is then a surrogate measurement of the level of glucose circulating in your blood 24/7 for that 2 to 3-month period. It’s like wearing a blood glucose monitor!

The advantage of the A1c over a fasting blood glucose is that the A1c test captures all 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, be absorbed in the blood, and be transported, by insulin secreted in the pancreas for the purpose, to the cells. That is how your body gets the “energy” from carbs delivered to, and hopefully into, your cells. In people with a “normal” metabolic function, the glucose moves from the blood into the cells. Then, after a couple of hours when all the circulating glucose has been “taken up,” the level of glucose (and insulin) in the blood lowers to where it began.

However, in people whose metabolism has developed a specific “dysregulation” called Insulin Resistance, the receptor cells on the surface of the destination cells refuse to open, and the level of both insulin and glucose in the blood remains “elevated.” The energy is not taken up. As a consequence, you get hungry and tired and lack energy, literally. So, these people will have a higher A1c, corresponding to the higher blood glucose that is circulating for hours/days, even continuously, if you regularly eat carbs at every meal and with in-between-meal snacks.

Now, the two examples I promised: Person #1 is the email correspondent referred to in Retrospective #195R. He was diagnosed a Type 2 diabetic (A1c 6.5%) about 9 months ago. In response, he changed his diet (“just stopped eating bread, potatoes, pasta and ice cream”). 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, 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 that his diabetes is almost “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 100mg/dl; A1c test = 5.0%. Note: this person has the same blood glucose value (+/-100mg/dl), but a “normal” A1c (for a 70 year old male) of 5.0% This person eats a typical American “balanced diet,” between 40% and 60% carbohydrate, and is not diabetic or even close to being Pre-diabetic, whereas Person #1 definitely is diabetic, even though both have identical fasting blood glucoses.

The A1c test is what differentiates #1 (controlled diabetic) from #2 (non-diabetic). And, the A1c is what made a diagnosis of incipient Type 2 diabetes possible in Person #1, and permitted him to take early action to address it.

Person #1 learned he could 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. If you have Insulin Resistance (as measured by your A1c), watch what you eat!

Retrospective #195: “I did it myself, with no help from my doctor”

The other day I had an email exchange with someone who reads The Nutrition Debate. 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 replied: “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 my doctor. Just made sense since I was a big white carb eater and knew that was a big sugar source.” A thinking man: eating refined carbs and sugars made his blood sugar rise!

There, you see. I’m not that crazy fanatic that you all think I am. And you don’t have to be one either. Here’s this guy, presumably with a regular work and family life, who saw what had happened to him (diagnosed a Type 2), he recognized he was a “big white carb eater”, and he envisioned the result (disease, meds, eventually complications).

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! His A1c’s returned to “normal” (clinically on the cusp of “non-diabetic” on the ADA scale), and his fasting blood glucose stabilized at the lower end of the pre-diabetic scale “over 3 (successive) blood works.” That, as I said, is a “good story.” And it could be yours, too, if you took the same steps as my correspondent.

Notice, though, that his doctor didn’t tell him to eat low carb. He just gave him 3 months to get his act together “before putting me on meds.” That’s the ADA protocol: “lifestyle changes” (“diet and exercise”) first, then start you on meds. The problem is that the ADA’s medical protocol doesn’t advocate the right dietary changes. Surprised? No? Doctors aren’t trained in nutrition. But a more cynical view is that your doctor is in business to treat illness, with medicine. Besides, exercise is not a good weight loss strategy. Personally, it just makes me sweaty and hungry.

In my opinion, though, It’s immaterial. What your doctor wants to see are results, i.e., good labs: A1c’s and fasting blood glucose, and other markers, like weight, waistline and BMI. And blood pressure. She is probably also testing your 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. They will all improve on a low carb diet.

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. And, he said proudly, “I did it myself with no help from my doctor.” I would argue, though, that the doctor did help. He made an explicit threat: “Dr. gave me 3 months to see what a diet might do before putting me on meds.” That’s motivational!

That kind of threat (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, and who don’t want to be dependent on other people or things. I remember thinking when I was in my 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 him!

Retrospective #194: Live Fermented Foods

Okay, I’m not an “expert” on this, 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, that’s good too. In our pursuit of healthy eating and “truth,” we are open to new ideas, and new foods. We hope you are too.

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, kefir, natto and kim chi.

The traditional process requires fermentation with salt (in brine); however, today many of the foods mentioned above are made by modern methods that do not involve fermentation. If a listed food is made from pasteurized products, it 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.” 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” 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.  He’s not advocating these foods; he just wants to explain how fermentation makes these foods “tolerable.”

Dr. Mercola, a high-profile osteopathic physician (DO) and web entrepreneur, 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.”

At the moment, kim chi is my favorite live fermented food. I’m lucky that I can buy mine from a local Korean green grocer in a town near my hometown. Curiously, there is none offered in the large farmers’ market that I visit every week in winter, but I found some in the Publix supermarkets that are ubiquitous in Florida. They’re always 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 in the dairy case is too. 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 many other states. And the vendor next to my egg/organ meat vendor (who also sells grass-fed, grass finished beef) 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 at the farmers’ market. Maybe veggies are just too inexpensive in Florida, 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.

Note: If you’re live 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 fermentation process down so you can eat it while it’s still at its best.

Retrospective #193: “We never changed our mind,” the “scientist” said.

The Los Angeles Times headlined, “High-protein diets: Bad for the middle-aged, good for the elderly.” 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.

The LATimes.com piece, and the journal Cell Metabolism where the “research” originally appeared, are complicit in this “sort-of-science.” Quoting from The Nutrition Debate #192, and referring to Taubes’s New York Times op-ed:

“The scientific method requires that a hypothesis be rigorously tested, with a skeptical bias, and… 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.’”

The problem with this “research,” 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 will be clear to the discerning reader. 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,’ quoting from Taubes’s 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, [since] 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 as researchers studying nutrition have decided that this is the best they can do,” Taubes concludes, kindly.

I would not be so kind. I would conclude, cynically, that the “scientists” (and the media) 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 questioned her objectivity (Is she vegan?), 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.”

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 such observational studies with a heavy dose of salt (which I like).

Then to nutrition scientists Taubes 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, leave your mind open, rather than “never changing” it, as this study author had and said. I’m doing my best to keep an open mind. 

Retrospective #192: Climate Change and “The Nutrition Debate”

It is ironic that many in the climate change consensus community, who view themselves as adherents to fact-based science, would deny dissent from climate change skeptics yet embrace the alternative view of nutritional science (as espoused here at “The Nutrition Debate”). That’s my take on an on-line opinion piece in SFGate by Debra J. Saunders. The San Francisco Journal article is titled, “Climate Change Consensus, no dissent allowed.”

The author quotes a CNN commentator that “some stories don’t have two sides.” CNN argued there’s no need to present climate-change dissenters 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.” Also, “Last year the Los Angeles Times revealed it won’t print letters that deny a human cause to global warming.” Well, I guess that settles it.

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 15.7 million hits, no doubt 97 percent in agreement with the happy conceit. What is “scientific consensus”? Everybody piles on to the “accepted wisdom,” which then constitutes “scientific proof.”

A commenter noted that One Hundred Authors Against Einstein, a 1931 book, 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 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.

19^th century physicist John Tyndall, referring to scientists who follow evolution, wrote, “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; If it doesn’t agree with experiment, it’s wrong.”

In Gary Taubes’s February 2014 NYT op-ed, “Why Nutrition Is So Confusing,” he asked. “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 answered, “may depend on which is the correct answer.” There are “two conflicting observations” at play here; “We know how to eat healthy and maintain a healthy weight,” or “something about the conventional thinking is… wrong.”

Since 1960 600k articles (and thousands of diet books) have been published, Taubes said. “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 noted, 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 was Taubes’s not-so-subtle pitch for support for the Nutrition Science Initiative, a 501c that he and Peter Attia, MD, started in 2012…and now, sadly, nearly defunct.

Taubes explained how long-term clinical trials are prohibitively expensive and exceedingly difficult. He jibes that “no pharmaceutical company stands to benefit” and laments “prospective sources of funding are limited, particularly when we insist the answers are already known,” Sounds like the climate change argument, doesn’t it?

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 continued, “Nutritionists have adjusted to this reality by accepting a lower standard of evidence on what they’ll believe to be true.” We have a field of sort-of-science in which hypotheses are treated as facts because they’re too hard or expensive to test.”

But Taubes isn’t ambiguous about what his personal bias is. He said, “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 truth.

Retrospective #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. I am a Type 2 diabetic with 33 years of 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, and died prematurely, was the impetus for “The Nutrition Debate.” His death was a totally unnecessary tragedy.

First, a little background. There are 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 dietary intake (food) was 90%+ fat.

Type 2 diabetes, formerly called “adult onset diabetes” but now found in children, 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 doesn’t get taken up into the cells and the level of glucose in the blood rises. The diagnosis of Type 2 diabetes is made with an elevated fasting blood glucose (on 2 consecutive office visits), or preferably one elevated hemoglobin A1c test, reflecting a 3-month average of circulating glucose as measured on the surface of 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 sugars and starches in foods (that all convert to glucose) as its primary energy source. It conserves body fat for use when food is not available. It’s a brilliant design, since fat is a very good storage vehicle. It is more than twice as dense in energy (9 calories per gram vs. 4 for carbs).

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,” and/or 2) prescribe an oral medication to help. If the patient is not successful in losing weight, the doctor adds another oral med and then maybe a 3^rd med to the “cocktail.” More recently, new injectable medications (GLP-1s) are sometimes prescribed. Insulin injections are usually reserved as a “last resort.”.

Many patients who are treated using the ADA’s standards for blood glucose control, which are much too lax, will eventually progress to becoming insulin-dependent Type 2s. 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. In reality, however, Type 2 diabetes is a dietary disease.

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 amputations; retinopathy (damage to the blood vessels of the retina, resulting in blindness); and nephropathy (end-stage kidney disease).

Insulin therapy for Type 2 diabetics usually begins with “basal” insulin, injected once 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 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.

If you are a Type 2 diabetic, what does this suggest to you? If your pancreas still makes insulin, couldn’t you do the same? 1) Eat only small amounts of carbohydrates and thus only need to use small amounts of the body’s precious supply of insulin? And 2) Avoid glucose spikes, and thus protect your pancreas from further damage.  I think you can! Remember: Type 2 diabetes is a DIETARY disease, and YOU control what you eat!

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

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

Two thoughts crossed my mind: How much had she had to drink? And why am I feeling on the defensive? Anyway, I said “sure.” It could be interesting, and, as my readers know, I do not guard my health and medical privacy. I am thrilled to share the news about how changes in what I eat over the last 17 years have transformed my health.

I won’t repeat all the statistics here. For new readers, though, I have been a Type 2 for 33 years, and 17 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 cholesterol also improved very dramatically, my blood pressure improved (on fewer meds) and my inflammation marker also dramatically improved. So, I said, “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. Short 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 wouldn’t like doing it and 2) I wouldn’t be able to do it indefinitely as a “lifestyle change,” which is needed if I am to succeed long term.

This is not just about my former glutenous and bibulous lifestyle. It’s true I had to change what I ate to save my health. But I am not an ascetic, so I had to find an “alternate” lifestyle with equal or greater gustatory rewards. Eating is not a volitional thing. This is about a driving force that controls the urge to “consume food just for pleasure” and not just to “maintain energy homeostasis.” This is called “hedonistic hunger.” I’m not making this up.

I had just read an article in the Journal of Clinical Endocrinal Metabolism titled, “Hedonic eating is associated with increased peripheral levels of ghrelin and the endocannabinoid 2-arachidonoyl-glycerol in healthy humans: a pilot study.” The story line: the hunger hormone (ghrelin) and opioid receptors in the brain regulate eating behavior based on palatability. It’s not will power, folks. 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 stomach (ghrelin) and the brain (hypothalamus) telling us to eat. The signals are, frankly, sometimes almost impossible to resist. Our response: to eat low energy density foods (carbohydrates) with high palatability. 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 hunger cravings.

The body will regulate energy homeostasis using different mechanisms. You body is “happy” to burn body fat for energy if you don’t eat carbs. It is designed to work that way. We didn’t 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’s natural.

This PubMed Abstract concludes: “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.”

I always ate for pleasure, but 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. In fact, I often skip lunch. 

Retrospective #189: The New Nutrition Facts Labels

My feed to Jimmy Moore’s Livin’ La Vida Low-Carb blog recently brought me a piece about the proposed new Nutrition Facts labels announced by first lady Michelle Obama at a White House press conference. It looked interesting, so I Googled the New York Times’ story on it. There are four major changes in the draft proposal.

1) The calorie count per serving will be displayed more prominently. That’s a good thing, 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 components (LDL, HDL and triglycerides) matter more than the total. So it is with calories.

2) “Added sugar” (from external sources not naturally found in the food) will be listed separately. This is a good first step, and it may have the effect of having food manufacturers lower the amount of added sugar in processed foods. It should make people 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 3^rd ingredient in a loaf of bread. Would the new labels consider this sugar “added sugar” or an essential ingredient in the basic recipe for bread? We’ll have to wait and see.

Of course, this change will not address nor change 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. Both “natural sugars” and “added sugars” will have the same effect on your blood glucose level. “So, what difference, at this point, does it make?” (Clinton/Benghazi reference; hehe).

Anyway, 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. Except for the trans fat change, enacted in 2002 that took effect in 2006, it’s been about 20 years since the last major changes.

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.” 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 favored carbohydrates, which includes sugars. Now, with the seeming shift from vilifying all fats to vilifying “added sugars,” the USDA/HHS is “turning the Titanic,” first addressed here by me in an eponymous column in 2011.

Regrettably, the USDA/HHS still lumps dietary cholesterol and saturated (good) fat and artificial trans (bad) fats together on the label and do not require that unsaturated fats (especially polyunsaturated) be listed on the label. They frequently are, but they, unlike cholesterol and saturated 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?

Finally, and most importantly, it is regrettable that this proposal is still based on the same macronutrient recommendations that have also long been outdated on the Nutrition Facts label: 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 Nutrition Facts label on it, wouldn’t we already be healthier? In the meantime, it is eerily scary but accurate, I think, to view these label changes as rearranging the deck chairs on the Titanic while our nation’s state of health continues to sink.

Retrospective #188: “Older Patients with T2DM and Co-morbidities…”

A story in DiabetesinControl.com, “Older Patients with T2DM and Co-morbidities Don’t Feel Heard,” got my attention. Diabetes in Control is a weekly digest of articles primarily for physicians who treat patients with Type 2 diabetes. The lede was, “Most adults with T2DM have at least one co-morbid condition, and almost half of them have three or more.” The most commonly reported chronic co-morbid conditions were hypertension, arthritis, retinopathy, hypercholesterolemia (high cholesterol), coronary artery disease, and neuropathy.

The source for the story, a study in Clinical Diabetes, was making an important point about patients being heard. All patients in the study were ≥ 60 years old, white, highly-educated and had good glucose control.  That’s me. It relates how difficult it is for a “new” patient to get the attention and cooperation of a physician when, in his or her professional opinion, the “proper care” differs from the patient’s opinion.

This is, after all, seen as justified by the physician. The patient is just a layman with no professional liability for malpractice, no risk of sanctions from medical practice boards, or loss of reimbursement from Medicare and supplemental insurance for not following professional practice standards and guidelines. But I’m spoiled. My doctor (now deceased), who treated me for over 20 years, set me on the course of eating Very Low Carb and oversaw the complete turnaround of my progressively worsening T2DM from “out-of-control-on-3-oral-diabetes-meds” to “in-remission” on a minimum dose of  just one oral (Metformin). He has my everlasting gratitude.

My “new” doctor is also great. He reviewed my “history” and told me to just, “Keep doing what you’re doing.”  That’s great! My physician (and I) determine the risks and benefits of me not 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.”

It 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 patient’s] preferences were not being listened to,” is a recurring theme. Two things came to mind. 1) 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. Today, however, especially with the new AHA/ACC guidelines, 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 lipid “labs,” but some would, and the new AHA/ACC guidelines dictate that I should take one. But “my preference” is a definite “NO!”

Then, 2) there’s 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) 145 pounds? Or, should I eat what the AHA or the Dietary Guidelines for Americans tell me to eat? Once again, “my preference” tells me that I know more about what diet I should eat than the USDA/HHS. My n = 1 experience, aided by frequent testing, has taught me what to eat.

As reported in the 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,” 5% a “Paleo” style diet and 11% various other diets. I suppose, Very Low Carb, LCHF, Keto or even Atkins Induction were included in the 11% various other diets, but most physicians wouldn’t admit to such heresy.

Retrospective #187: Chronic Systemic Inflammation

This is a primer for the layman (by a layman) on “Chronic Systemic Inflammation.” Chronic means “persistent, long-standing, long term.”  It is in contrast to “acute” which means “with a rapid onset and/or a short course.” Systemic means “throughout the body,” as when you have a fever. Inflammation is the body’s response to an “injury.” I put injury in quotes because, while we understand the outward manifestation of the body’s “acute” inflammatory response to stubbing a toe (pain, swelling, etc.), we are often unaware of the presence and dire consequences of “chronic, systemic inflammation.” It is a continuing “injury” that is often undetected, and can be very serious.

To be clear, our body’s response to an acute injury (i.e., pain and swelling), is actually a good thing. It means our immune system has swung into high gear to defend itself against the “injury.” The biological process is technical, so suffice it to say they involve a temporary mobilization of “hormone-like” proteins, e.g., cytokines and macrophages. But enough of that; my eyes glaze over when I write about those little buggers. The point is: when the body has completed a repair to the injury, the inflammation goes away and everything returns to normal.

Chronic systemic inflammation is a whole other thing and is mostly unrecognized. So, why should we care? Dr. Art Ayers, a PhD biomedical researcher with a special interest in inflammation and disease, puts it this way: “Inflammation is the foundation for cancer and degenerative/autoimmune diseases. Small changes in diet and exercise, e.g. omega-3 oils, vitamin D, low starch, and maintaining muscle mass, can dramatically alter predisposition to disease and aging, and minimize the negative impact of genetic risks.”

One of the most common markers of chronic systemic inflammation is a blood test: the high-sensitivity C-reactive protein (hsCRP). Results in the range of 3.1 to 10mg/L are considered “Higher Relative Cardiovascular Risk;” 1.0 to 3.0 “Average Relative Cardiovascular Risk;” and <1.0 “Lower Relative Cardiovascular Risk.” When I started eating Very Low Carb in September 2002, my hsCRP had never been tested. Here are my scores for the last 16 years:

3/03	10/03	12/06	4/09	7/10	4/11	11/12	4/13	4/14	8/15	8/17	8/19
6.4	5.8	2.5	1.8	0.7	1.5	0.1	1.3	0.4	0.6	0.8	1.7

Note that my doctor, an internist/cardiologist, shortly after starting me on Very Low Carb in September 2002, tested my CRP twice in the first year. Both times the result put me at a “Higher Risk” (6.4 & 5.8mg/L). He didn’t test me again for 3 years, and by this time my CRP-based risk had dropped to “Average” (2.5mg/L). The next test, 3 years later, my hsCRP had dropped further to 1.8mg/L. The next 5 years he tested my hsCRP just once a year, three of them <1.0 (0.7, <0.1 and 0.4), a “lower” CVD risk. I think my doctor had noticed the big difference that Dr. Ayers mentions in “Cooling Inflammation,” his blog. I think he was particularly interested in the effect the Very Low Carb diet (and my 170-pound weight loss) had on Chronic Systemic Inflammation. Now he tests only every other year.

How did I lose 170 pounds and lower my hsCRP? Well, you can start by reading my two previous blog posts, #185, “Your Diet is Very Restrictive” and #186, “Your Diet is Very Restrictive Part 2.” And there’s more to come.

Note 1: The Google heading “Inflammation” includes the following: “Chronic inflammation is widely observed in obesity. The obese commonly have many elevated markers of inflammation, including: CRP (C-Reactive Protein).” “Waist circumference correlates significantly with systemic inflammatory response,” and “C-reactive protein (CRP) is generated at a higher level in obese people.” VISCERAL FAT (abdominal fat around the internal organs) IS VERY INFLAMMATORY. “Mild elevation in CRP increases risk of heart attacks, strokes…and high blood pressure.”

Note 2: A common cause of Chronic Systemic Inflammation is periodontitis, an inflammatory disease affecting the tissues that surround and support the teeth. “Periodontitis is caused by microorganisms on the tooth's surfaces, along with an overly aggressive immune response by pro-inflammatory cytokines, lymphocytes & macrophages against these microorganisms.”

Retrospective #186: “Your Diet is Very Restrictive” Part 2

I realized, after writing the last column, I had told you only half the story. Yes, my diet is “very restrictive,” including in two additional ways I didn’t mention: 1) I try to avoid all vegetable and seed oils, specifically polyunsaturated soybean oil, corn oil, Canola, sunflower and cottonseed oil, etc.; and 2) I try to avoid all grains and everything made from them. That means I eat very little fried food and virtually nothing that has been made with flour.

I do eat monounsaturated oils (olive oil and avocado) and saturated fat oils (specifically coconut oil and MCT oil). I select fatty cuts of meat (beef, lamb and pork) and chicken with the skin on, and fatty cold-water fish (sardines, herring, tuna, char). I also eat lots of eggs from pastured hens raised by a local farmer. Forget about dietary cholesterol! I wish I could say I ate beef from grass-fed, grass-finished beef and even butter from grass fed cows, but alas, I do not. I also try to eat offal (liver or kidneys) once a week.

Is this a challenge? Sure, at times, especially when dining out. In restaurants the workaround is often to order from the appetizer menu. Sometimes I will order a salad and an appetizer, or two appetizers. That avoids the proverbial starch that seems to accompany most main dishes. Of course, almost every kitchen will gladly give you a double portion of vegetables instead of a vegetable and a starch, but I don’t want double of anything. It’s too much food. Small meals, remember? Also, when you order from the appetizer menu, you don’t get a bread basket. That helps.

At home, the workaround for all the “forbidden goodies” in the house is not to open the freezer (where my wife keeps ice cream), or the pantry where her chips and crackers are stored. Out-of-sight/out-of-mind really works for me. Our eyes are powerful hormone stimulators. I bet there’ve been more than a few scientific papers written on how visual stimulation excites the brain (think sex, guys) and prepares the glands.

But the shift in the balance from saturated fat (Lard) to polyunsaturated fats (Crisco) and manufactured oils over the last 50-100 years is wholly unrelated to carbohydrates. Of particular interest in the very heavy shift in the ratio of Omega 6 (linoleic acid) to Omega 3 (linolenic acid) in our diet from roughly 1: 1 to as much as 30:1 over this time period. That’s why it is important to seriously cut back on vegetable and seed oils (linoleic acid) and increase the Omega 3s (e.g. with supplemental fish oil). But you can’t “fix” this problem with fish oil alone; you have to cut back dramatically on the polyunsaturated vegetable and seed oils you eat, starting with fried foods.

It is also important to eliminate fried foods because “vegetable” oils, already damaged in manufacturing by pressure, heat and chemicals, are then reheated repeatedly in fryers. These oils are also damaged by daylight and quickly become rancid. Saturated fats do not. So, cook with butter, coconut oil and lard, not vegetable oils! Use olive oil as a salad dressing or drizzle to add flavor and richness, and you will be eating well indeed.

As Dwight Lundell, MD, in Jimmy Moore’s good book, Cholesterol Clarity (pg. 35), quoted in #185, said, “The population will become split between the smart and the dumb. The smart ones will begin taking their health into their own hands because they’re already seeing that what we are doing now is not working.”

Moore then commented as follows: “I am a huge proponent of people taking responsibility for their own health. We are all unique individuals with different needs and yet we are treated like lemmings by the medical profession when it comes to our health. I get why so many people abdicate personal responsibility with their health; it’s so much easier to just do what we’re told. But that approach clearly doesn’t work: Science changes all the time, and medical and nutrition specialists simply can’t keep up. How can they possibly have all the answers? There’s no way around it. If you want to be healthy, it’s up to you to make it happen! Educate yourself, and then act on what you learn. You must be the final arbiter of your own health.”

So, what are you waiting for? Want to be healthy? Take charge of what you eat. You will see a world of difference.

Retrospective #185: “Your Diet is Very Restrictive!”

A friend who saw my blog on Facebook said, “Your diet is very restrictive.” I objected! I was being defensive, of course, but my diet is very restrictive, especially to someone who eats “without restriction” and gets away with it. And that appears to be a fairly large segment of the population. It includes everyone who is of normal weight or who is not diagnosed as a Type 2 or Pre-diabetic or with Metabolic Syndrome. And who gets that diagnosis?

Lest those who appear to be healthy take comfort from this, Dr. Dwight C. Lundell, MD, author of The Cure for Heart Disease and The Great Cholesterol Lie, on pg. 36 of Cholesterol Clarity, by Jimmy Moore with Eric C. Westman, MD, says, “Our diet is not working because 70% of us are overweight and obese, we have 29 million diabetics and 75 million pre-diabetics, and the rest of us don’t even know we’re pre-diabetic”(my emphasis).

Lundell continues, “People are realizing that what we are doing is not working, and they are looking for other ways around this. That’s where do-it-yourself healthcare and self-monitoring will become the norm.”

And do-it-yourself healthcare begins with diet. Even if you’re overweight (the 70%), it is your diet that you should address to “fix” your health. And if you are among the 30% “who don’t even know [you’re] pre-diabetic,” then it is your diet that you need to address to “fix” that. If I haven’t made myself clear yet: Everyone needs to look at their diet and change it. But how? That’s the question. The best way is “self-monitoring” of your health markers.

The markers to monitor are blood glucose (fasting & A1c), HDL cholesterol, triglycerides, LDL particle size and type, and chronic systemic inflammation (hs C-reactive protein or hsCRP). Forget Total Cholesterol and LDL cholesterol. Of course, you’ll need to see a doctor to get these tests, so ask for a copy of your labs, and LEARN YOUR MARKERS.

So, how do you fix these markers? By changing your diet. I am not talking about eating less and exercising more. A growing consensus is emerging that the dietary advice we are still getting from our government and our healthcare providers is what is causing the diabetes and obesity (“diabesity”) crisis. Of course, I knew I was a Type 2 diabetic when I changed my diet 17 years ago (in 2002). I was diagnosed in 1986. And, at my cardiologist doctor’s suggestion, I changed my diet to Atkins Induction (20g of carbs a day) and lost 60 pounds in 9 months (without hunger). I later switched to Richard K. Bernstein's 6-12-12-Plan and lost 110 pounds more. Total: 170 pounds.

But the big change from eating Very Low Carb (VLC) was in my diabetes health and my lipid (cholesterol) chemistry. The first day on VLC I had a hypo (low blood sugar; symptoms: sweating, light-headedness), so my doctor eliminated one of the oral diabetes meds he had prescribed. The next day I had another hypo, so he cut the other two diabetes meds in half, and a few days later, he cut them in half again. Eventually I eliminated one of those two, and today I take just a minimum dose of Metformin. Of course, my A1c’s dropped to the mid 5s, and a new doctor today would say I was “non-diabetic.”

Even more amazing were the changes in my lipid chemistry. My average HDL more than doubled (from of 39 to 81). My average triglycerides declined by 2/3rds from 137 to 49. Total Cholesterol remained about the same, and my LDL inched up slightly but now they are Pattern A (the large/fluffy buoyant type). My latest TC: 207; LDL: 110.

So, how do I do it? By eating a “very restrictive” diet, obviously. I’m not perfect. I cheat all the time. But I have a paradigm that I strive to follow, My target macronutrient ratios: 75% fat; 20% protein; 5% carbohydrate. Just coffee with a little heavy cream for “breakfast.” One or 2 small meals a day, spaced at least 5 hours apart; no eating less than 3 hours before bedtime; no snacks, except sometimes a small VLC snack an hour or so before dinner.

Lunch (when I eat it): kippered (smoked) herring from a can, or a can of sardines in water or olive oil. Dinner: a small portion of protein and one serving of a low carb vegetable, tossed in butter or roasted in olive oil.

My cheats: a glass (or two) of red wine before supper and bread in a restaurant. At home I drink iced tea with stevia; in a restaurant, a cocktail (or two). Water would be better, of course, but my diet is not that restrictive. 

Retrospective #184: “VLC = Not So Much Thinking”

My editor made this comment in the margin of one of my columns recently, and it occurred to me she had made (as usual) a really cogent observation. The full comment was, “I suppose that making people think about food choices is the key, but VLC = not so much thinking. That’s a real plus for me.” It’s all the more interesting since neither she nor her husband is diabetic; but she really knows about good nutrition and metabolism.

Of course, making people think about food choices IS the key to healthy eating whether you’re diabetic or pre-diabetic or just overweight. I think it is also the way everyone should eat…in part because it is the way we all used to eat. We were healthier as a population before the advent of manufactured and processed foods. That’s a fact.

But I also know that what turns many people off about VLC is the prospect of counting carbohydrates. If it’s not counting calories, it’s counting carbs and fat and protein. I admit, I used to do it compulsively (which is my nature), but it’s not necessary. That’s my editor’s point. It’s not necessary to do that. (Am I repeating myself?) All you have to do with this Way of Eating is 1) understand the basic principles and 2) adhere to them.  Not so much thinking.

Of course strict adherence is a daunting prospect for some, but with an open mind (and strict adherence) you will learn that hunger will not be a driver of non-adherence. You will not be hungry, if you adhere to the principles. It’s that simple. It may take a few days, but your hunger will disappear. Your hormones will take over. They will detect that since you’re not eating carbs, there must be none available. Your hormones don’t know about your stash. With props to Claude Bernard, your hormones operate entirely within the milieu intérieur – inside the body.

Your hormones are acutely attuned to what you put in your mouth for energy. If you only eat a few carbs, your body uses those, with protein and fat, and then it will use your body’s stored carbs (liver glycogen) for energy. And then, if you don’t eat too much fat, it will use your body fat for energy. Voila! Bingo! You’re losing body fat and all you had to do was eat VLC and wait for your hormones to take over.

So, “not so much thinking” works, so long as you know what foods are carbohydrates and which foods have more and which have fewer. There is a learning curve for that, but it doesn’t require so much thinking. It just requires effort (strict adherence). I started on Atkins Induction and stayed on it for 9 months, losing 60 pounds. Notice I didn’t mention that Atkins Induction is just 20 net grams of carbohydrate a day. You don’t need to know that. You just need to strictly eat just what Atkins Induction says you can eat… and strictly avoid what foods you can’t eat.

And if you want to succeed, please don’t give yourself a “holiday” or day off. I don’t mean, nor do I expect, that you won’t cheat. I do. I just mean don’t plan on cheating. If you’re not hungry, you won’t have “cravings,” and you’ll actually have more energy, and you’ll feel better, and you’ll be losing weight and your lab tests will keep improving.

But don’t think that you can succeed if you only do this VLC 5 or 6 days a week. It won’t work. You can’t fool your body. It’ll think you found your stash, and everything is now hunky dory. It will stop burning your body fat and start saving it, and banking more for the next “famine.” It doesn’t know we now live in a veritable cornucopia of “food.”

And the trigger for this new “hunky dory” hormonal message will be that silly Reese’s Cup you picked up on the checkout line. “Eye candy.” It will trigger a glucose and then an insulin response, which means it will shut down your fat burning metabolism and restart the fat storage and glucose burning metabolism that causes the pancreas to secrete and pump insulin to carry the sugar energy (glucose) to your cells. I repeat: Your. Fat. Burning. Stops. And your body, thinking the cornucopia is flowing again, will expect more food by mouth and more “sugar.” Your hormones will send you “I’m hungry. Feed me” signals. And you’ll have to start all over again, and it could take a few days to lose the water retained by the kidneys with the sugar and start burning fat again. That discouraging.

Retrospective #183: My New “Lipidologist” and Me

I had an appointment recently with a “new” doctor – new to me, that is. He’s an established physician in a large group that is part of a larger consortium of groups. He practices “Family Medicine,” which means he’s a generalist.

I met my new doctor in a bar. He was having broiled salmon, and I was having a drink (while my wife shopped). Anyway, he told me he was a physician, and he mentioned the group. I told ­­­­­­­him I had just been “fired” (for being rude) by an endo in that group. His suggested I call his office the next day to make an appointment, so I did.

The appointment didn’t go well. In the clinic I told him I had been off my Very Low Carb eating plan off almost 2 months and had gained more than a few pounds. I expected my A1C would probably go up from 5.7% to +/- 6.0%. “My goal is to get it back to 5.6% or below,” I said. He replied, “That would be ‘non-diabetic.’” He added that if I lost 40 pounds, “You would be non-diabetic.” I replied that a few years ago I was 50 pounds lighter than I was now, and I added, with emphasis, “believe me, I was still diabetic,” because I would still be Insulin Resistant.

I then mentioned that when I am “on” my program, I eat between 10 and 15 grams of carbohydrates a day. He responded with a tone and air of certitude, “Twenty grams of carbohydrate a meal is what you should eat.” This really set me off. My new doctor knew everything there was to know about me without even taking a history. I had been a Type 2 diabetic for 28 years, the last 12 of which I have managed to get off virtually all my oral meds and keep (for the most part) good glucose control by diet alone, and now he was telling me how to manage my diabetes his way. I know. I know. He was just following clinical guidelines, as set down by the ADA, the AHA, etc., etc.

He then brought up the subject of statins, declaring he was a lipidologist. I told him I would refuse a statin if he ordered it, and I told him why. I mentioned my latest lipid panel (at the time): TC: 217; LDL: 122: HDL: 85; TG: 49; TC/HDL ratio: 2.6). I said I considered that stellar. He replied that the National Cholesterol Education Program (NCEP-4) Guidelines recommend a TC < 200 and an LDL < 100 (which was true; those were the old guidelines). The new ACC/AHA guidelines (see Retrospective #181) no longer set LDL targets in absolute numbers. I called the NCEP guidelines pure BS and said the gurus and guidelines that I follow are very happy with my lipid (cholesterol) panel.

Actually, I later recalled that one of my favorite books, Paul and Shou-Ching Jaminet’s “Perfect Health Diet” says, “The ideal serum lipid profile – the one that produces the best health and minimum mortality – looks like this:

·         Total Cholesterol level between 200 and 260 milligrams per deciliter

·         LDL Cholesterol level above 100 milligrams per deciliter

·         HDL Cholesterol level above 60 milligrams per deciliter

·         Triglyceride level around 50 to 60 milligrams per deciliter

I then repeated my exceptional HDL (85) and TG (49) numbers and added that my LDL (122) was Pattern “A.” His response was: “Define ‘Pattern A.’” I replied, “large, buoyant, fluffy, rather than small dense, to avoid having oxidized, small dense LDL particles get stuck in the eroded endothelial layer of my arteries. I added that my very low hs C-Reactive Protein scores suggest that my arteries were not inflamed. I showed him my history of CRPs, and he did admit it was “impressive.” They had gone from 6.4 when I started very low carbing to a recent low of 0.1.

But then he said something that shook my faith that my new doctor and I were going to work out. He said, “The latest science is that all LDL are alike. They all get stuck. I asked him for a citation for that. I said I read a lot of medical journals and scientific papers – probably more than he did. He didn’t like that, and replied I did not. How can he know? Anyway, when I asked him later for the “LDL are all alike” citation, he replied, “Give it up!”

What I gleaned from this appointment is that Family Medicine MDs are trained to diagnose “incipient” Type 2 diabetes and treat it with pharmacotherapy. They’ve learned by rote the clinical definition of “diabetic” and “non-diabetic.” They know what Insulin Resistance (IR) is and believe it can be reversed, and “non-diabetic” status achieved, by weight loss alone. But this one doesn’t understand that THAT DOES NOT REVERSE Insulin Resistance.