The Nutrition Debate #300: ‘Sugar’ in Food and Blood: a primer on carbohydrates

I heard an ad on TV last night for a diabetes drug. The ad explains that, “It (the drug) removes some sugar from your body.” I asked (I think audibly to the TV), “How did the sugar (that the drug removes) get into your body in the first place!!!?” And that suggested the corollary question, “If you didn’t eat so many carbohydrates, wouldn’t you have less “sugar” to “remove…from your body”? And this brings me back to the basic question: What foods become “sugar,” in the sense of the ad, in the first place? What foods convert to glucose? The answer, basically, is all carbohydrates.

“Sugar” is in quotes because I am not referring to cane (or table) sugar; I and the ad copywriter are referring to “blood sugar” (glucose), the compound that most carbohydrates break down into by digestion. It’s true that some carbs break down into fructose and glucose, and a few (dairy carbs) into galactose and glucose, and starches are all long-chain glucose molecules, but it is the simple monosaccharide glucose, commonly called “blood sugar” or just “sugar,” to which we refer.

If you have been diagnosed with pre-diabetes or Type 2 diabetes, it is because you first developed a precursor condition called Insulin Resistance (IR). Insulin from your pancreas is required to move the glucose and “open the door” to your cells to “take up” the glucose for energy. IR means the ‘door’ is blocked; glucose can’t get into your cells. It continues to circulate and builds up to high levels, damaging your organs and small blood vessels. You are at high risk for a multitude of diseases.

Most people who are newly diagnosed pre-diabetics or Type 2 diabetics are surprised to learn the “sugar” (glucose) content of common foods. But how much “sugar” (glucose) do carbohydrates make? To understand the answer in context you need to know how much blood “sugar” is “normal,” that is, normally circulating in the blood of a person (before a meal) who has a normal glucose metabolism. The answer is surprisingly low; it’s 1 teaspoon (5 grams equivalent) of “sugar.” See The Nutrition Debate #232, “A spoonful of sugar,” and, for an explanation of the math, the blog of Michael Eades, MD.

As Dr. Eades points out, a diagnosis of Type 2 diabetes is having a “sugar” (glucose) level in your blood equivalent to just 1¼ tsp. Yet, a McDonald's“small” Coke (16oz) has 8 tsp of “sugar,” a Big Mac 9 tsp of “sugar,” a large fries 13 tsp of “sugar,” a large chocolate McCafé shake (22oz) 28 tsp of “sugar,” a bagel 10 tsp of “sugar,” a low-fat chocolate milk 5 tsp of “sugar,” a baked potato 7 tsp and an 8 oz container of low-fat fruit yogurt 9 tsp of “sugar.”  There are hundreds more examples here.

If the door to your cells is partially closed by Insulin Resistance, can you really afford to eat 30, 40, 50 times more “sugar” in one meal (carbohydrates → glucose) than your body can handle? Do you really want to become more and more dependent on drugs to take the “sugar” out of your body that you put into it? You really do have a choice, you know. Self management works. You don’t have to go crazy. You just need to be aware of what your body can handle (by testing your blood sugar), and then be guided accordingly in your food choices. If you don’t, the disease you have acquired by eating too many foods too high in carbohydrates for too long (on the government’s advice!) will surely damage your body, and shorten your life… 

That’s the choice you have to make. I’m not trying to scare you. I’m trying to educate and inform you about how you can make better choices. You probably know this. I hope you feel more empowered now to take the steps you need to take. 

If you’ve read this blog to the end, it’s a safe bet that you’re a neophyte to diabetes, or at least to diabetes self-management. If that’s true, welcome. You might also want to visit Jenny Ruhl’s website, Blood Sugar 101. It’s excellent.

The Nutrition Debate #299: The Set Point: Why Maintaining Weight Loss is So Hard

The excerpt from the Lancet Diabetes and Endocrinology comment in The Nutrition Debate #297, “Obesity in Remission,” brought to mind a segment from “Choices,” the 2^nd of four hour-long videos reviewed in The Nutrition Debate #275, “Weight of the Nation,” published on 12/31/14. You might have missed it. But if you are having trouble losing weight or, having been successful in the past, are now putting weight back on (as I am), you should read #297, and this blog post.

Starting at minute 17:00 in “Choices,” Rudolph Leibel, MD, Co-Director of the New York Obesity Research Center at the Columbia University Medical Center, says, “Individuals losing weight are NOT metabolically the same as they were before they lost weight.” “The weight reduced individual will be requiring about 20% less (sic) calories per day relative to what somebody of that weight who’s never lost weight would eat…in order to keep at that body weight,” he says

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“Consider two individuals – same gender, same age, exactly the same body weight – one of whom is at that body weight as a result of let’s say a 10 or 15% weight reduction, the other who’s been at that weight for their entire adult life. If that reduced weight individual goes out to lunch with her friend, and they both order the same meal, that will represent a 20% overeating for the weight-reduced individual, and be quite normal for the individual who’s not in that state. Twenty percent might seem like a little, but 20% excess calorie intake a year will account for the inexorable weight regain.”

“As far as we know, this phenomenon does not go away,” Dr Leibel says. “So, being successful for a year or two doesn’t mean that you’re going to be able to go back to eating what would be appropriate for a person who’s never lost weight.”

“Does that seem unfair?” an off-camera voice asks an overweight woman. “Sure, it does seem unfair. It’s unfair that, you know, I just can’t lose the weight and go back to the way a normal thin person lives their life, but that’s part of the price you pay for allowing yourself to get overweight in the first place,” the woman responds. Okay, that’s the thinking of this well-meaning and very well-funded, widely-viewed and deeply-flawed HBO series. Forget for a minute who funded it.

You can choose to blame yourself for following the Government’s Dietary Guidelines since 1977, and your doctor’s advice at least since 1961 when the American Heart Association started telling you to eat less saturated fat and cholesterol. That’s when Agribusiness starting making more “low-fat” manufactured foods with added sugars and processed carbohydrates.

Or you can choose to eat many fewer carbs and more fat – both saturated and monounsaturated, but not polyunsaturated fats (vegetable and seed oils). You will feel fuller when you eat fatty meats and fish and a few low-carb veggies. Fat satiates. Protein digests slowly. Your blood sugar will stabilize, your blood lipids will improve, your inflammatory markers will too, and as you lose weight, without hunger, your blood pressure should come down too. All these good things happened to me.

And when I regained some of the weight I lost, but continued to eat low-carb, high-fat – just too much of it – the only thing that went up was the number on the scale. Like many of my readers, I have a “biological predisposition for energy storage” and I live in “an environment that promotes high energy intake” (both carbs and fat). The RESULT: an obesity–promoting interaction between the two (weight gain). This condition is both chronic and, at times, treatment-resistant. I like to eat.

The Nutrition Debate #298: “Obesity in Remission” Part 2

My hopes were up in #297, “Obesity in Remission,” because the powerhouses in obesity medicine whose long comment in Lancet Diabetes and Endocrinology I partially excerpted, appeared to understand the mechanism. Most doctors do not. They also included phrases like “promotes energy overconsumption” (due to habituation and dopamine signaling, palatable foods and reward deficits, etc.), and “increases fat storage capacity” (suggesting the importance of the hormone insulin). I was soon to be disappointed. Apparently, these guys have first-class cabins on the Titanic, and they’re not giving them up

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They’re right of course about all the things that promote “energy overconsumption,” so long as the energy referred to is carbohydrates. But they do not mention that word even once in their long comment. Alas! Would that they explain why!

The human body has two main sources of energy, both in food ingested and stored: Carbohydrates and fat. Carbs can be eaten (to make glucose) or can enter the blood as glucose from glycogen stored in the liver from previously eaten carbs. Fat can be eaten or enter the blood from triglycerides broken down from stored fat when serum insulin is low either because of fasting or when blood glucose is low. This includes people with a disregulated glucose metabolism (Type 2 diabetics, pre-diabetics and carb addicts, i.e. people who have Carbohydrate Intolerance from years of over consuming carbohydrates).

Protein is not considered a primary source of energy for the body because it cannot be stored. But it is needed and used every day for essential functions. The amino acids that protein breaks down into, that have NOT been “taken up” within 4-5 hours of being eaten, go to the liver and are later used to make glucose (blood sugar) in a process called gluconeogenesis.

However, the authors of the Lancet comment do not mention dietary fat as an energy source, much less one to be used for weight reduction since they associate its caloric density (9 calories per gram vs. 4 calories per gram for both carbs and protein) with weight gain and thus advocate avoiding “calorically dense food” as part of a weight reduction strategy. Maybe they’re afraid of saturated fat and cholesterol. If so, they have been wearing blinders and are out of touch with the evolving world of nutrition, perhaps dining in the first class salons as the Titanic continues on its course in the frozen North Atlantic

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They get SO close. They say, “Because sustained obesity is in large part a biologically mediated disease, more biologically based interventions are likely to be needed to counter the compensatory adaptations that maintain an individual’s highest lifetime bodyweight.” Okay, a candidate biologically based intervention would be carbohydrate restriction, allowing serum insulin levels to drop and thus triglycerides (body fat) to be broken down, enter the blood stream, and be used for energy.

But no. They say, “Current biologically based interventions comprise antiobesity drugs, bariatric surgery, and…intermittent intra-abdominal vagal nerve blockade.” (I suspect this 3^rd method is so new it may have been what this is all about.) “These interventions do not permanently correct the biological adaptations that undermine efforts for healthy weight loss but do, during use, alter the neural or hormonal signaling associated with appetite to reduce hunger and caloric intake.” Well, that’s exactly what Carbohydrate Restriction does! “During use,” it “alters the neural and hormonal signaling associated with appetite” and “reduces hunger and caloric intake.” And improves lipid profiles and other CAD and CVD risk markers!

And it does all these things without risk of surgery or the side effects of drugs. What don’t these people understand?

The Nutrition Debate #297: “Obesity in Remission,” a short series

“Obesity in Remission” is a new lexeme in my vocabulary. I discovered it in this long and provocative (for me) comment in Lancet Diabetes and Endocrinology published online (login req’d). A link to the Lancet summary and to the full text of the comment was provided by this Medscape Medical News piece. Why it was provocative for me will be the subject of Part 2 of this series. This post is a long excerpt from the beginning of the comment to explain in context “Obesity in Remission.”

“Many clinicians are not adequately aware of the reasons that individuals with obesity struggle to achieve and maintain weight loss,¹ and this poor awareness precludes the provision of effective intervention.² Irrespective of starting weight, caloric restriction triggers several biological adaptations designed to prevent starvation.³ These adaptations might be potent enough to undermine the long-term effectiveness of lifestyle modification in most individuals with obesity, particularly in an environment that promotes energy overconsumption. However, they are not the only biological pressures that must be overcome for successful treatment. Additional biological adaptations occur with the development of obesity and these function to preserve, or even increase, an individual's highest sustained lifetime bodyweight. For example, preadipocyte proliferation occurs, increasing fat storage capacity. In addition, habituation to rewarding neural dopamine signaling develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.⁴ Importantly, these latter adaptations are not typically observed in individuals who are overweight, but occur only after obesity has been maintained for some time.³ Thus, improved lifestyle choices might be sufficient for lasting reductions in bodyweight prior to sustained obesity. Once obesity is established, however, bodyweight seems to become biologically stamped in and defended. Therefore, the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely.

“Evidence suggests that these biological adaptations often persist indefinitely, even when a person re-attains a healthy BMI via behaviourally induced weight loss.³ Further evidence indicates that biological pressure to restore bodyweight to the highest-sustained lifetime level gets stronger as weight loss increases.⁵ Thus, we suggest that few individuals ever truly recover from obesity; individuals who formerly had obesity but are able to re-attain a healthy bodyweight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and bodyweight who never had obesity.^3, 5 For most individuals, these biological adaptations need to be addressed for weight loss to be sustained long-term. We believe these mechanisms largely explain the poor long-term success rates of lifestyle modification, and obligate clinicians to go beyond mere recommendations to eat less and move more.”

“Individuals who formerly had obesity but are able to re-attain a healthy bodyweight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and bodyweight who never had obesity.” Boy, who among us (overweight and obese) cannot relate to this statement? The authors of this “comment” in Lancet, who are all recognized, distinguished authorities in Obesity, have explained in understandable terms the dilemma that so many of us have experienced. I commend them for their efforts to share their understanding with other clinicians, urging that they should “go beyond mere recommendations to eat less and move more. For this: “Bravo,” as far as it goes.

These distinguished experts in obesity have described how “these mechanisms,” specifically “these biological adaptations,” “need to be addressed for weight loss to be sustained long-term.” I love that it that they think it should “obligate clinicians” to go further, and I look for them to explain how. My hopes soar with phrases like “promotes energy overconsumption” and “increases fat storage capacity” that suggest they might know the mechanism, but then they associate “avoiding calorically dense food” with a means of “seeking weight reduction.” Alas, my hopes are dashed. See Part 2 next to see how they did it.

The Nutrition Debate #296: Another Nail in the Coffin of the Dietary Guidelines

Zoe Harcombe, popular author and obesity researcher, got her first piece in the British Medical Journal’s Open Heart recently. The BMJ is perhaps the world’s most discriminating arbiter of medical science. Its Open Heart organ is an “open access, peer reviewed, online-only journal dedicated to publishing research in all areas of cardiovascular medicine.” This piece fit the requirements, and the conclusion was earthshaking. The title tells it all: “Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systemic review and meta-analysis.”

Harcombe conceived of this original research article and collaborated with several other credentialed authors in the data extraction, meta analysis and writing of the manuscript. All the authors were involved in the critical evaluation of content and reported no competing interests. The article has 32 linked references and was externally peer reviewed by the BMJ.

The full-text article came to my attention from a piece in Diabetes in Control: “Government Dietary Fat Guidelines Did Not Have Sufficient Supporting Evidence.” The subtitle restates the CONCLUSION of the Abstract of the paper: “Dietary recommendations introduced for 220 million U.S. and 56 million UK citizens by 1983 did not have sufficient supporting evidence from randomized controlled trials.” To be clear, the RCT studies evaluated were all published before 1983.

For the uninitiated, 1977 was the year where in the U.S a Senate Select Committee called the McGovern Commission held a few hearings and subsequently published the Dietary Goals for the United States. That document, prepared by Senate staffers, was the precursor to the 1980 Dietary Guidelines for Americans, which was revised and republished every five years thereafter. The Brits followed with their own dietary standards in 1983. These events have been chronicled in many places including briefly in The Nutrition Debate #4, “Big Government, Big Pharma and Poor Little Dr. Atkins.”

The dietary recommendations introduced in the U.S (1977) and in the UK (1983) were to reduce overall fat consumption to 30% of total energy intake and reduce saturated fat consumption to 10% of total energy intake. The protein recommendation was set at a meager 10% and the carbohydrates at a whopping 60%. That’s why starting around 1980 we (as a population) started to get fatter. That’s why diabesity skyrocketed and heart disease and many other diseases of “malnutrition” (for lack of fat-soluble vitamins from animal based foods) have plagued our nations.

In recent years, we have come to realize that the American public are participants in the largest uncontrolled experiment in history. This experiment hasn’t turned out very well, and we are still suffering the consequences. So, now the Titanic is slowly changing course. The limitation on the total percentage of fat in the diet has been omitted (#294), and now, hopefully (#295), in the 2015 Dietary Guidelines, cholesterol will “no longer be considered a nutrient of concern for overconsumption.” Think about it: All the shrimp, egg yolks, butter, etc. you have given up over the years, needlessly.

 I suspect the BMJ piece is but one of several initiatives in the non-conflicted medical and nutrition community to influence the members of the 2015 Dietary Guidelines Advisory Committee (DGAC). This group has had to endure a barrage of testimony from powerful Agribusiness. This list of oral presenters from 1 day of the 2^nd of 7 public hearings of the DGAC is just the tip of the iceberg and illustrates the immense pressure they are under. I’ve got my fingers crossed for their integrity.

The Nutrition Debate #295: Cholesterol: no longer “…considered a nutrient of concern…”

“NBC’s ‘Today Show’ had a story about dietary cholesterol,” my wife said at breakfast yesterday. Later we both heard a similar story on PBS’s “All Things Considered” as we drove to our separate engagements. So, today I did a Google News search on “dietary cholesterol” (the cholesterol in food, like eggs and shrimp, that we eat). The first story that came up was from Fox News. It wasn’t very good. The author puffed it up with off-message “contributions” from the AP and Reuters.

Still, the essence was that Marian Neuhouser, chair of the relevant subcommittee of the 2015 Dietary Guidelines Advisory Committee, announced a decision to the full DGAC committee at its final meeting in December 2014. She said it is their recommendation that dietary cholesterol no longer be ‘considered a nutrient of concern for overconsumption,’ according to the Fox News Report. A 6hr. 57min. indexed video of the full meeting, #7 (December 15), is online and can be seen here.

The final report, “2015 Dietary Guidelines for Americans,” will be published by the USDA/HHS later this year. “While those agencies could ignore the committee’s recommendations, major deviations are not common,” The Washington Post said.

“Five years ago, I don’t think the Dietary Guidelines diverged from the committee’s report,” Naomi K. Fukagawa, the 2010 vice chair, told The Washington Post. Fukagawa says she supports the change on cholesterol. “Walter Willett, chair of the nutrition department at the Harvard School of Public Health, also called the turnaround a ‘reasonable move,’” The Post reported. “There’s been a shift of thinking,” he said. (“…a shift of thinking”? Incredible that he said that!)

Well, la-di-da, the Titanic IS really changing course. (See: The Nutrition Debate #12: “Turning the Titanic,” also #162, #189, #202, and #292). And this is MAJOR, except that, with this report, saturated fat is left behind; it is still one of the bad guys. But it’s good news for people who long for shrimp. I actually know a few, including medical doctors, who have passed up shrimp being passed as h’ordeuvres at a cocktail party, and others who eat egg whites instead of whole eggs for breakfast. (See: The Nutrition Debate #176, “Eggs, Cholesterol and Choline,” #211, “Eggs and Satiety,” and #225, #228 and #265.

The danger, of course, with the Titanic changing course, is whether it is turning to port or to starboard. If it turns to starboard, it will run into a sea of ice flows and eventually solid sea ice. Think eroded endothelial layers, advanced glycation end products (AGEs), and clogged arteries from the rancid and oxidized LDLs (oxLDL) in overused and overheated vegetable and seed oils. (See: The Nutrition Debate #21, “The Dangers of Polyunsaturated Fats,” also #20, #22, #23, #24, and #49.)

That’s the outcome that can be expected 1) from the 2013 AHA/ACC recommendation that the target for total dietary fat consumption be omitted to allow fat to replace the formerly much too high Dietary Guidelines recommendation for carbohydrates, both simple sugars and highly processed carbs; and 2) that saturated fat consumption be further reduced from the previous 7% - 10% of total calories to 5% - 6%. With this 1-2 punch the resultant recommendation will be that we consume more Mono and Polyunsaturated fats. But, while monounsaturated fats are good, most PUFAs are BAD.

That’s exactly where the Titanic is headed, with the blessing of Robert Eckel, current co-chair of the ACC/AHA guidelines committee and past president of the American Heart Association. While he conceded that there is “insufficient evidence” to make a recommendation to support dietary restrictions of cholesterol, he said “a three-to four-egg omelet isn’t something I’d ever recommend to a patient at risk for cardiovascular disease.” Some myths die hard. 

The Post story recalls the origins of the cholesterol myth. A Russian scientist at the Czar’s Medical Institute in St. Petersburg fed cholesterol to rabbits for four to eight weeks in 1913 and saw that the cholesterol harmed them. Then in the 1960s an American graduate student, Lawrence Rudel, noted that when the Russian fed cholesterol to white rats, it had no effect. Later, Ancel Keys acknowledged the difference between obligate herbivores (rabbits) and mammals (rats and humans). In 1997, Ancel Keys, father of the diet/heart hypothesis (saturated fat + cholesterol → heart disease), infamously said:

“There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”

Then there’s this: Updated findings of the famous Framingham Study, published in Archives of Internal Medicine (2009):

“In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol. . . we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active.” Quote from Dr. William Castelli, Director.

The Nutrition Debate #294: “Saturated Fat and CAD: It’s Complicated”

Tricia Ward, Editorial Director of theheart.org at Medscape Cardiology, took on a challenging assignment with this long survey piece. I’m taking on the assignment too, but I will shorten and steer my review using my “selection bias.” The Medscape review is a good piece, generally, designed to educate doctors. It gets a lot of the basics about SFAs right and introduces the busy physician to many aspects of newer concepts from evidence-based-science. That’s a catch phrase that’s all the rage these days. It was deployed here, I think, to draw a stark contrast with the now widely disparaged diet/heart hypothesis.

The setup: “Dietary guidelines for the prevention or treatment of coronary artery disease (CAD) have emphasized a reduction in the consumption of saturated fat since the 1960s.” Here a footnote links to a 1961 piece in Circulation, the journal of the American Heart Association (AHA). Note: 1961 was the year that Ancel Keys, father of the diet/heart hypothesis, appeared on the cover of Time magazine and joined the board of the AHA. The setup continues: “Dietary saturated fat increases blood levels of low-density lipoprotein cholesterol (LDL-C) and subsequent risk of CAD, or so goes the conventional wisdom.” The “doubting Thomas” tone is appropriate, and an encouraging start.

The tension rises: “The disparate findings have led to calls to stop demonizing saturated fat and equally vocal cries to proceed with caution before we let lard back into the menu.” Now, the plot starts to thicken; Introducing the “bad” guys:

“Meanwhile, the 2013 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines on lifestyle management to reduce CVD risk omitted a target for total dietary fat but did recommend a goal of 5%-6% of calories from saturated fat.” Three points: 1) The lead author of the ACA/AHA guidelines is Robert Eckel, professor of medicine at the University of Colorado. He is one of the protagonists in this story but is not introduced by name into the narrative until more than half way through; 2) Note the significant omission of a target for total dietary fat. It was previously less than 30% of total calories; and 3) Note the limitation of SFAs to 5%-6%. It was previously 7%-10%. That’s a significant reduction. (This is about 11g or 2.25 teaspoons of butter for a person eating 2000 calories a day.)

The other protagonist in this set piece is Dariush Mozaffarian, dean of the Friedman School of Nutrition Science and Policy at Tufts University in Boston. He gets most of the science right (IMHO) – and I cannot emphasize that enough – but just cannot walk through the open door provided by the ACA/AHA’s omission of a target for total dietary fat. Instead, Ward quotes him as saying, “polyunsaturated fats are beneficial…” Perhaps this comment is taken out of context by Ward and reflects her personal bias. And by doing so, she becomes a third protagonist, representing the PUFA contingent.

Mozaffarian does disagree with Eckel’s 5%-6% limit on SFAs. “To derive a conclusion that saturated fat should be 5% of calories [from the DASH study, as Eckel does] is not evidence based,” he says. Other Mozaffarian gems include: “The School Lunch Program allows chocolate skim milk and banned whole milk. That’s absurd.” Another: “…the biggest driver of de-novo lipogenesis [where the liver makes body fat from large slugs of liquid or other highly processed carbs] is the dose and speed that the carb is delivered.” Ward explains, “In terms of foods, a bagel or soda consumed in isolation is more likely to trigger [the liver making fat] than a small amount of potato mixed with vegetables and oil.”

Mozaffarian’s comment that “The U.S. view on saturated fat is totally based on the effects on LDL-C, and that’s why we have dietary guidelines to lower our saturated fat intake…” begins a good discussion of LDL-C particle size, concentration, HDL-C and triglycerides.” The article gets into the weeds a bit but it's good and, as I said, it is written for a technically savvy reader.

My biggest gripe, and personal bias, besides giving Eckel and the ACA/AHA guidelines so much play, was Ward’s transparent injection of her own POV about PUFAs. I think she pushes both Eckel and Mozaffarian, and Marion Nestle whom she quotes a few times, toward the Mediterranean “dietary pattern” touted by the 2010 Dietary Guidelines for Americans. It and the ACA/ADA guidelines are widely expected to be repeated in the 2015 Guidelines due out in less than a year. Why, you ask?

Alice H. Lichtenstein, D. Sc., is Vice-chair of the 2015 Dietary Guidelines Advisory Committee and is in charge of drafting the document. Lichtenstein was also the lead author on the AHA’s current “Diet and Lifestyle Recommendations.” And she also served on the AHA committee in which Robert H. Eckel, M.D. was co-chair and lead author of the above mentioned “2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk. Together, they are a formidable force today.

On a lighter note, my favorite part of this Medscape piece is the comment section. You can link to it here.

The best one, from Dr. J M, was: “Will the ghost of Ancel Keys ever be exorcised?” There’s also a very good one by Dr. Robert Hansen on “replacing SFA with PUFA [will] result(s) in increased oxLDL and increased Lp(a) in humans.” BRAVO! Take a look, if you feel up to it. In my opinion, Hansen got it right, but alas, his is still just a voice in the wilderness.

So, there’s evidence out there that there are a few doctors who are paying attention to the evolving story of (dietary cholesterol), saturated fat and CAD, and many, sadly, who are not. The story, I think, is perhaps more complex than complicated.

The Nutrition Debate #293: The HEAL Clinics: Diabetes and Medical Weight Loss

As I said in #292, I am not angry at doctors, blah, blah, blah, “even though they are aware that how they are required to treat [Type 2 diabetic patients] will trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.”  These clinicians, I said, “are in a tough spot.” But, there exists on the fringes of mainstream medicine a few doctors who have broken from the pack. Among them are academics (what have they got to lose?), and a few lone wolves/mavericks. Until now.

Individual practitioners, even those working in an academic setting (research/teaching/clinic), can have only a limited influence. Frequent submissions to peer-reviewed journals and writing popular books can add to the effect. Leadership in professional organizations where you can “set the agenda” helps too. But the real impact – the “cavalry to the rescue” impact ala Jeb Stuart – can only be realized by someone who leads a band of raiders effectively attacking from the rear.

The army of sheep – the obese, pre-diabetic and diagnosed Type 2s out there who are being herded into a “lifelong regimen of drug management, obesity and escalating diabetes” – are ready to be rescued. And the rear guard today, the physicians who know that they “are in a tough spot” because they follow “the current treatment protocol” that the medical establishment has ordained as the “standard of care,” and know it doesn’t work for the majority of patients, are ready too. Many of these physicians are looking, as we are, for a “rescue.”

Well, the time may be right. Or the fruit ripe. There’s certainly plenty of it “low-hanging.” ;) It’s time to introduce to the “partisans” (all of us who are trapped with similarly aligned clinicians) someone known to all of us “LC followers” who have been looking for answers and leadership. It is Eric Westman, MD, MHS, Associate Professor of Medicine at Duke University and Director of the Duke Lifestyle Clinic. He is perhaps best known to “our crowd” as the co-author of both “The New Atkins for a New You” and “Cholesterol Clarity.” He is also currently president of the American Society of Bariatric Physicians.

Dr. Westman’s newest venture is as Co-founder, President and Chief Medical Officer of HEAL Clinics, a start-up being developed by Bruce Rossiter, Co-founder, CEO, Chairman and chief fund-raiser. Rossiter has startup and venture capital experience to balance Westman’s medical expertise. The heretofore unattributed quote (“will trap patients in a lifelong regimen of drug management, obesity and escalating diabetes”) is lifted from the Private Placement Memorandum (6-pages) at the Investors tab at healclinics.com. The best part from a “sufferers” POV is Dr. Westman’s 2 ½ page Manifesto titled, “Benefits of HEAL Clinic’s Low-Carb Lifestyle – Putting Diabetes in Remission.” The remainder of this blog post is selected quotes from the PPM. I encourage you to click on this link and read about HEAL.

“Type 2 diabetes occurs when a person consistently eats too many carbohydrates. All carbohydrates (except for the fiber content and small amounts of vitamins and minerals) convert to blood sugar (glucose). When one consumes excessive carbs, the pancreas produces excessive insulin. It is both the excessive levels of glucose and insulin that produces harmful and chronic inflammation, damaging our cells and organs.”

“Excessive carbohydrate consumption is encouraged by the U. S. Dietary Guidelines and the food industry, which provides tens of thousands of highly processed, sugar and other carb-laden foods to entice us. Studies show that sugar is more addictive than cocaine. It is this combination of our own desire to eat excessive carbs and the food industry’s desire to sell carb-filled products that has created our obese and unhealthy population….”

“Many people not yet diabetic or pre-diabetic are asymptomatically obese, meaning they are obese but do not have symptoms yet, though they are at high risk of developing pre-diabetes and subsequently diabetes by consuming excessive carbohydrates. A segment of our population is normal in weight but still suffers from Type 2 diabetes or pre-diabetes.”

“Since excessive eating of carbohydrates can cause Type 2 diabetes, it can be put into remission by following a Low-Carb lifestyle. The HEAL Low-Carb Protocol is far more preferable than doctors prescribe medications and insulin that are expensive and have potentially dangerous side effects. It is well documented that the standard ‘pills-and-needles’ treatment method rarely puts diabetes into remission. However, it is certain that following HEAL’s Low-Carb Protocol will put almost every person with Type 2 diabetes into remission.”

“A Low-Carb lifestyle is not the medical establishment’s standard of care for Type 2 diabetes even though it is a safe, effective, and well-researched way to put the disease into remission. Perversely, many of the prescribed medications, such as insulin, cause weight gain and increase food cravings, making it difficult for a patient to lose weight. Most of the blood sugar control medications have side effects, many of them serious. The current treatment protocols trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.” [The emphasis was added by me, of course.]