REtrospective #245: “…in patients on sulfonylureas”

Lots of Type 2 diabetes patients are on sulfonylureas (SUs). They were the first class of oral anti-diabetic medications approved in the U.S. (1955) and remained the only class until 1995 when metformin (Glucophage) was added. Metformin eventually took over and became the first-line drug, used even for the treatment of Prediabetes. 

Second generation SUs, approved in 1984, include the familiar generics glyburide (Micronase, Diabeta) and glipizide (Glucotrol). All SUs act by increasing insulin release from the beta cells in the pancreas. Some diabetes experts feel that SUs accelerate the loss of beta cells from the pancreas and should be avoided. Ralph DeFronzo, MD, in his 2008 ADA Banting Award keynote speech, said, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1c and progressive loss of ß-cell function”

The Wikipedia entry advises that SUs “decrease lipolysis [breakdown and release of fatty acids by adipose tissue] and decrease clearance of insulin by the liver.” Thus, “like insulin, sulfonylureas can induce weight gain…”). In addition, “All sulfonylureas carry an FDA-required warning about increased risk of cardiovascular death.” And that’s not all.

Wikipedia continues, “First line therapy with sulfonylureas significantly increases the risk for death in patients with Type 2 diabetes when compared with treatment with metformin. Additional research showed that the combination of metformin and a sulfonylurea was also associated with a significantly increased risk for death when compared with combination therapy with metformin and a dipeptidyl peptidase-4 (DPP-4) inhibitor

“Sulfonylureas are potentially teratogenic [think 2-headed] and cannot be used in pregnancy or in patients who may become pregnant. Impairment of liver or kidney function increases risk of hypoglycemia, and are contraindications.”

And then there are the Interactions. Wikipedia: “Drugs that potentiate or prolong the effects of sulfonylureas and therefore increase the risk of hypoglycemia include acetylsalicylic acid [aspirin] and derivatives, allopurinol, sulfonamides, and fibrates. Drugs that worsen glucose tolerance, contravening the effects of anti-diabetics, include corticosteroids, isoniazide, oral contraceptives and other estrogens, sympathomimetics, and thyroid hormones. Sulfonylureas tend to interact with a wide variety of other drugs, but these interactions, as well as their clinical significance, vary from substance to substance.” Sympathomimetics include caffeine and some decongestants.

Then there’s a 2014 report in JAMA Internal Medicine regarding interactions of sulfonylureas and antibiotics resulting in hospitalizations or emergency department visits. The lede: “Use of certain antimicrobial agents is linked to an increased risk of hypoglycemia in older patients on sulfonylureas, according to a study of Medicare claims.” The JAMA finding: “Physicians should definitely avoid using those antibiotics in patients on sulfonylureas.”

I was on a sulfonylurea (Micronase, then the generic glyburide) from my initial T2 diagnosis in 1986. When Glucophage (metformin) was permitted in the U.S., my doctor added it. As I continued to eat “one-size-fits-all” balanced diet, with 55% to 60% carbohydrates as recommended since 1980 for everyone by the USDA’s Dietary Guidelines for Americans, my diabetes got progressively worse. Eventually, I was “maxed out” on both metformin and glyburide and starting a 3^rd class of oral antidiabetic drugs. I knew that my drug “cocktail” was soon destined to be replaced by injected insulin.

That’s when my doctor, who had just read Gary Taubes’s “What If It’s All Been a Big Fat Lie,” the NYT Magazine cover story on July 7, 2002, suggested I try a Very Low Carb diet to lost weight. I did and the first day I got hypoglycemia. I ate a candy bar and called the doc. He told me to drop the new drug he had added.” The second day, hypoglycemia returned and he told me to cut the glyburide and metformin in half. I did, and the next day, he said, “Cut them in half again.” Eventually I stopped the glyburide and for the last 17 years, I have taken just one 500mg of metformin a day.

Doctors still prescribe SUs. They’re dirt cheap and they lower blood sugar and A1c’s (which are elevated because of the foods we eat). But metformin is now dirt cheap too. So, for patients still on sulfonylureas, I ask myself, in view of all the downside risks, why don’t they just change the foods they eat? They won’t need to take a sulfonylurea.

Retrospective #244: Diabetes on Rise but Complications Decline

“Diabetes on the Rise but Complications Decline” was the title of a video on my Medscape Alert a while back. The subtitle was “Diabetes on Rise as Waistlines Expand.” Sounds to me like it’s another epidemiological analysis.

Declining complications and expanding waistlines are “sentinel indicators of outcomes,” in Type2 diabetes, according to the narrator. The data were collected from several very large public databases which “…examined 5 complications of diabetes – acute myocardial infarction [heart attack], stroke, lower extremity amputation, end-stage renal disease, and death from diabetic ketoacidosis…” The story references an article from the New England Journal of Medicine.

“We are all aware that we have epidemics of diabetes and obesity in the United States,” the narrator observed, but he didn’t attempt to explain why. The NEJM ABSTRACT made a similar observation, and added that “preventive care for adults with diabetes has improved substantially in recent decades.” It concluded that “rates of diabetes related complications have declined substantially in the past two decades.” Translation: Treatment of the blood glucose symptoms of Type 2 diabetes have reduced morbidity and mortality from the disease, but not addressed the cause.

The specific findings: “The diagnosis of diabetes increased from about 6.5 million in 1990 to almost 21 million in 2010, but the rates of major complications actually fell in all 4 age groups.” There was a 69% reduction in MI cases, a 53% reduction in strokes, “but the rates of MI and strokes were about the same.” There were also fewer cases of amputations (“a reduction of more than 50%”) and fewer cases of end stage kidney disease (“a reduction of about 28%”), and hypoglycemic (sic) crises declined by 65%. (NEJM article reported on hyperglycemic crises.)

The Medscape author opined, “It is hard to pick any particular factor,” he sais, but noted that “studies have shown that risk factor control, how you organized your healthcare system, and patient support for issues such as smoking cessation are all important in improving care, but certainly new drugs (e.g. statins) and such cardiovascular procedures as revascularization might help as well.” [Did he really call statins “new drugs”? He must be living under a rock.]

The video concluded, “The idea of using team-based care is promoted and probably an important factor; then repeats, “Medications are better, especially for lowering cholesterol, as are treatment of risk factors and patient education.

What the good doctors failed to mention in either the ABSTRACT or the Medscape piece is that the increased patients with diabetes is in large part due to the changes made in the diagnostic criteria for Type 2 diabetes.  In 1997 the threshold for diagnosing Type 2 diabetes changed from a fasting glucose level of 140mg/dl to 126mg/dl. Then, in 2002, the American Diabetes Association defined, for the first time, Prediabetes, enlarging the patient population. Prediabetes is described as impaired fasting glucose (IFG,) defined as a fasting blood glucose of 100-125 mg/dl. People with Prediabetes are at increased risk for developing Type 2 diabetes and for heart disease and stroke.

So, if you want to define changing standards for defining a threshold diagnosis of Type 2 diabetes and Prediabetes as “preventive care for adults with diabetes has improved substantially,” so be it. But changing standards for screening for and treating Type 2 diabetes are reasons why the ratio of complications (numerator) to number of cases diagnosed (denominator) is improving. As the denominator gets larger, the fraction gets smaller. That’s 5^th grade math.

My beef with this report is that is both detached and delusional. If I were an MD clinician or PHD epidemiologist, I would take no comfort from this report. It is both detached and delusional in the sense that it’s like the deckhands rearranging the chairs on the Titanic as the ship sinks. Treating the symptoms of Type 2 diabetes is all these deckhands are doing. And deliberately creating misleading relative rather than absolute ratios is just a feel-good delusion.

In addition, the report doesn’t recognize that obesity itself is but a symptom of Type 2 diabetes, or rather of the larger Metabolic Syndrome, the mechanism of which is Insulin Resistance (IR). IR is the cause of the disregulated glucose metabolism and broken fat metabolism, that is the “sentinel indicator” of Type 2 diabetes that needs to be addressed.

But epidemiologists keep rearranging the deck chairs and clinicians keep writing scripts. It’s very sad. Tragic, really.

Retrospective #243: New York Times good; Fox News bad!

I was pretty excited to see in my inbox a study published in The Annals of Internal Medicine. Funded by the National Institutes of Health, it was a randomized controlled trial (RCT) to show the superiority of low-carb over low-fat dieting for losing weight. The result showed the superiority of low-carb over low-fat in the primary end point of the hypothesis being tested: improving heart disease risk, using all the classical markers for determining that risk.

The study, “Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial,” was performed at the Tulane University School of Public Health in New Orleans. It enlisted a diverse population of 148 men and women without either clinical cardiovascular disease or diabetes. The study DESIGN: “A randomized, parallel group trial. The OBJECTIVE: “To examine the effects of a low-carbohydrate diet compared with a low-fat diet on body weight and cardiovascular risk factors. I was able to read only the ABSTRACT, as full access cost $29.95.

The study participants were randomly selected to be placed in one of two groups and had no restrictions on calories. They were also told to make no changes in physical activity. The target for the low-carb group was to eat less than 40 grams of carbohydrate a day. The target for the low-fat group was to eat less than 30% of daily energy intake from total fat and less than 7% from saturated fat. Both groups received dietary counseling from an RD and were tested at baseline, three months, six months, and twelve months. About 80% of the participants finished the one-year study.

The CONCLUSION was succinct: just two sentences. The first is declarative and absolute: “The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet.” The second, “Restricting carbohydrates may be an option for persons seeking to lose weight and reduce cardiovascular risk factors,” is prospective and phrased more like an implied suggestion. This may be more palatable to physicians, who have not been trained in nutrition, and to nutrition professionals who, together with physicians, have all been misled.

The results, in layman’s terms, have now been broadcast widely. Andreas Eenfeldt (The Diet Doctor) and Jimmy Moore (Livin’ La Vide Low-Carb) were among the first. But The New York Times, The Wall Street Journal, National Public Radio, Time Magazine, CBS News, and the Washington Post, were all quick to follow. The NYT’s summarized it thus:

●     Triglycerides – the type of fat that circulates in your blood – “plunged” on the low-carb diet.

●     HDL – the so-called “good” cholesterol – rose more sharply than it did for people on the low-fat diet.

●     Total Cholesterol/HDL ratio – an important maker of heart disease risk – improved.

●     Chronic systemic inflammation – as measured by hs-CRP (C-reactive protein) also “plunged.”

●     Blood pressure, total cholesterol and LDL, the “bad" cholesterol, showed little change in both groups.

The NYT article was clearly open-minded and its view of the results positive. A professor of cardiology at McGill University in Montreal who was not associated with the study was quoted as saying that the decrease in [heart disease] risk on the low-carbohydrate diet “should translate into a substantial benefit.” He added,

“One important predictor of heart disease that the study did not assess was the relative size and number of LDL particles in the bloodstream. Two people can have the same overall LDL concentration, but very different levels of risk depending on whether they have a lot of small, dense LDL particles or a small number of large and fluffy particles.”

In contrast to the very well reported and balanced story in the New York Times, the Fox News Channel had a cardiologist on their “Fox and Friends” program who failed to mention, in terms of heart disease risk, all the clearly beneficial primary outcomes of the trial, including the 5 bullets above. He did, however, begrudgingly acknowledge, it seemed to me with genuine surprise, that Total Cholesterol and LDL (the so-called “bad” cholesterol) stayed about the same for people in each group. That was no surprise to me. Personally, I have seen all the listed cardiovascular risk benefits and more. In the course of a few years, I also managed to lose a tremendous amount of weight (170 pounds).

Maybe the more conservative Fox News Network was interviewing a more conservative cardiologist. Frankly, it seems to me that he (and most of the conservative medical establishment) has plaque on the brain, not in their arteries. 

Retrospective #242: God Favors Animal Fat

About one-third through Nina Teicholz’s, The Big Fat Surprise, possibly the best book yet on nutrition and healthy eating for the whole human race, I came across a reference I had never seen before. Nina describes herself as a tireless researcher with a nine-year obsession reading thousands of scientific papers, but she does not explain how she came upon this citation from the Old Testament, Genesis, Chapter 4, Verses 1-5 (New International Version):

[1] “Adam lay with his wife Eve, and she became pregnant and gave birth to Cain. She said, ‘With the help of the LORD I have brought forth a man.’ [2] Later she gave birth to his brother Abel. Now Abel kept flocks, and Cain worked the soil. [3] In the course of time Cain brought some of the fruits of the soil as an offering to the LORD. [4] But Abel brought fat portions from some of the first born of his flock. The LORD looked with favor on Abel and his offering. [5] but on Cain and his offering he did not look with favor. So, Cain was very angry and his face was downcast.”

Well, we all know what happened next: Cain killed Abel. How prophetic! Cain, who favored “the fruits of the soil,” killed his brother who favored animal fat. When I read this passage the NIV Study Bible to my wife, she said it sounded “paraphrased.” So, I went to her copy of “The Revised Standard Version” of The Holy Bible. Verse 4 there reads: “And Abel brought of the firstlings of his flock and of their fat portions. And the LORD had regard for Abel and for his offerings.” When I read this to my wife, she had to agree it was essentially the same: God favors animal fat.

But just to be sure, I searched online for the King James Version of the Bible (the one I grew up with). Verses 4-5 read as follows: “[4] And Abel, he also brought of the firstlings of his flock and of the fat thereof. And the LORD had respect unto Abel and to his offering: [5] But unto Cain and to his offering he had not respect. And Cain was very wroth, and his countenance fell.” So too, the Samaritan Pentateuch (Hebrew language version of the Torah), Septuagint, Vulgate, Syriac, even the Masoretic Text, all have the same ancient message: God looks upon animal fat with special favor.

When my wife was satisfied that Nina Teicholz had accurately cited the passage from Genesis in The Big Fat Surprise, she got the message and then contributed to the message with this: The New Testament’s Parable of the Prodigal Son (NIV Luke 15: 11-31), paraphrased: When the “lost” son, who had squandered his inheritance (while his father lived), and returns home to humbly ask for his father’s forgiveness, the father instead celebrates the return of his “lost” son, with these words: [23] “Bring the fattened calf and kill it. Let’s have a feast and celebrate.” God favors animal fat.

Has animal fat always been the preferred source of nutrients for optimal human health? That we evolved to select the “fat portions” of our “fattened” domesticated animals to eat first? Tribal peoples all over the world, who were neither Jews nor Christians, also preferred the fat and viscera (organs) rather than muscle meat. Teicholz writes (pg. 17) “…the Inuit [aka Eskimos] were careful to save fatty meat and organs for human consumption while giving leaner meat to the dogs. In this way, humans ate as other large, meat-eating mammals do. Lions and tigers, for instance, first eat the blood, hearts, kidneys, livers, and brains of the animals they kill, often leaving the muscle meat for vultures.”

Vilhjallmur Stefansson, the Harvard-trained anthropologist, learned this during the year he spent living with the Inuit in the arctic.  He ate the same meat and fat, including organ meat, as the Inuit. And when he returned home and was ridiculed for reporting his observations, he submitted to a year-long experiment eating just “the Eskimo diet.” And “during the ensuing year,” Teicholz wrote, “Stefansson fell ill only once – when experimenters encouraged him to eat only lean meat without the fat.” “Diarrhea and a feeling of general baffling discomfort,” Stefansson said, “were quickly cured by a meal of fat sirloin steaks and brains fried in bacon fat.”

But lions and tigers and even Eskimos are not part of our experience. We are products of what has come to be called Western Civilization. And we have become victims of our own prodigal past. We have abandoned our traditional ways of eating and have been led astray by “Cain” and a diet of mostly processed grains, sugars and “vegetable” (seed) oils.

By some accounts, you can’t get much earlier in the history of the human race than Adam and Eve, who begat Cain and Abel. And, “(I)n the beginning” God looked with favor on Abel and on animal fat. So, where did we go wrong? 

Retrospective #241: Should A1c Increase with Age?

The headline in Diabetes in Control reads “HbA1c Increases with Age.” Headlines like this are often evidence of confirmation bias and can be perilously misleading. So, I read the digest piece and then the abstract in the medical journal Diabetic Medicine. If you register and pay a big fee, you can get 24-hour online access to the full study from publisher Wiley.com. Such is the cost to society for dissemination of partially government-funded medical research.

Interestingly, it appears, on Diabetes in Control is guilty of confirmation bias. The medical journal is simply guilty of myopia. I say “it appears” because that is all I can afford. The full study could disabuse me of my take (and biases). That said, this study was a review of two data sets whose aim was “to determine whether using HbA1c for screening and management, in a “cross-sectional analysis in adults without known diabetes,” the effects of aging have an impact on diagnostic accuracy.” That’s reasonable, and the researchers found some interesting, but unsurprising RESULTS.

My quarrel, then, is not with the researchers. It is with Diabetes in Control, and with their headline writer in particular. It is not nit picking to point out that the headline and the Diabetes in Control story are contradictory. Neither is it consistent with the AIM, RESULTS or CONCLUSION of the actual paper, as reflected in the ABSTRACT. In addition, disparities like this just cause me to get a bit unglued and go off on a rant, so hold on to your seat. It’s a brief one.

The study adjusted for covariates for a multitude of factors, such as race, BMI, etc, but not for treatment modality. Here’s where the myopia, or maybe just ignorance comes in. Everyone in both data sets received the same or a similar failed treatment plan, the ADA Standard of Care of Type 2 diabetes. So, naturally, everyone’s A1c increased as they got older! BREAKING NEWS: It was supposed to increase as they got older! The establishment medicine definition of diabetes is that it is a PROGRESSIVE disease. That means: Your condition will get worse as you get older IF YOUR DOCTOR FOLLOWS THE ADA STANDARD OF CARE. And as your condition gets worse, your A1c will get worse. Duh!!!

So, that’s where the digest failed. It just saw this result the way it was predisposed to see it. Except it was also careless; it describes the data sets as “adults with known diabetes,” not “without known diabetes.” A typo?

Another quibble I have is with the characterization that “the researchers found a remarkable decrement in the performance of the predictive value of A1c as compared with a 2-hour Oral Glucose Tolerance Test (OGTT), with age. Well, la dee dah. It shouldn’t come as news that the OGTT is and will always be the “gold standard” for screening for Type 2 diabetes. I had one in the 1980s. Have you ever had one? Do you know anyone at all who ever has had one?

But my quibble is not with the obvious superiority of the OGTT; it is with the term “remarkable decrement.” The Abstract provides some specificity. In elderly subjects without diabetes, over 10 years, their HbA1c’s increased less that 1/10^th of one percent, whereas in an analysis of all elderly subjects, including those with diabetes on that failed treatment modality, their HbA1c increased by less than 1%. For reference, remember that the A1c Standard of Care for the general population of Type 2 diabetics is 7%, but in the elderly the ADA now sets the bar as high as 9% to “lessen the burden” on the patient. In my opinion, that’s just recognition and concealment of a failed medical policy.

Of course, the RESULT is that, bottom line, when treated to the ADA Standard of Care, as all the patients in both large subsets of data were, “both glucose intolerance and HbA1c levels increased with age.” In addition, “The specificity of HbA1c-based diagnosis criteria for prediabetes decreased substantially with increasing age.”

Clinical takeaway: one of the Diabetes in Control “practice pearls”: “Age should be taken into consideration when using HbA1c for the diagnosis and management of diabetes and prediabetes.” Is that because of a failed medical policy, your “progressive” disease will get worse with age, as everyone in the medical community has come to expect and accept? In other words, be prepared to raise the bar from an A1c of 7% to 9%. But it doesn’t have to be that way.

My recommendation: Everyone who has had 2 consecutive Fasting Blood Glucose tests ≥100mg/dl, or whose HbA1c is 5.7% or higher, is “Prediabetic” and should have a 2-hour Oral Glucose Tolerance Test to cement the diagnosis. Then, regardless of age, they should be advised to change their diet to dramatically reduce sugars and processed carbs.

Retrospective #240: Pottenger, his Cats and his Prophesy

A while ago a regular reader and friend of this blog suggested I read “Pottenger’s Cats, a Study in Nutrition,” originally published in 1983 and more recently republished in paperback by the Price-Pottenger Nutrition Foundation. So, I did. Francis M. Pottenger, Jr., MD, was a physician and researcher who, starting in 1932, conducted feeding experiments on cats in which he observed that cats on “deficient diets” developed changes in bone maturation that paralleled the degeneration that Weston A. Price, DDS, found in people who abandoned traditional foods.

In feeding experiments on more than 900 cats over 10 years, “Dr. Pottenger found that only diets containing 100% raw milk and raw meat produced optimal health. This was reflected in good bone structure, wide palates with plenty of space for teeth, shiny fur, reproductive ease, gentle disposition, and the absence of parasites or disease.” In his most startling observation, he gathered extensive evidence that on a poor diet, this physical degeneration “increased with each generation,” noting “the third generation did not even live long enough to reproduce.” Wow!

The publisher of a related film, “Pottenger’s Cats,” says: “If it is true with human beings, as it is with cats, that nutritionally-caused degeneration is passed down to our children, [then] a sobering challenge stands before us.” I think that this warning about nutrigenomics, an aspect of epigenetics, is increasingly getting our attention. How our individual genes express themselves depends on many environmental factors, the most important of which is what we choose to eat. And, in case you haven’t noticed, we are getting fatter and sicker on the highly processed carbs, sugars and vegetable oils in the “eating pattern” recommended by the USDA’s “Dietary Guidelines for Americans.”

Of course, Weston A. Price, himself a dentist who studied the role of whole, real foods and saturated fats in the diets of diverse cultures around the world that had not yet been exposed to the Western Diet, made similar observations in his groundbreaking magnum opus, “Nutrition and Physical Degeneration” (1939). Today, under founder Sally Fallon, the Weston A. Price Foundation (WAPF) carries on his work. The work of this foundation is worthy of your support.

I previously dealt with this subject in Retrospective #205 about “Deep Nutrition,” a book by Catherine Shanahan, MD. subtitled, “Why Your Genes Need Traditional Foods.” Her dogmata, the Four Pillars of Authentic Cuisine, are to “eat, as often as we can, preferably daily”: 1) meat cooked on the bone; 2) organs and offal; 3) fresh (raw) plant and animal products; and 4) better than fresh – fermented and sprouted. “These categories,” she says, “have proved to be essential by virtue of their ubiquitousness. In almost every country other than ours people eat them every day.”

“Pottenger’s Prophesy,” by Gray Graham, Deborah Kesten and Larry Scherwitz, is another good read. Subtitle: “How Food Resets Genes for Wellness and Illness.” Note the recurrent theme of Doctors Pottenger, Price and Shanahan.

In “Pottenger’s Prophesy” the authors address “the foods that launch your genes on a path toward illness, as well as the diet that can activate ‘healthy’ genes…to promote a longer, healthier life.” Here we see again: “the emerging new science of epigenetics – how the foods you eat switch genes on or off that can lead either to wellness or illness. It’s fair to say, I think, for followers, this is a new paradigm. It is ‘the medicine of the future.’ Personally, I believe it.

What these books and authors tell us is that not only can we affect our own health, wellness and longevity by what we eat now, but by changing the foods we eat, we will pass down to our children and their children a healthier set of genes. These authors provide hundreds of references in the more recent scientific literature related to both animals and humans to show conclusively that our destiny is in the food choices we make.

A trenchant and pithy blurb on the back cover says it well: “This book has again introduced us to concepts that we should have listened to decades ago. Perhaps this generation will pay attention! We will continue to die of obesity-related chronic illnesses until people begin to reclaim their health by understanding what and how to eat.” I wonder, will this generation pay attention? I hope so. We’re going to continue to do our part to see that outcome realized.

What’s your favorite meat-on-the-bone? Do you occasionally eat organ meat? Or a raw or fermented food?

Retrospective #239: “Low-Carb Diet Should Be First Approach for Diabetes”

Andreas Eenfeldt, M.D., founder of the very popular Diet Doctor, headlined a 2014 blog post with “Scientists: A Low-Carbohydrate Diet Should Be First Approach for Diabetes!” In it he provides a link to the full-text document (29 pages, with 99 foot-noted references). The paper was published in the mainstream journal Nutrition under the title, “Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base.”

Richard Feinman, PhD, was the lead author, among 26 co-authors. Eenfeldt comments, “Behind the article is a large group of scientists who have long focused on low-carb diets. But the name that stands out to me is Arne Astrup, the influential Danish professor and nutrition researcher who in recent years became convinced and changed sides in the debate. And dared to admit it. A scientist with integrity” (Eenfeldt’s emphasis).

Highlights from the “In Press Accepted Manuscript”:

·         We present major evidence for low-carbohydrate diets as first approach for diabetes.

·         Such diets reliably reduce high blood glucose, the most salient feature of diabetes.

·         Benefits do not require weight loss although nothing is better for weight reduction.

·         Carbohydrate-restricted diets reduce or eliminate medication.

·         There are no side effects comparable to those seen in intensive treatment with drugs.

The Abstract from the accepted manuscript:

“The inability of current recommendations to control the epidemic of diabetes, the specific failure of the prevailing low-fat diets to improve obesity, cardiovascular risk or general health and the persistent reports of some serious side effects of commonly prescribed diabetic medications, in combination with the continued success of low-carbohydrate diets in the treatment of diabetes and metabolic syndrome without significant side effects, point to the need for a reappraisal of dietary guidelines.”

The Abstract is followed by Definitions of Very Low and Low Carb diets and then by “12 Points,” each with fully footnoted exposition and links to references. There is then a Discussion, Conclusion and Recommendations.

Point 1. Hyperglycemia is the most salient feature of diabetes. Dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels.

Point 2. During the epidemics of obesity and type 2 diabetes, caloric increases have been due almost entirely to increased carbohydrate.

Point 3. Benefits of dietary carbohydrate restriction do not require weight loss.

Point 4. Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss.

Point 5. Adherence to low-carbohydrate diets in people with type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.

Point 6. Replacement of carbohydrate with protein is generally beneficial.

Point 7. Dietary total and saturated fat do not correlate with risk of CVD.

Point 8. Plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary lipids.

Point 9. The best predictor of microvascular and, to a lesser extent, macro-vascular complications in patients with type 2 diabetes, is glycemic control (HbA1c).

Point 10. Dietary carbohydrate restriction is the most effective method (other than starvation) of reducing serum triglycerides and increasing high-density lipoprotein (HDL).

Point 11. Patients with type 2 diabetes on carbohydrate-restricted diets reduce and frequently eliminate medication. People with type 1 usually require lower insulin.

Point 12. Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to the effects of intensive pharmacologic treatment.

The Diet Doctor concludes his commentary on this published scientific paper in Nutrition with this suggestion: “The article in Nutrition is excellent for print out and hand out to curious physicians and diabetes nurses. Recommended!”

I couldn’t agree more. It is a very well-made case and should be widely disseminated in the medical community.