The Nutrition Debate #231: Vitamin K-2 and Insulin Sensitivity

Weston A. Price called it “Activator X,” and for lack of further research Vitamin K-2 remained a mystery for 62 years. In this article on the Weston A. Price Foundations website, Christopher Masterjohn explains, “Vitamin K₂ works synergistically with the two other ‘fat-soluble activators’ that Price studied, vitamins A and D. Vitamins A and D signal to the cells to produce certain proteins and vitamin K then activates these proteins.”

Now, Vitamin K-2 supplementation is all the rage for the multiple benefits it appears to confer. This 6-year old piece, “Vitamin K-2, the Missing Nutrient,” by Chris Kresser, begins with a study of its benefit with relation to prostate cancer and is also a very good summation of its other salutary effects, including some related to type 2 diabetes.

My editor brought my current attention to Vitamin K-2 with this note: “Perhaps you saw ‘this post’ on Bernstein – a great reason to eat ghee.” The Bernstein Diabetes Forum, if you don’t know, is a diabetes help forum (registration required) at http://care.diabetesjournals.org/content/34/9/e147.full. It is where I received my basic (and advanced!) education in Very Low Carb eating. It is unthreatening – indeed, it is a very friendly resource for neophytes, and a good place to hang.

It just happens that my editor also introduced me to ghee, pure 100% butter fat (“clarified” butter) and in particular to the Ancient Organics brand made from Strauss Creamery Butter. This wonderful, burnished-flavored organic ghee, while admittedly expensive, is made from the cream of grass fed cows and is undoubtedly high in vitamin K-2. Butter made from cows confined to barns and feed-lot conditions is not.

Similarly, eggs produced by hens in confined, even so-called “free range” conditions, is not going to be high in Vitamin K-2, as explained by Stephen Guyenet at Whole Health Source in this 2009 piece, “Pastured Hens.” “The reason pastured eggs are so nutritious is that the chickens get to supplement their diets with abundant fresh plants and insects. Having little doors on the side of a giant smelly barn just doesn't replicate that,” Guyenet explains. Just take a look at the comparisons between conventional and pastured eggs for Vitamins A, D and E, beta carotene and omega 3 fatty acids in the link above.

But the ‘post’ my editor referred to was this rather arcane paper in Diabetes Care, the Journal of the American Diabetes Association: http://care.diabetesjournals.org/content/34/9/e147.full. The title, “Vitamin K-2 Supplementation Improves Insulin Sensitivity via Osteocalcin Metabolism: A Placebo Controlled Trial.” The 2011 study was conducted by a team from the Department of Internal Medicine at the Seoul National University College of Medicine in Seoul, Korea.

The “weeds”: “Undercarboxylated osteocalcin (ucOC) is reported to function as an endocrine hormone, affecting glucose metabolism in mice. Vitamin K, which converts ucOC to carboxylated osteocalcin (cOC), has been suggested to regulate glucose metabolism my modulating osteocalcin and/or proinflammatory pathway. We studied whether modulation of ucOC via vitamin K2 supplementation for 4 weeks affects ß-cell function and/or insulin sensitivity in healthy young male subjects.” So, 42 healthy young male volunteers received vitamin K-2 (menatetranome; 30mg; Eisai Co., Japan) or placebo t.i.d [three times a day] for 4 weeks. This is the MK-4 form of K-2, the short-lived artificial form of the vitamin.

“To summarize,” the researchers say, “we have demonstrated for the first time that vitamin K-2 supplementation for 4 weeks [significantly] increased insulin sensitivity in healthy young men, which seems to be related to increased cOC rather than modulation of inflammation.” Then, “We conclude that, unlike in rodents, cOC rather than ucOC, may be the endocrine hormone that increases insulin sensitivity in humans.” And, to review, vitamin K-2 is the catalyst that converts ucOC to cOC. So, vitamin K-2 is, once again, that mysterious “Activator X that synergistically works with and activates the other fat soluble vitamins and proteins.

Now, where do you get this magical stuff? Well, if you’re not eating eggs from pastured hens or ghee from grass-fed cows, you may not be getting enough K-2 to work synergistically with the other fat soluble vitamins. And, if you are trying to avoid saturated fat, you may not be getting enough of those other fat-soluble vitamins (A & D), and calcium, in the first place. Natto, the Japanese breakfast food made from fermented soy beans (an acquired taste, I’m told), is by far the best source of vitamin K-2. Hard and soft cheeses are also good sources. So are other fermented foods. And liver and other organ meats and fish eggs too. Or, if these food choices don’t appeal, you can consider supplementation.

Dr. Kate Rheaume–Bleue, in her authoritative book, "Vitamin K2 & the Calcium Paradox", recommends, that you consider supplementing with up to 200mcg (that’s micrograms) of the MK-7 form of vitamin K-2. This is the natural, long-lasting form of K-2, so the dosage is much, much smaller and needs to be taken only once a day. I haven’t read her book yet, but it is getting rave from the likes of Dr. Mercola. His interview of Dr. Kate (1hr -22 min) is worth listening to. Sample quote from the interview: “Vitamin K-2 is critical for keeping our bones strong and our arteries clear.”

For the time being (until I’ve read the book), I’m going to stick with my pastured hen’s eggs and Ancient Organics ghee.

The Nutrition Debate #230: Frustrated by Failure? Solution: Lower the Standard of Care!

“Tight Glycemic Control More 'Burden' Than Benefit for Many,” this Medscape Medical News piece proclaimed. It really got my blood boiling. Later, I recognized that “anyone with a clinical practice” would relate to this sentiment, as one of the authors says in the online article in JAMA Internal Medicine. But the proposed “solution,” in the salutary guise of “patient-centered care,” is to “personalize treatment.” Sounds promising, but look carefully at the confirmation bias in their hypothesis. Consider also the tendency to blame failure-to-successfully-treat on the patient (rather than the treatment) and then to assign the failure to the patient’s “burden” of treatment, thus relieving the patient of the moral burden for failure.

The primary end-point was “to estimate the treatment burden vs. benefits from intensive vs. moderate glycemic control in patients with type 2 diabetes.” The outcome: “Using a simulation model [carefully constructed by the researchers to confirm their hypothesis?], the researchers discovered that for patients with type 2 diabetes who are on metformin and have an HbA1c below 9%, adding other antidiabetic therapies to try to lower glucose further may only confer modest benefits 15 to 20 years later.” Even though, citing the UK Prospective Diabetes Study (UKPDS), the authors acknowledge that “Lowering HbA1c delays the onset and slows the progression of early microvascular disease.”

So, what do we learn here? The new standard of care “for many” is an A1c <9% for an average glucose reading of 212? And for these “many,” the treatment plan, described as having “a low-treatment burden,” is simply to prescribe metformin and do nothing else? Because the benefit gained, depending on age when diagnosed, is only “modest”? What, pray tell, could lead anyone with a clinical practice to reach this conclusion? Could it be the failure of the “treatment” modality?

This study was carried out by doctors from “the University of Michigan and the VA Ann Arbor Healthcare System.” Not to slam yet another VA facility, but – I have to wonder – are the vets at this VA facility subjected to this lower standard of care?   If true, shame, shame on these doctors. But, maybe I’m just piling on. Maybe, by JAMA Internal Medicine publishing this piece, they too are advocating a broader application of this lower standard of care. I’ll have to read the comments.

Why lower the standard of care? Because, “for patients older than 50, especially, any potential benefits are often outweighed by ‘burdens’ of lifelong treatment – such as substantial weight gain from sulfonylureas, the need to frequently inject insulin, or the risk of hypoglycemia.” Well, patients older than 50 includes “most” people initially diagnosed with type 2 diabetes, so this new paradigm would then thus apply to “most.” NB: The authors, to their credit, do make an exception for “the 15% to 20% of people who have very high HbA1c’s and require more aggressive treatment to manage the disease.”

The authors state that the decision to “start new medications” (beyond metformin, assuming metformin is tolerated) should be “based on individual circumstances and preferences.” “These are important decisions,” they say, “because type 2 diabetes is a chronic disease that requires lifelong treatment. Thus, shared decision making, in which patient preferences are specifically elicited and considered, appears to be the best approach to making most decisions about glycemic management in patients with type 2 diabetes.” Don’t doctors take primary responsibility for patient care anymore?

But the most disingenuous statement in this article was this: “What really surprised us was you end up with a reduction of quality of life for many patients – basically those who are a little bit older when they are diagnosed or those who really don’t like their treatments.” Don’t like their treatments? If the treatment “really bothers you, then you just need to understand that you have a slightly higher risk [according to the ‘simulation model’ they’ve constructed] of these complications, and it may not be worth treating to prevent that,” they concluded. Now that’s confirmation bias for you.

It’s true: Some people can’t tolerate metformin even if it is titrated. And some anti-diabetic meds do cause weight gain, and injecting insulin is a “bother” and certainly can cause weight gain and does entail a risk of hypoglycemia. But do these “constant annoyances of having to be on a medication and experience the side effects” constitute a “burden” that exceeds the benefits of having improved glucose control? Or is this construct just rationalization to justify a failed treatment plan?

And if the treatment plan included dietary changes such as carbohydrate restriction, would not the benefits of losing weight, taking less anti-diabetic oral medications, and stopping insulin injections altogether, far exceed the “burden”?

I know people who tell me they could “never” give up bread, pasta, rice, corn and potatoes, or beverages sweetened with sugar or HFCS. “I really wouldn’t like that treatment,” they say. But…you know what? It really works.

The Nutrition Debate #229: My Alternate Healthy Eating Index (MyAHEI)

In The Nutrition Debate #200 (here), I lament the fact that the term “Healthy Eating” has been co-opted by the Diet Dictocrats in the Federal Government and their cohorts in U.S. agriculture, food processing and manufacturing. IMHO, the United States Department of Agriculture (USDA), that produces the Dietary Guidelines for Americans every 5 years, does not have the health of the American consumer in mind; their job is to promote industry. If you want proof for this, read Minger’s Death by Food Pyramid.

In the latest iteration, the USDA Center for Nutrition Policy and Promotion (CNPP) has produced MyPlate, replacing the original Food Guide Pyramid and later MyPyramid. It has also produced the Healthy Eating Index (HEI) as “a measure of diet quality that assesses conformance to federal dietary guidance” and to “monitor the diet quality of the U.S. population and the low-income subpopulation.” The USDA’s CNPP first objective: 1) Advance and promote dietary guidance for all Americans, (emphasis mine). In other words, a one-size-fits-all eating plan for all Americans, regardless of health status.

The Harvard School of Public Health website The Nutrition Source (not to be confused with The Nutrition Debate, a much better “nutrition source”) says the USDA’s new MyPlate still falls short on giving people the nutrition advice they need to choose the healthiest diets. “Tragically,” the Harvard site says, “the information embodied in this pyramid didn’t point the way to healthy eating. Why not? Its blueprint was based on shaky scientific evidence, and it barely changed over the years to reflect major advances in our understanding of the connection between diet and health.” It also acknowledges that, frankly, “intense lobbying efforts from a variety of food industries also helped shape the pyramid and the plate.”

So, what was Harvard’s response? They created their own Healthy Eating Pyramid and Healthy Eating Plate. Then, they went one step further. They created their own Alternate Healthy Eating Index (AHEI) , a “110-point measure of dietary quality.” Unfortunately, neither the USDA’s HEI questionnaire nor Harvard’s AHEI questionnaire are in the public domain. They are closely held. Only the scorers of the eating patterns of the self-reporting participants know what the people ate.

Consequently, the outcomes of both indices are useful only for the promotion of their respective points of view about what constitutes “healthy eating.” This leads me to the conclusion that there is insufficient transparency in this type of reporting. I think what we need is yet another tool for assessing diet quality: one that I shall coin “My Alternate Healthy Eating Index” (MyAHEI)©. The principles of MyAHEI are listed below: You can self-report your own score in the comment section at the bottom of the blog post. Give yourself 5 points for each question you can answer affirmatively. Part scores are permitted.

The Nutrition Debate’s 20 Guiding Principles of “My Alternate Healthy Eating Index (MyAHEI)” © of Diet Quality

1.       Eat 3 small meals a day, equally sized and evenly spaced, over no more than 10 hours.

2.       Eat animal protein with saturated fat (and dietary cholesterol) with every meal.

3.       Eat 12 to 18 whole eggs from pastured hens each week.

4.       Eat no snacks between meals (except an occasional low-carb/high fat snack before dinner).

5.       Eat no fried foods and no vegetable or seed oils. Use butter, ghee, and coconut oil. No margarine or store-bought mayo.

6.       Eat no bread, rice, pasta or potatoes.

7.       Eat only nuts that are lowest in polyunsaturated fatty acids (Macadamias, almonds, hazelnuts).

8.       Eat sardines in olive oil or wild salmon at least 5 times a week.

9.       Eat no prepared foods and no food sold in boxes or bags (except some flash-frozen veggies and fish).

10.   Eat mostly fresh vegetables tossed in butter or roasted in olive oil.

11.   Eat fish oil capsules (2g/day).

12.   Eat organ meats (liver, kidneys, heart, brains, etc.) at least once a week.

13.   Eat only low-carb vegetables. Avoid corn, beets, peas and carrots.

14.   Eat no fruit, except berries with heavy cream on very special occasions only.

15.   Eat a salad at least twice a week with supper. Do not use store-bought salad dressings.

16.   Eat salt to taste; add salt to enhance the flavors of real foods.

17.   Drink copious amounts of water and stevia-sweetened iced tea, and coffee with breakfast only.

18.   Drink wine, or other alcoholic beverages, with (and/or before) dinner only.

19.   In restaurants, order from the appetizer or small plate menu only; avoid entrees, sides and desserts.

20.   In restaurants, eat from your own plate only!!!

The Nutrition Debate #228: A1c and your estimated Average Glucose (eAG)

The glycated hemoglobin (Hb) A1c test has become the new standard for assessing a patient’s diabetes or prediabetes status. It is measured in percent, as for example 7.0%, the default ADA target to be met or exceeded in your diabetes care plan. The percent is the amount of glycated hemoglobin on the surface of your red blood cells, that is, the amount of glucose attached to the hemoglobin molecule.

Red blood cells typically live 2 to 3 months, so this is a pretty good way of determining the level of glucose in your blood 24/7 over a 2 to 3 month period. The ADA recommends that your doctor test your A1c level at least 2 times a year and preferably 4. Medicare will pay for 4, unless more frequent testing is deemed “medically necessary” by your doctor.

Prior to the widespread use of the A1c test to assess your diabetes status, the clinician used two consecutive fasting plasma glucose tests that exceeded the ADA standard for a diagnosis of type 2 diabetes. Prior to 1997 that standard was 140mg/dl (U.S measurement). After 1997 the standard was lowered to 126mg/dl. In addition, a new standard for prediabetes was established: two consecutive fasting plasma glucose readings between 100 and 125/mg/dl. If your lab tests are between 100 and 125mg/dl, and your doctor hasn’t told you that you are prediabetic, you might want to ask him/her why?

The difference in units (% vs. mg/dl) has resulted in a disconnect between these two tests. Besides, knowing your fasting blood glucose only tells a small part of the picture of your diabetes health. What happens to your blood glucose after you eat is what really defines how impaired your glucose tolerance is and the degree of insulin resistance you have developed. And that is why the A1c test is a better indicator of your diabetes health than the fasting plasma glucose test. This is particularly true for middle aged women, oddly enough.

So, to resolve the disconnect and the confusion that has resulted, scientists have developed a table that creates a correlation between A1c % and estimated Average Glucose (eAG) in mg/dl. This table is copyrighted by diabeteschart.org.

As you can see on this chart, an A1c of 7% is equivalent to an estimated Average Glucose of 154mg/dl. This is stunning. An average of 154mg/dl means that, if you have an A1c of 7% (the ADA recommended target), your plasma blood glucose is higher than that for many hours each day, especially if your fasting blood glucose is in the 126mg/dl or lower range. Why is that important? Because it is generally understood and accepted that any time your blood glucose is above 140mg/dl, it is slowly but inexorably doing damage to your nerves and microvascular system. It may take years, but damage is being done.

My own A1c’s have been higher than I would like for the last year or so. I have not been as vigilant as I should be in watching what I eat. I am always scrupulous about breakfast and lunch; but at or after dinner, I have not always stuck to my plan. As a result my A1c’s are now almost always in the high 5s. An A1c of 5.8 is equivalent to an eAG of 120mg/dl, which means if my fasting blood sugars are in the low 100s, my postprandials are at or near 140mg/dl. i.e., borderline bad.

But my doctor, who adheres to the ADA standard, considers my blood sugar “in control.” He is wrong, of course, but how to convince him otherwise? So, I just have to establish my own standard, and hope he goes along with my self-management plan. So far, he’s “on board,” but if at some point we see it differently, I will just have to change doctors.

I currently have a prescription to test twice a day. When I was learning about low-carb eating, my previous doctor (now deceased) wrote a script for 4 test strips a day. But now, I can get by with 2 tests a day. I always do a fasting test and use the second strip for a 2 hour postprandial test or to test at other times.

I sometimes to do a “continuous” (@ 2 hour intervals) test all day. Recently, while on Doxycycline to treat a tick-borne infection, I had these results:  9AM (fasting): 128; 11AM (2hr pp): 120; 1PM (4hr pp, before lunch): 125; 3PM (2hr pp): 120; 5PM (before dinner): 118; and 7PM (2hr pp): 179. Here’s why. For dinner, I ordered 2 appetizers: 6 raw oysters, and then steak tartare with an egg yolk in the center. Then, I helped my wife eat the large order of sweet potato fries that came with her “steak frites.” Of course I should have ordered a side of roasted Brussels sprouts instead.

Result: my blood sugars were stable, if somewhat high, all day long due to my body helping the antibiotic fight the infection. Then, after dinner, I had a huge “spike,” or excursion (in the language of blood sugar monitoring), due to my indiscretion. I love sweet potato fries, but I paid a price for going “off the reservation.”

The Nutrition Debate #227: “One in 10 American Adults is Diabetic…”

“One in 10 American Adults is Diabetic; 1 in 4 is Unaware’ is the full title of this recent story in DiabetesinControl.com. The subtitle is “The United States has 3 million more diabetic patients today than in 2010.” These shocking headlines are all too familiar, and frightening, especially to the growing at-risk segment of the population. Is there any new news here?

“According to the 2014 National Diabetes Statistics Report, recently released by the Centers for Disease Control, at least 29 million people living in the U.S. have diabetes; 28% of these patients are undiagnosed. In a study done from 2009 to 2012, 37% of adults in the U. S. were considered pre-diabetic based on fasting glucose and A1c levels. This equates to 86 million Americans who will become diabetic if something doesn’t change.”  Of the pre-diabetics, only 7% know their status.

“…if something doesn’t change.” Hmmm… So what does the medical and public health establishment propose to do?

“Therefore, the American College of Cardiology (ACC,) in collaboration with the American Diabetes Association, the American College of Physicians and Joslin Diabetes Center, has announced a partnership and the launch of a new Diabetes Collaborative Registry that will help practitioners work together to track and improve the quality of care across the continuum.” In other words, close ranks, collect data, and hope, by studying the data, to improve patient outcomes…

So, who’s sponsoring, supporting and funding this new registry of patients? You guessed it. AstraZeneca, makers of Byetta, Bydureon, Onglyza, and a host of other pharmacotherapies, like Crestor, for diabetes and its related co-morbidities. The goal: to “allow primary care physicians and specialists who treat patients with diabetes to compare data and real-time metrics on patients in all stages of the disease.” Access to electronic medical records; now that’s doing something, huh?

The president and CEO of the Joslin Diabetes Center summed it up nicely. He said, the “center is pleased to be a founding partner of the first clinical diabetes registry. Not only will patients benefit with a registry of this kind; so will diabetes researchers who will gain access to numerous data from a variety of specialists. This will ensure that research is based on the most current data that is out there.” Did you miss how the patient will benefit?  I did too.  He doesn’t say.

But maybe the ACC guy does. The ACC president “believes there is a clear need for cross-specialty management of diabetes patients especially because cardiovascular disease is the leading cause of death for diabetic patients,” according to the Diabetes in Control piece. True enough. The ACC is a stakeholder in gaining access to your electronic medical records too.

Maybe the American Diabetes Association will be able to tell us how the patient will benefit – how something will change to prevent or deter or just slow down the rate at which, by the CDC’s Division of Diabetes Translation (?!) predicts “if we do nothing, and the numbers continue to rise, 1 in 5 Americans will have diabetes by 2025, and possibly 1 in 3 by 2050.”

Well, here’s what the Diabetes Association’s Chief Scientific and Medical Officer told Diabetes in Control: “Diabetes is not one disease but a complex set of diseases and too often leads to serious and potentially life-threatening complications, such as cardiovascular and kidney disease, as well as nerve damage, amputation, blindness and a multitude of other health problems. We hope that a cross-specialty, clinical registry will ultimately allow us to improve the quality of care – and therefore quality of life – for all people living with diabetes by giving researchers a clearer picture of what’s happening to patients at various stages of their disease. Improved data collection should help us to improve patient outcomes.”

Well, there you have it. Everyone wants to sit back and let researchers study the data “to get a clearer picture of what’s happening to patients at various stages of their disease,” like 86 million guinea pigs in one giant lab. I wonder why – no, I am dumbfounded that – no one responded proactively to the CDC’s warning, that “…if something doesn’t change… 86 million Americans will become diabetic.” Let’s see. What could possibly change to affect this outcome? Diet, do ya think?

Are the American College of Cardiology (ACC), the American Diabetes Association, the American College of Physicians and Joslin Diabetes Center all too hobbled by their vested interest in, and dependence on, pharmacotherapy?  Do they have any interest in, or curiosity about, a proven therapy that doesn’t involve taking any drugs?

The medical establishment is moving very slowly, and I’ve given up on our government doing “something.” The purpose of the United States Department of Agriculture (USDA) is to promote American agricultural and the food processing and manufacturing industries. And they are the ones who ordain what we eat; they write the Dietary Guidelines for Americans. The fox is in charge of the henhouse.   So, what can you do to manage diabetes or stave off pre-diabetes?  Keep reading.

The Nutrition Debate #226: Improved Glycemic Control and CV Risk

Last week, Marlene Busko (Medscape Medical News) reported on a poster presentation at the American Diabetes Association (ADA) 2014 Scientific Sessions in San Francisco. The “new, real-world study, based on real clinical practice,” demonstrated “a very strong effect” of glycemic control on cardiovascular outcomes, Busco reported. The lead author of the study was Dr. Nick Freemantle, professor of epidemiology and biostatistics at University College London.

The lede for the Medscape piece was, “Among patients with type 2 diabetes who start taking insulin, those who attain good glycemic control are less likely to have a major adverse cardiac event (MACE) in the medium term than those who fail to achieve this.” But the takeaway I got was that “it doesn’t appear to matter how you get to (glycemic) control; it’s getting to control that matters.” The message, as Dr. Freemantle said, is to “achieve improved HbA1c…by whatever means.”

“The study covered nearly 3,000 patients who had had diabetes for about 9 years but had hyperglycemia despite generally receiving oral antidiabetic agents.” [Weren’t eating a low-carb diet, were they?] “The patients had a mean age of 61, about half were women, and at baseline they had a median body mass index of 28.6.” Despite taking up to 3 oral antidiabetic agents, their median HbA1c was 9.3% (range 8.1 – 10.7%). Like me, nearly 12 years ago, these patients were obviously relying solely on their doctors to manage their type 2 diabetes. The result: their disease progressed to the point where their doctors started them on insulin.

So, what happened? “Patients whose HbA1c levels remained high had worse outcomes.” How much worse? “Specifically, a 1% higher HbA1c increased the risk of a major adverse cardiac event (MACE) during a 4-year follow-up by 25% compared with an otherwise similar patient with a 1% lower A1c.” The “1% increase in HbA1c above the mean was associated with a significant 36% increased risk of a first stroke, and a significant 31% increased risk of cardiovascular death. During the study follow-up, there were 44 nonfatal MIs (myocardial infarctions, or heart attacks), 57 nonfatal strokes, and 60 deaths from cardiovascular causes. There were 148 deaths from all causes.”

Seven percent were not taking any oral antidiabetic agents when they began insulin therapy. About a quarter were taking 1, half of the patients were taking 2, and a fifth were taking 3 orals. Two thirds of the patients were taking metformin, three-quarters a sulfonylurea (!), twenty percent were on a TZD, and the rest on other meds not commonly used in the U.S.

The starting dose of insulin was a low 0.20 U/kg body weight, which was then titrated upward as needed, Medscape reported. “The patients made substantial gains in glucose control,” Dr. Freemantle said. “The median HbA1c dropped to 7.4% (range 6.7% – 8.4%) at 1 year and remained around that level at years 2, 3 and 4.” “The results confirm that people with better blood glucose control have better cardiovascular outcomes,” Dr. Freemantle said.

The guided-poster-tour moderator, an MD, told Medscape Medical News, “This study suggests (that) getting glycated hemoglobin down with low-dose insulin in combination with other therapies is safe and might be beneficial by reducing CV events.” That sounds like a safe conclusion to me! He added, “Although it was not a prospective study with a comparator arm, nevertheless it reinforces that ‘good glycemic control is important to prevent cardiovascular events.’” Duh!

This study was funded by Sanofi, a major manufacturer of insulin (Lantus and Apidra), but that in no way, in my opinion, changes the outcomes. It just happens, not surprisingly, that the outcomes benefit them by promoting the use of “low-dose insulin in combination with other therapies.” So be it. But remember the takeaway:  “it doesn’t appear to matter how you get to (glycemic) control; it’s getting to control that matters.” To reiterate - “achieve improved HbA1c…by whatever means,” as Dr. Freemantle said.

Obviously, neither cohort in this study considered dietary choices as part of their diabetes care. They relied on their doctors to take care of them. They “had had diabetes for about 9 years but had hyperglycemia. And, despite taking up to 3 oral antidiabetic agents, their median HbA1c was 9.3% (range 8.1 – 10.7% or an average glucose level of 186 to 260). My HbA1c, after 16 years of letting my doctor prescribe progressively more anti-diabetic meds (3 total), and doing nothing on my own behalf, had been as high as 8.9%. Up until this point, I can see myself in their shoes. I was there.

But here’s the critical difference: their disease progressed to the point where their doctors started them on insulin; my doctor started me on a Low Carb diet. I not only lost a huge amount of weight. I was able to discontinue my meds!!!

The Nutrition Debate #225: Diet and Type 2 Diabetes Risk

I keep hoping that someday I will read in the scientific or mainstream media that eating a low-carb diet will reduce the risk for type 2 diabetes. I mean, it’s so obviously true that I am at a loss to explain why I don’t read it all the time. Then, a recent Diabetes in Control headline gave me renewed hope, until I read the “fine print.”

The headline, ADA: Improving Quality of Diet Reduces Risk for Type 2 Diabetes, was both true and hopeful. The sub-title, “Consuming healthier foods improves risk independently of other lifestyle changes such as weight loss or physical activity,” gave me further encouragement. Then, my hopes crashed. The lede provided all the detail needed to confirm the bias of the storyline. It began, “Researchers at the Harvard School of Public Health have found that patients who ate more whole grains, fruits, vegetables, and less sweetened beverages and saturated fats improved their diet quality index scores by ten percent over four years. This reduced their risk for developing type 2 diabetes by about 20% when compared to those who made no diet changes.” Presumably this diet is an improvement over the junk food filled SAD (Standard American Diet).

The bias is in the measurement tool that the Harvard “researchers” used. It is the “110 point Alternate Healthy Eating Index 2010” (AHEI) that was used to measure “dietary quality.” Harvard’s Walter Willett and colleagues developed the AHEI in 2010 to “improve on” the Healthy Eating Index (HEI) that was originally developed by the USDA in 1990 and updated every five years to conform to the changes in the USDA’s Dietary Guidelines for Americans.  “The Healthy Eating Index (HEI) is a measure of diet quality that assesses conformance to federal dietary guidance,” the USDA website explains.

A comparison of Harvard’s AHEI and the USDA’s HEI can be viewed on Yahoo here. This link’s main value, however, is that it provides links to both the 2010 AHEI and the HEI. In my view, obviously, both the AHEI and HEI are deeply flawed, not least for their views about fats, especially liquid fats (refined oils) from polyunsaturated sources (corn, soy bean, sunflower, peanut, canola and “other vegetable oils”). In addition, both Harvard’s AHEI and the USDA’s HEI regard a “move to a plant-based diet” an “important step in the right direction,” according to the AHEI link. They would have you view “solid” (saturated) fats as evil, and severely curtail your consumption of egg yolks, butter and red meat. Harvard is still hopelessly hamstrung by its Hammurabian bias. This “study” simply seeks to promote the “ancient” (50-year old) and totally erroneous bias against saturated fats.

The USDA’s Center for Nutrition Policy and Promotion [note the undisguised use of ‘promotion’ here] uses data collected via 24-hour recalls of dietary intake in national surveys to construct the HEI score. The methodology of Harvard’s 110 point AHEI uses “a scoring system similar to the USDA’s index…using information about daily diets collected from more than 100,000 female nurses and male health professionals taking part in two long-term studies.”

Harvard can’t be faulted for trying to improve on the “one-size-fits-all” Dietary Guidelines for Americans. But just tweaking it, as Harvard does, is not the solution. Neither, however, do I fault some of Harvard’s tweaks. My main gripe is with their intentional and, in my view, nefarious confounding of “more whole grains, fruits, vegetables,” with “less sweetened beverages and saturated fats.” And, in this last phrase, the conflating of “sweetened beverages and saturated fats.” Elsewhere, they (and the USDA) consistently conflate “saturated fats” and “trans fats.” These are egregious examples of knowingly and maliciously using a rhetorical device to confuse and mislead the public. And it is downright damnable. Damnable, I say.

With respect to this particular “study” (public policy press release), how can Harvard say that the 10% improvement in diet quality index scores (over those who made no self-reported diet changes), and which lead to about a 20% reduction in developing type 2 diabetes, was attributable to eating “more whole grains, fruits, vegetables,” or eating “eating less sweetened beverages and saturated fats.” Perhaps the 10% improvement in scores was attributable to the (self-reported) elimination of sweetened beverages without any change in saturated fat intake or whole grains, fruits and vegetables. Or eating more whole grains, fruits and vegetables and fewer sweetened beverages, but the same amount of saturated fat. Or any combination of variables. It is confounding, conflating and confusing.

But that’s about what I expected when I read that this “study” was a product of the Harvard School of Public Health. It is simply a promotional piece to advance their idea of a “healthy diet.” Harvard did, however, produce an interesting critique of the USDA’s Healthy Eating Index, based on the Dietary Guidelines for Americans, at their The Nutrition Source site.

The Nutrition Debate #224: Diabetic Foot: A Cinderella Condition?!!!

To be fair, the full title of this Medscape Medical News story is, “Diabetic Foot: A Cinderella Condition, Needs a Team Approach.” But really, the simpler title, “Diabetic Foot Needs a Team Approach,” would have been much better. That’s what the story was about, and from a medical perspective, it was a good story. The findings were reported at the ADA 2014 Scientific Session last week. A few points that caught my attention were:

●     There is a need for a “uniform, multidisciplinary approach,” with a “national treatment plan” for diabetic foot. To this end, a U.S. National Diabetic Foot Registry is now being established. (All four comments on the story agreed).

●     At one large “safety-net hospital system that serves a diverse patient population,” in “2000 there was nearly a 50-50 chance that if you came in with a diabetic-foot infection, you would lose your foot.” As a result of establishing a limb-salvage program at this institution, there has been a staggering reduction in the number of amputations.

●     The average age of the amputee population was 55.9 years, 72.5% of the patients were male, and the average H1c was 9%. Seventy percent of the patients also had coronary artery disease, and 14% end-stage renal disease.

●     Amputation was “a robust independent predictor of death, associated with a significant, almost 85% increased risk for mortality,” with “most of the deaths – just under 50% -- due to cardiovascular disease.”

●     “Even minor amputations were associated with an almost 50% increased mortality risk, a somewhat surprising finding.” And, “Once you have an amputation, you go down a not very healthy road.”

The session moderator told Medscape Medical News, “It was…disappointing... to see that minor amputations had no better outcome – you would expect that they would do better, but apparently not.” “But I think that if you look at the natural course of the disease, these patients die of cardiovascular disease – it doesn’t matter what you do to their extremity, they all die of CVD. I guess we should expect it, but we would hope it would be better,” he said.

Given this dismal, if no longer abysmal outlook, I would hardly call this a Cinderella Condition. Even having the amputation rate fall from 36% to 11% (after the limb-salvage program was implemented at that particular safety-net hospital system), “they all die of CVD” is not a story-book ending. It’s not like “they lived happily ever after,” unless it is to be inferred that the prospect going forward of a “uniform, multidisciplinary approach” with a “national treatment plan” for diabetic foot has the potential for “a happy ending.” I’ll try to imagine that that is what was intended by the stupid title.

I haven’t written about diabetic foot before except to mention that diabetic neuropathy (a precursor to diabetic foot), along with nephropathy and retinopathy, are the three major classes of diabetic complications, along with the above-mentioned cardiovascular disease (CVD) and related microvascular complications like erectile dysfunction. Hopefully, my readers are not there yet and never will be. Hopefully, your A1c is much, much lower than 9%, which is truly uncontrolled. An average glucose of 212 requires drastic action on the part of both the physician and the patient.

Of course, if you’ve somehow just been diagnosed with diabetes and have an A1c as high as 9% (or higher), you can do something dramatic to lower it. One thing you undoubtedly will do, and are doing, is your homework. If the doctor hasn’t scared the bejesus out of you, reading about the progressive nature of the disease is scary enough. Reading about the complications and the likely prognoses is likewise scary. Reading the five bullets above is downright terrifying. But you can do your homework and choose a course of action to avoid all this.

The first A1c that I ever had, long before that test was common, was given to me by an endocrinologist 21 years ago in 1993. It was 7 years after my initial diagnosis and probably many more since I had become a full-fledged type 2. My A1c was 8.9%. Curiously – inexplicably, really – I didn’t have another A1c test for 10 years, and by this time I had already been on a Very Low Carb diet (Atkins Induction) for almost a whole year (50 weeks). It was 5.4%. I would love to have known what it was just before I began to eat Very Low Carb. It could very well have been 9% or higher.

My editor says that I was very lucky. I sometimes forget. Many people develop early signs of complications in just a few years of “uncontrolled glucose control.” Others not. I guess I was, and continue to be, lucky. Do you want to take a chance that you’ll be lucky too? It’s up to you. Are you a gambler? Just be aware: Diabetes Foot is not a Cinderella Condition.

The Nutrition Debate #223: Adding Insulin to Metformin for T2s: a scary “outcome”

“Adding Insulin to Metformin for T2s May Increase Risk of Death” was the scary headline of a recent Diabetes in Control story that caught my attention. It stunned me, actually. The story was based on the full JAMA paper (now by payment only), “Association between Intensification of Metformin Treatment with Insulin vs. Sulfonylureas and Cardiovascular Events and All-Cause Mortality Among Patients With Diabetes.” The ABSTRACT can be viewed here.

Both the Diabetes in Control piece and the JAMA scientific paper are qualified and raise more questions than they answer. And so do the objectives and design of the study, in my mind. Why, for example, would anyone today want to compare adding insulin to adding a sulfonylurea? Haven’t the sulfonylureas as a class been thoroughly discredited? I cite Dr. Ralph DeFronzo’s Banting Lecture (keynote address) to the 2008 ADA Convention in San Francisco and his full paper published in Diabetes in which he wrote, “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.” Scripts are declining dramatically.

Perhaps because that was what they had to work with. The study took place in the Veterans Administration (VA) hospital system in Nashville.  The Vanderbilt University researchers reported more patients in the sulfonylurea cohort than in any other. (“Among 178,341 metformin monotherapy patients, 2,948 added insulin and 39,990 added a sulfonylurea.”) That reminds me of the story of the person who lost a ring in a dark alley and was looking for it under a street light. When asked why, he replied, “There’s more light here.” But couldn’t they have used a more current treatment modality than a sulfonylurea, like a TZD or GLP-1, rather than one that causes more harm than good to the pancreas (and the patient!).

The OBJECTIVE of the study was alarming in itself: “To compare time to acute myocardial infarction (AMI), stroke or death in a cohort of metformin initiators who added insulin or a sulfonylurea.” So, let me quickly dispel the most alarming of these outcome objectives: “Acute myocardial infarction and stroke risks were statistically similar.” Whew! That’s the good news. The bad news? The CONCLUSION (from the full-paper): “Among patients with diabetes who are receiving metformin, the addition of insulin compared with sulfonylurea was associated with an increased risk of a composite of nonfatal cardiovascular outcomes and all-cause mortality.”

Of course, this finding of an “association” was followed by, “These findings require further investigation to understand risks associated with insulin use in these patients…” Okay, that’s pretty much pro-forma these days. It also just a plea for more taxpayer funding for further investigations (a medical school research department jobs program). But that final sentence of the CONCLUSIONS section has a compound predicate; it continues, “…and call into question recommendations that insulin is equivalent to sulfonylurea for patients who may be able to receive an oral agent.” Okay, okay, but sulfonylureas aren’t the only oral agent available! And they overwork the remaining working beta cells that you have, leading to their destruction!

Sulfonylureas have been in use in the U.S. since the late 40s. Metformin was introduced in Britain in 1958, in Canada in 1972, and finally permitted by the FDA in 1994. Now, it is the preferred first course of treatment both in Europe and the U.S. for pre-diabetes and is used as a monotherapy by many full-blown T2s (like me), who rely primarily on diet for blood sugar control. But if I needed a 2^nd therapeutic, I WOULD NEVER AGAIN AGREE TO TAKE A SULFONLUREA, just as I would never agree to take a statin to lower my Total Cholesterol and LDL-C. I’m very happy with my lipid levels as they are, thank you very much.

So, where do we go from here? It’s confusing…in fact, it’s confounding. The first “Practice Pearl” in the Diabetes in Control raises a very good issue: “Many variables were not considered in choosing the participants in this study.” Their takeaway: “These findings require further investigation to understand risks associated with insulin use in these patients.” It must be noted, that “these patients” were all in the Veterans Administration (VA) hospital system in Nashville. To my knowledge, this particular VA hospital has not been implicated (so far) in the spreading scandal in our VA hospital system. Period.

But it comes as no surprise to me that that system is still administering sulfonylureas; or that the researchers at the Vanderbilt University Department of Medicine, Department of Biostatistics, and Department of Health Policy continue to advocate for this particular “oral agent” (a sulfonylurea). After all, it’s cheaper than an insulin regimen, and isn’t that what Health Policy is all about when the Federal Government gets involved in your health care? Am I piling on? I don’t think so.