Monday, October 14, 2019

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?

Sunday, October 13, 2019

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.

Saturday, October 12, 2019

Retrospective #238: Low-dose aspirin, a nuanced approach for Type 2s


Do you take an anti-platelet medication? It’s more commonly referred to as “low-dose aspirin therapy.” The most common regimen in the U. S. is an 81mg, enteric coated aspirin, taken once a day. A 2014 report published in Circulation, the journal of The American Heart Association (AHA), had updated findings. American Family Physician, re-published the findings under, “Updated Recommendations on Daily Aspirin Use in Patients with Diabetes.”
The guidelines and the supporting research are for the primary prevention of cardiovascular disease in diabetics. (“Primary” is medical jargon for those who do not already have CHD; “Secondary” prevention would be to prevent a heart attack in those who already have heart disease.) The lede in the Family Practice piece makes a compelling case:
Persons with diabetes mellitus have two to four times the risk of cardiovascular events compared with persons of the same age and sex who do not have the disease. Coronary heart disease (CHD) is responsible for more than two-thirds of deaths in persons with diabetes who are older than 65 years.”
The recommendations are, however, very nuanced:  “Low-dose aspirin therapy is reasonable in adults with diabetes and no history of vascular disease” who are at increased risk of CHD events based on an accurate assessment of CHD risk, “and who are not at increased risk of bleeding (i.e., no history of GI bleeding or peptic ulcer disease, and no concurrent use of other medications that increase bleeding risk).” You should consult your doctor.
“Adults with diabetes who are at increased risk of CHD events include most men older than 50 years and women older than 60 years who have at least one additional major risk factor (i.e., smoking, hypertension, dyslipidemia, or family history of premature cardiovascular disease). Aspirin should not be recommended in adults with diabetes who are at low risk of cardiovascular events (men younger than 50 years and women younger than 60 years with no additional major risk factors). The potential adverse effects from bleeding offset the potential benefits in these patients.”
The American Family Physician’s “Practice Guidelines” go still further: “Low-dose aspirin therapy may be considered for patients with diabetes who are at intermediate risk of CHD events (younger patients with at least one risk factor, older patients with no risk factors, or patients with a 10-year risk of 5 to 10 percent).” Again, ask your doctor.
They note also: “Not all patients with diabetes are at high risk, and the use of a risk prediction tool is essential. There are several Web-based tools available, such as the UK Prospective Diabetes Study Risk Engine (referenced) and the Atherosclerosis Risk in Communities CHD Risk Calculator” (also referenced). And that: “Risk should be reassessed periodically, because patients may acquire additional risk factors over time.”
After publication in Circulation, the paper appeared two months later in Diabetes Care, the journal of the American Diabetes Association, subtitled, “A Position Statement of the American Diabetes Association, a Scientific Statement of the American Heart Association, and an Expert Consensus of the American College of Cardiology Foundation.” Four months later, Family Practice Physician bought into it too and closed ranks with its “Practice Guidelines.”
Oddly enough, the time of day that aspirin is taken may make a difference. In 2013, a New York Times Well blog began, “Millions of adults take an aspirin every morning to ward off heart disease. But a new study suggests that the pills might be most effective if taken right before bed.” Why? “Cardiovascular events are about three times more likely to occur in the morning, when blood pressure and platelet activity are typically at their highest levels.” “Taking a daily aspirin helps thin the blood and prevent platelets from clumping, lowering the likelihood of heart attacks and stroke.”
The time-of-day study was done at Leiden University Medical Center in the Netherlands. The researchers found “that morning platelet activity was reduced to a much greater degree when the aspirin was taken at night. The timing of the aspirin, however, had no impact on morning blood pressure levels, which was something else the researchers measured.” The findings were presented at an American Heart Association (AHA) conference.
With my doctor’s approval, now that I’m “non-diabetic,” I discontinued my daily low-dose aspirin about 5 years ago. Up ‘till then, I took a low-dose aspirin with supper, so it could dissolve before I lay me down to sleep.

Friday, October 11, 2019

Retrospective #237: “…the ‘why’ behind my broken blood sugar.”

A loyal reader and faithful correspondent recently wrote to me that she was “always looking for the ‘why’ behind [her] broken blood sugar.”  I replied explaining the predisposition of some genomes to Insulin Resistance (IR), the predicate and the mechanism by which we slowly develop Type 2 diabetes. It begins with impaired glucose tolerance, advances to impaired fasting glucose, then progresses through beta cell failure and increased IR and full-blown Type 2 diabetes.
This “why” and “how,” however, is irrelevant, if we are already Type 2s. The fact is, if we were genetically susceptible and we ate a diet very high is sugars and processed carbs, as we were told, we became diabetic. It is instructive only to learn "what" to do to treat it effectively. The real question, then, is, "why" don't we change what we ate?
The “who” for this is all those who are 1) diagnosed Type 2s or 2) diagnosed (and undiagnosed) Pre-diabetics. The latter includes all those whose fasting blood glucose values have been between 100 and 125 on two consecutive lab tests or whose A1c’s are ≥5.7% and <6.5%. (Bear in mind that this A1c standard is the ADA’s lax measure; pioneer diabetologist Dr. Richard K. Bernstein and many other specialists regard an A1c of 5.7% to be full-blown Type 2.
If you’re either a diagnosed Type 2 or Prediabetic, you have a choice: 1) follow doctor’s orders: lose weight (if you’re overweight), eat the “healthy low-fat, high-carb diet” he or she likely prescribes, as defined by the Dietary Guidelines for Americans, the ADA, the AHA and the AMA, and take the medications your doctor prescribes while he or she monitors your progressively worsening condition. That’s not an unfair characterization. That is THEIR EXPECTATION.
Alternatively, if you’re either a diagnosed Type 2 or Pre-diabetic, you can lose weight (if you’re overweight), eat a “healthy low-carb, high-fat diet,” and take minimal or no medications while your doctor monitors your improving health (weight, blood pressure, lipids). As Michael Eades, M.D., commented on his popular Protein Power blog some years ago, "...the low-carb diet is the best way to shed weight and improve health for the vast majority of people."
The USDA’s one-size-fits-all low-fat, high-carb diet just doesn’t make sense for Type 2 diabetics or Pre-diabetics, (or anyone for that matter). It is the reason that we as a population, whether Pre-diabetic, Type 2 diabetic or not, are fat and getting fatter. It is how you fatten pigs and cows on the feedlot! Carb loading is how animals in the wild prepare to survive a long, hard winter when food is in short supply. You do too! You put on fat by eating grains, whether they’re “whole grains” or not. By the way, that “whole grain” loaf of bread with toasted whole grains on the outside? Those grains were brushed on and made sticky and brown using high fructose corn syrup (HFCS) or molasses.
My faithful reader and correspondent knows all this of course. It was just “wistful” thinking on her part (LOL). So, I am not writing this for her. I am writing this for those of you who still rely on your doctor to manage your diagnosed or undiagnosed Type 2 diabetes or Pre-diabetes. Read the Nutrition Debate #235: “Self vs. medical management of T2DM.” Self-management (under a willing doctor’s care) can avert the serious complications of Type 2 diabetes, both Micro and Macrovascular, including, ahem, men, erectile dysfunction. And lose weight and get off most meds to boot.
If you are officially or unofficially Pre-diabetic – with a fasting blood sugar between 100 and 125 – or with an A1c that is rising to or above 5.7%, you have a chance now to do something about it…BY CHANGING WHAT YOU EAT.
If you currently eat according to the government’s Dietary Guidelines for Americans, a one-size-fits-all prescription, and you’re a woman, you are eating about 300 grams of carbohydrate a day. That’s 60% of a 2,000 calorie a day diet. 60% is the Daily Value (DV), or Referenced Daily Intake (RDI), formerly called the “Recommended Dietary Allowance” (RDA), on the Nutrition Facts panel on packaged, processed food products. If you’re a man, you are eating 375 grams of carbs a day (60% of a 2,500 calorie a day diet). This is the high carb diet that the government recommends you eat.
I know. That’s shocking, but it’s a fact. The names have changed, but the percentage hasn’t. According to our USDA, we (all of us!) are supposed to be eating a diet that is 60% CARBOHYDRATE. Of course, you don’t have to do what the USDA tells you to do. You can take charge of your own health. Why not try 20% carbs (100g/day)? Can you do that?

Thursday, October 10, 2019

Retrospective #236: Inflammation and the Low Carb Diet

David Mendoza was a low-carb dieter and popular Type 2 blogger who in 2014 wrote an article about chronic systemic inflammation and low-carb dieting in Health Central. In it he referred to another article he wrote in Health Central in 2009. They were both interesting, but what really caught my attention was a link Mendosa provided to a PubMed abstract titled, “Advice to follow a low-carbohydrate diet has a favorable impact on low-grade inflammation in Type 2 diabetes compared with advice to follow a low-fat diet.” The full text is available from the Annals of Medicine.
His 2009 piece began, “More and more research pinpoints inflammation as a root cause of Type 2 diabetes.” He went on, “Type 2 diabetes generally results from the combination of impaired beta cell function and insulin resistance acting on susceptible genes.” In his 2014 piece, Mendosa relates these two disparate phenomena with a quote from Dr. Richard K. Bernstein, the Pied Piper of very low carb dieting and blood glucose monitoring to manage diabetes.
Mendosa, quoting Bernstein from his encyclopedic book, Diabetes Solution:
“To simplify somewhat, inheritance plus inflammation plus fat in the blood feeding the liver causes insulin resistance, which causes elevated serum insulin levels, which cause the fat cells to build even more abdominal fat, which raises triglycerides in the liver’s blood supply and enhances inflammation, which causes insulin levels to increase because of increased resistance to insulin.”
If that vicious cycle is too “geeky” and confusing for you – it is to me – then the “Advice to follow…” article above, a Swedish study, is not. The title says it all, very succinctly: “A low-carb diet has a favorable impact on low-grade inflammation in Type 2 diabetes compared with a low–fat diet.”
The Abstract’s BACKGROUND sets up the study: “Inflammation may play an important role in Type 2 diabetes. It has been proposed that dietary strategies can modulate inflammatory activity.”
The “low-carb” diet used in the study was 20% carbohydrates. That’s 100 grams of carbohydrate a day on a 2,000 calorie a day eating plan. The low-fat diet was 55-60% carbohydrate, or 275 to 300 grams of carbohydrate a day. This is the amount, if you didn’t know, that the Dietary Guidelines for Americans recommends for women of a certain age who eat 2,000 calories a day. It is also the amount on which the Nutrition Facts panel of packaged and processed foods is based. That’s a stunning revelation to most people. If you don’t believe me, check it out for yourself.
To my thinking, 100 grams of carbs a day is at the very high-end of low carb. Perhaps it was chosen as the “low-carb” amount for the study so as to be seen as “achievable” by people just starting out in low-carb eating. It is certainly achievable by anyone who gives it a good faith try. It certainly must be acknowledged that cutting carbohydrates by two-thirds, from 300g/day to 100, is no small feat. But it is enough reduction for most people who are not already diagnosed Type 2s. And it would make management with medications for diagnosed Type 2s much easier. Finally, it may make reversal of Pre-diabetes possible for people whose glucose tolerance is not already too badly impaired.
So, what did this randomized, real-world study reveal? RESULTS: “Both the low-fat diet and low carb diets led to similar reductions in body weight, while beneficial effects on glycemic control were observed in the low carb group only.” In addition, using various clinical laboratory measures, after 6 months, inflammatory markers “were significantly lower in the low-carb group than in the low-fat group.” Quod erat demonstrandum (Q.E.D.)
Note the C-Reactive Protein (CRP), a common inflammation blood marker, of the low-fat dieters actually increased 18% from1.41 to 1.67mg/L, while the CRP of the low carb dieters decreased 22% from 1.12 to 0.87mg/L.
CONCLUSION: “To conclude, advice to follow a low-carb diet or a low-fat diet had similar effects on weight reduction while effects on inflammation differed. Only the low carb diet was found significantly to improve the subclinical inflammatory state in Type 2 diabetes.”
Has your CRP level been checked recently? Has it ever been done? Ask your doctor. I have it done annually.

Wednesday, October 9, 2019

Retrospective #235: Self- vs. medical management of T2DM

A Google search on self-management of Type 2 diabetes got 1.75 million “hits” in 2014. That’s a lot of advice, the vast majority of which, in my opinion, was really bad. So, in this sea of flotsam and jetsam, there wouldn’t be much chance that you’ll find this little rubber ducky (#235). But my post is going to show you how almost any well-designed Type 2 diabetes self-management program is far superior to any ADA/AHA/AMA/USDA designed protocol.
To show superiority, we will need a basis for comparison. For Type 2 diabetes, that would be the Standard of Care as set by the American Diabetes Association (ADA).  They, in turn, will be tied into the U.S. government’s standards for insurance reimbursement for Medicare and Medicaid patients, to which both supplemental and private insurers also generally conform. And since Type 2 diabetes is a medical condition that is commonly associated with a raft of co-morbidities, including obesity, metabolic syndrome, dyslipidemia, hypertension, and cardiovascular disease, the Standards of Care and insurance reimbursements for these conditions must also be factored in.
So, when you “present” as an overweight middle-aged person, with elevated fasting glucose (>100 but <126mg/dL) or an A1c that is “increased risk of diabetes” (5.7-6.0%) or “higher risk of diabetes” (6.1-6.4%), if you’re lucky, you’ll get Metformin and be told to “lose weight.” Not so lucky? You’re told, “Your glucose is a little high” and “We’ll watch it.”
You’re probably already on a cocktail of blood pressure meds for your overweight-related hypertension, and if you’ve been eating a low-fat, high-carb diet, as recommended since 1980 by the Dietary Guidelines for Americans, you probably also have high triglycerides, low HDL, and high LDL, with a total cholesterol over 200mg/dL (i.e., “High Cholesterol”). So, you’re on a statin too, to lower your Total and LDL Cholesterol, because that’s what statins do.
Your doctor must treat you for this complex of conditions. For example, an endocrinologist (a hormone specialist!) that I went to recently (without a referral), wanted to prescribe a statin for me because my total cholesterol was over 200. It did not matter to him that my total cholesterol (207mg/dL) was over 200 BECAUSE MY HDL WAS 90. (Friedewald formula: TC = HDL + LDL + TG/5). My LDL was 110 and my triglycerides 34. All that mattered to him was, that, to conform to the NCEP Standard, I be on a statin. I refused. He probably wrote in my chart, “Noncompliant.”
The Dietary Guidelines for Americans (DGA) are similarly one-size-fits-all. The DGA guides to this day that everyone, regardless of metabolic status, should eat the same low-fat, high carb diet. But the pendulum is beginning to swing.
We’re now told to eat less sugar and highly processed carbs (that’s good advice). We’re also told it’s the quality, not the quantity, of fat that matters. They say shun trans fats (very good advice) and eat more vegetable and seed oils and less saturated fat (that’s very bad advice). The government’s one-size-fits-all standards are still way behind the curve.
The American Diabetes Association Standard of Care, to achieve an A1c ≤7.0%, is hopelessly lax. The reason for this catastrophic Standard of Care is that it is a function of a failed treatment protocol. And it is a failed treatment protocol because of the government’s insistence on a LOW-FAT, HIGH CARB ONE-SIZE-FITS-ALL DIET for all Americans.
Never mind that this dietary is what has made us fat. Never mind that all carbohydrates raise your blood glucose. When you “present” as an overweight middle-aged person, with elevated fasting glucose, or A1c, your doctor should tell you to drastically curtail your intake of carbohydrates. Mine did. He started me on 20 grams of carbohydrate a day to lose weight. I did. I lost lots of weight (170 pounds in the first few years). I also had to stop taking virtually all my oral diabetes meds in the first week! Over time my blood pressure went from 130/90 to 110/70 on fewer meds. My HDL more than doubled, and my triglycerides dropped by two-thirds. And I am no longer, of course, taking a statin.
I self-monitor my T2DM by carefully watching what I eat, weighing myself daily, and monitoring my fasting blood sugar daily, and A1c’s, to a much higher standard than prescribed by the American Diabetes Association and my doctor.
What’s your HDL level?  Or does your doctor even care? You see, there’s no ‘magic pill’ to get your HDL up above the 40mg/dL range (50 for women), considered “borderline.” Only a low-carb diet does that…and lowers triglycerides too.

Tuesday, October 8, 2019

Retrospective #234: You begin to secrete insulin when…


Whether you’re a Type 2 diabetic or not, your body’s mechanism for regulating the level of glucose in your blood begins the same. It is far beyond my pay grade to explain it in detail, but I can give you an overview of how it works.
Everyone has a brain and a functioning autonomic nervous system, and while we’re alive, they work basically the same way. We breathe, our hearts beat, our temperature is regulated, and we are driven by elemental forces within us to eat, procreate and sleep. For survival, optimum health, and longevity, the body tells us what to do and when to do it. One of those elemental drives is eating. The body needs food to sustain itself. And grow. So, we seek food.
We seek food and learned through the ages what to eat. Through an evolutionary process we became omnivores. Eating both animal and vegetable foods allowed the human species to spread far and wide. Populations adapted to the variety of foods available in different climates and seasons and in times of both feast and famine. To kill, catch or gather food, we used our senses and motor skills and our developing intellectual powers. But first, before all the rest, when our bodies told us we were hungry, our senses kicked in. Our senses provided the message to seek and find food.
First among our senses was sight. By some estimates, ninety percent (90%) of what we sense is visual. The sight of food excites our brain and sends a signal to the pancreas to secrete insulin. Insulin is required to transport and enable uptake of glucose, from digested starches and sugars (carbs) in the blood. That energy replaces glycogen that has been stored in muscle and the liver and has been used, both to maintain our basal metabolism and for motor activities like hunting, fishing or gathering. As much as 10% of energy from protein is used just in digesting and absorbing it.
In addition, the smell and sound of food (e.g., a sizzling steak) excites our brain and sends a signal to the pancreas to secrete insulin. And personally, I think the smell of food is a more powerful stimulant to eat (and therefore possibly a more powerful stimulant to secrete insulin) than the sight of food. The smell of food being cooked is closer in time to eating it, and more of a certainty than just seeing food “on the hoof” with the prospect of a kill.
Even THINKING about food, which many dieters say they do all the time, excites our brain and sends a signal to the pancreas to secrete insulin. My serum insulin is probably somewhat elevated when I write about nutrition. Having a constantly elevated serum insulin, as carboholics do, can be problematic. Insulin is the fat storage hormone. When insulin is elevated, the body stores food energy and does not burn energy by breaking down energy stored as body fat.
Finally, there’s the taste of food, the digestive enzyme amylase from the salivary glands in the mouth excites the brain and sends a signal to the pancreas to secrete insulin. In the “normal” (healthy) metabolism, this is a burst of insulin that prepares your digestive system to ramp up to secrete more insulin to handle food passing through the stomach and on to the small intestine where the final digestion and absorption processes occur.
All these sensory processes are normal. In fact, they are elemental survival traits. And they are autonomic, meaning they happen automatically without conscious initiation. However, we do have total awareness of them, and we act on them. We seek food to feed our bodies to sustain life and to grow. It is fundamental to survival.
But what happens when these normal metabolic mechanisms break down? When the supply of insulin is lessened because our pancreatic beta cells which secrete insulin don’t function or die? Or when the insulin we have been able to produce circulates with the glucose from digested food but does not open the body’s cells to take up the glucose and replace the glycogen that’s been used? Answer: With a “broken” metabolism, your blood sugar rises abnormally.
Today, if you allow your blood sugar to rise to the point where you have “uncontrolled” blood sugar levels, you are diabetic. But if you are just Pre-diabetic, and you don’t want your disease to progress to that point, there is a natural way to manage and control without medication, your elevated blood sugar levels. There is something you can do to preserve what function your pancreas has left to make insulin and your cells’ ability to take up glucose. You can change what you eat. You can adapt what you eat for survival. You can eat fewer carbs. Your life may depend on it.

Monday, October 7, 2019

Retrospective #233: Multifactorial Approach to Prevent CVD in T2DM

Michael Marre, a French physician who heads the diabetes department at a Paris hospital, gave an oral presentation at the 2014 American Diabetes Association 74th Scientific Sessions in San Francisco. It was reported on in Medscape Medical News, an aggregator of medical news for physicians. The title of his talk: “Multifactorial Approach to Prevent Cardiovascular Disease in Type 2 Diabetes,” subtitled “Identifying Diabetes and Cardiovascular Risks.” The risk part was okay, the multifactorial approach to prevent CVD ho-hum, and the comment section priceless. Here’s my précis.
Dr. Marre’s definitions: “Diabetes mellitus is a metabolic disorder caused by both a defect in insulin secretion and in insulin action. It is an important contributor to vascular damage. Remember that, by definition, diabetes induces microvascular complications, and it is also a huge risk factor for macrovascular complications.” I might quibble with “caused by” and argue that it is diabetes controlled to the ADA Standard of Care that induces microvascular complications, but still, his view conforms to the medical establishment’s, so you can’t blame him for their dereliction.
To his credit, Dr. Marre states that “you can take some prevention measures, which include lifestyle interventions that can reduce the risk for diabetes by 50%.” He adds, though, “If that’s not enough, you can add some pharmacotherapy” and then launches into a litany of meds that can possibly “delay or postpone the progression to diabetes mellitus.” His primer continues: “In fact, an individual evaluation must include an assessment of the classic risk factors, the glycemic status, the macrovascular disease, and the microvascular disease:
     The classic risk factors are family history, lifestyle, smoking, hypertension and dyslipidemia (cholesterol issues).
     Macrovascular disease: coronary status, cerebral vascular disease, peripheral arterial disease, and heart failure.
     Microvascular disease: retinopathy, nephropathy, and neuropathy, and
     Don’t forget arrhythmias, especially atrial fibrillation
To his credit, Dr. Marre says “Cardiovascular risk requires multifactorial management, with an emphasis on lifestyle intervention. Look at what the patient eats and drinks.” He advocates “a Mediterranean diet from your birth date.” Okay, I’ll admit a Mediterranean diet would be a better choice of what to eat and drink than the Standard American Diet (SAD), but hey, so would almost any way of eating. And Dr. Marre says, he is “from the Mediterranean area.”
Summarizing, Dr. Marre’s management and control recommendations are pretty much pro forma “establishment”:
     Maintain blood pressure below 140/85 mm Hg. This is the objective for patients without any renal impairment. If the patient has a slight increase in microalbuminuria, then the blood pressure objective must be below 130/80.
     Look at the low-density lipoprotein (LDL) cholesterol level, which must be below 1.8 mmol/L (70 mg/dL).
     Glycemic control, as assessed by A1c, must be below 7%.
Dr. Marre cautions, “For blood pressure lowering, do not forget to prescribe as first-line therapy a rennin-angiotensin-aldosterone inhibitor. This is mandatory.” That’s an ACE inhibitor, like Enalapril. Whew! I take one.
For lipid control, use a statin for first-line therapy, and prescribe an appropriate dose. [another pill]. Antiplatelet therapy [low-dose aspirin] is recommended for secondary prevention of cardiovascular disease. “Often,” he said, “you have to combine several antidiabetic agents [more pills or injections] to achieve good glycemic control, but as most of our patients are overweight or obese, use Metformin as much as possible in first-line therapy.” Again, whew!
But wait a minute! What happened to those lifestyle interventions? To “looking at what the patient eats and drinks”? Here is a doctor lecturing on the basics of clinical care for the overweight or obese Type 2 diabetic patient, to avoid the co-morbidities of micro and macrovascular disease, and all he has to offer, except lip service, is a cocktail of pills?
There were just five comments. The first four were “the usual”; the fifth, most unusual: “This is rubbish and when I open it, I am struck by several ads for Victoza I cannot get rid of. What can I expect from a site that is financed by industry? Oh, Eric Topol, how can you possibly work here and look yourself in the mirror every morning.” Signed: Anders Hernborg, Swedish GP. Anders Hernborg is a mostly retired, MD, “independent researcher” and “activist.” Of the 22 published scientific papers which he has co-authored, one is titled “Advertising or Science?” Being “mostly retired” makes time for research and writing. Telling the truth may also be a certain way to become “mostly retired.”

Sunday, October 6, 2019

Retrospective #232: “A spoonful of sugar”

“A spoonful of sugar” is the title of a 14-year old and still popular blog post of Dr. Michael R. Eades. Eades, in his own words, is a “sort of traditional M.D. with an eye to what works to get patients well whether it is traditional or not.” He and his physician wife, Mary Dan Eades, are the authors of “The Protein Power LifePlan” and before that “Protein Power,” two of the best books I have read on the subject of optimal health, low carb eating and Type 2 diabetes.
The one-teaspoon-of-sugar metric refers to the amount of “sugar” (glucose) that is dissolved in the 5 liters of blood in the circulatory system of a typical human. In the article Dr. Eades explains that a blood glucose reading of 99mg/dl, “the highest fasting blood sugar you can have and not be diagnosed as pre-diabetic,” means that you would have just 4.95 grams of grams of sugar in your blood. One teaspoon of sugar is equivalent to, i.e., weighs just 5 grams.
The American Diabetes Association established the current Type 2 diabetes diagnostic thresholds in 2009. They are 70-99mg/dL being a “normal” fasting blood glucose, 100-125mg/dL being prediabetic, and ≥126mg/dL being diabetic.
Quoting Dr. Eades: “If you run the calculations for 126 mg/dl, the amount of sugar in the blood of someone just over the line into the diagnosis of diabetes, you find out that it is 6.25 grams, or 1 1/4 teaspoon. So, the difference between having a normal blood sugar and a diabetic blood sugar is about a quarter of a teaspoon of sugar.” He continues:
“What really gets kind of scary is when you look at the amount of carbohydrate in, say, a medium order of McDonald’s fries compared to the sugar in your blood. Remember, it is the job of your digestive tract to breakdown the starch and other complex carbohydrates, which are nothing more than chains of sugar molecules, into their component sugars so that they can be absorbed into the blood. An order of medium fries at McDonald’s contains 47 grams of carbohydrate*. 47 grams of carbohydrate converts to about 47 grams of sugar, which is almost 10 teaspoons. So, when you eat these fries you put 10 times more sugar into your blood than that required to maintain a normal blood sugar level. If you figure, as we did above, that one quarter of a teaspoon is all the difference between a normal blood sugar and a diabetic blood sugar, the 10 full teaspoons would be 40 times that amount.”
And if that isn’t scary enough, Dr. Eades then hits you with his coup de grâce:
“Since your metabolic system has to work very hard to deal with the sugar load from an order of fries, imagine what it has to do when you add a large soft drink, a hamburger bun, and maybe an apple turnover for dessert.”
I have to admit I never thought about my pancreas and its declining ability to make insulin, and my body’s declining ability to process that insulin, and the “sugar” attached to it in my blood, when I drove up to McDonalds and ordered my large order of fries, as a side order. For 16 years, before my doctor suggested I try very-low-carb eating to lose weight, I just relied on him to deal with my progressively worsening type 2 diabetes. I didn’t know any better!
Boy, what a difference eating very-low carb made, both in my weight (at one point I had lost 188 pounds) and in my diabetes status. Although I have since regained some of that 188 pounds (I continue to maintain at least a 150-pound weight loss), I am still able to stay off almost all the diabetes meds I had been taking. I had been maxed out on two orals (Metformin and glyburide) and had been started on Avandia. Today, I just take one small dose of Metformin a day. And my blood sugars are now “non-diabetic.” My A1cs are in the low to mid 5s, once even reaching 5.0%
The takeaway? In a person with a “healthy” metabolism, your body gives itself a shot of insulin the moment you see or even think about eating. A metabolism compromised by enough Insulin Resistance to give you an impaired glucose tolerance (IGT) can no longer do that. Then, when something starchy or sweet (carbs) contacts your saliva, the brain signals the pancreas to immediately secrete more insulin… but for some of us it’s too late. Your damaged or clogged pancreas can no longer make as much insulin as it did before, and the insulin that it does make is not “taken up” by the cells as it circulates around your body. The “not taken up” is the Insulin Resistance (IR) part.
The result: Your body is overwhelmed by the sugar (glucose) circulating in your blood after digesting the carbs (starches and sugars) you just ate, and your blood sugar rises above healthy levels, and the silent damage to your organs and your Microvascular and Macrovascular systems continues…
 * The McDonalds table has been updated. A medium French fries is now 44g of carbs. A large French fries is 67 grams. 

Saturday, October 5, 2019

Retrospective #231: Vitamin K-2

Weston A. Price called it “Activator X,” and for lack of further research Vitamin K-2 remained a mystery for 62 years. In an article on the Weston A. Price Foundation’s website, Chris Masterjohn explains, “Vitamin K2 works synergistically with the two other fat-soluble vitamins that Price studied, Vitamins A and D, which Vitamin K activates.
Vitamin K-2 supplementation is now all-the-rage for the multiple benefits it appears to confer. A now 11-year old article, “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 good summation of its other salutary effects, including some related to Type 2 diabetes.
My editor brought my 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), where I received my basic education in Very Low Carb eating. It’s a friendly resource for low-carb neophytes.
My editor also introduced me to ghee, pure 100% butter fat (“clarified” butter) and in particular to the Ancient Organics brand. This 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 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 a 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.
But the ‘post’ my editor referred to was a paper in Diabetes Care, the Journal of the American Diabetes Association. The title, “Vitamin K-2 Supplementation Improves Insulin Sensitivity via Osteocalcin Metabolism: A Placebo Controlled Trial.” The 2011 study was conducted by a team at the Seoul National University College of Medicine in Korea.
“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 K-2 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 or placebo for 4 weeks.
“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.” “We conclude that, unlike in rodents, cOC rather than ucOC, may be the endocrine hormone that increases insulin sensitivity in humans.” Vitamin K-2 is the mysterious “Activator X,” the catalyst that synergistically works to convert ucOC to cOC 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. 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 raw 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 book, "Vitamin K2 & the Calcium Paradox", recommends 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. In it, she says, “Vitamin K-2 is critical for keeping our bones strong and our arteries clear.” For the time being, though, (until I’ve read the book), I’m going to stick with my pastured hen’s eggs and Ancient Organics organic ghee.

Friday, October 4, 2019

Retrospective #230: Frustrated by Failure? Solution: Lower the Standard of Care!

“Tight Glycemic Control More ‘Burden’ Than Benefit for Many,” a Medscape Medical News piece proclaimed. Reading this online article later in JAMA Internal Medicine really got my blood boiling. The proposed “solution,” in the guise of “patient-centered care,” is to “personalize treatment.” Sounds nice, but consider also the potential to blame failure-to-successfully-treat ON THE PATIENT, rather than on the WRONG TREATMENT PLAN, and then to assign the failure to the patient’s “burden” of treatment, thus relieving the patient of the moral burden for failure. Neat, huh?
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, 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, the authors acknowledge, “Lowering HbA1c delays the onset and slows the progression of early microvascular disease.”
So, what did we learn here? The new Standard of Care “for many” would be an A1c <9%, equal to an AVERAGE glucose of 212mg/dl? And that 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 is only “modest”? What could lead anyone with a clinical practice to reach this conclusion? Could it be THE FAILURE OF THE TREATMENT PLAN?
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 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. A new paradigm!
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.” But, “patients older than 50” includes most people initially diagnosed with Type 2 diabetes, so this new paradigm would then thus apply to almost everyone!
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. [only on the wrong treatment plan]. 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….” Get patient “buy in” of less “burden.” Sounds appealing!
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 constructed] of these complications, and it may not be worth treating to prevent that,” they concluded. That’s confirmation bias!
It’s true: Some people can’t tolerate Metformin. And some anti-diabetic meds (e.g.SUs) do cause weight gain, and injecting insulin is a “bother” and 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 or no anti-diabetic oral medications, and stopping insulin injections, 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 plan,” they say. But…you know what? IT REALLY WORKS

Thursday, October 3, 2019

Retrospective #229: My Alternate Healthy Eating Index (MyAHEI)


In Retrospective #200, 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. 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. Read Minger’s Death by Food Pyramid.
In its latest iteration, the USDA’s Center for Nutrition Policy and Promotion 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.” Their first objective: 1) Advance and promote dietary guidance for all Americans. 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 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, “intense lobbying efforts from a variety of food industries also helped shape the pyramid and the plate.”
So, Harvard’s response was to create 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.” I think we need another tool for assessing diet quality: one I coin “My Alternate Healthy Eating Index” (MyAHEI)©. The principles of MyAHEI are listed below: Read it and self-report your own score in the comment section. Give yourself 5 points for each question you can answer affirmatively. Part scores 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 a window of no more than 10 hours.
2.      Eat animal protein with animal fat (and dietary cholesterol) with every meal, and to your heart’s content.
3.      Eat 12 to 18 whole eggs from pastured hens each week.
4.      Eat no snacks between meals (except perhaps a low-carb/high fat snack before supper).
5.      Eat no fried foods and vegetable or seed oils, margarine or store-bought mayo. Eat butter, ghee, and coconut oil.
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-caught salmon, char, or turbot at least 5 times a week.
9.      Eat no store-prepared foods and no food sold in boxes or bags (except flash-frozen fish and veggies).
10.   Eat mostly fresh low-carb 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, only on very special occasions.
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 (1 or 2 glasses only), or other alcoholic beverages, with (and/or before) supper 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!!!

Wednesday, October 2, 2019

Retrospective #228: A1c and your estimated Average Glucose (eAG)


The glycated hemoglobin (Hb) A1c has become the new standard for assessing a patient’s diabetes status. It is a percentage, as for example the ≤7% default ADA target for a diagnosis of Type 2 diabetes. The percent is the amount of glucose attached to the surface of a hemoglobin molecule within a red blood cell.
Red blood cells typically live 2 to 3 months, so this is a surrogate way of determining the level of glucose in your blood 24/7 over that 2 to 3-month period. The ADA recommends that a Prediabetic’s A1c be tested at 2 times a year and, if you’re a diagnosed Type 2, 4 times a year. Medicare will pay for 4, unless more is deemed “medically necessary.”
Prior to using the A1c test, a clinician used two consecutive fasting plasma glucose tests that exceeded the ADA’s Standard of Care for Type 2 diabetes. Until 1997 that Standard was ≥140mg/dl. After 1997 it was lowered to ≥126. In addition, a new standard for Prediabetes was established: readings between 100 and 125mg/dl. If your lab tests are between 100 and 125mg/dl, and your doctor hasn’t told you that you’re Prediabetic, you might want to ask why?
The difference in units (% vs. mg/dl) has understandably led to some confusion and a disconnect. 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 are developing. That is why the A1c test is a better indicator of your diabetes health than the fasting glucose test.
So, to resolve the disconnect and the confusion that has resulted, a copyrighted table has been developed at diabeteschart.org that creates a correlation between A1c % and estimated Average Glucose (eAG) in mg/dl.
From this chart, an A1c of 7% is equivalent to a whopping eAG of 154mg/dl. This is stunning. That means that, if you have an A1c of 7% (the AD’s recommended GOAL), your plasma blood glucose is higher than 154mg/dl 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 MICRO AND MACRO VASCULAR SYSTEMS.
Because I have not been as vigilant as I should be in watching what I eat, my own A1c’s have been higher than I would like for the last year or so. Breakfast and lunch are easy for me, but at or after dinner, I have not always stuck to 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 near or above 140mg/dl. That’s bad.
But my doctor, who adheres to the ADA Standard of Care, considers my blood sugar “in control.” How can I convince him otherwise? He is following the ADA’s Standard. So, I just have to establish my own Standard, and hope he goes along with my plan. So far, he’s “on board,” but in the future, if we see it differently, I’ll 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 get by fine with 2. I always do a fasting test and use the second strip to test at other times, or just renew the prescription later.
Recently, while on an antibiotic to treat a tick-borne infection, I did a “continuous” (@ 2-hour intervals) test all day. 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. Dinner was in a restaurant. I ordered 2 appetizers: 6 raw oysters, and then steak tartare with an egg yolk in the center. Then (here’s the bad), I helped my wife eat her large order of sweet potato fries that came with her “steak frites.” I should have ordered/eaten a side of roasted Brussels sprouts instead.
Result: all day long my blood sugars were higher than usual for me due to my body helping the antibiotic fight the infection, but they were stable. Then, after dinner, they “spiked” due to my indiscretion. I love sweet potato fries, but I paid a big price for going “off the reservation.” To see if it normalized, I should have tested 4 hours postprandial, but didn’t. I’m still on a single dose of Metformin (with the evening meal) to suppress postprandial gluconeogenesis.