The Nutrition Debate #240: Pottenger, his Cats and his Prophesy

Some time ago a regular reader and friend of this blog suggested that I read “Pottenger's Cats, a Study in Nutrition,” originally published in book form in 1983 and more recently republished in paperback by the Price-Pottenger Nutrition Foundation. So I did. Francis M. Pottenger, Jr., M.D., 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.

Quoting from the jacket, in feeding experiments of 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, indeed prescient 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.” If you’d like to see images, this video presents an overview.

The publisher, quoting from the 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, a sobering challenge stands before us.” And I think that this warning about nutrigenomics, an aspect of epigenetics, is increasingly getting our attention. How our individual genes express (or do not express) themselves depends on many environmental factors, the most important of which is what we choose to eat. And, have you noticed, we are getting sicker on the diet of highly processed vegetable oils and carbohydrate laden and sugary foods based on the recommendations of the USDA’s “Dietary Guidelines for Americans”?

Of course, Weston A. Price, himself a dentist who studied the role of whole, living foods and essential 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 the leadership of Sally Fallon, the Weston A. Price Foundation (WAPF) carries on his work. The work of this foundation is worthy of your support.

I have previously dealt with this subject in a blog post on “Deep Nutrition” (2009), a book by Catherine Shanahan, MD, and Luke Shanahan. The subtitle of the book: “Why Your Genes Need Traditional Foods.” The Shanahans’ 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” (2011,) by Gray Graham, Deborah Kesten and Larry Scherwitz, is another recent read. Sherwitz, a PhD, is founder of the Nutritional Therapy Association (NTA), a holistic nutritional therapy training organization. Graham is a Nutritional Therapy Practitioner (NPT) and Kesten an MPH and nutrition researcher. The subtitle of their book is, “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.” We are reminded once 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 – (is the) ‘new paradigm’ and ‘the medicine of the future.’ Personally, I believe that. I like to say, “I am living proof” (albeit n=1).

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. That Pottenger demonstrated that convincingly with his cats was but a harbinger. 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.” Tyne Moore, ND, DC.

Will this generation pay attention? I hope so. We’re going to continue to do our part to see that outcome realized.

Your favorite way to eat “meat on the bone?”

The Nutrition Debate #239: Low-Carb Diet Should Be First Approach for Diabetes

Diet Doctor Andreas Eenfeldt, M.D., the very popular Swedish blogger and low-carb advocate, recently headlined a post with “Scientists: A Low-Carbohydrate Diet Should Be First Approach for Diabetes!” He provides a link to the full-text paper (29 PDF pages, with 99 foot-noted references). It is to appear in the respected mainstream journal Nutrition under the title, “Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base.”

Eight of the twenty-six co-author’s names are familiar to me, including Richard Feinman, PhD, the lead author. 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 linked version of 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. After the 12 points there is a Discussion and then 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 the newly 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. This paper is a very well made case and should be widely disseminated in the medical community.

The Nutrition Debate #238: Type 2 Diabetics: Do you take a low-dose aspirin?

Do you take an antiplatelet medication? If you’re not sure, 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. Here, from American Family Physician, are “Updated Recommendations on Daily Aspirin Use in Patients with Diabetes,” confirming the findings. The report was originally published in Circulation, the journal of The American Heart Association (AHA), here.

The guidelines and the supporting research are for the primary prevention of cardiovascular disease in diabetics. (“Primary” means for those who do not already have CHD; “Secondary” prevention would be to prevent a heart attack in those who already have heart disease.) Is it justified? The lede in the Family Practice piece makes a pretty 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 is, however, somewhat 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).” Obviously, you should consult a doctor to make that determination.

“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, albuminuria, 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 (here) and the Atherosclerosis Risk in Communities CHD Risk Calculator (here).” And that: “Risk should be reassessed periodically, because patients may acquire additional risk factors over time.”

After its publication in Circulation, the paper appeared two months later here in Diabetes Care, the journal of the American Diabetes Association. The subtitle of both: “A Position Statement of the American Diabetes Association, a Scientific Statement of the American Heart Association, and an Expert Consensus Document of the American College of Cardiology Foundation.” Family Practice Physician bought in to it and closed ranks with its “Practice Guidelines” four months later.

Oddly enough, the time of day the aspirin is taken may make a difference. A New York Times health blog last year 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.”  

The reason: “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,” therefore, “helps thin the blood and prevent platelets from clumping, lowering the likelihood of heart attacks and stroke,” the Well blog says.

The 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.

So, the lead author of the study said, “it may make more sense for daily aspirin users to take the medication before turning in each night, rather than first thing in the morning.” I take it with supper, so it can dissolve before I lay me down to sleep.

The Nutrition Debate #237: “…the why behind my broken blood sugar.”

A loyal reader and faithful correspondent recently wrote to me, as an aside, that she is “always looking for the ‘why’ behind my broken blood sugar.” I’ve didn’t reply directly to her, but I have addressed the subject in myriad posts on this blog. I have explained the predisposition of some genomes to type 2 diabetes, the mechanism by way of insulin resistance (IR) wherein one comes to have impaired glucose tolerance and impaired fasting glucose, and then progresses through beta cell failure and increased IR to full-blown type 2 diabetes. If you’re interested, About.com offers this excellent explanation.

But, this “history” of how we have become type 2 diabetics is really irrelevant, if we are already. The fact is that if we were susceptible, either 1) we are already or 2) we are slowly becoming type 2 diabetics. So, if either is so, the real question is, what can we do about it? This requires a 2-part answer: 1) for diagnosed type 2s and 2) for diagnosed or 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 Hb A1c’s are = or > 5.7%. (Bear in mind that this A1c standard is the ADA measure; pioneer diabetologist Dr. Richard K. Bernstein and many other specialists regard an A1c of 5.8% to be full-blown type 2 diabetes. Check your post prandial glucose and see what you think; don’t wait for your next appointment.)

If you’re a diagnosed type 2, you can either 1) follow doctor’s orders: lose weight (if you’re overweight), eat a “healthy diet” (which is low-fat, high-carb, as defined by the Dietary Guidelines for Americans), and take medications while your doctor monitors your progressively worsening condition. That’s not an unfair characterization on my part. That is their expectation.

Alternatively, if you’re a diagnosed type 2, you can lose weight (if you’re overweight), eat a “healthy diet” (which is low-carb, high-fat, as common sense would dictate), 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."

Now, if you’re an “undiagnosed or diagnosed pre-diabetic” (“those whose fasting blood glucose values have been between 100 and 125”), or have a slightly elevated A1c that’s climbing out of the healthy 4 range into the mid-5s and higher as you continue to eat the Standard American Diet (SAD), what can you do? Again, you have two options: 1) continue eating the diet recommended to you by the USDA (think about that: the U. S. Department of Agriculture’s Center for Nutrition Policy and Promotion produces the Dietary Guidelines for Americans); or 2) start eating a diet much lower in carbohydrates.

The USDA’s one-size-fits-all low-fat, high-carb diet just doesn’t make sense for diabetics or pre-diabetics (or anyone at all for that matter). It is the reason that we as a population, whether pre-diabetic, diabetic or not, are fat and getting fatter. It is how you fatten pigs and cows in 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 purportedly “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, or some such.

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 who still rely on their doctor to manage their diagnosed type 2 diabetes. If you don’t know how seriously misguided you are to do this, read The Nutrition Debate #235: "Self- vs. medical management of T2DM." And continue reading this blog for guidance on how self-management (under a willing doctor’s care) can avert the numerous, serious complications of type 2 diabetes, both micro and macro vascular, including erectile dysfunction.

And if you are pre-diabetic – whether officially diagnosed or undiagnosed (with a fasting blood sugar between 100 and 125) or with an A1c rising to and above the mid 5s, you have a splendid chance to do something about it…by changing your diet. And the sooner you start, the better.

If you currently eat according to the government’s one-size-fits- all prescriptive diet, you are probably eating about 300 or more grams of carbohydrate a day. That’s 60% of a 2,000 calorie a day diet and the amount of carbohydrate that the Nutrition Facts panel on packaged, processed food products says is the Daily Value (DV), formally the Referenced Daily Intake (RDI), according to Wikipedia. These were formerly called the “Recommended Dietary Allowance” (RDA). And that’s shocking, but a fact. The name may 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 government tells you to do. You can take charge of your own health and eat lower carb. Why not try a 20% carb diet (100g/day)? Can you do that?

The Nutrition Debate #236: Inflammation and the Low Carb Diet

Low-carb dieter and popular type 2 blogger David Mendosa recently wrote an article about chronic systemic inflammation and low-carb dieting inHealth Central. He referred to another inflammation piece 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 favourable 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 here.

Mendosa begins his 2009 piece with this: “More and more research pinpoints inflammation as a root cause of type 2 diabetes.” He added, “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 this new Swedish study – the “Advice to follow…” link above – is not. The headline says it simply: 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 and the amount on which the Nutrition Facts panel of packaged and processed foods is based. That’s stunning to most people. If you don’t believe me, check it out for yourself.

In “my book,” 100 grams of carbohydrate a day is very high-end low-carb. Perhaps it was chosen as the “low-carb” amount for the study so as to be seen as an “achievable” amount by people just starting out in the low-carb Way of Eating. It is certainly achievable by anyone who gives it a good faith try. But, it must be said that cutting carbohydrate consumption by two-thirds (from 300g/day) is no small feat. It is undoubtedly a sufficient reduction for the majority of people who are not already diagnosed type 2s. It would make management with medications for diagnosed type 2s so much easier. And 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.”

Table IV from the full-text of the study, showing data for all the inflammation markers tested, is reproduced here. Note the CRP 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.”

Wikipedia tells us that CRP has a half life of 48 hours, so the anti-inflammatory effects of a diet change can begin quickly.  Have your CRP levels been checked?

The Nutrition Debate #235: Self- vs. medical management of T2DM

1,750,000 “hits” on the subject of self-management of type 2 diabetes in my initial Google search; that’s lots of advice, the vast majority of which is, in my humble opinion, really bad. So, in this sea of flotsam and jetsam, there wouldn’t be much chance of your finding my little rubber ducky (#235). Besides, this post is going to show you how almost any well-designed program of self management of type 2 diabetes is far superior to any ADA/AHA/AMA/USDA designed protocol. The differences will astound you, I promise. And the benefits to you, “the patient,” will be demonstrable.

To show superiority, we will need a basis for comparison. In the case of type 2 diabetes, that would be the Standard of Care set by the American Diabetes Association.  They, in turn, will comply with the government’s standards of “insurance” reimbursement for Medicare and Medicaid patients, to which private insurers also generally conform. And since type 2 diabetes is a medical condition that is generally associated with a raft of other disorders and conditions, including obesity, metabolic syndrome, dyslipidemia, hypertension, and cardiovascular disease, the Standards of Care and standards of insurance reimbursements for these conditions must also be factored.

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’re given metformin and told to “lose weight.” Not so lucky and you’re only 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 obesity-related hypertension, and if you’ve been eating a low-fat, high-carb diet as recommended by the Dietary Guidelines for Americans since 1977, you probably also have high triglycerides, low HDL, and high LDL, with a total cholesterol over 200mg/dL. So, you’re on a statin too, to lower your LDL and Total Cholesterol (because that’s what statins do) in conformance with the National Cholesterol Education Program (NCEP) Standard of Care (another one of those government standards).

Your doctor, whether he or she is a general practitioner or a specialist, has to treat you for this complex of conditions. For example, an endocrinologist (a hormone specialist!) that I went to see recently (without a referral), wanted to prescribe a statin for me because my total cholesterol was over 200 (and I have other risk factors: hypertension and type 2 diabetes). It did not matter to him that my total cholesterol (207mg/dL) was over 200 because my HDL was 90. My LDL was 117 and my triglycerides 34. I wonder if he knew about the Friedewald formula: TC = LDL + HDL + TG/5. All that mattered to him was, to conform to the NCEP Standard of Care (and insurance payment/review criteria), that I be on a statin. I refused.

The Dietary Guidelines for Americans are similarly one-size-fits-all. Everyone, regardless of metabolic status, should eat the same low-fat, high carb diet. But the pendulum is beginning to swing. Now we’re told to eat less sugar and highly processed carbs (that’s good advice). We’re now also told that it’s the quality, not the quantity, of fat that matters. They say shun trans fats (good advice) and eat more vegetable and seed oil and less saturated fat (that’s bad advice). Still, the government’s one-size-fits-all standards are way behind the curve. In addition, they have been hopelessly corrupted by industry influence at the USDA. It’s bad news, period.

The American Diabetes Association has similar standards. It used to be one-size-fits all, and the Standard of Care, to achieve an A1c of < or = to 7.0%, hopelessly lax. This catastrophic Standard of Care was and still 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 the American population. And now they want to lower the Standard of Care. See #230 here.

Never mind that that this dietary is what has made the population fat. Never mind that all carbohydrates raise your blood glucose. At the very least, once you “present” as an overweight middle-aged person, with elevated fasting glucose (>100 but <126mg/dL) or an A1c that is at “increased risk of diabetes” (5.7-6.0%) or “higher risk of diabetes” (6.1-6.4%), your doctor should tell you (as mine did) to drastically curtail your intake of carbohydrates. My doctor suggested I start on 20 grams of carbohydrate a day to lose weight. I did. I lost lots of weight.

 And I also was able to give up virtually all of my oral diabetes meds. And my blood pressure went from 130/90 to 110/70 on the same meds. And my HDL more than doubled. And my triglycerides dropped by two-thirds. And I no longer, of course, need a statin. This treatment protocol, which I self-monitor by watching what I eat and monitoring my blood sugar to a much higher standard than prescribed by the American Diabetes Association and my doctor, is clearly far superior to the one-size-fits-all medical standard that our government and the medical establishment continue to use to treat T2DM.

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, which is considered borderline ‘bad’ for men (45mg/dL for women). Only a low-carb diet can do that. And lower your triglycerides too.

The Nutrition Debate #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 circulating in your blood begins the same way. It is a complex process, and far beyond my pay grade to explain in detail, but I can give you an overview of how it works and affects your health. If you’re interested enough, you can follow the links to learn more.

Everyone has a brain and a functioning autonomic nervous system, and, as long as 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 grow and sustain itself. So, we seek food.

We have learned through the ages what to eat. Through an evolutionary process, by adaptation, 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 and foremost, 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 perceive is visual. The sight of food excites our brain and sends a signal to the pancreas to secrete insulin in preparation to transport glucose (energy converted from food) throughout our circulatory system. That energy replaces glycogen that has been stored in muscle and the liver and has been depleted by use, both to maintain our basal metabolism and for motor activities like hunting, fishing or gathering, and for preparing food and eating it. As much as 10% of food energy is used just in digesting and absorbing it.

The smell of food excites our brain and sends a signal to the pancreas to secrete insulin. Everybody knows that. (Does this sound like a Geico commercial?) 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. Thus, it is a more physiologically appropriate time to have an elevated level of insulin circulating in the blood.

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. I imagine, as I think about and write two columns a week for The Nutrition Debate, my serum insulin must always be somewhat elevated. And since insulin is the hormone that type 2 diabetics have issues with, having a constantly elevated serum insulin, can be problematic. Do you know what your fasting insulin level is? Mine has only been tested once, in 2013. It was 7.8mU/L (range 3.0-25.0).

Then, of course, the taste of food, associated with the response of the digestive enzyme amylase mixed with mucus from the three pair of salivary glands in the buccal cavity (mouth), excites the brain and sends a signal to the pancreas to secrete insulin. In the “normal” metabolism, this is a burst of insulin that prepares your digestive system to ramp up to secrete a bunch more to handle the food passing into the alimentary canal and on to the small intestine where the final digestion and absorption processes occur. Mysteriously, most type 2s havelost the ability to generate this anticipatory burst of insulin.

All of these sensory processes are normal. In fact, they are, as we said at the beginning, 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 and water to feed our bodies to sustain ourselves. It is fundamental survivalism.

But what happens when some part of these metabolic mechanisms breaks? When the supply of insulin is lessened because our pancreatic beta cells (in the Islets of Langerhans which secrete insulin) die? Or when the insulin we have been able to produce circulates with the glucose from digested food but is not taken up by the body’s cells to replace the glycogen that’s been used up by ordinary living? Answer: With a “broken” metabolism, your blood sugar rises, you get type 2 diabetes, and your risk factors for microvascular and macrovascular diseasesincrease dramatically.

What happens when we can no longer produce enough insulin to transport and allow the “uptake” of blood glucose? Until synthetic insulin was developed in 1922, you died from hyperglycemia. The only “therapy” for those unfortunate souls was to eat a strict ketogenic diet, in which virtually no carbohydrates were consumed. Today, if you allow your type 2 diabetes to progress to the point where you have “uncontrolled” blood sugar, you can inject insulin to regulate your blood sugar.

But if you are pre-diabetic (or a diagnosed type 2), and you don’t want your diabetes to progress to that point, is there an alternative for you to injecting insulin? Is there something else you can do to preserve what function your pancreas has left to make insulin? Answer: You can adapt what you eat for survival. You can eat fewer carbs. Your life may depend on it.

The Nutrition Debate #233: Multifactorial Approach to Prevent CVD in T2DM

The Nutrition Debate #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 (with transcription) at the recent American Diabetes Association 74th Scientific Sessions in San Francisco. It was shownhere in Medscape Medical News, an aggregator of medical news designed for physicians. His title, “Multifactorial Approach to Prevent Cardiovascular Disease in Type 2 Diabetes,” was subtitled “Identifying Diabetes and Cardiovascular Risks.” The risk part is 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.” You can quibble with “caused by” and argue that it is diabetes that is controlled to the ADA standard of care that induces microvascular complications, but still, his view conforms to the medical establishment’s current standard of care, 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 is not enough, you can add in 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

Again, to his credit, Dr. Marre states “Cardiovascular risk requires multifactorial management, with an emphasis on lifestyle intervention. Look at what the patient eats and drinks” (emphasis mine). He blithely 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 healthy way of eating. Let’s just say that Dr. Marre, who says he is “from the Mediterranean area,” is just being chauvinistic. We can forgive him. He is, after all, a Frenchman.

Once again, however, Dr. Marre’s management and control recommendations are pretty much pro forma “establishment”:

● Maintaining blood pressure below 140/85 mm Hg. This is the objective for patients without any renal impairment. If the patient has a slightincrease in microalbuminuria , then the blood pressure objective must be below 130/80 mm.

● Look at the patient’s 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. [I had to look this one up; 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. [another pill]

Often, you have to combine several antidiabetic agents [yet 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.”

Wait a minute! Whatever happened to those lifestyle interventions? To looking “at what the patient eats and drinks”? Here is a doctor giving out the basics of clinical care for 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?

At this writing, there are 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, M.D., Dr. h.c ., “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 (LOL). For some, telling the truth may also be a quick way to become “mostly retired.”

The Nutrition Debate #232: “A spoonful of sugar”

"A spoonful of sugar" is the title of a 9-year old and still very popular post on the blog of Dr. Michael R. Eades, a “sort of traditional M.D. with an eye to what works to get patients well whether it is traditional or not,” in his own words (comment #12). He and his physician wife, Mary Dan Eades, are the authors of “The Protein Power LifePlan,” one of the first and best of the almost 50 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 he goes through the calculations to demonstrate 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 (weighs) just 5 grams.

The American Diabetes Association established these diagnostic thresholds in 2009. They are based on a “normal” fasting blood glucose being 70-99mg/dL, a prediabetic fasting blood glucose being 100-125mg/dL, and a fasting blood glucose reading of 126mg/dL or higher being “frank” type 2 diabetes. See The Nutrition Debate #228, “A1c and your estimated Average Glucose (eAG),” to see how the inexpensive A1c test has more recently become a more reliable standard for diagnosing pre-diabetes and type 2 diabetes status.

“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,” Dr. Eades tells us. He goes on to slam home his point:

“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, he then hits you with this coup de grâce:

“Since your metabolic system has to work very hard indeed 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 and ordered my large order of fries (as a side order!) to my meal at McDonalds. For 16 years (before my doctor suggested I try low-carb eating to lose weight and help with my type 2 diabetes), I just relied on him to deal with my progressively worsening blood sugar condition. I didn’t know, frankly, that I could treat my own diabetes by the choices I made in what I ate.

Boy, what a difference it made, both in my weight (at one point I had lost 170 pounds) and in my diabetes status. Although I have since regained some of that lost weight (I continue to maintain a 125 pound weight loss), I am still able to stay off almost all of 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 500mg of metformin once a day. And my blood sugars are “under control,” according to my doctor and the ADA standard of care, so long as I continue to eat low carb.

The takeaway? Just remember that, 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 impaired glucose tolerance (IGT) no longer can do that. Then, when something sweet or sugary (carbs) contacts your saliva, the brain signals the pancreas to prepare to secrete more insulin… but it’s too late. Your damaged 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. You have insulin resistance (IR).

The result: Your body is overwhelmed by the sugar (glucose) your body has made by digesting the carbs you just ate, and your blood sugar rises above healthy levels, and the damage to your organs and microvascular system inexorably begins…

 * The McDonalds table has been updated. A medium French fries is now 44g of carbs. A large French fries is 67 grams.         Check the sugar content of your McDonalds choices at http://nutrition.mcdonalds.com/getnutrition/nutritionfacts.pdf.