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.