Type 2 Diabetes, a Dietary Disease #337: Facts and Fallacies About the Nutrition Facts Panel

Probably more than half my readers are women, but I’ll venture that almost all (both men and women) are deceived, I believe intentionally, by the USDA’s design of the Nutrition Facts Panel on manufactured “food” products. Many women especially have been handicapped by their refusal to use their intelligence to do a little simple math. Claiming a “block” just doesn’t cut it with me.

The most recent example came to light when my pre-diabetic friend (and new LCHF acolyte) thought she was in compliance with her announced plan to eat only 15-30g of carbohydrates per meal. For her convenience, she wants to continue to drink a meal replacement or “snack” beverage called Glucerna Hunger Smart Shakes, which, according to their website, is “specially designed for people with diabetes.” The Nutrition Facts Panel on the product says it contains 180 calories, with 8g of fat, 15g of protein and 16g of carbohydrate.

I told my friend that this beverage was 35% carbohydrates and that that was a higher percentage of carbs than I thought she wanted to eat (on her new LCHF 60/20/20 eating plan). She replied by sending me the percentages on the label that she apparently believed were the percentages of calories in that serving: FAT 12%; CARBS 5%, and PROTEIN 30%. I inferred that she thought that the product she drank was just 5% carbs. In fact, the actual percentages of calories in that serving are 40% FAT, 27% CARBS (see footnote*) and 33% PROTEIN.

How can that be? Well, for starters, the percentages on the Nutrition Facts panel are the percentages of the USDAs catastrophic recommendations for “% Daily Values (%DV)”: That recommendation is CARBOHYDRATES: 300g a day for women and 375g a day for men; PROTEIN: 50G; and FAT: 67g. By percentage of calories, that’s 60% CARBOHYDRATE for both men and women, 10% PROTEIN AND 30% FAT. The USDA doesn’t care if you’re diabetic or pre-diabetic, young, old, active, or sedentary. USDA’s Nutrition recommendation is one-size-fits-all.

The % Daily Value then – the % that appears on the label on the Nutrition Facts panel – is a percentage of our government’s horribly flawed dietary regimen that is WHOLLY UNHEALTHY FOR ANYONE, much less someone with Insulin Resistance who has been told they are pre-diabetic. What matters is the percentage of calories by macronutrient in the product in hand. The Nutrition Facts panel doesn’t tell you that. You have to do the math.

●     Protein contains 4 calories per gram, so to get protein calories, multiply the protein grams by 4 and then divide that by the total calories to get the percentage of protein in the product.

●     Carbs also contain 4 calories per gram, so to get the carb calories, multiply the carb grams by 4 and then divide that by the total calories to get the percentage of carbohydrate in the product.

●     Fat contains 9 calories per gram, so to get the fat calories, multiply the fat grams by 9 and then divide that by the total calories to get the percentage of fat in the product.

I do these in my head to get a rough number, which is always good enough. But if you don’t want to do that, you could just buy and eat real food. Real food doesn’t need a Nutrition Facts panel to tell you it’s good to eat.

The new changes coming in the Nutrition Facts panel will reshuffle the numbers and change the font size and where they appear on the label. They will not, however, make any substantive changes in the content, and they will not change the % Daily Value of the macronutrients. A “mostly plant based” diet that is 60% carbohydrate is still the USDA’s/HHS/FDA’s recommended “eating pattern” – with the same macronutrient distribution that has made many of us sick. Does this sound to you like rearranging the deck chairs on the Titanic? It does to me.

* The micronutrients listed on the label added up to 196 kcals (not 180) so I had an online chat with a Glucerna nutritionist who said “some sugar alcohols in the product contain fewer than 4 kcal/gram and some fiber is not absorbed.” So, I calculated that the number of carb grams contributing to the 180 calories was not 16 but 12.)

Type 2 Diabetes, a Dietary Disease #336, Noakes: “It’s the fatty liver disease, stupid.”

Continuing my theft of Dr. Tim Noakes' excellent post on South African blogger Marika Sboros’s FOODMED.NET, Dr. Noakes relates how “more support for Gerald Reaven’s unifying hypothesis of chronic disease has come from an unexpected source – from those doctors, hepatologists, who specialize in…diseases of the liver.”

Dr. Noakes continues, “It has been known for some time that the added risks associated with obesity depend, in part, on where that extra fat is stored in the body.  Thus fat that accumulates under the skin – subcutaneous fat – is far less unhealthy than is fat that accumulates within and between the organs in the abdomen, so-called visceral obesity.

“The hepatologists have now gone one step further to show that the real killer in visceral obesity is the fat that accumulates within the liver causing NAFLD, a disease that is now reaching epidemic proportions.

“Their work shows that it is NAFLD and not obesity per se that produces the abnormal metabolic state – the atherogenic dyslipidemia (Table 2) – that causes heart disease in those with insulin resistance and the metabolic syndrome.

“Table 2: The metabolic features of atherogenic dyslipidemia present in those with NAFLD and insulin resistance

●    Elevated blood glycated hemoglobin (HbA1c) levels

●    Elevated fasting blood insulin levels

●    Elevated fasting blood glucose levels

●    Hyperinsulinemia and hyperglycemia (elevated blood glucose levels) in response to carbohydrate ingestion

●    Low blood HDL-cholesterol concentrations

●    High blood triglyceride concentrations

●    Elevated numbers of small dense LDL-particles

●    Elevated blood Apo lipoprotein B concentrations

“The absolutely key point is that dietary carbohydrates and not dietary fat cause NAFLD. For when the insulin resistant eat excess carbohydrates including fructose found in sugar and fruits, they must convert into fat any extra carbohydrate they cannot either use as a fuel or store immediately as carbohydrate in liver or muscles.

“Note that all these options are severely reduced in those with insulin resistance.  Instead under the action of insulin – the fat-building hormone – that fat is stored, initially as fat in the liver.  But as NAFLD develops, insulin resistance worsens, hyperinsulinemia increases, atherogenic dyslipidemia deteriorates and the seeds for the chronic diseases of obesity, diabetes, heart disease, NAFLD and perhaps cancer and dementia are sown.

“Thus it is that dietary carbohydrates and not dietary fat are the direct cause of this group of chronic diseases in those with insulin resistance.

“Summary:

●    The work of Dr Gerald Reaven is as revolutionary to the understanding of medicine as were the works of Newton, Galileo and Darwin to their disciplines.

●    By producing a unifying theory for perhaps six chronic diseases and by presenting the initial evidence that these conditions are initiated by high carbohydrate diets in those with insulin resistance, he has fundamentally changed our understanding of how these conditions develop and how best they should be treated.  And also how they might be prevented.

Our challenge is to incorporate this new understanding into our teaching and practice of medicine.”

Type 2 Diabetes, a Dietary Disease #335, Implications of Reaven’s Unified Hypothesis: Part 2

Last week’s column was heavily cribbed, with attribution, from Dr. Tim Noakes' recent post on South African Marika Sboros’s excellent blog FOODMED.NET. This week I’m going to continue it with an almost verbatim extraction. It is so well written, and so profound in its implications, I don’t want to botch it by editing a thing!

We left off with Noakes explaining how endocrinologist and Stanford professor Dr. Gerald Reaven presented at the 1988 ADA annual Banting lecture a unified hypothesis of chronic disease, which he called Syndrome X but which thereafter became known as Reaven’s Syndrome. Today it’s simply called Metabolic Syndrome.

Noakes continues, “To determine whether nutritional factors contribute to the development of the metabolic syndrome, beginning in the 1980s, Reaven completed a number of RCTs of the effects of low-carbohydrate diets in patients with this condition. Without exception his studies showed that removing carbohydrates from the diet uniformly improved all measures of health in those with insulin resistance and metabolic syndrome.

“So besides establishing the fundamental role of insulin resistance in these chronic diseases, Reaven also discovered the optimum treatment – carbohydrate restriction. By any measures, Reaven should be a shoe-in for the Nobel Prize in Medicine.  But perhaps not.  For he failed subsequently to emphasize the curative effects of low-carbohydrate diets in insulin resistance.

“Why not,” Noakes asks?

“I suspect that during his daily work at Stanford Medical School, Reaven was in close contact with some of the more important cardiologists in the USA and perhaps in the world. They would not have taken kindly to their colleague’s suggestion that, to prevent heart attacks, cardiologists should be prescribing high fat diets instead of the low fat diet dictated, then as now, by the American Heart Association.

“Had he chosen that route, Reaven’s colleagues would have excommunicated him, his research funding would have dried up, and his career would have been over, exactly as happened to Dr John Yudkin in England for his (correct) suggestion in the 1970s that sugar, not saturated fat, causes heart disease.

“So it seems to me that Reaven kept quiet, choosing rather to continue researching insulin resistance without paying much attention to how a low-carbohydrate, high-fat diet might – simply, effectively and at low cost – prevent and reverse all the medical disguises through which insulin resistance reveals itself.

“One disease, one cause, many symptoms:” Reaven’s unified hypothesis of chronic disease.

“Reaven’s problem is not unlike that faced by Darwin and Galileo whose findings estranged each from religious orthodoxy.  For Reaven’s unifying hypothesis of chronic disease must offend not just his colleagues in cardiology.  For his hypothesis strikes at the very heart (pun intended) of the pharmacological model that we practice in modern medicine.

“For if obesity, diabetes, heart disease, NAFLD and high blood pressure (and perhaps also cancer and dementia) are in fact all symptoms of the same underlying condition, insulin resistance, then our current model of medical management must be wrong, requiring as it does, specific but different pharmacological treatments for each separate condition, overseen by different hierarchies of medical specialists.

“BUT WHAT IF THE CORNERSTONE FOR THE TREATMENT OF ALL THESE CONDITIONS IS A LOW-CARBOHYDRATE DIET – the very diet that has now been vilified by my profession for the past 50 years?  That must be an extremely frightening thought for very, very many.  How does one come to terms with the possibility that, by following medical orthodoxy, one may have harmed very many patients?”

What indeed?! Think about it…

Thank you, Dr. Tim Noakes, for the courage to speak out. Note: all CAPS, bold and italics added by this blogger.

Type 2 Diabetes, a Dietary Disease #334: A Unifying Hypothesis of Chronic Disease: Part 1

I don’t remember how I landed on South African blogger Marika Sboros’s site, FOODMED.NET; but I love it, and I have signed up for regular delivery. Her blog’s subtitle is “Let food be your medicine,” so you can readily see my affinity. I first read a post in the “Managing Your Blood Sugar” series titled NOAKES: "IT'S THE FATTY LIVER DISEASE, STUPID' PART 2, tagged “LCHF.” Interestingly, Marika explains, LCHF in her lexicon means “Low Carb Healthy Fats.” I like it. It’s time to take on the PUFAs!

The author of this particular post is world-renowned scientist and University of Cape Town Professor Emeritus Dr. Tim Noakes. Noakes introduces his subject via the misunderstood term “risk factors” as taken from epidemiology and “observational” or “associational” studies. He delves briefly into “hazard ratios” (HRs), relative and absolute risk, and related subjects to show how data is commonly manipulated and abused.

“This is intellectually absurd,” Noakes says. “How can everything be a risk factor for everything else?” he asks. He answers, “The answer can be found in the ignored work of Dr. Gerald Reaven, Emeritus Professor of Medicine at Stanford University.” “Reaven has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance.”

Reaven’s interest in insulin resistance was piqued by the distinction between Type 1 and Type 2 diabetes. Type 1 is characterized by the total absence of endogenous insulin; Type 2, insulin resistant diabetes, by “abnormally high amounts [of insulin] because the target cells on which the insulin normally acts are resistant to its action; hence the condition of insulin resistance or carbohydrate intolerance. Persons with insulin resistance have blood insulin concentrations that are elevated most of the time, a condition known as hyperinsulinemia.”

Noakes says, “Reaven’s great contribution has been to show this persistent hyperinsulinemia in insulin resistance, whether or not associated with T2DM, produces a collection of grave secondary consequences.”

“But Reaven’s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinemia are the necessary biological precursors definitely for four and perhaps for all six of the most prevalent chronic conditions of our day: 1) Obesity; 2) Arterial disease (local: heart attack or stroke; disseminated: T2DM; 3) High blood pressure; 4) Non-Alcoholic Fatty Live Disease (NAFLD); Cancer; and Dementia (Alzheimer’s Disease, also known as Type 3 Diabetes).”

Reaven gave the  keynote Banting lecture at the 1988 American Diabetes Association annual meeting. His talk explained the underlying factor for a constellation of abnormalities: glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension.  He named it “Syndrome X; it was also given the moniker Reaven’s syndrome. Today it is simply called Metabolic Syndrome.

“The key finding from Reaven’s work,” Noakes says, “is that these conditions are not separate – they are different expressions of the same underlying condition. Thus a patient should not be labeled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).”

“Instead,” Noakes continues, “the patient should be diagnosed with the underlying condition – insulin resistance – with the realization that the high blood pressure, the obesity, the diabetes, the NAFLD, or the heart attack or the stroke are simply markers, symptoms if you will, of the basic condition.”

“And that basic condition,” Noakes concludes, “is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day. “

Thus we have it: Reaven’s unifying hypothesis of chronic disease: “One disease, one cause, many symptoms.” Tune in next week for a glimpse at the profound implications of this fundamental advance in medical science.

Type 2 Diabetes, a Dietary Disease #333: NAFLD, Supplements, Fructose and PUFAs

A friend recently asked me to look over a list of supplements suggested as “interventions” for a diagnosis of NAFLD (Non-alcoholic fatty liver disease). I’ve been helping her with concerns about appropriate prophylaxes for other health issues – Insulin Resistance (IR) and Alzheimer’s Disease (AD) – so she sent me a link from Life Extension (LE), a supplement seller recommended by her doctor. I agreed to look it over and get back to her.

Life Extension’s “suggestions” include eight (8) supplements, all but one of which – a drug, metformin – they sell. All “have been shown to boost liver health and help manage NAFLD,” and “prevent progression to the more deadly NASH, which is a precursor of liver failure.” Pretty scary stuff! How many of these supplements should I buy? Then, at the bottom of the page, I saw that the tab on the link my friend sent was pg. 2. I clicked on pg. 1.

“Roughly one-third of the American population suffers from nonalcoholic fatty liver disease or NAFLD. NAFLD can go undetected for years and may eventually progress to inflammation and scarring of the liver (cirrhosis) and, in some cases, full-blown liver failure. A formerly rare condition, its rapid emergence has been linked to skyrocketing rates of metabolic syndrome and diabesity, the term many experts use for co-occurring diabetes and obesity.

My friend is not obese, but her IR and abnormal lipid profile puts her squarely in the Metabolic Syndrome “X.”

 “While poor dietary choices are often to blame, cutting-edge research suggests that hidden genetic factors may also play a role, and some people do not metabolize polyunsaturated fats properly, resulting in fatty deposits in the liver.”

Life Extension’s “fix,” of course, is predictable: They offer to sell you some supplements.

“As mainstream medicine continues to struggle in the search for drugs to manage this widespread condition, emerging scientific evidence has shed light on effective natural interventions that may halt or even reverse its progress.”

But wait, these “interventions” are just surrogates for drugs, and the best “treatment” for a condition that was caused by poor dietary choices and polyunsaturated fats is to make good dietary choices and eat healthy fats.

While you can’t change your genes, you can change the way they “express” themselves, even after being exposed to a barrage of the poor dietary choices advocated by our government going on 50 years now!

And, Life Extension has identified the likely causes of NAFLD: poor dietary choices and polyunsaturated fats.

What are those “poor dietary choices”? Life Extension hones in on the main one, a simple sugar, fructose. Fructose is half of every (cane) sugar molecule, and it is shunted directly to the liver to be metabolized. If the liver is already full of stored carbs (glycogen), it makes, via de novo lipogenesis, new fat molecules in the liver.

“Of course, what we eat is as important as the calories it contains. One of the major bad actors in today’s world is fructose, found in high quantities in high-fructose corn syrup. Fructose promotes formation of new fat molecules in the liver, blocks breakdown of existing fats, stimulates free radical production, and promotes insulin resistance. Increasing numbers of studies are linking increased fructose consumption with NAFLD, and even with its deadlier consequence, NASH. Patients with NAFLD consume 2-3 times as much fructose as do control patients, even corrected for body weight.”

The other dietary choice LE cites as a probable cause of NAFLD is “polyunsaturated fats,” or PUFAs, found in highly processed vegetable oils (canola, corn and soy bean oil, among many others). These are unnatural food oils that did not exist before technology was developed to extract them. I have written about the harm PUFAs do many times, but Life Extension’s citation was refreshing to see because liquid fats are still recommended to us to by the Dietary Guidelines for Americans (2015-2020)!

A small amount of PUFAs are “essential,” meaning the body can’t make them; however, the ratio of the “essential” ones (Omega 6s and Omega 3s) is important. Historically this has been 2:1 to 4:1. With the proliferation of “industrial” food oils over the last half century, and the USDA’s advocacy of them (and Cargill’s and ADM’s production and marketing of them), the ratio for most Americans is now 20:1 to 30:1.

You can’t fix this ratio by just supplementing the denominator with fish oil. You need to cut back dramatically on the numerator: on all fried foods and processed foods, like commercial baked goods, containing PUFA’s.

Replace PUFAs with monounsaturated fats (e.g., from olive oil and avocados) and saturated fats, such as coconut oil and grass-fed butter, lamb and beef, full-fat dairy and wild-caught fin and shellfish. All Real Foods!

Type 2 Diabetes, a Dietary Disease #332: “Pre-Diabetic” or un-diagnosed Type 2?

I recently talked for an hour or so to a friend who knows that I know a lot about Type 2 Diabetes. He sought me out to ask me what he should do. I asked him, “What is your situation?” Here’s what he told me:

His fasting blood sugars (FBG), he said, are consistently running in the 140s. That’s 140mg/dl. I told him that was “out of control.” I asked him what his postprandials were. He didn’t know “postprandial” so I said your blood sugar 1 or 2 hours after starting breakfast. He said he didn’t know. He didn’t do postprandials.

I asked him what his latest A1c was. He replied 6.9. That’s 6.9%, but he said it was almost 2 years ago. I asked him if his doctor had told him that he was diabetic. He said “No,” and I said, “Well, you are!” The American College of Endocrinologists define Type 2 Diabetes as an A1c of ≥6.5%, and the American Diabetes Association as ≥7.0%, but that definition is part of the problem. Some clinicians today regard an A1c of ≥5.7% as full-blown Type 2 diabetes.

I asked my friend if he was currently taking any medications to control his blood sugar. He said, “Yes.” He was taking two 500 mg tablets of metformin twice a day, plus glyburide (a sulfonylurea). He didn’t remember how much, and I don’t remember how often he takes it, because this set me off on a rant.

I said, “You are already maxed out on metformin” at 2000 mg/day, and you are taking a sulfonylurea (SU), a class of medications that pumps the pancreas to produce insulin to cover the carbs you are eating, AND IT’S NOT ENOUGH!” SUs ARE A DRUG THAT, WHILE STILL PRESCRIBED BY UNKNOWING PHYSICIANS (BECAUSE ITS CHEAP AND “EFFECTIVE” IN REGULATING BLOOD SUGAR BY SECRETING INSULIN), BEAT UP AND WEAR OUT THE BETA CELLS IN THE PANCREAS THAT MAKE THE INSULIN, AND THEY EVENTUALLY DIE!!! RESULT: YOU WILL SOON BE TAKING BOTH LONG ACTING AND MEALTIME INSULIN (INJECTING IT) TO CONTROL YOUR BLOOD SUGAR.

He said, “What should I do?” I didn’t hesitate to tell him: “You’ve got to change what you eat, I mean seriously change what you eat.” “What do you have for breakfast,” I asked? “Oatmeal,” he said, “with milk and a little sugar.” “Switch to eggs,” I said, “any way (fried, scrambled, poached).” “How many”, he asked? “One, two or three; add a strip of bacon if you like,” I said, “but no juice, cereal, bread or jelly. Only heavy cream and artificial sweetener in your coffee, if you must.” I told him he wouldn’t be hungry. He wouldn’t need a mid-morning snack. (He had mentioned he ate an apple in mid-morning “’cause he was starving.” I just rolled my eyes in horror.)

I also told my friend that he had to get off the SU. But the effect could be that his A1c will go up unless he instead replaces it with a drug that acts in a different way, sparing the pancreas. There are now several more modern classes of drugs, both oral and injectable (not insulin). Many clinicians would even argue reasonably that a temporary course of exogenous insulin would perhaps be the best course of treatment in his case to get his blood sugar under “good control.” But I would argue that the best course of “treatment,” and the only one that addresses the cause of Type 2 Diabetes (which is Insulin Resistance), is to radically change what you eat, NOW.

My own experience supports this course of action. In 2002 I weighed 375 pounds and I was maxed out on metformin and a sulfonylurea and starting a DPP-4 inhibitor (Avandia). In retrospect, I was on my way to injecting insulin. My doctor wanted me to lose weight, of course, so he “prescribed” a radical change of diet, a Very Low Carb diet called Atkins Induction. The surprising result was that on the 1^st day of strict compliance I got a hypo (a low blood sugar). The doc ordered me to stop the Avandia. The next day, another hypo, and he told me to cut the metformin and the glyburide (the SU) in half. A few days later I had to cut them in half again. Still later I cut out the SU altogether. Eventually, I transitioned to Dr. Richard K Bernstein’s 6-12-12 program for diabetics.

After a few years or eating this entirely different way, I had lost 170 pounds, my blood pressure was 110/70 (on the same meds), my HDL-C more than doubled and my triglycerides dropped by 2/3rds. And all I did was change what I ate.

Type 2 Diabetes, a Dietary Disease #331: Dear Max: Don’t Eat Oatmeal for Breakfast!

(Note: This is a Universal Fill-in Form. Just change the name of the person and the carb food as appropriate.)

I know you’re busy, Max, but…your health is at stake, so pay attention: You’re Pre-Diabetic, and in all likelihood, you’re will become a full-blown Type 2, unless you change what you eat. Type 2 Diabetes is a Dietary Disease.

Doctors treat Type 2 Diabetes by treating one symptom, high blood sugar. They give you vapid advice (lip service, really) to undertake “lifestyle changes” like “eat less and exercise more,” to lose weight! Then, for your high blood sugar, they treat it (you) with meds. They follow up by monitoring your blood sugars at intervals to see that they are “well controlled” (by Diabetic Association standards), and, when they are not, they add meds.

Their response, to treat you with more meds (too little, too late, and all wrong!), will only result in wearing out your pancreas, the organ that makes insulin. In the end (literally), you are likely to have to inject insulin. You will eventually die from one of the micro or macrovascular complications of the disease.

Doctors should advise you to treat the cause of your Type 2 Diabetes, which is Insulin Resistance (IR). If they advise you with respect to diet, the advice you get is likely to be just plain wrong. If you follow it, you will do so at your personal risk. They are also treating your disease to much too lax a standard. They will regard your blood sugars as “well controlled” at a level where they are doing you harm. To repeat, if you don’t change what you eat, your Type 2 Diabetes will progress, with increased risk for all the attendant complications.

Insulin Resistance means that insulin receptors in your cells are refusing to take up the glucose that is being transported in your blood by the carrier insulin. Glucose is the fuel that your body makes from digesting carbs, (and to a lesser extent from excess protein returned to the liver). Result: your blood sugar rises. Solution: eat fewer – many fewer, carbs. Did you know, there is no (zero) nutritional requirement for carbs? And your IR means you are becoming, or have become, Carbohydrate Intolerant. Insulin Resistance = Carbohydrate Intolerance.

Your body needs some glucose (not carbs).  Some glucose is so essential to the body that the body has multiple ways to make it from protein and fat. And your body does need both protein and fat, and that is what you have to eat if you want to treat the cause of your Pre-Diabetes. Takeaway: Eat mostly fat and protein.

Hunger is the principal (but not the only) biological driver of eating. It is both intrinsic and autonomic. Your conscious will pales by comparison. You are a slave to your hunger – especially if you are carb dependent. If you eat carbs at every meal, and between meals eat carbohydrate snacks, your body will come to biologically expect that since carbs are abundant, you can depend on them as an easy and quick source of energy. In today’s world, carbs are abundant, and ubiquitous. And they are a quick and easy and cheap source of energy 24/7/365.

Biologically, when your body becomes dependent on carbs, it blocks access to an alternate and totally complete source of fuel that everyone has: stored body fat. Stored body fat is packed full of energy: 9 calories per gram vs. 4 for carbs and protein. But, your body can’t access that dense stored energy source because added insulin, accompanying the glucose still circulating in your blood, sends a signal to the brain that you don’t need to use your body fat to maintain the body’s steady energy state (homeostasis). The fact is, as a Pre-Diabetic, because of your Insulin Resistance, both your plasma glucose and your plasma insulin are continually elevated.

Translation: when the carbs you last ate are quickly digested, your body tells you that you are hungry again! You crave carbs. It tells you to eat more.

SOLUTION: After an overnight fast, just eat protein and fat (with ‘zero’ carbs) for breakfast. That means: no juice, no cereal, no bread, no jelly. You will feel full. After a few days, your body adjusts its internal metabolism and you will never be hungry again in the morning, mid-morning or even at lunch. If you continue with protein and fat for lunch, you will not be hungry again until the cocktail hour. And if you eat a small supper of mostly protein and fat, with a serving of low-carb veggies, you will not need to eat again until breakfast (or lunch). Repeat this every day and before long your fasting blood sugars will drop back into the “normal” range, and after a few months, your A1c’s will too. And your doctor will be happy because you lost weight. He or she will also likely reduce or eliminate your meds! And all you did was change what you ate!