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!

Type 2 Diabetes, a Dietary Disease #330: My FBGs have been transformed, Part 2

In #329 here, I related two major changes in self-management of my 30-year Type 2 Diabetes that marked the beginning of a transition – a transformation really, in my blood sugar control. Like many Type 2s who treat their disease as a “dietary disease” (as I do), worsening blood sugar control is hard to attribute. There is always the question: is it a “compliance” issue with the Low Carb Way of Eating (WOE) or, as is the conventional wisdom, is it a “natural progression” of worsening Insulin Resistance (IR), especially if carb restriction is not the main means of BS control.  Whichever the case, the Type 2 needs to be both vigilant for changes in control and flexible. I was prepared to change my regimen, first by improved compliance, and if necessary, as a last resort, my medications. After all, my health is at stake, and control of blood sugar levels, starting with a low fasting blood sugar, is critical.

So, In January I started Andreas Eenfeldt’s 5-part program that I described in #329, and at my April appointment, my doctor agreed to increase my prescription for Metformin to 1500mg/day. I chose that level because I had read somewhere, sometime in the past (then quickly buried the memory) that 1500mg/day is where Metformin really begins to work. (So, “Why,” I’m asking myself now, “have neither I nor any of the doctors I have seen for the past 10 years ever suggested that I increase my dose from 500mg?” For myself, I have already answered that question in #329: it was pride from having given up virtually all my oral antidiabetic meds, and not wanting again to be “drug dependent.” I cannot answer, however, for the doctors. Perhaps it is because they thought that I wanted to manage my type 2 diabetes. Or perhaps they just don’t know much about type 2 meds.

Or perhaps – and this is what I suspect is the most likely reason – all the doctors I have seen have considered my type 2 diabetes already “well controlled.” After all, my A1c’s were always below the level of concern of the American Diabetes Association guidelines for clinical care. And as for my current doctor, I love him, but except for my insisting on it, he would not even have me testing my blood sugars once a day, much less twice. He’s only interested now in my A1c and wouldn’t even order a fasting glucose if I didn’t ask for it. And when I first went to see him (after he “inherited” me from my previous doctor who had died), he suggested I only come to see him once a year. I was, in his mind, “well controlled” and thus “healthy” and just needed an annual checkup!

3) The 3^rd “tweak” in my routine (for #1 and #2 see #329) was to add 6 grams of MCT oil (in gel form) to my daily supplements, as a prophylactic and therapeutic treatment for insulin resistance (IR) in regions of the brain. The brain uses about 20% of the glucose the body makes. Alzheimer’s Disease (AD), like type 2 diabetes, develops over many years, before its symptoms become apparent. The brain simply can’t get the glucose it needs due to the Insulin Resistance. Alzheimer’s has thus been described as Type 3 Diabetes. MCT oil, which is 100% Medium Chain Triglycerides extracted from coconut oil and palm kernel oil, go directly to the liver which converts them to ketone bodies. Ketones are an alternate fuel for the brain, and the brain loves them. I wrote about AD and Supplemental Ketones in The Nutrition Debate #322 here and in #323, #324 and #325.

So, what’s all the hullabaloo about? What’s the breakthrough? The answer: My fasting blood sugars have been TRANSFORMED. They are now ALL below 100mg/dl. WELL below 100. Two weekly AVERAGES in a row of 79mg/dl, range 68 to 92. This transformation began in mid-March, with increasingly regular FBGs in the 90s. By mid-April it was in full swing: Now virtually all my FBGs are in the 70s and 80s, with only an occasional outlier.

And I’ve not been “perfect.” I have even had a little French bread, with butter, at one restaurant meal. And 3 thin French bread slices slathered with rillette at another, both with no discernible effect on my fasting blood sugar the next morning! Previously, any transgression as “egregious” as this would definitely have shown up 12 hours later in my FBG (and for a few days after!) THIS IS VERY LIBERATING.

In addition, the impact of starting the day with a FBG in the “normal” range will surely have a lowering effect on my next A1c. And the lower blood sugars mean a lower circulating insulin level, which means more breakdown and burning of body fat, as long as I don’t overeat fat. After all, for most people, losing weight is as powerful, or more powerful, a motivator as blood sugar control. But when you’re not hungry (because your body is chugging along on its own fat), you really don’t have a good excuse to overeat…not that I ever needed one!

Type 2 Diabetes, a Dietary Disease #329: My FBGs have been transformed, Part 1

I believe a combination of recent “tweaks” to my self-treatment of Type 2 Diabetes has resulted in a blood sugar control “breakthrough.” It may be too soon to say definitively that I have found “the secret” for me, but I think I have. Below are the variables that have changed in recent months.

1) I am now adhering with a high level of compliance to the following 5 guidelines that Andreas Eenfeldt (www.thedietdoctor.com) mentioned in a video I watched in January:  I now a) follow strictly a low carb diet, b) eat only when hungry, c) sleep 7-8 hours a night, d) weigh myself daily, and e) practice intermittent fasting. The two IF methods Dr. Eenfeldt “prescribes” are 5:2 and 16:8. I chose 16:8, seven days a week! I skip breakfast because I’m not hungry at breakfast (see #326). I also sometimes skip lunch, or eat a very light one (one or two hard boiled eggs). As a result of the IF, I think I am in a mild form of nutritional ketosis for more hours every day.

2) For the last 10-12 years, as my only oral anti-diabetes medication, I have been taking 500mg of Metformin once a day. (Before that, I had titrated off a sulfonylurea (Glyburide) from 5mg to 2½ to 0 after starting the Bernstein Diet. Before that, after starting Atkins Induction in September 2002, to avoid hypos, I quickly had to stop taking Avandia, which I had just started, and then had to cut my Glyburide from 20mg to 10 to 5 and my Metformin from 2000mg to 1000 to 500).

I provide this history to explain why I had been reluctant to increase my oral anti-diabetes meds. It was pride, and the fact that no one had suggested that I increase my Metformin or add a new oral anti-diabetes med, until last year. (And, if they had, I’m not sure I would have agreed to either.) The conventional wisdom is that type 2 diabetes is a condition that is “progressive.” I am not saying here that I agree. However, my A1c was creeping up (at one point to 6.5%), and it was becoming increasingly difficult for me to get fasting readings below 100mg/dl. In fact, it had been a few months since I had seen even one below 100. As a result, my resolve not to increase the Met or add a new med, and my pride, were both slipping. After all, my health (the risk of all the microvascular and macrovascular complications) was at stake.

So, I decided that the first step for me was more vigilant self-management. After all, type 2 diabetes is a dietary disease. (Here’s where I do a little shameless self-promotion: Read my blog at www.thenutritiondebate.com where the theme, starting with #306, has evolved to “Type 2 Diabetes, a Dietary Disease.”) That’s why I began the steps described in 1) above, and they had an effect. But that still left the question: If my disease was in fact progressing (not a case entirely of my “compliance” slipping), should I consider increasing my medication from just 500mg of Metformin once a day or adding another class of meds? I pondered this question for months.

For years I have attended classes offered by a Certified Diabetes Educator, both to support her as well as try to persuade her to subscribe to and teach a Low Carb Way of Eating for diabetics. Last year she suggested I try a SGLT2 inhibitor. SLGT2s block the re-absorption of glucose in the kidney, increase glucose excretion, and thus lower blood glucose levels. I read all the latest research and decided I was not ready to go there. So, last December, I asked my doctor to increase my Metformin to 1000mg once a day, and he said, “okay.”

Then in January I attended a conference on Metabolic Therapeutics and discovered that a sub-set of attendees, all of whom were very healthy athletes/body builders, were taking supplemental ketones to help lose weight and stay in ketosis. Some of them, including the PhD researcher who was the conference organizer, were also maxed out on Metformin, taking 2000mg/day, to increase their insulin sensitivity and suppress gluconeogenesis, thus minimizing body fat by promoting breakdown and burning of fat cells and maximizing muscle synthesis. This was an eye-opener for me. Of course, Metformin is a wonder drug. It’s mechanism of action is still not completely understood, but as I wrote about here, in this recent JAMA article, it has been seriously advocated for everyone. And, unlike the SLGT2s, is has been around for over 50 years, is demonstrably safe, and really cheap. So, after the conference, with supplies on hand, in February I decided to increase my Metformin dose to 1500mg/day.

In the weeks following implementation of that decision, my fasting blood sugars slowly began to transition. And by the second half of March, after a long hiatus, I was beginning to get fasting readings below 100mg/dl again (mostly in the 90s). What happened next, however, was quite remarkable. See Part 2 of this story next week.

Type 2 Diabetes, a Dietary Disease #328, “…the most sustainable diet ever!”

I am so sick and tired of hearing the public health and medical professions declare that eating Low Carb (LC), or heaven forbid, Very Low Carb, is “not sustainable” over the long haul; that most people don’t have the will power to restrict their diet to primarily foods that are comprised of protein and fat. Well, I doubt these PhDs and MDs were themselves ever obese or, if they were, had tried LC. But now that the “science” behind the diet/heart hypothesis has been debunked, and dietary cholesterol is no longer verboten, the reasons not to try it are gone.

Let’s face it: The reason people eat is because they are hungry. More accurately, the reason people eat is because their bodies are hungry. The brain, specifically, is the nerve center for messages from the blood and digestive system that tells you to eat. It wants you to think about, look for and eat food. It’s a primordial thing.

And why is the body hungry? Because it needs to maintain a constant flow of energy to keep everything running and in balance. This condition is called “homeostasis.” The body works relentlessly to also maintain your set point weight. These are very powerful forces. And they are autonomous, which means they work automatically without your conscious input. In fact, as you know, they fight your conscious efforts to lose weight. And they have a built-in evolutionary bias to add weight, for unforeseen events (an unproductive hunt, a poor harvest, or winter).

So, when you think it’s all about your “will power,” you are deluding yourself. You have an overly optimistic bias toward your ability to not eat. It’s not about your conscious will. Hunger is driven by forces beyond your control. It’s driven by your biology, which is more powerful than your conscious you. But, once you understand how your biology works, you can work with it. You can “defeat” the message that drives you to eat when you have plenty of fat stores hanging on your body. And you know you do. And you want to get rid of that extra fat, right?

Of course, you can stay with the restricted calorie, balanced diet and see how it works for you. But, you know in your heart of hearts that that regimen doesn’t work. And if you want to figure out how to get your body to naturally burn its own fat, stay with me. I am not selling snake oil or anything else; just a dietary idea that works.

How would you feel about a diet that works without hunger? That’s right, the hunger is gone. There will no longer be physiological signals and messages telling you to put something in your mouth. Why, because your body is satisfied with the available food source: your body fat. How did this condition come to pass?

“Just one word…Insulin” (apologies to “The Graduate”). Insulin is both the glucose-transporter hormone and the fat storage hormone. When you eat carbohydrates, they all break down to simple sugars – glucose primarily – and are “escorted” in your blood by insulin secreted for the purpose. If you’re pre-diabetic or a type 2, you have a degree of insulin resistance (from eating too many carbs for too many years), so your blood glucose and your blood insulin stay elevated. If you eat carbs at every meal (even a small, calorie restricted meal), they (glucose and insulin) are at a continuously “high” level. Result: You don’t lose weight, and you’re still hungry!!! Why?

Insulin is also the fat storage hormone. That means, it regulates when to make fat (when you eat too many carbs or too much fat), and when to burn fat…to maintain homeostasis. And your brain reasons that if you have a high level of insulin circulating in your blood, you must have glucose availability (from carbs, mostly) for energy to maintain homeostasis. It doesn’t recognize, unfortunately, that your glucose metabolism is disregulated by insulin resistance (your Pre-Diabetes or Type 2 Diabetes). It just looks at your elevated blood insulin level.

 Your body (not you) then “reasons” that it doesn’t need your body fat for energy, and so it blocks its breakdown. Your body would be very happy to burn your body fat for energy, but your elevated blood insulin level is blocking the signal. You simply can’t lose weight if your blood glucose and blood insulin remain high. Your body won’t let you. You have to lower your circulating blood glucose and blood insulin levels. How? By not eating carbohydrates.

When you abstain from eating carbs for a few days, your body’s blood glucose and blood insulin will decrease and unblock the path to burning body fat for energy, making free fatty acids and ketones. Your body will be happy and you will have been launched on “…the most sustainable diet ever” because THE HUNGER IS GONE!