Retrospective #12: Turning the Titanic: Who’s in Charge of Your Health?

Turning a gigantic ship like the Titanic, under way with a full head of steam, is said to take a lot of time and miles of open sea. Turning the Nutritional Guidelines for American is proving to be equally difficult and time consuming. But Americans are changing their Way of Eating, slowly but surely. And this in spite of obdurate resistance from the cabal of forces united in opposition: the USDA/HHS, Agri-Business, Big Pharma, and the Medical Establishment.

That is hopeful, because we all know what happened to the Titanic. And we are a nation of individuals of free will. We are not confined together on the deck of a ship. We are free to choose our own course. Admittedly, however, in the absence of the certain knowledge of our impending doom (metabolically speaking), combined with the lack of an assurance of the safety and efficacy in choosing an Alternative course, we are reluctant to change our Way of Eating. Most of us “go along for the ride,” blindly willing to follow the course determined by our captains of public health and guided by the pursers of the processed food industry. We are marshaled by the stewards (the media) who serve us our daily reminders -- avoid saturated fats, now called solid fats, and dietary cholesterol -- and the clinicians who bus up after them all with myriad medications for our mounting metabolic maladies (see #8).

Never mind that the course that we have been following was based on a hypothesis that was based on a flawed epidemiological study (Ancel Keys’s cherry-picked studies of 6, later 7, nations out of 22: see #3). Never mind that Keys, the father in 1953 of the Lipid Hypothesis, admitted in 1997: “There’s no connection whatsoever between cholesterol in food and cholesterol in blood.  We’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.” Never mind that “Epidemiological studies can only go to prove that an agent could have caused, but not that it did cause, an effect in any particular case.” From the beginning, the dissenters never had a chance once the AHA got behind the hypothesis with public advertising (and a fundraising effort) promoting their “risk factors” for heart disease. Never mind that Keys and the AHA were wrong all along!

Never mind that the body synthesizes its own cholesterol to compensate for the amount that we don’t eat. Cholesterol is essential for all animal life. It is the essential structural component of all cell membranes, and it repairs damage from inflammation in our blood vessels. Did you know that the brain is the most cholesterol-rich organ in the body, most coming from in situ synthesis? And, that human breast milk contains loads of cholesterol? And that it is needed to make bile acids, steroid hormones, and absorb the fat-soluble Vitamins A, D, E and K.

Never mind that the evidence supporting saturated fat in the diet has been convincingly documented. Never mind that those pursuing low-fat diets in The Framingham Study had a higher incidence of all-cause mortality. Never mind that after 40 years the director of The Framingham Study had to admit (July 1992, Archives of Internal Medicine): "In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum [blood] cholesterol.” This startling message has been drowned out by the drum-beat from public health officials to lower cholesterol, especially LDL-C, led by the AHA, Big Pharma, industrial food processors, Medicare, Medicaid and by the clinical practitioners who peddle Big Pharma’s statin drugs.

Never mind that… Well, you get the idea. If you are interested in reading the evidence-based science out there, there are many good books out by real science writers (not “hacks” like me) who look closely at the evidence, even in early 2011 when this blog was originally written,. Maybe the best is Gary Taubes’s “Good Calories – Bad Calories” (2007). His more “accessible” “Why We Get Fat: And What to Do About It” (Knopf, 2010) is an easy read.  Sally Fallon and Mary Enig’s “The Truth About Saturated Fats,” is also a good read. And, Malcolm Kendrick’s “The Great Cholesterol Myth” and Uffe Rafnskov’s “The Cholesterol Myths.” And, adding just one of many books written since 2011: Nina Teicholz’s “Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” (2014).

These writers would create a food pyramid very different from the most recent HHS/USDA “Guidelines.” But the latest guidelines do show signs of change. The Titanic has begun to turn. You’ll see how in the next Retrospective.

Retrospective #11: Why We Get Fat

If memory serves me correctly, Gary Taubes’s book, “Why We Get Fat: and What to Do About It” was published after Christmas 2010. This column was written in anticipation of its publication and is re-written here as part of a daily Retrospective series begun 10 days ago. In an earlier tome, “Good Calories – Bad Calories” (2007), Taubes proffered his “Alternative Hypothesis” (scroll down Retrospective #5) to the Conventional Wisdom about “why we get fat.” His Book, “Why We Get Fat,” was written to be “more accessible,” and to be read by the lay public.

The previous Retrospective #10 was on the role of insulin as the transport vehicle for glucose in the bloodstream. As Taubes describes in #5, and we recap in #10, insulin levels in the blood rise whenever there are elevated levels of glucose present. Insulin transports the glucose to the cells for energy uptake, but at the same time blocks the breakdown and entry of energy from stored fat into the bloodstream. This is insulin’s role in “fuel partitioning.”

The fat stored in our bodies are triglycerides. A triglyceride molecule is big, comprised of three fatty acid molecules linked to one glycerol molecule. When the enzyme lipase in fat tissue is activated by insulin (and other) hormones, triglyceride molecules break down into their component parts. The fatty acids are released into the blood and are then available for cellular uptake. Ketone bodies, produced as a byproduct of the breakdown (lipolysis), and the glycerol, are used for energy too. This process can occur at night during an overnight fast and is called ketosis.

That being said, our bodies burn “sugar” (glucose) when it is available. And that’s the problem. That is “why we get fat.” Glucose is always available! In the Standard American Diet (SAD), our “balanced” diet is heavily weighted towards carbohydrates, all of which become glucose in the blood stream. Your body can’t be a fat burner and a sugar burner at the same time, and glucose is the preferred fuel when and BECAUSE it is available.

This is a conservation strategy by design.  The body will run on glucose for so long as 1) we eat things that will break down into glucose – that includes all carbohydrates and all sugars (which are carbs) – or 2) we have glucose stored (as glycogen) in the liver and the muscles. And if it runs out of eaten or stored glucose, the body can also make small amounts of glucose from “glucogenic” amino acids (from protein) or from glycerol from fats (lipolysis).

Since insulin must be present in the bloodstream to transport glucose to the cells for energy, so long as there is an elevated level of insulin in the bloodstream, the unneeded food energy from any of the excess fat or carbohydrates consumed (that cannot otherwise be stored in the liver and muscles) must be accumulated as body fat (by de novo lipogenesis). We’re living on sugars and processed carbs, and saving and accumulating more fat for “hard times.”

For almost half a century we’ve done this to avoid dietary fats, and particularly saturated fats and dietary cholesterol. We’ve been told that they are bad for us. The low-fat diet was supposed to protect us from “killer diseases” like heart disease, stroke and cancer. Ironically, today there is little evidence that it provides protection and mounting evidence that limiting saturated fats in the diet may do more harm than good. Obesity is the precursor for Metabolic Syndrome and many other Diseases of Western Civilization: CVD, AZ and many cancers.

In the late 1990s I recall reading a New York Times front-page, column-1 story reporting on a new treatment modality being recommended for patients presenting with hypertension, hypercholesterolemia, and Type 2 Diabetes or Pre-diabetes with obesity. The impetus for the new modality was the failure of clinicians to treat obesity effectively, and this was due, they said, to “patient noncompliance”! (not the wrong low-fat, balanced “diet and exercise” prescription (“eat less and move more”). The new paradigm they recommended was a workaround: using just pharmacological solutions: High blood pressure and high cholesterol both respond to medications!

Unfortunately, this solution often results in the Pre-diabetic developing Type 2 diabetes (25% within 3-5 years), then the T2 getting progressively worse until they become insulin dependent (multiple daily injections!) and eventually develop one of the complications or co-morbidities (CVD), from which they will, most assuredly, die. 

Retrospective #10: Carbohydrates, Insulin and Pre-diabetes

Why do we get fat? We eat too much and don’t exercise enough, you say. Well, if you do, you’ve got company. That’s the conventional wisdom. It was reinforced by the just-revised “Dietary Guidelines for Americans, 2010.” (This post was originally written in early 2011.) The joint press conference promoting this Low-Fat, High-Carb, mostly plant-based Pattern of Eating, was held by the Secretaries of the USDA and HHS, both former farm state governors.  It also means that you probably haven’t read or accepted the Alternative Interpretation of the Energy In – Energy Out formulation explained in Retrospective #5 in this series. (To see #5 on this blog, just scroll down, or on Face Book, click on my name and scroll through my timeline.)  It flat-out refutes the Low-Fat, High-Carb WOE.

Gary Taubes, in his very good book, “Good Calories – Bad Calories,” introduced in Retrospective #4, makes the case convincingly. In #5 of his “certain conclusions,” in the Epilogue of that book (p. 454), he states, “Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior. Obesity is a disorder of excess fat accumulation.” But why do we get hungry and eat and accumulate more fat rather than burn body fat for energy balance? What makes us hungry and eat too much and too often when we have plenty of stored body fat to use? The answer, according to Taubes, is too many dietary carbohydrates, especially sugars and highly processed carbs.

All of Taubes’s ten “certain conclusions” merit re-reading (scroll down to #4), but his last two speak directly to these questions:  9) “By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be;” and 10) “By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.”

The mechanism at work here is the effect that all carbohydrates exert on the hormone insulin. That includes all sugars and all processed carbs, regardless of their glycemic index or glycemic load. When carbs are eaten by a healthy person with normal glucose metabolism and regulation, in the initial response the enzyme amylase, in saliva in the mouth, triggers a quick burst of ready-made insulin previously produced by the pancreas. Then, in the small intestine, additional enzymatic action further breaks down the sugars and starches to simple glucose, which are then absorbed through the wall of the small intestine and into the bloodstream. In a healthy person, with normal insulin sensitivity and non-impaired glucose response, the additional insulin, produced by the pancreas in response to elevated glucose levels in the blood, slowly “mops up” the glucose (takes it to the muscles, etc.) over a one to two-hour period. Then, the levels of both glucose and insulin in the blood decline.

Thus, one of primary functions of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with Impaired Glucose Tolerance (IGT): Insulin Resistance. These impairments are the first signs, usually undetected and overlooked, of the metabolic disorder called Pre-diabetes.

Until recently, the fasting blood glucose (FBG) test was the most common test for diagnosing Pre-diabetes. The diagnosis was sometimes confirmed with a more expensive test, the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year (this was written back in 2011), however, there has been a change in protocols. Now, a test called the A1c is coming to be the norm (again, 2011).

In addition, in 1997 the “then” diagnostic standard for Type 2 Diabetes Mellitus was lowered: FBG from ≤140mg/dl to 126. In 2002, the A1c test for Type 2 Diabetes was established at 6.5%, and later at 5.7% for Pre-diabetes. Some clinicians (Richard K. Bernstein, MD: “The Diabetes Solution”) and researchers (Ralph A. DeFronzo, MD, UTHSCSA) have always used a lower standard. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks. If your blood glucose doesn’t return to “normal” two hours after you begin eating, you have Insulin Resistance. This can be done at home – no appointment required – with a meter and test strips.

In the next Retrospective, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When this hormone is “out of balance,” the result is fat synthesis and accumulation. We get fat. We’ll explain how, next.

Retrospective #9: Metabolic Syndrome, the American Disease of Civilization

What is Metabolic Syndrome? There are various definitions but all include having at least 3 of the following 5 medical conditions. The first always is central obesity (what I have coined “omental adiposity”), or a Body Mass Index (BMI) ≥30, or an elevated waist circumference (men ≥40 inches, women ≥35 inches). The other four “risk factors” are elevated triglycerides (≥150mg/dl), reduced HDL, the “good” cholesterol (men ≤40mg/dl, women ≤50mg/dl), elevated blood pressure (≥130/85mm Hg, or use of medications for hypertension) and elevated fasting glucose (≥100 mg/dl, or use of medications for hyperglycemia). Now ask yourself: Do I have Metabolic Syndrome?

Metabolic Syndrome is just one of a larger class of disorders that have become known as the Diseases of Modern Civilization. Metabolic Syndrome, because it is increasingly affecting our and other Westernized populations at younger and younger ages, especially in the last fifty years, has been closely identified with diet and lifestyle factors. Gary Taubes (of “Good Calories-Bad Calories” repute) and many others, including (humbly) me, associate Metabolic Syndrome exclusively with diet. And as a “lifestyle” condition, all five risk factors are remediable, by you.

To support the “lifestyle” or “diet” association, let’s look at how the American diet has changed in modern times. These are only associations -- not causal relationships – but overwhelming anecdotal data support the association.

When this post was written in 2011, annual sugar consumption in the US was estimated to be in excess 160 pounds per capita, and most of that was triglyceride-raising high fructose corn syrup (HFCS). HFCS is 55% fructose and 45% glucose. It was first introduced into the food supply in 1978 and today is ubiquitous. Look for it on food labels, in soft drinks, and also in breads, cereals, breakfast bars, lunch meats, yogurts, soups and condiments, and avoid it like the plague. Americans consumed only about 100 pounds of sugar (sucrose) per person in 1920 and only about 15 pounds in 1830, most of that molasses, according to the Diet Heart Publishing timeline cited in Retrospective #3.

Older readers will remember Vitamin D rich lard, the rendered fat from pigs. It was once the #1 cooking fat with 70% of the market. And McDonald’s French fries used to be cooked in beef tallow. Today, highly processed soybean oil has a 70% share of the market, and zero vitamin D. And, again as Diet Heart Publishing points out, “now the experts who told us not to eat lard, because it is a saturated fat, are telling us we are deficient in Vitamin D!”

Per capita butter consumption in 1910 was 18 pounds. By 2000 it was less than 4 pounds. By 1957 margarine outsold butter for the first time. We gave up butter’s beneficial vitamin A for the excess, inflammation-inducing omega 6 fatty acids found in margarine, vegetable shortening and processed vegetable oils. Interestingly, as the trans fat danger of margarine became apparent, by 2005 butter had started to enjoy a comeback and for the first time was outselling margarine, again according to the Diet Heart Publishing timeline.

Finally, we Americans, for the last half century in particular, have been buying and eating more and more refined, highly processed carbohydrates, starches and sugars included as ingredients in the prepared foods that increasingly dominate the choices available to us. We choose them largely for convenience as we go about our busy lives. These daily dietary choices portend our own destruction, metabolically speaking. The Metabolic Syndrome has become the American Disease of Civilization, and it is associated with a long list of related conditions, or “co-morbidities.”

 Research has yet to firmly establish the causal relationship, but it is common for a patient with Metabolic Syndrome to progress to T2 diabetes and cardiovascular disease (CVD). In the United States, CVD is the leading cause of death among both men and women, and the presence of type 2 diabetes doubles the risk. In fact, over 50% of deaths in patients with type 2 diabetes are due to CVD. People with Metabolic Syndrome have a greater risk of CVD, particularly men over age 45 and women over 55, and a 5-fold risk of developing type 2 diabetes.

Metabolic Syndrome, a silent condition, thus poses a significant public health threat. Left unchecked, it will have a staggering effect on healthcare costs in the United States in the years ahead. So, what can be done to check this “epidemic”? If overweight and obesity is the most common risk factor, then we have to ask, why do we get fat?

Type 2 Nutrition #474: “Taking aim at belly fat”

Most people are more motivated to lose weight than to control their type 2 diabetes (T2D). We’ve come to think 1) that being overweight or obese is a personal failure best addressed with self-discipline, “diet and exercise,” and 2) that T2D is a medical condition that is best left to doctors. In my opinion, both ideas are wrong. Why?  Because 1) T2D is a dietary disease, and 2) obesity is also a “dietary disease, the results of a metabolic disorder developed over a period of many years from eating the “wrong” foods”!

Has “diet and exercise” worked for you? If not, is it because the diet and exercise program you followed didn’t result in permanent weight loss? Could it be that the “healthy eating” patterns recommended by the USDA/HHS, and endorsed by the AMA, AHA and ADA, are the same ones that got us fat in the first place? Their solution is to “eat less and move more” using the same balanced diet, loaded with refined carbs and sugars.

Did you really expect to permanently lose weight without hunger eating a high-carb diet? And did you think exercising more would not make you hungry? Exercise is healthy, but it is not a good weight loss strategy.

Maybe the composition of your diet is where the problem lies. Have you considered that by just changing the macronutrient proportions of your diet you could lose weight easily, and without hunger? And keep it off so long as you continue to eat that way. By now you surely must know that I am suggesting you eat a Low Carb diet. If you do, you will lose weight. And you can do it without hunger, and without exercise (if you want to).

Likewise, treating type 2 diabetes as a condition that is within the purview of the medical profession is a surefire way to assure that you remain sick. Consider this: The Standard of Care goal of the American Diabetes Association (ADA) is that your A1c be ≤7.0%. That means the ADA’s goal is for you to always be “diabetic” since the threshold for diagnosis of type 2 diabetes is ≥6.5%. Your doctor will consider that you’re “in good control” if, with quarterly tests, and more meds as needed, you have an A1c of ≤7.0%. Wahoo!

That’s all your doctor can do in a clinical setting. Besides, most know zilch about nutrition and what they do know is mostly wrong. It is guided by USDA/HHS’s ChooseMyPlate.gov and ADA’s Create Your Plate. They just want maximum reimbursement (w/o penalty) under Medicare and other insurance rules, and to do that they must advocate for the USDA/HHS “lifestyle formulary” to eat a “plant-based diet” and “move more.”

Do you see what’s wrong with this picture? Do you see that YOU, by making just one change, can address both obesity and type 2 diabetes? Type 2 diabetes and obesity are both dietary diseases! YOU can treat them both yourself. Your doctor only sees you in the office, but YOU can manage both diseases EVERY DAY, just by what you eat. You have a choice: let your doctor monitor your diseases, or YOU take control of them.

The “dietary solution” for weight loss (eating Low Carb) is the same “prescription” for T2D management. You will both 1) lose weight generally but specifically visceral fat in your liver and pancreas, thereby improving their function and 2) lower your high blood sugar (caused by Insulin Resistance) and improve your A1c.

If you’re a man, take a look at these pics (Type 2 Diabetes #355, Before and After), for how I managed to lose my “beer belly” and recently achieve an A1c of 5.0%. By the government’s measure, I am now “non-diabetic.”

If you’re a woman, read this Harvard Women's Health Watch article.  Belly fat creates serious health risks, but if you follow the advice to eat a Low Carb Diet (not the same-old, same-old establishment advice that Harvard still dishes out, you can achieve the same result (without hunger), and TAKE AIM AT YOUR BELLY FAT.

If you go Low Carb, your doctor will be very happy the next time the nurse weighs you in and takes your blood. The scale and lab tests will show you made a good decision. You lost weight and improved your blood sugar control in the same way, and YOU did it YOURSELF, without hunger…and even without exercise (if you want).

Retrospective #8: Epidemiologically Speaking: Patterns of Health and Illness

The Diseases of Modern (Western) Civilization began about 10,000 years ago, co-incident with the transition from the Paleolithic to the Neolithic era. The nomadic hunter-gatherer discovered he could lead a more stable and stationary existence on a diet largely comprised of cereal grains. This was a major shift in the human dietary.

In 1880, with the transition from stone-ground to steel-rolled flour, it accelerated. After the turn of the 20^th century, Crisco introduced fake “vegetable oil” fats and later the highly processed corn and soy bean oils high in Omega 6 fatty acids. In the latter half of the last century processed foods became ubiquitous. Today, many believe these shifts are the principal cause for the patterns of illnesses and medical disorders with which we are now beset.

In modern times, epidemiologists, who by definition look for statistical patterns of health and illness in populations, have examined this change and associated factors in myriad retrospective studies.  They have observed the health and illnesses of populations exposed to the “Western diet” and compared them to peoples who have lived in relative isolation without exposure to the changing dietary patterns of the industrialized world.

Epidemiology, however, is a statistical “science,” and can only go so far. These studies typically show correlations in similar populations and differences in dissimilar populations. As we’ve noted earlier, however, correlation does not imply causation. According to Wikipedia, “Epidemiological studies can only go to show that an agent could have caused, but not that it did cause, an effect in any particular case” (emphasis added by me).

Nevertheless, in the early 1950’s noted physiologist Ancel Keys proffered his Lipid Hypothesis, based on selected data from a 22-country epidemiological study. In his original Six Country Analysis (1953), and later the Seven Countries Study, launched in 1956 and first published in 1978, Keys’s hypothesis implicated dietary fat, particularly saturated fat and cholesterol, in heart disease. Acceptance of his hypothesis grew quickly and allowed others, like the American Heart Association, to promulgate the AHA’s now well-known “risk factors” for heart disease.

It also led to the controversial “Dietary Guidelines for Americans” (see Retrospectives #2 & #3). The USDA/HHS Committee to write the latest of these 5-year guidelines (for 2020) was formed just three days ago (2/21/2019).

All of these “prescriptions” dispensed to the consumer were still, however, nothing more than simple hypotheses and assertions. Hypotheses must be tested and retested by randomized controlled trials to independently reproduce similar outcomes. And if the outcomes aren’t reproducible, they must be rejected as false.

There have been many large, lengthy (in time) and costly trials such as the Framingham Heart Study. These studies have continuously been revised, updated and reinterpreted and their outcomes disputed. Along the way, many medical researchers have come increasingly to view with skepticism the Lipid Hypothesis and its resultant restrictions on consuming fats, particularly saturated fat and dietary cholesterol. Many in the medical and nutrition professions now view those recommendations as deeply flawed and based on inadequate scientific proof.

Conversely, the Standard American Diet (SAD), and in particular the USDA’s Dietary Guidelines for Americans, which is 60% carbohydrate, have increasingly come to infer a causal relationship with various diseases and metabolic disorders, chief among them Metabolic Syndrome. But, again, correlation does not imply causation.

The term Metabolic Syndrome is relatively new on the scene. When first described in 1988 by Gerald Reaven in his AHA Banting Lecture, he called it Syndrome X. It is, Wikipedia says, “a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes. It affects one in five people, and prevalence increases with age. A 11/23/10 CNBC story in Reuters (this blog post was originally written in January 2011), said “More than half of Americans will have diabetes or be prediabetic by 2020.” “More than half. “I think they nailed it.

In the next Retrospective we’ll learn the clinical definition of Metabolic Syndrome and how is it diagnosed (and treated.) In fact, the next +/- 500 posts will suggest ways to treat it, to “Lose the Weight…and Save Your Life.”

Retrospective #7: Are you a “Sugar Burner” or a “Fat Burner”?

A restricted or reduced-calorie, balanced diet, we have all learned ruefully, is a “starvation” diet. It doesn’t work because your body tells you that you are starving. You feel weak and tired and hungry, and your metabolism slows down.  Your body is screaming for more “energy in,” and your hunger eventually overpowers your will power. The result: you shovel “in” more energy, by mouth! The problem, of course, is that you are not allowing your body to get the energy it needs from the body fat you stored for that very purpose.

This would be a good time to go back and re-read Gary Taubes’s 10 “certain conclusions” in Retrospective #4 of this series. If you’re on the website, http://danbrown-thenutritiondebate.blogspot.com, just scroll down. If you’re reading this on Face Book, just click on my name, open and scroll down on my timeline. When you find #4, pay special attention to Taubes’s conclusions 2, 8, 9 and 10.

Now, back to The Nutrition Debate. The food we eat is rapidly digested and absorbed -- sugars and starches more rapidly than fats and proteins. Sugars and starches are all carbohydrates and all become “sugar” (glucose) in the blood stream when they are completely broken down by the digestive process. The sugars and starches that break down most rapidly are 1) the smaller molecules (sugars) and 2) the most highly processed foods, like bread.

The body prefers to use sugars and starches for energy because most of them are easy to break down and “burn” for energy. Fat takes a little longer, and has less precedence, as it was designed to be stored for times of famine. Protein takes the longest, remaining in the stomach for several hours. The good thing about fat, though, and protein too to a lesser extent, is that it provides a feeling of fullness (satiety). Carbs give us a quick “spike” of energy, but are then quickly followed by a “crash” and then that “hungry feeling” one gets (on a high-carb diet) between meals. This “craving” is the result of a hormonal signal calling for more energy (from sugars and starches) to quickly supply glucose to the blood stream. Protein or fat would be more satisfying, but sugar and starch will give you that quick “boost.” Some processed foods, like white bread, which converts to 100% glucose, actually digest more quickly than table sugar (sucrose), which is just 50% glucose (and 50% fructose)!

When you eat a diet that is largely comprised of carbohydrates, such as the Standard American Diet (SAD) which is 60% carbohydrate (Retrospective #2), you are, in metabolic slang, a “sugar burner.” You may eat healthy proteins and fats too, but your body is running on glucose (“sugar”) and storing fat. It calls for you to eat more (carbs for the quickest effect) whenever your blood sugar crashes, which is just a couple of hours after you last ate carbs.

Because you are primarily burning carbs for energy, most of the fats you eat, plus any extra carbs, and any excess protein (to be explained shortly), will be stored. The fats (and ultimately the extra carbs) will become triglyceride molecules and will be deposited within the fat cells of the adipose (fat) tissue on your body.

The protein, which all breaks down to amino acids, will be “taken up” by the muscles and other body tissue to repair and restore them within 4 to 5 hours after it is eaten. Any “leftover” amino acids, not taken up by the body, are sent to the liver where they are stored. Later, when there is a low blood sugar signal, the liver will reconstitute some of those amino acids (from the excess protein) as glucose, through a process of called gluconeogenesis.

So, how do you get away from this endless cycle of “sugar” (glucose) spikes and crashes that characterize the SAD? How do we get away from this diet that is making all of us fatter and sicker? And, if you need to lose weight, how do you become a “fat burner” instead of a “sugar burner”?  I think you know where I am going with this, but in the next installment I will first tell you about the consequences of the dietary program our government has advocated and we have now been mainstreaming for over 40 years. It is the story of the emblematic Disease of Civilization first described by Gerald Reaven in 1988 as Syndrome X and now more commonly known as Metabolic Syndrome.

Retrospective #6: “Energy In = Energy Out”: An Alternative Interpretation

The one universally held truth in the common understanding of human metabolism is the Energy Equation: “Energy In = Energy Out.” It is generally endorsed by most doctors, even some medical researchers, and universally by the popular press and the public at large. Why? Because it is so easy to understand.  It is, simply, “common sense.”

It also gains gravitas by its association with one of the basic laws of science, the First Law of Thermodynamics, as described in Wikipedia: “The total energy of an isolated system is constant. It can be transformed from one form to another, but it can neither be created nor destroyed.” Now, who’s gonna argue with “The First Law”! You’d have to be some kind of kook to even try, and you would be laughed at, all the way to (and in) the grave (viz: Atkins).

Okay. I’ll try. I get the courage because Gary Taubes, in his seminal opus “Good Calories – Bad Calories,” introduced in the last column, has convinced me. So, with apologies to Taubes for any errors in my understanding, I will try to recapitulate his explanation here to help convey an “Alternative” Interpretation of the immutable First Law of Thermodynamics, as it applies to the “Energy In = Energy Out” formulation for “energy balance,” or Homeostasis.

The problem with the conventional interpretation of the “Energy In = Energy Out” formula is that it measures “Energy in” in the wrong place, i. e., from outside the body, as something done to the body. Thus, the common-sense, universally believed understanding is as follows: Energy In (food eaten) = Energy Out (basal metabolism plus the added energy expenditure of activities, including exercise). Therefore, to lose weight (“improve” the energy balance) you must decrease calories (i.e., reduce “Energy in”) and/or exercise more (increase energy expended, i.e., “Energy out”). Sound familiar? Of course! It’s the ubiquitous “diet and exercise” prescription dished out by the medical and public health establishment. But this interpretation of how the Energy Equation works, with respect to where “Energy in” is measured, is fundamentally wrong, according to Gary Taubes, et. alia, Including now… me.

According to Taubes, the operative place to observe and measure Homeostasis (how the body itself modifies energy intake and expenditure to maintain a balanced state), is in the blood stream. The sources of all energy to the blood stream – the “Energy in” or left side of the equation – are basically three-fold: 1) energy from food eaten and digested, 2) energy stored in the liver and muscles, and 3) energy from our fat cells (adipose tissue aka triglyceride molecules), if allowed to break down when needed for energy. Take note in particular of this last source on the “Energy in” side of the equation, the very important “if allowed.” There’s a conditional aspect to it.

This 3^rd source of “Energy in” – our body fat – is the critical difference. With it you can 1) avoid the starvation aspect of conventional reduced calorie, balanced diet programs, 2) prevent that always hungry feeling, including cravings and the need to snack between meals and 3) give your body all the energy it needs, avoiding that drained, weak feeling. It is also an easy way to lose weight and keep it off, as long and so long as you stay with it.

The body itself balances the energy equation. That energy can include body fat, if allowed, through complex signals from various hormones, putting on the right side of the equation however much energy it needs. It will meet the needs of our basal metabolism plus whatever our activity level requires, if it can get access to that body fat. It will use the first two sources on the left side of the equation (1) food eaten and 2) energy stored in the liver and muscles), and then, if it is “allowed,” energy from the 3rd source, our body’s own fat cells. This last energy source, however, is, as we said, conditional, and it is critical to understand how the body can get access to it.

Once understood, and with knowing the Macronutrient composition of the foods we eat and the key role of the hormone insulin, we can learn how to use all three sources on the “Energy In” side of the equation.

Next, we’ll discuss what “if allowed” and “access” means, that is, how the mechanism works. It worked for me; it will work for you too. After all, it’s the frickin’ First Law of Thermodynamics, as correctly understood and applied.

Retrospective #5: Gary Taubes and the Alternative Hypothesis

Gary Taubes first came to my attention in 2002 as a result of the New York Times Sunday Magazine July 7th cover story entitled, “What If It’s All A Big Fat Lie?” Taubes had won the Science in Society Award of the National Association of Science Writers three times, but his 2002 article was the first widely read refutation, for a popular readership, of the “high dietary fat/cholesterol/heart disease” (lipid) hypothesis. It also posited his “Alternative Hypothesis,” which is predicated on a Very Low Carb (VLC) Way of Eating (WOE). I didn’t know it at the time, but my doctor, an internist/cardiologist, had read the article and tried the recommended diet himself to lose weight. He succeeded and suggested that I try to eat Very Low Carb, also to lose weight. I weighed 375 pounds at the time. As an afterthought, he said, “By the way, it will probably help your Type 2 diabetes.” Boy, was he ever right!

Following the publication of his 2002 NYT Magazine cover story, Taubes was besieged to write a book detailing his findings and touting the “alternative hypothesis.” He refused and instead spent the next five years researching and writing “Good Calories – Bad Calories” (Alfred A. Knopf, 2007). He refused to write a book for the popular readership because he said he did not want to produce a polemic. He wanted instead to research and present a history and analysis of all that has transpired in the field of obesity research and “science” – a word he uses sparingly and advisedly.  This book is a dense read, but getting through it is well worth the slog. In the end, in the Epilogue (pages 453-454), Gary Taubes proffers 10 “certain conclusions,” which I reproduce verbatim below.

“As I emerge from the research…certain conclusions seem inescapable to me, based on the existing knowledge:

1.       Dietary fat, whether saturated or not, is not the cause of obesity, heart disease, or any other chronic disease of civilization.

2.       The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis – the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.

3.       Sugars – sucrose and high-fructose corn syrup specifically – are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

4.       Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic disease of civilization.

5.       Obesity is a disorder of excess fat accumulation, not overeating and not sedentary behavior.

6.       Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

7.       Fattening and obesity are caused by an imbalance – a disequilibrium – in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses the balance.

8.       Insulin is the primary regulator of fat storage. When insulin levels are elevated – either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.

9.       By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.

10.   By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.”

I’ve read large parts of “Good Calories – Bad Calories” twice, and re-read Taubes’s “certain conclusions” a dozen times. I am convinced that he’s got it right. But, after failing to get the reception he had hoped for in the medical community, Taubes finally relented and agreed to write a book that would be more accessible to the general public. “Why We Get Fat: And What to Do About It” (2010). Hardcover: $19.38. Softcover: $13.38. Kindle: $11.99.

Retrospective #4: Big Government, Big Pharma, and Poor Little Dr. Atkins

In 1972 Dr. Robert Atkins published his “Diet Revolution” advocating a Very Low Carbohydrate diet. In response the AMA attacked Atkins calling his “high fat” diet a “dangerous fraud.” When Atkins was called before a Congressional Committee to defend himself, he was publically ridiculed and humiliated. Meanwhile, just two years later (in 1974), The Framingham Study reported that there was no association between high cholesterol and sudden death, but men with low cholesterol had a strong association with colon cancer and premature death. The water was muddy, but nobody outside the research community paid attention to the research findings and nuanced data.

Enter Senator George McGovern, chairman of a U. S. Senate Select Committee on Nutrition and Human Needs (“the McGovern Committee”). He had been a staunch supporter of agriculture since beginning his Congressional career. He was also convinced that fat made us fat and was responsible for “killer diseases” like cancer and heart disease. In 1977, after only two days of very contentious hearings, his committee published the “Dietary Goals for the United States,” aka “The McGovern Report.” The first “Dietary Guidelines for Americans,” published jointly by HHS and USDA, followed soon after in 1980. It has since been revised and reissued, with only incremental changes, every 5 years. The die had been cast. There was now no going back, in spite of mounting evidence. Government appointed scientists and processed food industry representatives would henceforth decide what to recommend we eat. What we eat had become Big Government’s business, and the province of Agri Business and Big Pharma.

In that same year as The McGovern Report (1977), the National Institutes of Health (NIH) reported on five diet-heart studies suggesting that a depressed level of HDL was the most reliable predictor of heart disease for men and women at all ages, but this went virtually unnoticed. This finding was studied further by the NIH, but only after a substantial delay. It wasn’t until 1999 that a large scale, long-term study confirmed that increasing HDL lowers CVD risk. This old link from 2009 indicates that it also lowers cancer risk, approximately 36% with every rise of 10 mg/dl.

In the meantime, NIH’s MRFIT study (1982, 13,000 men followed for 6 years) studied a low-fat, high-carbohydrate diet with a focus on vegetable fat, which effectively lowered total cholesterol. Participants had more heart disease deaths than their “usual care” cohort. In addition, the lowest cholesterol levels were associated with mortality levels equivalent to the highest cholesterol levels. They were also associated with significantly more strokes, digestive diseases and cancers. This study was also ignored, but the focus did shift to lowering LDL-C instead of Total Cholesterol, perhaps due to the desire for a simple public health message.

Now, enter Big Pharma. By the late 1980’s sales of the first LDL cholesterol lowering statin drug had begun. As a result of public advertising campaigns, people became familiar with their cholesterol numbers, and the difference between “good” and “bad” cholesterol entered the public consciousness. These campaigns were very effective. A recent AMA editorial suggested that world-wide sales of statins may approach $1 trillion by 2020.; they are the most successful drug of all time. However, there is no evidence that statins help women or anyone over 65.

Meanwhile, Ancel Keys, father of the lipid hypothesis, retired to Southern Italy, coming home to die in 2004 at age 100. However, according to Malcolm Kendrick, author of “The Great Cholesterol Myth,” Keys admitted in 1997 that cholesterol in the diet has no effect on cholesterol levels in the blood. Keys is said to have said, “There's no connection whatsoever between cholesterol in food and cholesterol in blood. And we've known that all along.”

What is that he said, you ask? Is it then possible that dietary cholesterol does not have to be limited at all? That Total Cholesterol is irrelevant? That high LDL-C is not a critical metric, and that high HDL-C and lower triglycerides are more important for heart health? And finally, that higher HDL-C and lower triglycerides are achievable, with weight loss, by eating low-carb, with fish oil supplementation (to lower triglycerides), and without taking statins?

Yes, it is, and when my doctor saw my most recent blood tests, including my lipid panel, he called me to tell me the results. He concluded, exultant: “You’re going to live to be 105!” Hmmm, I thought, that’s longer than Ancel Keys.

Retrospective #3: Ancel Keys and the Lipid Hypothesis

Ancel Keys, a prominent University of Minnesota physiologist who was keenly interested in diet and nutrition, was attending a medical conference in Rome in 1951 where he learned that “heart disease was rare in some Mediterranean populations who consumed a lower fat diet.” He noted, too, that “the Japanese had low fat diets and low rates of heart disease. He hypothesized from these observations that fat was the cause of heart disease.”¹ These observations and associations about dietary fat have since come to be known as the Lipid Hypothesis.

Just two years later, Keys, now convinced that dietary fat was the cause of heart disease, published his “Six Country Analysis” (1953), an epidemiological study. Years later, with his hypothesis now firmly entrenched, he published an updated version (Harvard University Press, 1980) as the “Seven Countries Study.” In this study Keys points out an association between dietary fat and mortality from heart disease. Critics pointed out then, and with increasing traction today, that Keys had data for 22 countries, but selected data from just 6 (later 7). As an example, Keys excluded France, a country with a high fat diet and low rates of heart disease. His detractors then and now claim that Keys had selected only data to support his hypothesis, and that that was bad science. Further, his was a retrospective analysis, not a prospective study, and thus did not prove causality. This distinction is an important and fundamental precept of scientific investigation, but one that is often overlooked by the media and lay public.

Meanwhile, the American Heart Association (AHA), founded in 1924 by cardiologists, had “re-invented” itself in 1948 as a fundraising organization. In 1956 their TV fundraiser on all three networks (that was all there was at the time) urged Americans to reduce their intake of total fat, saturated fat, and cholesterol. Then, when President Eisenhower had his first heart attack in 1958, the AHA recommended Americans eat “heart-healthy” margarine, corn oil, breakfast cereals and skim milk, a diet that the President (and millions of us) unhappily complied with.

Today, most “health-conscious” Americans still largely follow this diet, perhaps with the exception of margarine, which was basically a partially hydrogenated vegetable oil made with trans fats. We are now told, and I certainly agree, that trans fats are really bad for us.  But, we still (many of us) largely avoid eggs, butter, marbled beef and other fatty cuts of meat, and high-cholesterol-containing foods like liver and shrimp (and eggs, butter and cream!).

Meanwhile, by 1961 Ancel Keys was on the Board of the AHA, the AHA had adopted Keys’s low-fat diet, and Ancel Keys made the cover of Time Magazine under the banner “Diet and Health.” Fat became public health enemy #1.

That same year the famous Framingham Heart Study, another epidemiological study of 5209 people begun in 1949, noted that men under 50 with elevated serum (blood) cholesterol were at greater risk of heart disease. However, these men were also more likely to smoke, be overweight, not exercise, and, although not noted, have high blood sugar. These first three observations became the famous “risk factors” that, to this day, are the mantra of the the public health establishment, the medical community, and the media who trumpet it. Little noted was the finding that for men over 50 there was no association between elevated serum cholesterol and heart disease.

There were, of course, opposing voices in the medical community, including senior researchers at Rockefeller and Yale and the U. of Pennsylvania. They and others pointed out that elevated triglycerides (and low HDL) were associated with increased risk of heart disease and that low-fat, high-carbohydrate diets caused elevated triglycerides, but their findings were disregarded and their voices ignored. By 1972 the federal government’s WIC program only allowed skim or low-fat milk for kids over age 2. The die was cast. We had started down the road of government Dictocrats intervening in what we eat. Still more ominous interventions were to come. Stay tuned.

¹ The Timeline History of Heart Disease in this and succeeding columns draws heavily from a piece by the same title published by Diet Heart Publishing  at http://dietheartpublishing.com.

Retrospective #2: Nutrition 101: A Primer on the Fundamentals of Nutrition

Food has three principal nutrients, called Macronutrients. They are: Fat, Protein and Carbohydrate, hereafter sometimes referred to as “carbs.” All of the energy derived from food comes from these three components.

Foods also have non-caloric nutrients, namely vitamins and minerals, or Micronutrients, as well as water and ash. In addition, foods have essential but not yet well understood (or discovered) Phytochemicals, such as antioxidants.

The energy content of either a gram of protein or a gram of carbohydrate is four (4) calories. The energy of a gram of fat is nine (9) calories, making it thus more than twice as “dense” in calories as either protein or carbs. A gram of ethyl alcohol in an alcoholic beverage has seven (7) calories but, alas, no nutrient value, hence “empty” calories.

Most “sugar-free” candies and “energy bars” contain “sugar alcohol,” which does not elevate blood sugar levels, making them tempting to diabetics. They do, however, raise blood insulin levels, because the body senses sweet.

The total available energy of a food is therefore the sum of the products of the weight (in grams) times the calories per gram of each of its macronutrients. If you wanted to do the math (or use a software program) you could calculate how many calories of each macronutrient, and the total percentage energy in calories, are contained in each portion of food. But for this primer, it is only necessary to establish an understanding of the basic science.

If you are interested in healthy eating and a long life, you should be informed about the macronutrient distribution and balance of your diet. It was not so in the Paleolithic Era, referenced in the 1^st installment. It was then just about survival. It was through “survival of the fittest” and that we learned what to eat to be healthy and evolve.

Almost half a century ago in the U. S., some big-government advocates thought that heuristic learning (by trial and error) was fraught with too much risk. That’s when politicians and public health officials decided to get involved in establishing Dietary Goals (1977), and later Dietary Guidelines (1980) for Americans. The HHS/FDA created these standards and later the “Nutrition Facts” panel that is on all manufactured and processed food.

This is known today as the “Standard American Diet,” or SAD, for short, prophetically. It contains a “% daily value” (previously the “Recommended Daily Allowance”) for carbs, for an adult woman, of 300 grams (x 4 calories per gram = 1,200 calories, or a whopping 60% of a 2,000-calorie diet). The “daily value” for protein is 50g (x 4 = 200 calories or 10% of 2,000 kcal). And the “daily value” for fat is 65g (x 9 = 585 calories or +/- 30% of a 2,000 kcal. diet.

This means that our government currently, to this day, recommends that an American woman eat a diet comprised of 60% carbs, all of which break down to “sugars” in the blood. Simultaneously, beginning in 1980, most of us have become fatter, and many of us have become Type II diabetics (like me). Does anyone see a correlation here? Does anyone think maybe this is a vast public health experiment gone wrong? Many people now agree. It was a mistake.

But I don’t blame our doctors. For more than 50 years – longer than the entire time that virtually any doctor still in practice has been working – the prevailing wisdom passed down from the powers-that-be has wavered but little. The sources of information that the medical practitioner has relied on are, writ large, our public health officials and, derivatively, the practitioner’s medical community, through their specialty practice standards, medical journals and conventions, and the ubiquitous pharmaceutical salesperson. For the most part, practicing physicians were not trained much (if at all) in nutrition, except for basic biochemistry; they have had little time to “bone up” on an area that isn’t being pushed by big pharma because there is no money to be made in nutrition. So, I do not blame the clinician for treating symptoms of disease by prescribing medications. I sympathize with (most of) them. They are stuck in the status quo of the mainstream mantra and, and the dictates of government regulations, insurance, and reimbursement policies. They are unable to turn around in the face of these compelling drivers.

This suggests to me that it may be time for the patient to assume some responsibility and take charge of his (or her) own health.  What you eat is up to you. It’s in your hands. You can do it, if you take the trouble to “bone up.”

Retrospective #1: A Very Brief (and Necessarily Selective) History of Human Nutrition (and Dieting)

In the beginning, there were the hunters and the gatherers. In the History of Nutrition this was the Paleolithic Era, hence the Paleo Diet. In most cultures, men hunted and women and children gathered food as it was available to them. Early humans adapted to periods of feasting and starvation (fed and fasting states, in dieting terms).

We humans were of necessity omnivorous. It was a survival thing. We ate every part of the animals we were lucky or skilled enough to trap, club or impale. Every part of the animal (or fish), including the organ meats (offal), the blood, and even the marrow within the bone cavity, was eaten. Some of us still enjoy these foods today.

We also ate the things we could gather from in-season fruit trees and vines, and the leaves, roots and fungi that didn’t kill us. It was a trial and error thing. We learned that to survive we had to take risks, both in hunting and gathering, and to make the most of what was available. This is why children have a natural aversion or “distaste” for “new” foods and only increase the scope of what they will eat as they mature. Remember when you wouldn’t eat x – fill in the blank. For me, it was Brussels sprouts, which today I love, especially tossed in olive oil and roasted.

Then, as we became more “civilized” and gathered together for socialization and protection, we wandered about less. This undoubtedly fostered the beginnings of agriculture. We saw that cereal grains, that is, the seed heads of grasses such as corn, wheat, and rice, grew naturally where nature planted them. We reasoned, why wander about when we could plant our food supply and water and cultivate and harvest it where we lived? This also enabled us to build more permanent shelters and live in fertile places with good fresh water supplies and abundant game and vegetative life. We also learned that we could catch certain animals and domesticate them for a steady food supply as they multiplied naturally in captivity. Wunderbar! Surely, this was a milestone of human evolution.

Could life get any better? Perhaps. But, in the view of many students of these developments, this was also the beginning of mankind’s downfall, nutritionally speaking. It was the dawn of the onset of the age that was to bring us the dreaded Diseases of Civilization. It was the advent of the Neolithic Age, and it began about 10,000 years ago.

Fast forward to about 150 years ago. William Banting¹, in 1863 a retired London undertaker, wrote and published a 16-page pamphlet titled Letter on Corpulence – Addressed to the Public. In it, the 5-foot 5-inch, 200-pound Banting – surely a fat man – described a program of eating in which he “scrupulously avoided eating any…food that might contain either sugar or starch.” On Banting’s diet, he ate 5 or 6 ounces of meat or fish at each of three meals every day, together with a fair amount of wine and spirits, avoiding altogether “bread, milk, beer, sweets and potatoes.”  Banting lost about 50 pounds in 18 months. His pamphlet became a best seller in England and on the Continent.

William Banting credited his diet to William Harvey, an aural surgeon in London who had recently been to Paris where he had heard the great French physiologist Claude Bernard debate on diabetes. Voila! So, there you have it.

Now, fast forward again to about 50 years ago, to include the impact of the Industrial Revolution, the new roller-milling technology for making flour, trans-fat-loaded Crisco and “vegetable” oils made from soy beans and corn.  

On January 13, 1961, Ancel Keys, an assertive University of Minnesota physiologist (after whom WWII’s K-Rations were named), was on the cover of Time Magazine. Since the 30’s Keys had been interested in the influence of diet on health. His epidemiological work on the etiology of heart disease would later be published in his 2nd seminal tract, the “Seven Countries Study” (Harvard University Press, 1980). In it he advanced his hypothesis associating saturated fat and dietary cholesterol with heart disease. This was the genesis of the Diet-Heart (Lipid) Hypothesis.

Keys’ Lipid hypothesis led the nation and the world to the Low-Fat diet. Lamentably, the study was later discovered to have been “cherry picked.” It will be the subject of the third essay of this series, but first will be a primer for non-scientists (and physicians) on “The Basics of Nutrition: Macronutrients, Vitamins, Minerals and Phytochemicals.”

¹ “Prologue: A Brief History of Banting” from Gary Taubes’ Good Calories – Bad Calories, 2007, Alfred A. Knopf

Type 2 Nutrition #472: Is the Vedda Blood Sugar Remedy Credible?

A friend of 40 years, who used to follow my blog, thenutritiondebate.com, recently emailed me to ask, “Does the Vedda Blood Sugar Remedy have any credibility?” I’d never heard of Vedda before so I looked it up. It’s a Sri-Lanka herbal product and diet program that’s being promoted here in a new book.

The website Contra Health Scam says the Vedda Blood Sugar Remedy is a scam. Quoting from their conclusion, “Vedda Blood Sugar Remedy is nothing but a well-produced scam, complete with paid actors, stock photos, stock videos, twisted scientific studies and outright lies.” So, I sent the link to my friend and suggested instead that he look up the Virta Health program (see the name similarity?) for managing his weight and blood sugar.

My friend thanked me and later emailed me, “The Keto rage sure evidences your research! The weight loss results are phenomenal. This is totally counter to the food pyramid we grew up with, or Michelle Obama’s new school she tried to promote.” I replied, “Yes, that’s all true,” and asked if he would like to be added back to my distribution list.” He replied, “Yes, I am definitely still struggling to get to my goal weight. Thanks.”

Later, while working in the garden I got to thinking about this “conversation.” I found it very depressing. I’ve been proselytizing about how to manage weight and blood sugar about ten years and have written almost 500 columns (472 published with this one), and even my long-time friends (and my own wife!) pay no attention to me. How frustrating is that? So, I told my wife about the conversation and she said, “You have no bona fides.”

I understood what she meant, of course. I’m not a medical doctor. But, with exasperation, I replied, I have personally lost 170 pounds (and maintained most of the loss) BY DIET ALONE, WITHOUT EXERCISE, AND WITHOUT HUNGER. Not only that but I have turned my diabetes health around, from a progressively worsening disease to the point where, from a clinical standpoint, I am “cured,” and in complete remission.

In addition, my lipid (cholesterol) profile is also completely reversed, I’m no longer on a statin, my blood pressure is “normal” (with meds), and my inflammation non-existent (hsCRP ≤1.0). I am so full of energy and so much healthier and happier than I was 17 years ago when my doctor first suggested I try a Very Low Carb diet to lose weight. He didn’t call it LCHF or Keto, but that is what is was and IT WORKS!

So, it seems, my personal example only works for me – “you’re not like other people,” my wife says – until you read somewhere in the mass media about “the Keto rage” with “weight loss results [that] are phenomenal.” And then you realize that it’s “totally counter to the food pyramid we grew up with,” the one our government has been promoting for more than half a century.

My wife said I should be grateful that my friend has come back into the fold. I said I was, but still, I was stunned at the resistance of some people…by which I mean most people, not my friend in particular…to rational change. We just don’t want to change, until perhaps we reach a tipping point in our personal life. For me it was the shock of learning that I weighed 375 pounds. My doctor’s scale only went to 350, so one morning before an appointment, I stopped at the Fulton Fish Market in New York City and weighed myself on a commercial scale. I thought I was going to die. I looked around and I didn’t see any really fat, old people. I didn’t want to die.

What will it take for you? What combination of fear, courage, and a glimmer of a chance that changing your diet could work? That it might be easy to lose weight and improve all the markers associated with death?

What will it take for you to realize you became overweight because of what, you ate? To realize the way to reverse that condition is to change what you eat – to eat in a way “totally counter to the food pyramid we all grew up with,” that we’ve been following our whole lives and that got us into this mess in the first place. Think about it. If that’s what it takes, then maybe you’ll become a follower too, and we can grow old together…