The emphasis in the previous installment was on the role of insulin as the transport vehicle for glucose in the bloodstream. Insulin has an equally important role in fat accumulation (synthesis and storage) which relates to obesity. Insulin must be in the bloodstream whenever there are elevated levels of glucose present. Insulin transports the glucose to the cells for energy, and at the same time acts to block the breakdown and entry of energy from stored fat into the bloodstream. The reason is this: The body prefers to burn glucose as a quick and readily available source of energy. So, if glucose energy is available, that is, if we can eat it (any/all sugars and starches), or the body can find it (glycogen) in storage, or synthesize it (by gluconeogenesis) in the liver, the body will do that. If there is energy available from any one of these sources, then there is no need for energy from fat. So, the fat stays locked up in storage, awaiting famine, as in Paleolithic times.
The fat in storage in our bodies, as well as the fat we eat, is in the form of triglyceride molecules. A triglyceride molecule is comprised of three fatty acid molecules linked to one glycerol molecule. The triglyceride molecule is too big to get into the blood stream intact. Lipolysis is the breakdown of fat molecules. When the protein lipase in the adipose tissue is activated by any of numerous hormones, the triglyceride molecule breaks down into its component parts and the fatty acids are released into the blood and are then available for cellular uptake. Ketone bodies, produced as a byproduct, and the glycerol molecule, are used for energy too. This process occurs at night during an overnight fast and is called ketosis.
So, to summarize and repeat: We can’t be a fat burner and a sugar burner at the same time. Our body prefers to burn sugar (glucose) and will do so as long as 1) we eat things that will break down into glucose (all sugars and all carbohydrate foods), or 2) we have glucose stored (as glycogen) in the liver and the muscles, or 3) the liver can make glucose from excess amino acids (stored in the liver) from eating too much protein. 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) will be accumulated as body fat (by de novo lipogenesis), instead of broken down and burned for energy. That is why we get fat. We’re living on refined sugars and starches, and saving our fat (and accumulating more) for “hard times.”
This is particularly easy for us to do today - get fat – by eating a so-called “balanced” diet that is heavily skewed towards carbohydrates (see installment #2 at http://danbrown-thenutritiondebate.blogspot.com). And we’ve done this to avoid dietary fats, and particularly saturated fats and dietary cholesterol that we’ve been told erroneously are bad for us. The low fat diet was supposed to protect us from “killer diseases” like heart disease, stroke and cancer; today there is little evidence that it provides protection and mounting evidence that limiting fats in the diet may do more harm than good. Obesity is the precursor (but not necessarily a requisite) condition for Metabolic Syndrome and other Diseases of Civilization, including many cancers.
A couple of years ago a New York Times page -one story reported on a new treatment modality being recommended for patients presenting with hypertension, hypercholesterolemia, and Type 2 diabetes or prediabetes 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 “prescription” of “diet and lifestyle changes,” meaning a restricted-calorie, balanced diet and more exercise.) The new paradigm they recommended was a “workaround” using just pharmacological solutions. High blood pressure and high cholesterol both respond to medications. And many more new medications are now available for Type 2 diabetes.
Unfortunately, this solution often results in the pre-diabetic developing full-blown Type 2 diabetes (25% within 3-5years) and the diabetic patient getting progressively worse until they become insulin dependent (multiple daily injections!) and eventually develop one of the complications or co-morbidities, from which they will most likely -- almost assuredly, die.
Gary Taubes’s new book, “How We Get Fat: And What to Do About It” (Knopf, 2010), offers a different approach. I can’t wait to see how well this more “accessible” book is received, both by the medical community and the lay public.
© Dan Brown 2/13/11
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Wednesday, February 16, 2011
Tuesday, February 15, 2011
The Nutrition Debate #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 most recently reinforced by the release on 1/31/11 of the “revised” “Dietary Guidelines for Americans, 2010.” This was at a joint press conference held by the Secretaries of the USDA and the HHS, both former farm state governors. It also means that you probably haven’t read, or certainly haven’t accepted, the Alternative Interpretation of the Energy In – Energy Out formulation explained in Installment #5 in this series. (To see previously published installments, go to http://danbrown-thenutritiondebate.blogspot.com.) It flat-out refutes the Lipid Hypothesis.
Gary Taubes, in his serious and rather heavy read, “Good Calories – Bad Calories,” introduced in Installment #4, makes the case convincingly. In number 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” (emphasis added by me). The “obesity is a disorder of excess fat accumulation” is not a tautology; the operative word here is “disorder.” Why do we accumulate (synthesize and store) fat rather than break down and burn (catabolize and oxidize) the fat calories we eat? What drives our hunger to the point of eating too much and too often? The answer, according to Taubes, is carbohydrates.
All of Taubes’s ten “certain conclusions” merit rereading now and again (see Installment #4 in the archives), 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 starches, 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. The digestive process continues in the stomach where acids assist in starting to break down all the sugars and starches. 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 and then, with glucose, declines in level in the blood.
Thus, the primary function of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with impaired glucose tolerance and/or insulin resistance. These impairments are the first signs, often undetected and overlooked, of the metabolic disorder called pre-diabetes.
Until recently, the fasting blood glucose test was the most common test for diagnosing pre-diabetes. The diagnosis was confirmed with a more difficult and expensive test, called the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year, however, there has been a change in protocols, and now a test called the Hb A1c, or simply the A1c, is becoming the norm.
In addition, the diagnostic standard for Type 2 Diabetes Mellitus has been lowered, from 7.0 to 6.5, and to 6.0 for pre-diabetes. Some physicians set a much lower standard. Dr. Richard K. Bernstein, himself a Type 1 diabetic and a pioneer in blood test monitoring to achieve “normal” blood sugars, uses an A1c of 5.8 to diagnose full-blown Type 2 diabetes. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks after eating, that is, post-prandial. This can be done at home on your own schedule, no appointment required. Just eat to the meter.
In the next installment, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When the regulation of this hormone is out of balance, the result is fat synthesis and accumulation. We get fat. We’ll explain next.
© Dan Brown 2/6/11
Gary Taubes, in his serious and rather heavy read, “Good Calories – Bad Calories,” introduced in Installment #4, makes the case convincingly. In number 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” (emphasis added by me). The “obesity is a disorder of excess fat accumulation” is not a tautology; the operative word here is “disorder.” Why do we accumulate (synthesize and store) fat rather than break down and burn (catabolize and oxidize) the fat calories we eat? What drives our hunger to the point of eating too much and too often? The answer, according to Taubes, is carbohydrates.
All of Taubes’s ten “certain conclusions” merit rereading now and again (see Installment #4 in the archives), 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 starches, 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. The digestive process continues in the stomach where acids assist in starting to break down all the sugars and starches. 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 and then, with glucose, declines in level in the blood.
Thus, the primary function of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with impaired glucose tolerance and/or insulin resistance. These impairments are the first signs, often undetected and overlooked, of the metabolic disorder called pre-diabetes.
Until recently, the fasting blood glucose test was the most common test for diagnosing pre-diabetes. The diagnosis was confirmed with a more difficult and expensive test, called the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year, however, there has been a change in protocols, and now a test called the Hb A1c, or simply the A1c, is becoming the norm.
In addition, the diagnostic standard for Type 2 Diabetes Mellitus has been lowered, from 7.0 to 6.5, and to 6.0 for pre-diabetes. Some physicians set a much lower standard. Dr. Richard K. Bernstein, himself a Type 1 diabetic and a pioneer in blood test monitoring to achieve “normal” blood sugars, uses an A1c of 5.8 to diagnose full-blown Type 2 diabetes. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks after eating, that is, post-prandial. This can be done at home on your own schedule, no appointment required. Just eat to the meter.
In the next installment, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When the regulation of this hormone is out of balance, the result is fat synthesis and accumulation. We get fat. We’ll explain next.
© Dan Brown 2/6/11
Friday, February 4, 2011
The Nutrition Debate #9: Metabolic Syndrome, the American Disease of Civilization
What exactly is Metabolic Syndrome and how is it diagnosed? There are several definitions but most have five “risk factors” in common, with the first always being obesity. It is variously defined as “central obesity” (what I have coined “omental adiposity”), or a Body Mass Index (BMI) ≥30, or 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).
Metabolic Syndrome is just one of a larger class of disorders that have become known as the Diseases of Civilization. Metabolic Syndrome, because it is increasingly affecting Westernized populations at younger and younger ages, especially in the last fifty years, is more closely identified with diet and lifestyle factors. Gary Taubes (of “Good Calories-Bad Calories” fame) and many others, including (most humbly) me, identify Metabolic Syndrome primarily, I would say exclusively, with diet alone. To support this assertion, let’s look at some statistics of how the Western, and specifically the American diet, has changed in modern times. Granted, these are also only associations -- not causal relationships – and so need to be closely examined.
Annual sugar consumption in the US is now in excess 160 pounds per capita, and most of that is 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 it molasses, according to the Diet Heart Publishing timeline cited in Installment #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. Today, highly processed soybean oil has 70% of the market, and zero vitamin D. And, again as the Diet Heart Publishing timeline points out, “now the experts who told us not to eat lard 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 dangers of margarine have become 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 is becoming, indeed has become, the American Disease of Civilization and it is associated with a long list of related conditions, known as 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 cardio vascular 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 double the risk. In fact, over 50% of deaths in patients with type 2 diabetes are due to CVD. People with Metabolic Syndrome have a significantly greater risk of CVD, particularly men over age 45 and women over 55. These people also have a fivefold risk of developing type 2 diabetes.
Metabolic Syndrome, a growing and commonly silent condition, thus poses a significant public health threat. Left unchecked, it will have a staggering effect on healthcare in the United States in the years ahead. So, what can be done to check this “epidemic”? If overweight and obesity is the common risk factor, then we have to ask, why do we get fat?
© Dan Brown 1/30/11
Metabolic Syndrome is just one of a larger class of disorders that have become known as the Diseases of Civilization. Metabolic Syndrome, because it is increasingly affecting Westernized populations at younger and younger ages, especially in the last fifty years, is more closely identified with diet and lifestyle factors. Gary Taubes (of “Good Calories-Bad Calories” fame) and many others, including (most humbly) me, identify Metabolic Syndrome primarily, I would say exclusively, with diet alone. To support this assertion, let’s look at some statistics of how the Western, and specifically the American diet, has changed in modern times. Granted, these are also only associations -- not causal relationships – and so need to be closely examined.
Annual sugar consumption in the US is now in excess 160 pounds per capita, and most of that is 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 it molasses, according to the Diet Heart Publishing timeline cited in Installment #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. Today, highly processed soybean oil has 70% of the market, and zero vitamin D. And, again as the Diet Heart Publishing timeline points out, “now the experts who told us not to eat lard 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 dangers of margarine have become 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 is becoming, indeed has become, the American Disease of Civilization and it is associated with a long list of related conditions, known as 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 cardio vascular 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 double the risk. In fact, over 50% of deaths in patients with type 2 diabetes are due to CVD. People with Metabolic Syndrome have a significantly greater risk of CVD, particularly men over age 45 and women over 55. These people also have a fivefold risk of developing type 2 diabetes.
Metabolic Syndrome, a growing and commonly silent condition, thus poses a significant public health threat. Left unchecked, it will have a staggering effect on healthcare in the United States in the years ahead. So, what can be done to check this “epidemic”? If overweight and obesity is the common risk factor, then we have to ask, why do we get fat?
© Dan Brown 1/30/11
Wednesday, February 2, 2011
The Nutrition Debate #8: Epidemiologically Speaking: Patterns of Health and Illness
The dreaded Diseases of Civilization were first referenced in Installment #1 in this series. (See previously published installments archived at http://danbrown-thenutritiondebate.blogspot.com.) We began on that track about 10,000 years ago with the advent of agriculture, marking the transition from the Paleolithic era to the Neolithic. The nomadic hunter-gatherer discovered he could lead a more stationary existence on a diet largely comprised of cereal grains. This was a major shift in the human dietary. In the latter half of the last century this shift greatly accelerated. Today, many believe that this shift alone accounts for the emergent patterns of illnesses and medical disorders with which we are now beset.
In modern times, epidemiologists, who by definition look for 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 dietary of the industrialized world.
Epidemiology, however, 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. “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” (emphasis added by me), according to the Wikipedia entry.
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 1970, 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 make educated, informed assertions. This in turn led to the AHA’s now well-known “risk factors,” the McGovern Report’s “Dietary Goals” and the now infamous (to me) “Dietary Guidelines for Americans” (see Installments #2 & #3). The latest of these guidelines were due to be finalized by HHS/USDA in December 2010 as I wrote this.
All of these “prescriptions” dispensed to the consumer “with an interest in eating” were still, however, nothing more than simple hypotheses and assertions. Hypotheses must be tested and retested by randomized controlled trials to produce and independently reproduce similar outcomes, and if they don’t, they must be rejected as false. There have been many large, lengthy 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, other aspects of the so-called Western diet, and in particular the specific dietary recommendations I have previously referred to as the Standard American Diet (SAD), which is 60% carbohydrate, have increasingly come to infer a causal relationship with various diseases and metabolic disorders. Chief among these is the Metabolic Syndrome.
The Metabolic Syndrome is relatively new on the scene and was first recognized in 1988 when it was mysteriously named Syndrome X. The Metabolic Syndrome, again according to Wikipedia, “is 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. Some studies estimate the prevalence in the USA to be up to 25% of the population.” A recent CNBC.com story from Reuters, posted on 11/23/10, is headlined, “Half of Americans Facing Diabetes by 2020.” The lead-in then clarifies the headline as follows: “More than half of Americans will have diabetes or be prediabetic by 2020…” That is a daunting (and expensive) prospect.
In the next installment we’ll learn the clinical definition of Metabolic Syndrome and how is it diagnosed.
© Dan Brown 1/23/11
In modern times, epidemiologists, who by definition look for 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 dietary of the industrialized world.
Epidemiology, however, 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. “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” (emphasis added by me), according to the Wikipedia entry.
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 1970, 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 make educated, informed assertions. This in turn led to the AHA’s now well-known “risk factors,” the McGovern Report’s “Dietary Goals” and the now infamous (to me) “Dietary Guidelines for Americans” (see Installments #2 & #3). The latest of these guidelines were due to be finalized by HHS/USDA in December 2010 as I wrote this.
All of these “prescriptions” dispensed to the consumer “with an interest in eating” were still, however, nothing more than simple hypotheses and assertions. Hypotheses must be tested and retested by randomized controlled trials to produce and independently reproduce similar outcomes, and if they don’t, they must be rejected as false. There have been many large, lengthy 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, other aspects of the so-called Western diet, and in particular the specific dietary recommendations I have previously referred to as the Standard American Diet (SAD), which is 60% carbohydrate, have increasingly come to infer a causal relationship with various diseases and metabolic disorders. Chief among these is the Metabolic Syndrome.
The Metabolic Syndrome is relatively new on the scene and was first recognized in 1988 when it was mysteriously named Syndrome X. The Metabolic Syndrome, again according to Wikipedia, “is 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. Some studies estimate the prevalence in the USA to be up to 25% of the population.” A recent CNBC.com story from Reuters, posted on 11/23/10, is headlined, “Half of Americans Facing Diabetes by 2020.” The lead-in then clarifies the headline as follows: “More than half of Americans will have diabetes or be prediabetic by 2020…” That is a daunting (and expensive) prospect.
In the next installment we’ll learn the clinical definition of Metabolic Syndrome and how is it diagnosed.
© Dan Brown 1/23/11
Monday, January 31, 2011
The Nutrition Debate #7: Are you a “Sugar Burner” or a “Fat Burner”?
A restricted-calorie, balanced diet we have learned is a “starvation diet.” They don’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 eventually overrules your will power. The result: you shovel more energy in! The problem, of course, is that you are not letting your body get the energy it needs from the body fat you have stored for this purpose.
This would be a good time to go back and re-read Gary Taubes’s 10 “certain conclusions” in installment #4 in this series. If you didn’t save it, I have begun a Blog on Google’s Blogger site to post installments in this series after they are published. The URL is http://danbrown-thenutritiondebate.blogspot.com. A Google search using the URL in the Internet Explorer (IE) search engine works. I understand that a search in the Firefox browser or the Google Chrome search engine will also bring it up. When you find it, pay special attention to conclusions 2, 8, 9 and 10.
Now, let’s get back to The Nutrition Debate. The food we eat, when digested, is rapidly 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 which break down most rapidly are said to have a high glycemic index, a term now familiar to us all.
The body prefers to use sugar and starches for energy because most of them are quick and easy to break down and burn. 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 followed by a similarly precipitous “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 glucose (more sugars and starches) to supply more quick energy (in the form of glucose) to the blood stream. It’s not signaling for protein or fat. It wants sugary foods and carbs that quickly become sugar (glucose) in the bloodstream. Some starch, like white bread, actually digest more quickly (have a higher glycemic index) than table sugar (sucrose)!
When you eat a diet that is largely comprised of carbohydrates, such as the Standard American Diet (SAD) which is 60% carbohydrate (see installment #2), you are, in metabolic slang, a “sugar burner.” You may eat healthy proteins and fats too, but your body is running on glucose and storing fat. It calls for you to eat more carbs 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 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 your adipose tissue. The protein, which 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. Beyond that, they can’t be utilized by the body so they are sent to the liver where they are stored. Later, when there is a low blood sugar signal, the liver will reconstitute these amino acids (from the excess protein) as glucose, through a process of gluconeogenesis. And, as we know, the body uses glucose as its preferred source of energy, after stored carbs and before stored fat.
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 us fatter, and sicker? And, if you need to lose weight, how do you become a “fat burner?” I think you know by now where I am going with this, but in the next installment I will first tell you something of the consequences of the dietary program our leaders have advocated and we have now been mainstreaming for the last fifty years. It is the story of one of the Diseases of Civilization, first described as Syndrome X and now more commonly known as the Metabolic Syndrome.
© Dan Brown 1/16/11
This would be a good time to go back and re-read Gary Taubes’s 10 “certain conclusions” in installment #4 in this series. If you didn’t save it, I have begun a Blog on Google’s Blogger site to post installments in this series after they are published. The URL is http://danbrown-thenutritiondebate.blogspot.com. A Google search using the URL in the Internet Explorer (IE) search engine works. I understand that a search in the Firefox browser or the Google Chrome search engine will also bring it up. When you find it, pay special attention to conclusions 2, 8, 9 and 10.
Now, let’s get back to The Nutrition Debate. The food we eat, when digested, is rapidly 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 which break down most rapidly are said to have a high glycemic index, a term now familiar to us all.
The body prefers to use sugar and starches for energy because most of them are quick and easy to break down and burn. 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 followed by a similarly precipitous “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 glucose (more sugars and starches) to supply more quick energy (in the form of glucose) to the blood stream. It’s not signaling for protein or fat. It wants sugary foods and carbs that quickly become sugar (glucose) in the bloodstream. Some starch, like white bread, actually digest more quickly (have a higher glycemic index) than table sugar (sucrose)!
When you eat a diet that is largely comprised of carbohydrates, such as the Standard American Diet (SAD) which is 60% carbohydrate (see installment #2), you are, in metabolic slang, a “sugar burner.” You may eat healthy proteins and fats too, but your body is running on glucose and storing fat. It calls for you to eat more carbs 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 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 your adipose tissue. The protein, which 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. Beyond that, they can’t be utilized by the body so they are sent to the liver where they are stored. Later, when there is a low blood sugar signal, the liver will reconstitute these amino acids (from the excess protein) as glucose, through a process of gluconeogenesis. And, as we know, the body uses glucose as its preferred source of energy, after stored carbs and before stored fat.
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 us fatter, and sicker? And, if you need to lose weight, how do you become a “fat burner?” I think you know by now where I am going with this, but in the next installment I will first tell you something of the consequences of the dietary program our leaders have advocated and we have now been mainstreaming for the last fifty years. It is the story of one of the Diseases of Civilization, first described as Syndrome X and now more commonly known as the Metabolic Syndrome.
© Dan Brown 1/16/11
Saturday, January 29, 2011
The Nutrition Debate #6: “Energy In = Energy Out”: An Alternative Interpretation
The one universally held truth in our understanding of human metabolism is the Energy Equation: Energy In = Energy Out. It is accepted by most doctors, even some medical researchers, and universally by the popular press and the entire general public. Why? Because it is so easy to understand, and it’s just plain good “common sense.”
It also gains gravitas by its association with one of the basic laws of science, the First Law of Thermodynamics, paraphrased here just a bit: “the net (energy) supplied to the system equals the net work done by the system.” Who can argue with that? You’d have to be some kooky doctor or maverick scientist to even try, and you would be laughed at all the way to (and in) the grave (viz: Atkins).
Okay. I’m crazy enough to try. I get the courage because Gary Taubes, in his seminal opus “Good Calories – Bad Calories” introduced in the last installment, makes the argument convincingly for me. So, with apologies to him for any errors in my understanding, I will attempt to regurgitate his explanation here to help convey his Alternative Interpretation of this immutable law of thermodynamics, as applied to the Energy In = Energy Out formulation for weight control.
The problem with the conventional interpretation of the Energy In = Energy Out formula is that it measures “energy in” and “energy out” in the wrong place, i. e., exclusively outside the body, as something done to the body. Thus, the common-sense, universally accepted understanding is as follows: Energy In (food ingested) = Energy Out (basal metabolism plus the added energy expenditure of activities, including exercise). Therefore, to lose weight (“improve” the energy balance) you must restrict calories (i.e., reduce “energy in”) and exercise more (increase energy expended, i.e., “energy out”). Sound familiar? Of course! It’s the ubiquitous “diet and exercise” prescription. This interpretation of how the Energy Equation works, that is, where to measure “energy in” and “energy out,” is fundamentally wrong. Here’s why.
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. There, “Energy In” is the sum of the products of digestion and absorption (of nutrients from foods eaten), plus “quick” energy from food previously eaten, digested and stored (primarily as glycogen in the liver and muscles), and lipolysis, the breakdown and then oxidation (burning) of the body’s own fat cells. Thus, the source of our energy in the blood stream (the “energy in” or left side of the equation) is basically three-fold: 1) the small intestine (where digested food is absorbed into the blood stream), 2) stored carbohydrate energy (glycogen) available to the blood stream from the liver and muscles, and 3) our adipose tissue (fat cells, or triglyceride molecules), which, if allowed to break down, can move into the blood stream and contribute to “energy in.” Particularly take note of this last additional source on the “energy in” side of the equation, and the very important conditional aspect of it.
Thus, the body balances the equation itself, through complex signals from various hormones, putting on the right side of the equation however much energy it needs for our basal metabolism plus what our activity level requires. It uses the first two sources on the left side of the equation (food eaten and carbs stored), and then, providing it is “free” to take it, energy from the third source: it uses our fat cells for energy. This last energy source, however, is conditional and absolutely critical. This source of “energy in” is the critical difference that 1) avoids the starvation diet aspect of conventional restricted calorie but balanced diet programs, 2) prevents that always hungry feeling, including cravings and the need for between meal snacks, 3) gives the body all the energy it needs, avoiding that drained, and weak feeling that people get from balanced, starvation diets. It is also an easy way to lose weight (body fat) and keep it off, if you stay with it, for life.
When understood from this perspective, and with some additional insights from our knowledge of the macronutrient components of the foods we eat, and the key role of the hormone insulin, we can gain an understanding of how to use all three sources on the “Energy In” side of the equation to meet our body’s total requirements for “Energy Out.” In the next installment we’ll discuss what “free to use it” means, and how the mechanism works.
© Dan Brown 1/9/11
It also gains gravitas by its association with one of the basic laws of science, the First Law of Thermodynamics, paraphrased here just a bit: “the net (energy) supplied to the system equals the net work done by the system.” Who can argue with that? You’d have to be some kooky doctor or maverick scientist to even try, and you would be laughed at all the way to (and in) the grave (viz: Atkins).
Okay. I’m crazy enough to try. I get the courage because Gary Taubes, in his seminal opus “Good Calories – Bad Calories” introduced in the last installment, makes the argument convincingly for me. So, with apologies to him for any errors in my understanding, I will attempt to regurgitate his explanation here to help convey his Alternative Interpretation of this immutable law of thermodynamics, as applied to the Energy In = Energy Out formulation for weight control.
The problem with the conventional interpretation of the Energy In = Energy Out formula is that it measures “energy in” and “energy out” in the wrong place, i. e., exclusively outside the body, as something done to the body. Thus, the common-sense, universally accepted understanding is as follows: Energy In (food ingested) = Energy Out (basal metabolism plus the added energy expenditure of activities, including exercise). Therefore, to lose weight (“improve” the energy balance) you must restrict calories (i.e., reduce “energy in”) and exercise more (increase energy expended, i.e., “energy out”). Sound familiar? Of course! It’s the ubiquitous “diet and exercise” prescription. This interpretation of how the Energy Equation works, that is, where to measure “energy in” and “energy out,” is fundamentally wrong. Here’s why.
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. There, “Energy In” is the sum of the products of digestion and absorption (of nutrients from foods eaten), plus “quick” energy from food previously eaten, digested and stored (primarily as glycogen in the liver and muscles), and lipolysis, the breakdown and then oxidation (burning) of the body’s own fat cells. Thus, the source of our energy in the blood stream (the “energy in” or left side of the equation) is basically three-fold: 1) the small intestine (where digested food is absorbed into the blood stream), 2) stored carbohydrate energy (glycogen) available to the blood stream from the liver and muscles, and 3) our adipose tissue (fat cells, or triglyceride molecules), which, if allowed to break down, can move into the blood stream and contribute to “energy in.” Particularly take note of this last additional source on the “energy in” side of the equation, and the very important conditional aspect of it.
Thus, the body balances the equation itself, through complex signals from various hormones, putting on the right side of the equation however much energy it needs for our basal metabolism plus what our activity level requires. It uses the first two sources on the left side of the equation (food eaten and carbs stored), and then, providing it is “free” to take it, energy from the third source: it uses our fat cells for energy. This last energy source, however, is conditional and absolutely critical. This source of “energy in” is the critical difference that 1) avoids the starvation diet aspect of conventional restricted calorie but balanced diet programs, 2) prevents that always hungry feeling, including cravings and the need for between meal snacks, 3) gives the body all the energy it needs, avoiding that drained, and weak feeling that people get from balanced, starvation diets. It is also an easy way to lose weight (body fat) and keep it off, if you stay with it, for life.
When understood from this perspective, and with some additional insights from our knowledge of the macronutrient components of the foods we eat, and the key role of the hormone insulin, we can gain an understanding of how to use all three sources on the “Energy In” side of the equation to meet our body’s total requirements for “Energy Out.” In the next installment we’ll discuss what “free to use it” means, and how the mechanism works.
© Dan Brown 1/9/11
Friday, January 28, 2011
The Nutrition Debate #5: Gary Taubes and the Alternative Hypothesis
Gary Taubes first came to my attention as a result of the New York Times Sunday Magazine cover story of July 7, 2002, entitled, “What If It’s All A Big Fat Lie?” Taubes has 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 way of eating. I didn’t know it at the time, but my doctor, an internist/cardiologist, had read the article and tried such a diet himself to lose weight. He succeeded and recommended that I try low carb eating too, also to lose weight. As an afterthought, he said, “By the way, it will probably help your Type 2 diabetes.” Boy, was he ever right about that!
Following the publication of his 2002 NYT article, 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 produce 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 very dense read, but getting through it is well worth the slog. In the end, in the Epilogue (pages 453-454), he proffers 10 “certain conclusions,” which I present in full below.
“As I emerge from the research, though, 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 “Good Calories – Bad Calories” twice, and re-read Taubes’s “certain conclusions” at least 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 a little more accessible to the general public. Gary Taubes’s “Why We Get Fat: And What to Do About It” was published by Alfred Knopf last week (December 28, 2010). I’ve pre-ordered a bunch. Hardcover: $24.95. Amazon (hardcover): $13.41.The Kindle (Amazon) eBook edition is $9.99.
Next installment: The “Energy In – Energy Out” theorem: an alternate interpretation.
© Dan Brown 1/2/11
Following the publication of his 2002 NYT article, 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 produce 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 very dense read, but getting through it is well worth the slog. In the end, in the Epilogue (pages 453-454), he proffers 10 “certain conclusions,” which I present in full below.
“As I emerge from the research, though, 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 “Good Calories – Bad Calories” twice, and re-read Taubes’s “certain conclusions” at least 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 a little more accessible to the general public. Gary Taubes’s “Why We Get Fat: And What to Do About It” was published by Alfred Knopf last week (December 28, 2010). I’ve pre-ordered a bunch. Hardcover: $24.95. Amazon (hardcover): $13.41.The Kindle (Amazon) eBook edition is $9.99.
Next installment: The “Energy In – Energy Out” theorem: an alternate interpretation.
© Dan Brown 1/2/11
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