I’ve been avoiding this topic because I was afraid I was going to learn “the bitter truth” as I researched and studied synthetic sweeteners. You may feel the same way after learning about them. But increasing public awareness about human nutrition and health issues is why I write this column, so here goes.
An artificial sweetener is a food additive that is not natural and that duplicates the effect of sugar (sucrose) in taste, texture and “mouthfeel.” The primary compounds used as sugar substitutes in the United States are sucralose (e.g., Splenda), aspartame (e.g., Equal, NutraSweet), and saccharin (e.g., Sweet’n Low). The good news is none of these products contain any fructose. The bad news: 1) the little yellow, blue and pink packets all contain bulking agents which are mostly sugars, and 2) the effect on the body’s hormonal system of a high-intensity artificial sweetener is as bad or worse than “natural” sugar, as in refined sugar cane, even allowing that cane sugar is 50% fructose!
Not a big deal? You say it’s just a little. Not so. Splenda, for example, is usually just 5% high-intensity artificial sweetener (sucralose) and 95% bulking agents, specifically dextrose (D-glucose) and maltodextrin, a polysaccharide containing from 3 to 20 glucose molecules in a chain. The body easily and quickly metabolizes both of these sugars as energy, while most (85% to 95%) of the non-nutritive sucralose passes unchanged out of the body through the feces or, after some is absorbed into the blood, through the kidneys as urine. Reviewing then, that’s 5% non-nutritive sweetener and 95% nutritive sweeteners, all basically absorbed and metabolized as glucose.
How much energy are we talking about in the 95% part? Each 1 gram packet of Splenda contains almost a gram of carbohydrate (3.36 calories). That compares to 10.8 calories in a 2.8 gram packet of sugar, 15 calories in a level teaspoon of table sugar or 25 calories in a heaping teaspoon. The 5% sucralose part is non-nutritive (zero calories), but sucralose, the artificial “sugar,” is about 600 times sweeter than sucrose (table sugar). That’s a lot of sweetness.
Is this important? If you’re diabetic or pre-diabetic and need to limit or restrict sugars, then “sure.” We know that glucose induces an insulin response, and we are trying not to wear out our pancreas which produces insulin. There is in addition, however, also the well-established scientific fact that the taste of sweetness, perceived in the mouth by the salivary glands, induces an insulin response. As such, even a high-intensity artificial sweetener that contains no glucose (I know of none) would induce an insulin response. Chronic high insulin levels in the blood (hyperinsulinemia), which occurs when there is little glucose to transport, leads to insulin resistance, and eventually to Metabolic Syndrome and Type 2 diabetes. Wide use of artificial sweeteners, in this respect, could be worse for your health than real sugar.
An Equal packet, containing the artificial sweetener aspartame, is made with dextrose (D-glucose), acesulfame potassium, starch, silicon dioxide, maltodextrin and an unspecified flavoring. Equal tablets contain the sugar lactose.
Sweet’n Low is a compound of granulated saccharin, dextrose and cream of tartar. In Canada, Sweet’n Low is made from sodium cyclamate because saccharin has been banned there since the 70’s. In the U. S., cyclamate was banned in 1970.
A similar and closely related sugar substitute is a natural sweetener from the herb stevia. Four years ago Cargill and the Coca Cola Company introduced the stevia-based product Truvia. It is made from rebiana, an extract of stevia, pus erythritol, a sugar alcohol, and natural flavors. More recently, Pepsico and the Whole Earth Sweetener Company introduced PureVia. It contains the stevia extract, plus dextrose, cellulose powder and natural flavors. These extracts are relatively new to the market and are used both as tabletop sweeteners and as food ingredients, especially in beverages.
Other natural sweeteners include the sugar alcohols. Maltitol and sorbitol are often used in tooth paste, mouth wash, and in foods such as “no sugar added” ice cream. Erythritol is gaining momentum as a replacement for these other two sugar alcohols in foods as it is much less likely to produce gastrointestinal distress when consumed in large amounts. Xylitol is an especially non-fermentable sugar alcohol that is tooth friendly and is used in chewing gum. Possessing approximately 40% less food energy than sucrose, xylitol is another low-calorie alternative to table sugar.
So, the bitter truth is “there’s no such thing as a free lunch.” Bitter is better. (Butter is better too.) Weaning myself off Splenda isn’t going to be easy. I take it in my coffee and in my iced tea every day. But bitter will be better for my health.
© Dan Brown 11/20/11
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Sunday, November 20, 2011
Sunday, November 13, 2011
The Nutrition Debate #31: Carbohydrates and Sugars
Are all carbohydrates sugars? Are all sugars carbohydrates? What is a carbohydrate? And what is a sugar? This is not chemistry class, but I think we all need to know the answers to these basic questions if we are going to guard our health. So, I’ll try to keep it simple and interesting. After all, we all have to eat, and making wise choices requires us to be well informed. There’s a lot of misinformation going around so listen up.
All carbohydrates are saccharides. The word saccharide comes from the Greek word meaning sugar. Carbohydrates are divided into four types: monosaccharides, disaccharides, oligosaccharides, and polysaccharides. Monosaccharides and disaccharides are smaller compounds, composed of one or two molecules, and are commonly referred to as sugars. These compounds very often end in the suffix –ose. Examples include glucose (as in blood sugar), sucrose (as in table sugar), fructose (fruit sugar), and lactose (milk sugar).
Polysaccharides store energy (e.g. glycogen and starch) and as structural components (cellulose in plants). The term carbohydrate is often used to mean any food that is rich in complex carbohydrates such as cereals, bread, rice or pasta, or simple carbohydrates, such as candy, jams, jelly and ice cream.
Glucose, fructose and galactose are the three monosaccharides. They are the simplest carbohydrates in that they cannot be broken down into smaller molecules. They are the major source of fuel for metabolism, being used as an energy source (glucose being the most important). When not immediately needed for energy, they are converted into its storage form, glycogen, mainly in liver and muscle cells.
The disaccharides include sucrose (composed of one glucose and one fructose molecule), lactose (composed of one glucose and one galactose molecule) and maltose (two glucose molecules bonded in a special way). Oligosaccharides and polysaccharides are just longer chains of monosaccharides bound together. Oligosaccharides contain between three and ten monosaccharides and polysaccharides contain greater than ten monosaccharide units.
The human diet contains many foods high in carbohydrates: fruits, sweets, soft drinks, breads, pastas, beans, potatoes, rice and cereals. Carbohydrates are a common source of energy in living organisms; however, no carbohydrate is an essential nutrient in humans. Carbohydrates are not necessary building blocks of other molecules, and the body can obtain all its energy from protein and fats.
The brain and neurons generally cannot burn fat for energy, but use glucose or ketones. Humans can synthesize some glucose (in a process called gluconeogenesis) from specific amino acids, from the glycerol backbone in triglycerides, and in some cases from fatty acids. Glucose is a nearly universal, accessible and preferred source of calories. It is used first, either directly or indirectly from glycogen in storage. Polysaccharides are also a common source of energy. Many organisms can easily and quickly break down starches into glucose.
A commonly held belief among the general public, and even among nutritionists, is that complex carbohydrates (polysaccharides, e.g. starches) are digested more slowly than simple carbohydrates (sugars) and thus are healthier. However, there appears to be no significant difference between simple and complex carbohydrates in terms of their effect on blood sugar. Some simple carbohydrates (e.g. fructose) are digested very slowly (and very differently from glucose), while some complex carbohydrates (starches), especially that in processed food, raise blood sugar rapidly.
It is not sufficient, therefore, to buy foods that trumpet “whole grain ingredients.” The primary ingredients of these foods (those listed first) may be “bleached all purpose flour” (a highly processed food), sugar, dextrose, molasses, sucrose or HFCS (all highly processed sugars), before any “whole grains” are added. When you see grain sprinkled on the surface of that loaf of bread, just realize that it’s been brushed with HFCS to give it a nice brown color and make it sticky.
Always a wiser choice is to choose whole, unadulterated foods from the meat, dairy and produce aisles. Avoid the center of the store; shop the perimeter. Avoid food sold in a box or a bag, except perhaps flash frozen fish and veggies, in which case always check the ingredients list. Avoid anything refined or heavily processed. In other words, eat real food.
N.B.: For the record and for those who would doubt my authority of make some of the claims herein, this column has been largely cribbed – much of it lifted verbatim – from the Wikipedia entry “Carbohydrate.” Credit them. Check it out.
© Dan Brown 11/13/11
All carbohydrates are saccharides. The word saccharide comes from the Greek word meaning sugar. Carbohydrates are divided into four types: monosaccharides, disaccharides, oligosaccharides, and polysaccharides. Monosaccharides and disaccharides are smaller compounds, composed of one or two molecules, and are commonly referred to as sugars. These compounds very often end in the suffix –ose. Examples include glucose (as in blood sugar), sucrose (as in table sugar), fructose (fruit sugar), and lactose (milk sugar).
Polysaccharides store energy (e.g. glycogen and starch) and as structural components (cellulose in plants). The term carbohydrate is often used to mean any food that is rich in complex carbohydrates such as cereals, bread, rice or pasta, or simple carbohydrates, such as candy, jams, jelly and ice cream.
Glucose, fructose and galactose are the three monosaccharides. They are the simplest carbohydrates in that they cannot be broken down into smaller molecules. They are the major source of fuel for metabolism, being used as an energy source (glucose being the most important). When not immediately needed for energy, they are converted into its storage form, glycogen, mainly in liver and muscle cells.
The disaccharides include sucrose (composed of one glucose and one fructose molecule), lactose (composed of one glucose and one galactose molecule) and maltose (two glucose molecules bonded in a special way). Oligosaccharides and polysaccharides are just longer chains of monosaccharides bound together. Oligosaccharides contain between three and ten monosaccharides and polysaccharides contain greater than ten monosaccharide units.
The human diet contains many foods high in carbohydrates: fruits, sweets, soft drinks, breads, pastas, beans, potatoes, rice and cereals. Carbohydrates are a common source of energy in living organisms; however, no carbohydrate is an essential nutrient in humans. Carbohydrates are not necessary building blocks of other molecules, and the body can obtain all its energy from protein and fats.
The brain and neurons generally cannot burn fat for energy, but use glucose or ketones. Humans can synthesize some glucose (in a process called gluconeogenesis) from specific amino acids, from the glycerol backbone in triglycerides, and in some cases from fatty acids. Glucose is a nearly universal, accessible and preferred source of calories. It is used first, either directly or indirectly from glycogen in storage. Polysaccharides are also a common source of energy. Many organisms can easily and quickly break down starches into glucose.
A commonly held belief among the general public, and even among nutritionists, is that complex carbohydrates (polysaccharides, e.g. starches) are digested more slowly than simple carbohydrates (sugars) and thus are healthier. However, there appears to be no significant difference between simple and complex carbohydrates in terms of their effect on blood sugar. Some simple carbohydrates (e.g. fructose) are digested very slowly (and very differently from glucose), while some complex carbohydrates (starches), especially that in processed food, raise blood sugar rapidly.
It is not sufficient, therefore, to buy foods that trumpet “whole grain ingredients.” The primary ingredients of these foods (those listed first) may be “bleached all purpose flour” (a highly processed food), sugar, dextrose, molasses, sucrose or HFCS (all highly processed sugars), before any “whole grains” are added. When you see grain sprinkled on the surface of that loaf of bread, just realize that it’s been brushed with HFCS to give it a nice brown color and make it sticky.
Always a wiser choice is to choose whole, unadulterated foods from the meat, dairy and produce aisles. Avoid the center of the store; shop the perimeter. Avoid food sold in a box or a bag, except perhaps flash frozen fish and veggies, in which case always check the ingredients list. Avoid anything refined or heavily processed. In other words, eat real food.
N.B.: For the record and for those who would doubt my authority of make some of the claims herein, this column has been largely cribbed – much of it lifted verbatim – from the Wikipedia entry “Carbohydrate.” Credit them. Check it out.
© Dan Brown 11/13/11
Sunday, November 6, 2011
The Nutrition Debate #30: Is Fructose a Liver Toxin? Is it Really Poison?
Fructose is ubiquitous in the food supply. It is 67% of the natural sugar found in an apple as well as 50% of table sugar (sucrose), 55% of high fructose corn syrup (HFCS) in sweetened soft drinks, and 42% of the HFCS used in many baked goods, For a fuller exposé, take a look at the last column, #29, “Fructose: Formerly Known as Fruit Sugar,” also archived on my blog at www://danbrown-thenutritiondebate.blogspot.com.
The amount of all sugars is increasing each year in the American diet. Since 2000, however, the amount of fructose has leveled off and even declined slightly, precipitating the Corn Refiners’ Association recent TV ad campaign to repair the image of HFCS. In it, a pretty young woman says, “I learned, whether it’s corn sugar or cane sugar, your body can’t tell the difference. Sugar is sugar.” I agree. HFCS is essentially not much worse than (table) sugar made from sugar cane or beet sugar. HFCS and sucrose are basically the same, and both are equally bad for you.
The problem is not with the glucose component of sucrose. Once absorbed through the wall of the small intestine, glucose goes to virtually all the cells of the body and is used for energy or it is stored mostly in the muscles and liver as glycogen, a ready form of quick energy. Either way – used quickly or stored and used later – it is metabolized (broken down and “burned”). Glucose is the preferred and most commonly and readily used form of energy.
Fructose is different. It cannot be metabolized by the body for quick energy. Once it enters the bloodstream it goes directly through the portal vein to the liver and is stored there. Scientists, noting that the liver’s function is to filter out toxins, think that fructose is toxic. Remember, before modern agriculture, fruits were available seasonally and were far less sweet because they had not been hybridized. In addition, refined processed sugars were nonexistent. When we eat large doses of sugar the liver becomes overloaded with fructose. Is fructose toxic to the liver? Not in the sense of an acute toxin. It is, these scientists claim, a “chronic hepatotoxin.” In the words of Robert H. Lustig, MD, presenter of UCSF’s YouTube video, “Sugar: The Bitter Truth” in their Mini Med School for the Public series, fructose is “alcohol without the buzz.” No wonder that excess fructose consumption over a long period of time is frequently thought to be a cause, and is certainly associated with, non-alcoholic fatty liver disease (NAFLD), also on the rise.
Lustig adds: “Fructose increases de novo lipogenesis (fat formation), triglycerides and free fatty acids in most adults.” Fructose is a carbohydrate, but “it is metabolized like fat,” he says; therefore, “a high sugar diet is a high fat diet”.
In addition to Dr Lustig’s work, a 2005 a scientific paper titled “Fructose, insulin resistance and metabolic dyslipidemia,” from the Clinical Biochemistry Division, Department of Laboratory Medicine and Pathobiology, Hospital for Sick Children, University of Toronto, Toronto, Canada, concludes: “An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup...” A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis...” Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia... Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption...”
Dr. Lustig’s video presentation includes a slide entitled “Fructose is Not Glucose,” with five bullets, summarized here:
1. Fructose is 7 times more likely than glucose to form Advanced Glycation End Products (AGE’s).
2. Fructose does not suppress Ghrelin, the hunger hormone.
3. Acute fructose does not stimulate Insulin (or Leptin: The brain doesn’t see that you ate, so you eat more).
4. Hepatic fructose metabolism is different. (rather than forming glycogen, de novo lipogenesis occurs).
5. Chronic fructose exposure promotes the Metabolic Syndrome.
But Dr. Lustig says that because fructose is a chronic toxin, not an acute toxin, the USDA/FDA “won’t touch it.” That may be, but personally I think Cargill and Archer Daniels Midland may have some influence in Washington as well.
© Dan Brown 11/6/11
The amount of all sugars is increasing each year in the American diet. Since 2000, however, the amount of fructose has leveled off and even declined slightly, precipitating the Corn Refiners’ Association recent TV ad campaign to repair the image of HFCS. In it, a pretty young woman says, “I learned, whether it’s corn sugar or cane sugar, your body can’t tell the difference. Sugar is sugar.” I agree. HFCS is essentially not much worse than (table) sugar made from sugar cane or beet sugar. HFCS and sucrose are basically the same, and both are equally bad for you.
The problem is not with the glucose component of sucrose. Once absorbed through the wall of the small intestine, glucose goes to virtually all the cells of the body and is used for energy or it is stored mostly in the muscles and liver as glycogen, a ready form of quick energy. Either way – used quickly or stored and used later – it is metabolized (broken down and “burned”). Glucose is the preferred and most commonly and readily used form of energy.
Fructose is different. It cannot be metabolized by the body for quick energy. Once it enters the bloodstream it goes directly through the portal vein to the liver and is stored there. Scientists, noting that the liver’s function is to filter out toxins, think that fructose is toxic. Remember, before modern agriculture, fruits were available seasonally and were far less sweet because they had not been hybridized. In addition, refined processed sugars were nonexistent. When we eat large doses of sugar the liver becomes overloaded with fructose. Is fructose toxic to the liver? Not in the sense of an acute toxin. It is, these scientists claim, a “chronic hepatotoxin.” In the words of Robert H. Lustig, MD, presenter of UCSF’s YouTube video, “Sugar: The Bitter Truth” in their Mini Med School for the Public series, fructose is “alcohol without the buzz.” No wonder that excess fructose consumption over a long period of time is frequently thought to be a cause, and is certainly associated with, non-alcoholic fatty liver disease (NAFLD), also on the rise.
Lustig adds: “Fructose increases de novo lipogenesis (fat formation), triglycerides and free fatty acids in most adults.” Fructose is a carbohydrate, but “it is metabolized like fat,” he says; therefore, “a high sugar diet is a high fat diet”.
In addition to Dr Lustig’s work, a 2005 a scientific paper titled “Fructose, insulin resistance and metabolic dyslipidemia,” from the Clinical Biochemistry Division, Department of Laboratory Medicine and Pathobiology, Hospital for Sick Children, University of Toronto, Toronto, Canada, concludes: “An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup...” A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis...” Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia... Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption...”
Dr. Lustig’s video presentation includes a slide entitled “Fructose is Not Glucose,” with five bullets, summarized here:
1. Fructose is 7 times more likely than glucose to form Advanced Glycation End Products (AGE’s).
2. Fructose does not suppress Ghrelin, the hunger hormone.
3. Acute fructose does not stimulate Insulin (or Leptin: The brain doesn’t see that you ate, so you eat more).
4. Hepatic fructose metabolism is different. (rather than forming glycogen, de novo lipogenesis occurs).
5. Chronic fructose exposure promotes the Metabolic Syndrome.
But Dr. Lustig says that because fructose is a chronic toxin, not an acute toxin, the USDA/FDA “won’t touch it.” That may be, but personally I think Cargill and Archer Daniels Midland may have some influence in Washington as well.
© Dan Brown 11/6/11
Sunday, October 30, 2011
The Nutrition Debate #29: Fructose, Formerly Known as Fruit Sugar
What is fructose? Fruit sugar, right? Well, yes and no. It is found in copious amounts in fruit, of course, but so are other sugars. Free fructose, the monosaccharide form, is 57% of the total sugars found in an average apple, but free glucose, another monosaccharide, is 23% of the total sugar. Sucrose, a disaccharide composed of equal parts fructose and glucose, is the remaining 20% of the sugar. So, combining the free fructose with the fructose bound up in sucrose, the total fructose in an apple is 67% of the sugars. (Trust me on the math here.) The remaining one-third is glucose.
Apples and pears are on the high end of the fructose scale. Apricots, at 39%, are at the low end. The sugar in bananas is 50% fructose, grapes 53%, and peaches 46%. Honey is 50.5% fructose (free and combined). Besides tree and vine fruits, fructose is also found in other foods found in nature, for example, berries, sweet corn and sweet red peppers and most root vegetables (e.g., red beets, carrots, onions and sweet potatoes).Generally, most of the fructose is bound up in sucrose (equal parts fructose and glucose).
Sucrose in its processed form is what we know as table sugar, which is made from refining sugar cane or sugar beets. Table sugar is therefore 50% fructose. So is the sucrose, or simply “sugar,” listed near the top in the ingredients list of more and more processed foods.
According to Wikipedia, “Commercially, fructose is usually derived from sugar cane, sugar beets and corn, and there are 3 commercially important forms:” 1) processed crystalline fructose, 2) high-fructose corn syrup (HFCS), as a mixture of both glucose and fructose as monosaccharides, and 3) sucrose. All forms of fructose, according to Wiki, are commonly added to foods and drinks for palatability, taste enhancement and improved browning of foods such as baked goods.
Starting in the early 70’s, as total consumption of sugar rose in the U.S., HFCS eroded the sucrose market. By 2000 they were consumed in the U.S. in equal amounts. HFCS is commonly found in food and drink in two forms: The 55% fructose/41% glucose form is in use in the U.S. in non-dietary soft drinks. The 42% fructose/53% glucose formulation is used primarily in processed foods and baked goods. (The balances in both forms are “other sugars.”)
“The primary reason fructose is used commercially in foods and beverages, besides its low cost, is its high relative sweetness. It is the sweetest of all naturally occurring carbohydrates; at room temperature it is 1.73 times as sweet as sucrose,” but when heated it loses this advantage, again according to Wiki. The sweetness of fructose is “perceived earlier,” has a “higher peak,” “exhibits a synergy effect when used in combination with other sweeteners,” has “greater solubility,” “increases starch viscosity more rapidly and achieves a higher final viscosity than sucrose,” “retains moisture for a long period of time even at low relative humidity,” and therefore “can contribute to improved quality, better texture, and longer shelf life to the food products in which it is used,” all as reported in the Wiki entry. Ever wonder why a Twinkie or a Devil Dog stays soft forever? It’s the HFCS!
If you haven’t noticed how ubiquitous HFCS has become in the processed food supply, let me give you a snapshot. In the bread aisle at my local supermarket I found it in most of the “soft” goods and long shelf life items: Devil Dogs and Twinkies, of course, and fruit pies and muffins; also in hot dog and hamburger rolls and, naturally, in Wonder Bread. I also found it listed as 4th ingredient in Weight Watchers 100% Whole Wheat bread, just before molasses!
Fundamentally, however, regardless of whether the formulation of fructose you consume is 55%, 42%, or 50% fructose as in table sugar (sucrose), we all consume ever increasing amounts of fructose each year, whether we know it or not. We eat much more fructose than we think, and much more than the amount that is found in fresh fruit. Sugar -- ordinary table sugar, made from sugar cane -- remember, is half fructose.
So, why does it matter? Because fructose, in the words of Robert H. Lustig, MD, is “poison.” Dr. Lustig is professor of Clinical Pediatrics in the Division of Endocrinology at the University of California San Francisco. His research focuses on childhood obesity. He contends that, in the amounts we are eating it, fructose is toxic to the liver.
Want to know why? You can watch his 90 minute 2009 video, “Sugar: The Bitter Truth,” from UCSF’s “Mini Med School for the Public” on YouTube. Or stay tuned. In the next installment I will present my ‘Executive Summary’ of his evidence.
By the way, all of my columns are archived on my blog: www://danbrown-thenutritiondebate.blogspot.com.
© Dan Brown 10/30/11
Apples and pears are on the high end of the fructose scale. Apricots, at 39%, are at the low end. The sugar in bananas is 50% fructose, grapes 53%, and peaches 46%. Honey is 50.5% fructose (free and combined). Besides tree and vine fruits, fructose is also found in other foods found in nature, for example, berries, sweet corn and sweet red peppers and most root vegetables (e.g., red beets, carrots, onions and sweet potatoes).Generally, most of the fructose is bound up in sucrose (equal parts fructose and glucose).
Sucrose in its processed form is what we know as table sugar, which is made from refining sugar cane or sugar beets. Table sugar is therefore 50% fructose. So is the sucrose, or simply “sugar,” listed near the top in the ingredients list of more and more processed foods.
According to Wikipedia, “Commercially, fructose is usually derived from sugar cane, sugar beets and corn, and there are 3 commercially important forms:” 1) processed crystalline fructose, 2) high-fructose corn syrup (HFCS), as a mixture of both glucose and fructose as monosaccharides, and 3) sucrose. All forms of fructose, according to Wiki, are commonly added to foods and drinks for palatability, taste enhancement and improved browning of foods such as baked goods.
Starting in the early 70’s, as total consumption of sugar rose in the U.S., HFCS eroded the sucrose market. By 2000 they were consumed in the U.S. in equal amounts. HFCS is commonly found in food and drink in two forms: The 55% fructose/41% glucose form is in use in the U.S. in non-dietary soft drinks. The 42% fructose/53% glucose formulation is used primarily in processed foods and baked goods. (The balances in both forms are “other sugars.”)
“The primary reason fructose is used commercially in foods and beverages, besides its low cost, is its high relative sweetness. It is the sweetest of all naturally occurring carbohydrates; at room temperature it is 1.73 times as sweet as sucrose,” but when heated it loses this advantage, again according to Wiki. The sweetness of fructose is “perceived earlier,” has a “higher peak,” “exhibits a synergy effect when used in combination with other sweeteners,” has “greater solubility,” “increases starch viscosity more rapidly and achieves a higher final viscosity than sucrose,” “retains moisture for a long period of time even at low relative humidity,” and therefore “can contribute to improved quality, better texture, and longer shelf life to the food products in which it is used,” all as reported in the Wiki entry. Ever wonder why a Twinkie or a Devil Dog stays soft forever? It’s the HFCS!
If you haven’t noticed how ubiquitous HFCS has become in the processed food supply, let me give you a snapshot. In the bread aisle at my local supermarket I found it in most of the “soft” goods and long shelf life items: Devil Dogs and Twinkies, of course, and fruit pies and muffins; also in hot dog and hamburger rolls and, naturally, in Wonder Bread. I also found it listed as 4th ingredient in Weight Watchers 100% Whole Wheat bread, just before molasses!
Fundamentally, however, regardless of whether the formulation of fructose you consume is 55%, 42%, or 50% fructose as in table sugar (sucrose), we all consume ever increasing amounts of fructose each year, whether we know it or not. We eat much more fructose than we think, and much more than the amount that is found in fresh fruit. Sugar -- ordinary table sugar, made from sugar cane -- remember, is half fructose.
So, why does it matter? Because fructose, in the words of Robert H. Lustig, MD, is “poison.” Dr. Lustig is professor of Clinical Pediatrics in the Division of Endocrinology at the University of California San Francisco. His research focuses on childhood obesity. He contends that, in the amounts we are eating it, fructose is toxic to the liver.
Want to know why? You can watch his 90 minute 2009 video, “Sugar: The Bitter Truth,” from UCSF’s “Mini Med School for the Public” on YouTube. Or stay tuned. In the next installment I will present my ‘Executive Summary’ of his evidence.
By the way, all of my columns are archived on my blog: www://danbrown-thenutritiondebate.blogspot.com.
© Dan Brown 10/30/11
Sunday, October 23, 2011
The Nutrition Debate #28: Sugar in the Diet: What does it mean?
I ran into a friend at the supermarket the other day and asked her how she was. She replied, “Fine,” but “tired a lot.” Not wanting to miss an opportunity to proselytize, I suggested, “sugar crash.” She protested, “I don’t eat sugar!” So, I asked her what she ate for breakfast. Therein lies a tale of folly that deserves to be more widely known and understood.
Sugar, as she and virtually the “whole world” thinks of it, is table sugar, as in “added sugar” such as that sprinkled on cereal. It is also an ingredient in candy and ice cream. Soft drinks usually are sweetened with high fructose corn syrup.
Table sugar, the “added” sugar, is cane sugar and chemically is known as sucrose. It is a disaccharide, meaning it is composed of two simple sugar molecules. One of those molecules is fructose and the other is glucose. All chemical compounds ending in “ose” are sugars. Most break down in the digestion process to glucose, some to fructose, and a few to galactose, the third monosaccharide, before entering the blood stream through the wall of the small intestine.
Sugars in this “whole-world” sense do not include those found in fruits, which are a combination of free fructose, free glucose and sucrose. Fruit sugars are regarded in this “whole-world” view as good for you, because they are an inherent component of this “real” or whole food. Forget that for centuries hybridizers have been making fruits sweeter than those found in nature to appeal to our sweet tooth.
Carbohydrates, one of the three basic elements of nutrition (the other two being protein and fat), are all saccharides. Carbohydrates, including fruits, cereals, bread, potatoes, rice and pasta, are somewhat more complex compounds, meaning composed of many molecules. Nevertheless, they virtually all break down in the digestion process to the simple sugars glucose and fructose. Glucose goes to the cells for quick energy. Fructose goes directly to the liver and is stored.
Back to the question I asked of my friend: “What did you eat for breakfast?” Her answer: “A glass of orange juice, a whole grain cereal ‘with 3 grams of protein’ [in reduced-fat milk, I assumed], toast and jelly.” “All sugar,” I exclaimed! Obnoxiously, I said, “if you eat a lot of ‘sugar’ – read any food except fat and protein -- all at once, your blood stream will be flooded with sugar (glucose) sooner or later (up to a few hours, depending on the food and the condition of your metabolism), and insulin pumped from the pancreas (if it is still working well). And then, after the ‘sugar’ gets delivered to the muscles and organs by the insulin, your blood sugar level will crash and you will ‘feel tired’ (and hungry) again.”
You will feel hungry again because another hormone, ghrelin (first reported in Nature in 1999!), will send a signal from cells lining the fundus of the stomach to the hypothalamus in the center of your brain, that the “quick energy” in your blood (glucose) is low again. So, when your “all sugar” breakfast is digested, in mid-morning your body will again crave “sugar” (anything that will break down to glucose) to “feed the beast.” “Sugary snack” doesn’t mean a candy bar. It means any carbohydrate, including fruit, or a glass of milk (lactose), all of which will break down to glucose and again raise the level of sugar in the blood. It will also overwork the pancreas again to produce more insulin. A vicious cycle.
Over a course of years the cell wall of the destination cells in many people will develop insulin resistance, requiring more insulin to get the job of delivering glucose energy to our muscles done. Eventually, in many of these people, the pancreas will slowly burn out. The islets of langerhans that produce the beta cells in the pancreas will stop working. They will die. By the time your doctor discovers this, up to 80% of your pancreatic function will probably already have been lost. That was the stunning conjecture made by Dr. Ralph DeFronzo, American Diabetes Association keynote speaker at their annual meeting in San Francisco in 2008. You will be diagnosed with full-blown Type 2 Diabetes. You will be drug dependent for the rest of your life. You will then be watchful for, or worse, diagnosed with the “dreaded complications.”
As a result, in recent years the standards and methodology for diagnosing Metabolic Syndrome and Type 2 diabetes has evolved. The old standard was two consecutive elevated plasma blood glucose tests above 140mg/dl, lowered to 126 in 1997, where it remains today. Fasting blood glucose between 100 and 125mg/dl is now regarded as pre-diabetes.
The new diagnostic standard for T2 diabetes is the Hemoglobin (Hb) A1c test. The diagnostic standard was formerly 7.0%. A few years ago it was lowered to 6.5%, and a 6.0% level added for pre-diabetes. Some activist endocrinologists, such as Dr. Richard K. Bernstein, use a much lower standard, regarding an A1c of 5.8% as indicating full-blown Type 2.
So, to stay healthy, watch your total sugars and remember: All carbohydrates are sugars. Your body breaks sugars down into glucose, the simplest sugar. Glucose induces insulin secretion. If you still think you don’t eat sugar, read this again!
© Dan Brown 10/23/11
Sugar, as she and virtually the “whole world” thinks of it, is table sugar, as in “added sugar” such as that sprinkled on cereal. It is also an ingredient in candy and ice cream. Soft drinks usually are sweetened with high fructose corn syrup.
Table sugar, the “added” sugar, is cane sugar and chemically is known as sucrose. It is a disaccharide, meaning it is composed of two simple sugar molecules. One of those molecules is fructose and the other is glucose. All chemical compounds ending in “ose” are sugars. Most break down in the digestion process to glucose, some to fructose, and a few to galactose, the third monosaccharide, before entering the blood stream through the wall of the small intestine.
Sugars in this “whole-world” sense do not include those found in fruits, which are a combination of free fructose, free glucose and sucrose. Fruit sugars are regarded in this “whole-world” view as good for you, because they are an inherent component of this “real” or whole food. Forget that for centuries hybridizers have been making fruits sweeter than those found in nature to appeal to our sweet tooth.
Carbohydrates, one of the three basic elements of nutrition (the other two being protein and fat), are all saccharides. Carbohydrates, including fruits, cereals, bread, potatoes, rice and pasta, are somewhat more complex compounds, meaning composed of many molecules. Nevertheless, they virtually all break down in the digestion process to the simple sugars glucose and fructose. Glucose goes to the cells for quick energy. Fructose goes directly to the liver and is stored.
Back to the question I asked of my friend: “What did you eat for breakfast?” Her answer: “A glass of orange juice, a whole grain cereal ‘with 3 grams of protein’ [in reduced-fat milk, I assumed], toast and jelly.” “All sugar,” I exclaimed! Obnoxiously, I said, “if you eat a lot of ‘sugar’ – read any food except fat and protein -- all at once, your blood stream will be flooded with sugar (glucose) sooner or later (up to a few hours, depending on the food and the condition of your metabolism), and insulin pumped from the pancreas (if it is still working well). And then, after the ‘sugar’ gets delivered to the muscles and organs by the insulin, your blood sugar level will crash and you will ‘feel tired’ (and hungry) again.”
You will feel hungry again because another hormone, ghrelin (first reported in Nature in 1999!), will send a signal from cells lining the fundus of the stomach to the hypothalamus in the center of your brain, that the “quick energy” in your blood (glucose) is low again. So, when your “all sugar” breakfast is digested, in mid-morning your body will again crave “sugar” (anything that will break down to glucose) to “feed the beast.” “Sugary snack” doesn’t mean a candy bar. It means any carbohydrate, including fruit, or a glass of milk (lactose), all of which will break down to glucose and again raise the level of sugar in the blood. It will also overwork the pancreas again to produce more insulin. A vicious cycle.
Over a course of years the cell wall of the destination cells in many people will develop insulin resistance, requiring more insulin to get the job of delivering glucose energy to our muscles done. Eventually, in many of these people, the pancreas will slowly burn out. The islets of langerhans that produce the beta cells in the pancreas will stop working. They will die. By the time your doctor discovers this, up to 80% of your pancreatic function will probably already have been lost. That was the stunning conjecture made by Dr. Ralph DeFronzo, American Diabetes Association keynote speaker at their annual meeting in San Francisco in 2008. You will be diagnosed with full-blown Type 2 Diabetes. You will be drug dependent for the rest of your life. You will then be watchful for, or worse, diagnosed with the “dreaded complications.”
As a result, in recent years the standards and methodology for diagnosing Metabolic Syndrome and Type 2 diabetes has evolved. The old standard was two consecutive elevated plasma blood glucose tests above 140mg/dl, lowered to 126 in 1997, where it remains today. Fasting blood glucose between 100 and 125mg/dl is now regarded as pre-diabetes.
The new diagnostic standard for T2 diabetes is the Hemoglobin (Hb) A1c test. The diagnostic standard was formerly 7.0%. A few years ago it was lowered to 6.5%, and a 6.0% level added for pre-diabetes. Some activist endocrinologists, such as Dr. Richard K. Bernstein, use a much lower standard, regarding an A1c of 5.8% as indicating full-blown Type 2.
So, to stay healthy, watch your total sugars and remember: All carbohydrates are sugars. Your body breaks sugars down into glucose, the simplest sugar. Glucose induces insulin secretion. If you still think you don’t eat sugar, read this again!
© Dan Brown 10/23/11
Sunday, October 9, 2011
The Nutrition Debate #27: “…the strongest predictor of a heart attack”
The contemporary medical literature is replete with macro and other large studies that attempt to extrapolate a correlation between heart attack risk and blood lipids. The last two columns, “Understanding Your Lipid Panel” and “The Cause and Treatment of Heart Disease” address this issue from different directions. In this column we will attempt to put a fine point on the critical matter of lipid ratios.
In the 1960’s Total Cholesterol (TC) became a common and inexpensive test. As the principal metric of “the Lipid Hypothesis” popularized by Ancel Keys and then the American Heart Association, it became the universal marker for predicting heart disease risk. But that was more than half a century ago. We’ve come a long way since then.
The “treatment,” i. e. medical advice, then and now for high TC was to eat less saturated fat and other animal foods with high cholesterol content. This was the modality even though the body needs cholesterol for many essential purposes and makes up what we don’t eat by manufacturing it as needed. The threshold for TC was and remains today 200mg/dl.
Low density lipoprotein (LDL) is a component of TC. Even though the common test used to determine LDL was and is a calculated value, not a direct measurement, it became a popular target in the 80’s when big pharma developed drugs – statins – that lowered it. By lowering LDL, statins also lowered total cholesterol. So, doctors prescribed statins to anyone and everyone whose TC was over 200. Today, Lipitor, Crestor, Zocor, and its generic Simvastatin, account for $20 billion in world-wide annual sales.
In recent decades the other components of the Lipid Panel – High Density Lipoproteins (HDL) and Triglycerides (TG) – have taken on increased importance in understanding Cardio Vascular Disease (CVD) risk.Unfortunately, these developments have garnered little attention since the pharmaceutical industry has not yet developed blockbuster drugs to influence them. Fish oil lowers Triglycerides, but fish oil cannot be patented.
Most lipid panel lab results these days do however include a ratio of TC to HDL with a recommendation that it should be less than 5.0. In other words, if TC is 200, then HDL should not be less than 40. While this at least recognizes the importance of HDL, it is hardly a standard to be emulated. It is, in fact, borderline dangerous. Optimal is ≤3.5.
A somewhat higher standard coming into wider use is the inverse of this fraction, i.e. HDL/TC. However, the standard for this fraction is ≥0.24 = ideal. Translated, that is closer to a ratio of 4.0, versus 5.0 in the TC to HDL ratio cited above.
Many enlightened practitioners today, however, use the ratio of Triglycerides to HDL (TG/HDL) as “the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined,” according to just one of many articles in the literature. The study I quote is in Clinics at PubMed Central 2008 August 63(4) 427-432. Note, by the way, that neither TC nor LDL is a factor in this formula. This ratio is considered by informed clinicians today as more reliable than LDL, or TC/HDL, or high sensitivity (hs) C-reactive protein (CRP), the marker my internist/cardiologist uses.
Using this new gold standard, a TG/HDL ≤ 1.0 is considered ideal, a ratio of ≤2.0 is good, a ratio of 4.0 is considered high and 6.0 much too high. My recent TG/HDL = 0.35, which is interpreted to mean a very low probability of heart attack.
As the patent on Lipitor is about to expire, and the other name-brand statin drug patent expirations are not too far behind, big pharma is hard at work looking for the next blockbuster drug to lower Triglycerides or raise HDL. Alas, so far, diet -- that is, our dietary intake (as in, “we are what we eat”) -- is the only thing that seems to work, and big pharma isn’t in that business.
Agribusiness, however, has seen the potential for a big piece of the action here. Unfortunately, there isn’t much profit in “real food.” Ask your local farmer. The increasingly popular processed foods -- the so-called “heart healthy” foods we are being encouraged to eat in large quantities -- do not improve the TG/HDL ratio. They make it worse!
In the coming weeks we will return to the subject of healthy eating. Subjects will include “Sugar: What do we mean?” “Fructose: Where and what is it?,” “Intermittent Fasting: Is it a good idea?,” “Ketosis and Autophagy,” and “Cooking with Oils: good and bad choices,” Our goal will be to help the reader improve their TG/HDL ratio. Of course, to do that, you will need to have a baseline Lipid Profile. If you haven’t had a Lipid Panel done, or don’t know yours, ask your doctor to do one. And ask him to see how yours shapes up using the new gold standard for CVD risk: the TG/HDL ratio.
© Dan Brown 10/9/11
In the 1960’s Total Cholesterol (TC) became a common and inexpensive test. As the principal metric of “the Lipid Hypothesis” popularized by Ancel Keys and then the American Heart Association, it became the universal marker for predicting heart disease risk. But that was more than half a century ago. We’ve come a long way since then.
The “treatment,” i. e. medical advice, then and now for high TC was to eat less saturated fat and other animal foods with high cholesterol content. This was the modality even though the body needs cholesterol for many essential purposes and makes up what we don’t eat by manufacturing it as needed. The threshold for TC was and remains today 200mg/dl.
Low density lipoprotein (LDL) is a component of TC. Even though the common test used to determine LDL was and is a calculated value, not a direct measurement, it became a popular target in the 80’s when big pharma developed drugs – statins – that lowered it. By lowering LDL, statins also lowered total cholesterol. So, doctors prescribed statins to anyone and everyone whose TC was over 200. Today, Lipitor, Crestor, Zocor, and its generic Simvastatin, account for $20 billion in world-wide annual sales.
In recent decades the other components of the Lipid Panel – High Density Lipoproteins (HDL) and Triglycerides (TG) – have taken on increased importance in understanding Cardio Vascular Disease (CVD) risk.Unfortunately, these developments have garnered little attention since the pharmaceutical industry has not yet developed blockbuster drugs to influence them. Fish oil lowers Triglycerides, but fish oil cannot be patented.
Most lipid panel lab results these days do however include a ratio of TC to HDL with a recommendation that it should be less than 5.0. In other words, if TC is 200, then HDL should not be less than 40. While this at least recognizes the importance of HDL, it is hardly a standard to be emulated. It is, in fact, borderline dangerous. Optimal is ≤3.5.
A somewhat higher standard coming into wider use is the inverse of this fraction, i.e. HDL/TC. However, the standard for this fraction is ≥0.24 = ideal. Translated, that is closer to a ratio of 4.0, versus 5.0 in the TC to HDL ratio cited above.
Many enlightened practitioners today, however, use the ratio of Triglycerides to HDL (TG/HDL) as “the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined,” according to just one of many articles in the literature. The study I quote is in Clinics at PubMed Central 2008 August 63(4) 427-432. Note, by the way, that neither TC nor LDL is a factor in this formula. This ratio is considered by informed clinicians today as more reliable than LDL, or TC/HDL, or high sensitivity (hs) C-reactive protein (CRP), the marker my internist/cardiologist uses.
Using this new gold standard, a TG/HDL ≤ 1.0 is considered ideal, a ratio of ≤2.0 is good, a ratio of 4.0 is considered high and 6.0 much too high. My recent TG/HDL = 0.35, which is interpreted to mean a very low probability of heart attack.
As the patent on Lipitor is about to expire, and the other name-brand statin drug patent expirations are not too far behind, big pharma is hard at work looking for the next blockbuster drug to lower Triglycerides or raise HDL. Alas, so far, diet -- that is, our dietary intake (as in, “we are what we eat”) -- is the only thing that seems to work, and big pharma isn’t in that business.
Agribusiness, however, has seen the potential for a big piece of the action here. Unfortunately, there isn’t much profit in “real food.” Ask your local farmer. The increasingly popular processed foods -- the so-called “heart healthy” foods we are being encouraged to eat in large quantities -- do not improve the TG/HDL ratio. They make it worse!
In the coming weeks we will return to the subject of healthy eating. Subjects will include “Sugar: What do we mean?” “Fructose: Where and what is it?,” “Intermittent Fasting: Is it a good idea?,” “Ketosis and Autophagy,” and “Cooking with Oils: good and bad choices,” Our goal will be to help the reader improve their TG/HDL ratio. Of course, to do that, you will need to have a baseline Lipid Profile. If you haven’t had a Lipid Panel done, or don’t know yours, ask your doctor to do one. And ask him to see how yours shapes up using the new gold standard for CVD risk: the TG/HDL ratio.
© Dan Brown 10/9/11
Monday, September 5, 2011
The Nutrition Debate #26: The Cause and Treatment of Heart Disease
Just in case the publisher is on vacation this week, let me be the one to state here and again, unequivocally, that I am not a doctor. In fact I have no medical training whatsoever and only took four years of both high school science and high school math on my way to becoming an architect. So, nothing in my columns is intended nor should be construed as medical advice. I offer only my opinions and the opinions of those medical doctors and scientists cited with attribution.
This is the fifth and last in the mini-series on “knowing your fats.” In this series I have quoted extensively, from “The Skinny on Fats,” originally published in 2000 by the Weston A. Price Foundation and then incorporated into a cookbook, “Nourishing Traditions”, by Mary Enig, PhD. and Sally Fallon, president of the Foundation. The quotation that follows is from “The Skinny on Fats.” It is titled, “The Cause and Treatment of Heart Disease.”
“The cause of heart disease is not animal fats and cholesterol but rather a number of factors inherent in modern diets, including excess consumption of vegetables oils and hydrogenated [read “trans”] fats; excess consumption of refined carbohydrates in the form of sugar and white flour; mineral deficiencies, particularly low levels of protective magnesium and iodine; deficiencies of vitamins, particularly of vitamin C, needed for the integrity of the blood vessel walls, and of antioxidants like selenium and vitamin E, which protect us from free radicals; and, finally, the disappearance of antimicrobial fats from the food supply, namely, animal fats and tropical oils.52 These once protected us against the kinds of viruses and bacteria that have been associated with the onset of pathogenic plaque leading to heart disease.
While serum cholesterol levels provide an inaccurate indication of future heart disease, a high level of a substance called homocysteine in the blood has been positively correlated with pathological buildup of plaque in the arteries and the tendency to form clots—a deadly combination. Folic acid, vitamin B6, vitamin B12 and choline are nutrients that lower serum homocysteine levels.53 These nutrients are found mostly in animal foods.
The best way to treat heart disease, then, is not to focus on lowering cholesterol—either by drugs or diet—but to consume a diet that provides animal foods rich in vitamins B6 and B12; to bolster thyroid function by daily use of natural sea salt, a good source of usable iodine; to avoid vitamin and mineral deficiencies that make the artery walls more prone to ruptures and the buildup of plaque; to include the antimicrobial fats in the diet; and to eliminate processed foods containing refined carbohydrates, oxidized cholesterol and free-radical-containing vegetable oils that cause the body to need constant repair.” End of quote. Please see the Foundation website referred to above for the footnote references.
While there is not perfect concordance among the various leaders in the medical and scientific community (and even popular authors like Michael Pollan) on what to eat to avoid the Diseases of Civilization, there are remarkable similarities. Gary Taubes, and Kurt Harris, M. D., and Mary Enig, PhD, are among my favorites, but they are just a few of hundreds of authoritative resources in this emerging field. If we keep an open mind, we should all benefit from the knowledge that is becoming available. But, sad to say, it is difficult to turn the ship of state from its present course.
This is especially true 1) when convenience dictates labor-saving prepared foods, and fast-food solutions, 2) when cost is the primary driver of decisions we make at the supermarket, 3) when deceptive, misleading advertising influences the food choices we make, and 4) when agri-business has so much at stake in promoting the sale of new versions of processed foods. The result: the very foods that are billed as “heart-healthy” are in fact the ones that will lead us down the path to the modern Diseases of Civilization: metabolic syndrome, type 2 diabetes, hypertension and heart disease.
To avoid these outcomes, we need to take control of our own health. We have to learn how to “eat healthy.” And then we have to do it. In upcoming columns, we will continue to explore real food: What to eat, what not to eat, and why.
To get started and to monitor your progress, you should have a baseline lipid profile. I urge you to ask your doctor for a copy of your most recent lipid panel, or order one for you. Then show him column #25 in this series: “Understanding Your Lipid Profile” and discuss your profile in that context. Ask your doctor is he agrees with the analysis I offered. And ask if it would matter to him what you ate so long as you achieved that kind of turnaround in the course of say a year. I did, and you could too, if you change what you eat and follow that way of eating carefully.
© Dan Brown 9/5/11
This is the fifth and last in the mini-series on “knowing your fats.” In this series I have quoted extensively, from “The Skinny on Fats,” originally published in 2000 by the Weston A. Price Foundation and then incorporated into a cookbook, “Nourishing Traditions”, by Mary Enig, PhD. and Sally Fallon, president of the Foundation. The quotation that follows is from “The Skinny on Fats.” It is titled, “The Cause and Treatment of Heart Disease.”
“The cause of heart disease is not animal fats and cholesterol but rather a number of factors inherent in modern diets, including excess consumption of vegetables oils and hydrogenated [read “trans”] fats; excess consumption of refined carbohydrates in the form of sugar and white flour; mineral deficiencies, particularly low levels of protective magnesium and iodine; deficiencies of vitamins, particularly of vitamin C, needed for the integrity of the blood vessel walls, and of antioxidants like selenium and vitamin E, which protect us from free radicals; and, finally, the disappearance of antimicrobial fats from the food supply, namely, animal fats and tropical oils.52 These once protected us against the kinds of viruses and bacteria that have been associated with the onset of pathogenic plaque leading to heart disease.
While serum cholesterol levels provide an inaccurate indication of future heart disease, a high level of a substance called homocysteine in the blood has been positively correlated with pathological buildup of plaque in the arteries and the tendency to form clots—a deadly combination. Folic acid, vitamin B6, vitamin B12 and choline are nutrients that lower serum homocysteine levels.53 These nutrients are found mostly in animal foods.
The best way to treat heart disease, then, is not to focus on lowering cholesterol—either by drugs or diet—but to consume a diet that provides animal foods rich in vitamins B6 and B12; to bolster thyroid function by daily use of natural sea salt, a good source of usable iodine; to avoid vitamin and mineral deficiencies that make the artery walls more prone to ruptures and the buildup of plaque; to include the antimicrobial fats in the diet; and to eliminate processed foods containing refined carbohydrates, oxidized cholesterol and free-radical-containing vegetable oils that cause the body to need constant repair.” End of quote. Please see the Foundation website referred to above for the footnote references.
While there is not perfect concordance among the various leaders in the medical and scientific community (and even popular authors like Michael Pollan) on what to eat to avoid the Diseases of Civilization, there are remarkable similarities. Gary Taubes, and Kurt Harris, M. D., and Mary Enig, PhD, are among my favorites, but they are just a few of hundreds of authoritative resources in this emerging field. If we keep an open mind, we should all benefit from the knowledge that is becoming available. But, sad to say, it is difficult to turn the ship of state from its present course.
This is especially true 1) when convenience dictates labor-saving prepared foods, and fast-food solutions, 2) when cost is the primary driver of decisions we make at the supermarket, 3) when deceptive, misleading advertising influences the food choices we make, and 4) when agri-business has so much at stake in promoting the sale of new versions of processed foods. The result: the very foods that are billed as “heart-healthy” are in fact the ones that will lead us down the path to the modern Diseases of Civilization: metabolic syndrome, type 2 diabetes, hypertension and heart disease.
To avoid these outcomes, we need to take control of our own health. We have to learn how to “eat healthy.” And then we have to do it. In upcoming columns, we will continue to explore real food: What to eat, what not to eat, and why.
To get started and to monitor your progress, you should have a baseline lipid profile. I urge you to ask your doctor for a copy of your most recent lipid panel, or order one for you. Then show him column #25 in this series: “Understanding Your Lipid Profile” and discuss your profile in that context. Ask your doctor is he agrees with the analysis I offered. And ask if it would matter to him what you ate so long as you achieved that kind of turnaround in the course of say a year. I did, and you could too, if you change what you eat and follow that way of eating carefully.
© Dan Brown 9/5/11
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