Wednesday, March 20, 2019

Retrospective #32: Artificial Sweeteners

I’ve been avoiding this topic because I was afraid that as I researched and studied synthetic sweeteners I was going to learn “the bitter truth.” You may feel the same way after learning about them. Nevertheless, increasing public awareness about human nutrition and health 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 that 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 highly processed table sugar, i.e. refined sugar cane, even allowing that this cane sugar is 50% fructose!
Not a big deal? You think there’s just a little bulking agent? 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 the dextrose and/or maltodextrin as energy, while most (+/-90%) of the non-nutritive sucralose passes unchanged out of the body through the feces, the balance absorbed into the blood and excreted as urine via the kidneys. Reviewing then, that’s 5% non-nutritive sweetener and 95% nutritive sweeteners, all of the latter absorbed and metabolized as glucose.
How much nutritive 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 a Type 2 or Pre-diabetic and trying to limit “sugar,” then sure. Besides, it is sweetness per se that induces an insulin response, perceived in the mouth by the salivary glands. As such, even a high-intensity artificial sweetener that contains no glucose would induce an insulin response. Chronic high insulin levels in the blood, which occurs here even when there is much less glucose to transport, leads to insulin resistance, and eventually to Metabolic Syndrome and Type 2 diabetes. Wide use of artificial sweeteners, thus, 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.
There are alternatives to artificial sweeteners. When this column was originally written in late 2011, a natural sweetener made from rebiana, an extract from the herb stevia was gaining popularity. In 2007 Cargill and the Coca Cola Company introduced their stevia-based product, Truvia: stevia extract plus erythritol, a sugar alcohol, and natural flavors. A while later Pepsico and the Whole Earth Sweetener Company introduced PureVia. It is stevia extract, plus dextrose, cellulose powder and natural flavors. Both were used as tabletop sweeteners and as food ingredients, especially in beverages.
Other popular 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 candy 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.
So, the bitter truth is, “there’s no such thing as a free lunch.” Bitter is better. (Butter is better too.) In 2011 I thought that weaning myself off Splenda wasn’t going to be easy. I used it in my coffee and iced tea every day N.B.: 2019 update: Weaning myself off artificial sweeteners was easy; however, I now use pure powdered stevia in my coffee and liquid stevia extract in my iced tea. Alas, because they’re sweet, they still have an insulin response. So, see #481 next Sunday.

Sunday, March 17, 2019

Type 2 Nutrition #477: “Deprescribing antihyperglycemic meds…”

Okay, I admit it. I was predisposed to riff on and dis the headline in Medscape Medical News, “Diabetes Medications: Should You Deprescribe Them in the Elderly?” By posing a question, the headline was written, I thought, to suggest a hypothesis that tight control was neither necessary nor desirable in the elderly generally. It turns out, I am in general agreement with the author’s ideas and her specific recommendations.
When I first saw this headline I told my wife that if, when I read the piece later, the first paragraph didn’t de-sensationalize the subject, I was going to write a rant condemning it on the principal that such an idea should be advocated only on a very limited basis. Well, the first paragraph did de-sensationalize the subject.
The thrust of the article was “lowering the dose of ‘these’ drugs in patients at risk of hypoglycemia or other antihyperglycemic adverse effects, or in whom the drug’s benefit is uncertain, due to frailty, dementia, or limited life expectancy. Since the authors define “elderly” as age ≥ 65 years, I might pick a fight over the definition of “limited life expectancy,” Haven’t the authors heard that 85 is the new 65? I guess not. ;-)
It turns out Medscape was reporting on yet another deprescribing project of the Bruyère Research Institute (BRI) in Ottawa, Canada. This deprescribing idea, in general, sounds like a laudatory objective, especially since the primary antihyperglycemic target of this report was sulfonylureas (SUs), specifically Glyburide. In this, I totally agree. Glyburide pumps the pancreas dry to secrete insulin, thus lowering the patient’s blood sugar but depleting the organ’s capacity and putting the patient at high risk of hypoglycemia, which is BRI’s point.
The secondary target of the report is injected insulin, specifically an old-fashioned, “high risk” form, NPH. The BRI report suggests instead “deprescribing” NPH and substituting insulin detemir or glargine. And instead of prescribing glyburide, it suggests that doctors switch their patients to “short or long acting gliclazide.”
Where the BRI report, and Medscape, miss the mark, in my opinion, is in the overly broad statement that “many older patients with diabetes are still being treated to A1c <7%.” They explicitly accept the suggestion that people over 65 should be held to a more lax standard: <7.5% in healthy older adults and <8.5% in the very frail elderly. BRI’s purpose is to avoid “those medications that can contribute to a low blood sugar” Hypos.
Regrettably, this relaxed standard is only necessary because of the Standards of Medical Care, the failed treatment protocol dictated by the medical establishment. Such high A1c’s are totally unnecessary.
But the report provides evidence of the adverse clinical effects associated with tight glycemic control on the elderly: cardiovascular events, cognitive impairment, fractures, reduced quality of life, increased emergency room visits, and hospitalization for hypoglycemia associated with a poor prognosis. All of these are outcomes of medication regimens, and all can be mitigated by “deprescribing” in the way BRI advocates, they assert.
There is, however, another way, a way that achieves a safe and low blood sugar control without the high risk associated with SU’s like glyburide, and injected insulins like NPH, or even detemir or glargine. The article suggests various antihyperglycemic agents that have no risk of hypoglycemia, such as DPP-4s, GLP-1s agonists, and Metformin. My doctor actually laughed when I asked him if I could get a hypo from Met while fasting. ;-)
There is also another way for the “elderly” to manage their blood sugar and also to completely avoid the risk of hypoglycemia: eating in a way that doesn’t raise your blood sugar: eating Very Low Carb (VLC). I was able to quickly stop all my diabetes meds (except Metformin) and lower my A1c from the mid 6s to 5.0, by eating VLC. My doctor had to immediately deprescribe my diabetes meds to “treat” several hypos in the first week! That was almost 17 years ago, and I haven’t had a hypo since, and I am now considered, clinically, non-diabetic. Now, that’s an even better outcome than switching from one antihyperglycemic med to another, no?

Thursday, March 14, 2019

Retrospective #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 too, 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, respectively, 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), and lactose (milk sugar).
Polysaccharides are long strings of glucose molecules. Think of them as stored energy (e.g. as glycogen in humans and starch in plants) and as structural components (cellulose in plants). The term carbohydrate includes any food that is composed of long-chain glucose molecules -- the so-called “complex carbohydrates,” such as cereals, bread, rice or pasta, or the mono and disaccharides (“sugars”), such as those found in 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 further into smaller molecules. Glucose is also, along with fat, a source of fuel for metabolism, glucose being always being the first used. When not immediately needed for energy, glucose is converted into its storage form, glycogen, mainly deposited in the liver and muscle cells.
The disaccharides (two molecule compounds) include sucrose (one glucose and one fructose molecule), lactose (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 have more than ten monosaccharide units.
The human diet contains many foods high in carbohydrates: fruit, 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 and other nutritional requirements 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, however, a nearly universal and 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. Human beings can easily and quickly break down starches into glucose.
A commonly held belief among the public, and even among nutritionists, is that complex carbohydrates (e.g. starches) are digested more slowly than simple carbohydrates (sugars) and thus healthier, especially for Type 2 diabetics. However, sugar (sucrose, a disaccharide), contains 50% fructose which is does not raise blood sugar, while some carbohydrates (e.g. breads), are 100% processed and refined glucose, and raise blood sugar rapidly.
It is not sufficient, therefore, to buy foods that trumpet their containing “whole grains.” The primary ingredients (those listed first) may be “bleached all purpose flour” (a processed food), water and some form of sugar: dextrose, molasses, sucrose or HFCS (all highly processed), before whole grains are added. If you see them sprinkled on the surface of a loaf of bread, that surface has been browned and the whole grains adhered with brushed-on HFCS.
 N.B.: For the record, for those who would doubt my authority to make some of the representations made herein, this Retrospective was largely cribbed in 2011, some of it verbatim, from the Wikipedia entry for “Carbohydrate.”

Retrospective #30: Is Fructose a Liver Toxin?

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 bread and other baked goods. For a fuller exposé, scroll down to Retrospective #29, “Fructose: Formerly Known as Fruit Sugar,” also archived on my blog at
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 2011 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. HFCS and cane sugar (sucrose) are basically the same, and both are equally bad for you.
Part of the problem is the unique way fructose is metabolized. Glucose, once it has been absorbed through the wall of the small intestine, is distributed throughout the body for energy. It is also stored as glycogen, mostly in the liver and muscles, to be ready for quick energy. Either way – used quickly or stored and used later – it is metabolized (broken down, “burned” or stored). Glucose is thus the most commonly available 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 processed there. Scientists, noting that the liver’s function is to filter out toxins, think that fructose is toxic. In this context, remember, before modern times, fruits were only seasonal and were far less sweet because they had not been hybridized. In addition, refined sugar didn’t exist.
When we eat large doses of sugar, the liver becomes overloaded with fructose. In the words of Robert H. Lustig, MD, presenter of UCSF’s YouTube video, “Sugar: The Bitter Truth,” fructose is “alcohol without the buzz.” Fructose is a “chronic hepatotoxin.” Excess fructose consumption over a long period of time is thus now thought to be the cause, and is certainly closely associated with, non-alcoholic fatty liver disease (NAFLD), also on a very steep rise.
In addition to Dr Lustig’s work, a 2005 a scientific paper titled “Fructose, insulin resistance and metabolic dyslipidemia,” from Department of Laboratory Medicine and Pathobiology, Hospital for Sick Children, University of 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…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...”
Simply put, Lustig says: “Fructose increases de novo lipogenesis (fat formation), triglycerides and free fatty acids.”  Fructose is a carbohydrate, but “it is metabolized like fat,” So, when the liver detoxifies fructose by making glucose, and has all the glycogen it can hold from a big slug of fructose, the liver makes fat (triglycerides) from fructose. Fat!
Dr. Lustig’s video 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 have some influence in Washington as well.

Retrospective #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, is 57% of the total sugar found in an average apple, but free glucose, another monosaccharide, is 23%. Sucrose, a disaccharide sugar, composed of equal parts fructose and glucose, is the remaining 20%. 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 (berries), fructose is also found in other foods found in nature, for example, 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, which as we said is equal parts fructose and glucose. Sucrose in its processed form is table sugar, which is made from refining sugar cane or sugar beets. Table sugar is therefore 50% fructose.
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), and 3) sucrose. HFCS is also used in baked goods to “improve browning, for palatability and taste enhancement.”
Starting in the early 70’s, as sugar consumption peaked in the U.S., HFCS began to erode 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 reasons fructose is used commercially in foods and beverages is its low cost and 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, according to Wikipedia.  The sweetness of fructose is “perceived earlier,” has a “higher peak,” and “exhibits a synergy effect when used in combination with other sweeteners.” It has “greater solubility,” “increases starch viscosity more rapidly, and achieves a higher final viscosity than sucrose.” It also “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,” according to Wikipedia. Now you know 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. Remember, sugar -- ordinary table sugar, made from sugar cane -- is half (50%) 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. It’s had over 8 million views. Or stay tuned. In the next Retrospective I will summarize Lustig’s answer to the question, “Is Fructose a Liver Toxin.” My original post in 2011 had over 1,000 hits. And the next, “Carbohydrates and Sugars,” about 10,000.

Retrospective #28: “I don’t eat sugar,” she protested.

I ran into a friend at the supermarket the other day and asked her how she was. She replied, “Fine…tired a lot.” Not wanting to miss an opportunity to proselytize, I suggested, “Sugar crash.” “I don’t eat sugar!” she protested. So, I asked her what she ate for breakfast. Therein lies a tale of folly and self-deception that deserves to be debunked.
Sugar, as she and virtually the whole world thinks, is just table sugar, as in “added sugar” such as that sprinkled on cereal. It’s also a major ingredient in candy, ice cream and, formerly, soft drinks (high fructose corn syrup, today).
Table sugar, the “added sugar”, is cane sugar and is chemically known as sucrose. It is a disaccharide, meaning it is composed of two simple sugar molecules: fructose and 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 (single molecule sugar), before entering the blood stream through the wall of the small intestine.
Sugars in this “added sugar” sense do not include those found in fruit. But sugar in fruit is a combination of free (single-cell) fructose, free glucose and sucrose, a disaccharide. Fruit sugars are thus not regarded as “added sugar” because they are an inherent or integral component of this “real” or whole food found in nature. Forget that for centuries, to appeal to our sweet tooth, hybridizers have been making fruit sweeter than those found in nature.
All carbohydrates are saccharides. Sugars, as found in fruit, are the simple, single and double-celled saccharides. Other carbohydrates, including cereals, bread, potatoes, rice and pasta, are more complex compounds, called polysaccharides, meaning composed of many molecules, most of them glucose. Nevertheless, these long chains of glucose molecules all break down in the digestion process to the simple sugar glucose. Glucose goes to the cells for energy. Fructose goes directly to the liver and is stored, if there’s room, as glycogen, or as fat. That’s right, fat!
Back to the question I asked 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], toast and jelly.” That’s all sugar,” I exclaimed!
I continued, explaining, “If you eat a lot of “sugars” – carbohydrates → glucose, thus ANY FOOD EXCEPT FAT AND PROTEIN -- all at once, your blood stream will, sooner or later (1 to 2 hours, generally, depending on the food and condition of your metabolism, be flooded with “sugar” (glucose). Then, after the glucose gets delivered to muscles and organs by the hormone insulin, your blood sugar will CRASH and you will ‘feel tired’ (and hungry) again.”
So, when your “all sugar” breakfast is digested, in mid-morning your body will again crave “sugar” (i.e., anything that will break down to glucose) to “feed the beast.” A “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” (glucose) in the blood. It will also overwork your pancreas to produce more insulin. A vicious cycle.
Over a course of years, the cellular receptors of “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 people, the pancreas will slowly burn out. The beta cells in the pancreas that produce insulin will stop working. They will clog up or 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, in his 2008 keynote address to the American Diabetes Association at their annual meeting in San Francisco.  You will be diagnosed with full-blown Type 2 Diabetes and likely drug dependent for the rest of your life. You will then be watchful for, or worse still, diagnosed with a “dreaded complication”: neuropathy, retinopathy, and nephropathy (end-stage kidney disease).
The “new” (2010) diagnostic standard for T2 diabetes is an A1c of 6.5%. Previously (from 2002), the diagnostic standard for Pre-diabetes was a FBG of 100-125mg/dl and for Type 2, ≥126mg/dl (cut from 140mg/dl in 1997). Some endocrinologists today use a lower standard, regarding an A1c of 5.7% as indicating full-blown Type 2.
So, to stay healthy, watch your total “sugars” and remember: All carbohydrates are saccharides (“sugars”). Your body breaks all carbs down into glucose, or “blood sugar.” If you still think you “don’t eat “sugar,” read this again!

Retrospective #27: “…the strongest predictor of a heart attack”

The contemporary medical literature is replete with macro analyses and other epidemiological studies that attempt to show 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 Retrospective we’ll put a fine point on the subject of lipid ratios.
In the 1960’s Total Cholesterol (TC) became a common and inexpensive test. As the main metric of “the Lipid Hypothesis,” created by Ancel Keys and popularized by the American Heart Association, it became the universal marker for predicting heart disease risk. That was more than half a century ago. We’ve come a long way since then.
The dietary advice then and now for high Total Cholesterol was to eat less saturated fat and other animal foods high in dietary cholesterol. This was the modality even though the body needs cholesterol for many essential purposes (see Retrospective #24), and it makes up what we don’t eat by manufacturing it as needed. The threshold for high Total Cholesterol was established at 200mg/dl. It remains today at 200mg/dl.
Low density lipoprotein (LDL) is a component of TC. Even though the common test developed and used then and now 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. A recent AMA editorial suggested by 2020 Lipitor, Crestor, Zocor, and their generics will approach $1 trillion in world-wide annual sales.
At the same time medical science has come to have an increased understanding of other components of the Lipid Panel – High Density Lipoproteins (HDL) and Triglycerides (TG) –and their role in Cardio Vascular Disease (CVD) risk. Unfortunately, these developments have garnered little attention since Big Pharma hasn’t developed blockbuster drugs to influence them. Fish oil lowers Triglycerides (see Retrospective #22), but fish oil can’t be patented.
Most lipid panel lab results these days do however include a ratio of TC to HDL (TC/HDL) with a recommendation that it should be less than 5.0. So, if your TC is 200, then HDL should not be less than 40. While this at least recognizes the importance of HDL, it is not a standard to be emulated. It is dangerous. A good ratio is ≤3.5.
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, importantly, that neither TC nor LDL is a factor in this formula. This ratio is considered by informed clinicians today to be more reliable than LDL, TC/HDL, or chronic systemic inflammation, hsCRP, the marker my doctor 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, interpreted to mean a very low probability of heart attack.
Big Pharma is hard at work looking for the next blockbuster drug to lower Triglycerides or raise HDL. Alas, so far, diet -- that is, the food we eat -- is the only thing that seems to work, and Big Pharma isn’t in that business.
Agribusiness, however, sees the potential for a huge piece of the action here, but there isn’t much profit in “real food.” Ask your local farmer. But processed foods – that can be labelled and marketed as “heart healthy, have gained the stamp of approval of the American Heart Association, whose budget is largely supported by the very same Agribusinesses. These processed foods, however, do not improve your TG/HDL ratio. They make it worse!
In the coming weeks we will return often to the subject of so-called “healthy eating.” Our goal will be to help YOU to improve your TG/HDL ratio. Of course, to do that, you will need to have a baseline Lipid Profile. If you haven’t had a Cholesterol Panel done lately, or you don’t know yours, ask your doctor to do one and send you a copy. And ask him to see how yours shapes up using the new gold standard for CVD risk: the TG/HDL ratio.