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Sunday, October 30, 2011

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.

Sunday, October 23, 2011

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.

Sunday, October 9, 2011

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.

About Me

I was diagnosed a Type 2 diabetic in 1986. I started a Very Low Carb diet (Atkins Induction) in 2002 to lose weight. I didn’t realize at the time that it would put my diabetes in clinical remission, or that I would be able to give up almost all of my oral diabetes meds. I also didn’t understand that, as I lost weight and continued to eat Very Low Carb, my blood lipids would dramatically improve (doubling my HDL and cutting my triglycerides by 2/3rds) and that my blood pressure would drop from 130/90 to 110/70 on the same meds.
Over the years I changed from Atkins to the Bernstein Diet (designed for diabetics) and, altogether lost 170 pounds. I later regained some and then lost some. As long as I eat Very Low Carb, I am not hungry and I have lots of energy. And I no longer have any of the indications of Metabolic Syndrome.
My goal, as long as I have excess body fat, is to remain continuously in a ketogenic state, both for blood glucose regulation and continued weight loss. I expect that this regimen will continue to provide the benefits of reduced systemic inflammation, improved blood lipids and lower blood pressure as well.