Saturday, March 23, 2019

Retrospective #35: The Diet Doctor and the LCHF Diet

Back in 2011, butter was in great demand in Norway, and the new Swedish Diet Doctor website was getting 19,000 hits a day. The “real food” revolution had come to Scandinavia, according to Andreas Eenfeldt, MD, Diet Doctor founder, speaking at the 1st meeting of the Ancestral Health Symposium in Los Angeles, CA, that August. Today (March 2019), dietdoctor.com gets 350,000 visits a day, and Andreas Eenfeldt is still leading the “diet” revolution.
Dr. Eenfeldt came to my attention from a video link on Jimmy Moore’s Livin’ la Vida website.  Eenfeldt told how physician Annika Dahlqvist, who pioneered Low Carb High Fat (LCHF) diets in Sweden after failing to lose weight herself, was reported to the authorities for not adhering to the government’s healthy eating program in her practice. She was turned in for malpractice! So, the Swedish National Board of Health and Welfare, Sweden’s highest medical authority, decided to investigate. Fortunately, after a thorough investigation, they declared the LCHF diet was “compatible with scientific evidence and best practice.” Dr. Dahlqvist became an instant sensation and national hero. “Today,” Dr. Eenfeldt said in 2011, “twenty-three percent of Swedes are trying to eat low carb.”
The Swedish National Board of Health and Welfare deserves a lot of credit for their evidence-based determination. They made what amounts to a paradigm shift in national nutrition policy. In this country, we have not made nearly as much progress, despite the fact that most respected scientific journals now openly trumpet the news that there is “… no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD” and “…there were no clear effects of dietary fat changes on total mortality and cardiovascular mortality.”
The 2010 USDA’s Dietary Guidelines for Americans (DGA), published January 2011, govern school breakfasts and lunches, the WIC program, food stamps, and prison and military dietary programs. And they still call for Americans to avoid saturated fat and substitute instead processed “vegetable” oils. See Retrospective #21 below. And our media and most clinical practitioners still preach the low-fat, high-carbohydrate, “mostly plants” gospel.
In Sweden, Dr. Eenfeldt reports that Göran Berglund, Professor of Internal Medicine at Lund University, said, “Two generations of Swedes have been given bad dietary advice and have avoided fat for no reason. It’s time to rewrite the dietary guidelines and base them on modern science.” Fredrik Nyström, Professor of Internal Medicine at Linköping, said, “People have been recommending low fat diets for 30 years, and then it turns out to be completely wrong! There is no proven correlation between saturated fats and cardiovascular disease.”
Peter Nilsson, Professor of Cardiovascular Research at Lund, said, “It’s time to face the facts. There is no connection between saturated fats and cardiovascular disease.” Dr. Eenfeldt, who provided these quotes in his video presentation to the Ancestral Health Symposium meeting, then states: “Fear of saturated fats and cholesterol is the foundation for what has become known at the diet-heart or lipid hypothesis.” Eenfeldt continued, “When the foundation falls, the entire low-fat advice falls.” In other words, the Low-Fat diet that we have been misled into following, NOT the currently surging LCHF diet, is the fad diet.
What we are seeing, Dr. Eenfeldt says, is a paradigm shift. Saturated fat which was bad…is now good. Carbohydrates that were once thought to be good…now make us fat and sick when we eat too many. Diabetics are getting sicker every year, based on the bad dietary and medical advice they are getting. And it is getting worse.
Under the current circumstances, Dr. Eenfeldt asks on the video, who thinks that the U.S. Department of Agriculture, under whose auspices the Dietary Guidelines are prepared, is going to stop recommending that we eat grains anytime soon. The diet doctor website (in 2012 when this was originally written) lists fourteen randomized controlled trials that show significantly more weight loss with low carb diets than low fat diets. All have links to the respected peer-reviewed journals that published them. The dietdoctor.com site is an evidence-based resource.
Dr. Eenfeldt’s presentation was well received by a like-minded audience of scientists, doctors and interested lay people. He concluded with a quote from Victor Hugo: “All the forces in the world are not so powerful as an idea whose time has come.” “The paradigm shift is coming,” he said. “We can change the world.” And he has.

Friday, March 22, 2019

Retrospective #34: Foods that Raise HDL

“HAPPY HOLIDAYS TO YOU ALL,” my doctor, an internist and cardiologist, wrote in an email that he broadcast to his patients in January 2012. I returned the wish and requested ideas for subjects for my blog, which he followed.
To my delight he replied with some pithy titles, the first of which was “Foods that raise HDL.” HDL is “the good cholesterol” in your lipid profile. He was interested because my HDL had almost doubled from 43 average to 78 average since he suggested that I begin eating Very Low Carb (VLC) 10 years earlier. And he observed the changes.
The desired range for men is ≥40mg/dl, and for women ≥ 50mg/dl. Before I started to eat VLC my HDLs averaged 43 (16 values over 22 years: 48, 44, 61, 53, 50, 42, 41, 39, 38, 37, 38, 38, 39, 41, 39 & 42). Since I began eating VLC my HDLs have averaged 78 (14 values: 67, 92, 78, 71, 78, 81, 86, 91, 98, 67, 57, 63, 79 & 86). I don't know what has caused my HDL to go up since I started eating Very Low Carb, but it's gotta be the foods I eat. What else?
The other lipid test that has dramatically improved over the same period is triglycerides.  Before I started Very Low Carb, my triglyceride average of 21 previous lipid tests was 137. My triglycerides average for the last (most recent) 21 lipid tests has been 54. I attribute this dramatic improvement mostly to taking fish oil supplements (4 grams/day initially, then down to 2 grams/day). I also eat a can of sardines packed in olive oil almost every day for lunch.
At the time (2012), for breakfast I ate 2 fried eggs, 2 strips of bacon, and a big cup of coffee with full cream and two Splenda. For lunch I usually ate a can of sardines in olive oil and some Splenda sweetened iced tea. Note: both meals, all protein and fat; No juice or fruit or bread or cereal or jelly or milk or sugar, all high in carbohydrates.  
I ate no snacks mid-morning or mid-afternoon. I didn’t need them. I wasn’t hungry. The fat and protein provided satiety and supported my other needs.  My body was running on fat, my fat, both the fat I ate and my body fat.  I was now a ‘fat burner,’ not a ‘sugar burner.’ The body gets the small amount of glucose it needs from the small amount I eat and from ketone bodies from the breakdown of fat cells (triglycerides) and from gluconeogenesis.
Gluconeogenesis occurs when the amino acids from the protein I ate that was not taken up by muscles, etc. is stored in the liver and is then reconstituted as glucose (“gluco-neo-genesis”) when the body needs it.
For dinner I ate a small portion of protein (roasted, baked or broiled, not deep fried), a selected vegetable, and sometimes a glass or two of red wine. I avoided carrots, peas, corn or beets. They all contain too much sugar. And, of course, I don’t eat pasta or starchy root vegetables like potatoes, or winter squash, or grains like rice and couscous. I also try to avoid everything made with or cooked in vegetable oil, -- any “vegetable” (seed) oil. The oils I use are olive oil, butter, ghee and coconut oil, a very good “Medium Chain Triglyceride,” It’s a saturated fat, but because of its medium chain length, it ‘burns’ quickly and easily for energy, instead of being stored as body fat.
I intentionally select fatty meats and fish, eat chicken with the skin on (the skin is mostly monounsaturated fat), and like to slow cook (braise) grass-fed cuts of meat (brisket, osso bucco, shanks, hocks, etc. I do not limit dietary saturated fats or cholesterol. I eat all the shrimp and liver and free-range, pastured chicken eggs I want. And the result? Well, go back to the beginning of this Retrospective. My HDL has gone from 43 to 78 and my triglycerides from 137 to 54, on account of what I eat. My LDL and Total Cholesterol have both remained essentially constant.
So, doc, my answer to your question is that I really don’t know what SPECIFIC foods have raised my HDL and lowered my triglycerides. My answer is it’s the Way of Eating YOU SUGGESTED 10 years ago after you read Gary Taubes’ cover story, “What If It’s All Been a Big Fat Lie” in The New York Times Sunday Magazine.  You told me that after you read that article, you tried the diet yourself for 6 weeks and lost 17 pounds. You then suggested I do it too. And, as you know, I lost 170 pounds!

Thursday, March 21, 2019

Retrospective #33: Omental Adiposity

I coined that phrase. Dontcha love it? What I’m talking about is the increasingly common “beer belly” on men of a certain age -- men who look nine months pregnant before the baby has “dropped:” A high, hard abdomen, which is actually your peritoneal cavity filled with visceral fat around your organs. Your jacket button doesn’t button any more. You can’t hug without first bumping into the huggee. I know. I was “there” once, before I lost 170 pounds.
I first came across the noun form “omentum” about 2005 in, “You on a Diet,” a book by a Canadian doctor, Michael Roizen, popularized by Oprah and a PBS series. The omentum is a sheet of fat that is covered by the peritoneum. The greater omentum is attached to the bottom edge of the stomach, and hangs down in front of the intestines. The other edge attaches to the transverse colon. The lesser omentum is attached to the top edge of the stomach, and extends to the undersurface of the liver. In humans, especially men who make bad food choices, the omentum is a mass of fat around and especially in front of the stomach, liver, spleen, pancreas, kidneys and intestines.
This “visceral fat, also known as organ fat or intra-abdominal fat, is located inside the peritoneal cavity, packed in between internal organs and torso. It is differentiated from subcutaneous fat which is underneath the skin, and intra-muscular fat which is interspersed in skeletal muscle. Other distinctly different types of body fat include bone marrow fat and epicardial fat, which is deposited around the heart and found to be a metabolically active organ.
The common understanding of obesity is a net energy imbalance. The fundamental cause of obesity, however, is a metabolic disorder of fat regulation. There is a growing consensus that, in humans, central obesity is related to the excessive consumption of fructose. It is also associated with elevated levels of the hormone insulin. In a large study (NHANES III), excessive waist circumference appears to be more of a risk factor for metabolic syndrome than BMI (Body Mass Index). The Central Obesity Index (CBI) is another measure more predictive of increased risk than BMI.
Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Type II diabetes. Belly fat is a symptom of Metabolic Syndrome. (Scroll down to see Retrospective #9). Central obesity is also associated with glucose intolerance and dyslipidemia (“high cholesterol”), as well as a group of diseases that are either inherited or due to secondary causes (Cushing’s syndrome, PCOS, and treatment for AIDS).
Central obesity is known to predispose individuals for insulin resistance and Type 2 diabetes. Discoveries in recent decades have revealed that abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Central obesity seems to be the foremost type of fat deposit contributing to rising levels of serum resistin, one such hormone. Conversely, serum resistin levels have been found to decline with weight loss, especially decreased central obesity. Central obesity is metabolically very unhealthy!
Of course, there are sex differences in fat accumulation. Female sex hormones cause fat to be stored in the buttocks, hips and thighs. Men are more likely to have fat stored in the belly. When a woman reaches menopause and estrogen production declines, fat migrates from the buttocks, hips and thighs to the waist and belly.
So, what can be done about “omental adiposity”? Low fat and restricted calorie diets have not proven to be an effective long-term intervention. Most people regain the weight that was lost and many regain still more. Spot exercises, such as sit-ups, crunches and other abdominal exercises are useful in building abdominal muscles, but they have little, if any, effect on the adipose tissue located there. And, just for the record, there is little evidence that beer drinkers are more prone to abdominal adiposity than non-drinkers or drinkers of wine or spirits.
The best way to lose and keep off excess omental weight – the “pot belly” – is a diet that provides satiety (a high fat diet), that digests slowly and restores skeletal muscle (moderate protein), and that allows you to burn body fat for energy. That diet is a low carbohydrate diet. See Retrospective #11 (scroll down), or, on Facebook, search my Time Line. After the body burns the “sugars” (glucose) in carbs for energy, it turns to fat for energy, both dietary and body fat. I know. I’ve regained some of the 170 pounds that I lost, but I have lost my “beer belly” forever.

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 www.thenutritiondebate.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 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.