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.

Retrospective #26: The Cause and Treatment of Heart Disease

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.” It was written by Sally Fallon, founder and president, and Mary Enig, PhD. This quotation from “The Skinny on Fats” 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 [i.e  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.
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. Thus, 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 (cholesterol) profile. Ask your doctor for a copy of your most recent lipid panel, or have him/her order one for you. Then show them column #25 in this series: “Understanding Your Lipid Profile” and discuss your profile in that context. Ask your doctor is he/she agrees with my analysis. And ask if it would matter to them what you ate so long as you achieved that kind of outcome in just a few months. I did, and you could too, if you change what you eat and follow a LCHF Way of Eating carefully.

Wednesday, March 13, 2019

Retrospective #25: Understanding Your Lipid (Cholesterol) Panel

I am not a doctor or other health care professional, but I can read a lab test report, especially one that provides a “Reference Range” and declares a result “IN range” or “OUT OF range,” plus other guidance, for each test ordered.
At each office visit, my doctor always orders a complete blood count (CBC) and a metabolic series, including a lipid panel, plus an A1c. And from time to time, he orders other specialty tests (High Sensitivity CRP, liver, thyroid, kidney, etc.). This column is going to be about understanding the lipid panel. That includes Total Cholesterol, HDL-C, LDL-C (calculated), Triglycerides, and the Total Cholesterol/HDL Ratio. Some panels now also include non-HDL-C.
Most people know the drill: “high” Total Cholesterol is not a good thing, and that there is “good” cholesterol (HDL-C) and a “bad” cholesterol (LDL-C), and that we should try to get our circulating triglyceride levels down. If we aren’t successful at doing this, by following the doctor’s advice to limit saturated fat and cholesterol containing foods, he (ort she) is going to prescribe a statin drug, which will lower LDL-C and, thereby, Total Cholesterol as well. We are going to be asked to support this gazillion dollar annual statin industry by taking Crestor, Lipitor, Zocor, or Simvastatin, the Zocor generic equivalent. (Remember, the original of this Retrospective was written in 2011.)
This column is not about the efficacy or safety of prescribing a statin. Personally, I disagree with the current practice. I do not think statins should be prescribed to anyone without diagnosed heart disease, or anyone over 75 or any woman whatsoever.  There is no proven benefit. But this column is about “understanding your lipid panel.”
 So, let us suppose that two people (or the same person, in two “snapshots” of lipid panels taken at different times) have identical Total Cholesterol, i.e.: 200mg/dl (milligrams per deciliter). One has an HDL-C = 40mg/dl, an LDL-C = 130mg/dl (calculated), a Triglyceride count of 150mg/dl, and a Total Cholesterol/HDL ratio of 5.0ALL FIVE OF THESE VALUES ARE BORDERLINE OUT-OF-RANGE. They would appear in BOLD in the “OUT-OF-RANGE” column on your lab report. Your doctor would tell you, according to my understanding of the “Standards of Medical Practice,” to cut down on all those saturated fat and cholesterol containing foods, and immediately start taking a statin.
Now let’s look at another lipid panel: Total Cholesterol also 200mg/dl, HDL-C = 80mg/dl, LDL-C = 110mg/dl (calculated), Triglycerides = 50mg/dl, and a Total Cholesterol/HDL ratio of 2.5. The only value that is borderline high in this panel is Total Cholesterol at 200mg/dl. Everything else is textbook WUNDERBAR! The LDL-C is above optimal (<100mg/dl), but it is a derived (calculated) value, not a DIRECT value (and in 2018 the formula changed).
The formula for LDL-C in the lipid panel, until 2018, was the Friedewald formula: LDL-C = Total Cholesterol – HDL-C – Triglycerides/5. And, if your doctor was worried about your less than optimal LDL’s (because of existing heart disease, other cardiac risk factors such as hypertension, obesity, metabolic syndrome or higher than “normal” fasting plasma glucose or A1c) he could order an LDL direct measurement or an even more sophisticated VAP test of LDL-C particle size (“A”= “large and buoyant” or “B” =“small and dense.”) Regardless, this lipid panel would NOT lead your doctor to prescribe a statin or suggest a dietary change. He would tell you, “Everything looks great!” and “Continue with whatever you are doing.” Think about that. Both TC’s (Total Cholesterols) are the same: 200mg/dl.
To recap: A Total Cholesterol test score of 200mg/dl on your lipid panel, with the first set of values above, will put you on dietary restrictions, and when that “prescription” doesn’t work, on a statin. That’s what happened to me. I followed my doctor’s dietary advice, it failed, and I was on a statin for 5 years, until I changed my diet…
But if you have a lipid panel like the second example, you’ll be your doctor’s “poster boy,” as I was after I’d been on a Very Low-Carb, High-Fat Way of Eating for a year, again on my doctor’s advice. Even though he started me on LOW-CARB, HIGH-FAT to lose weight, he doesn’t want to know what I eat. My doctor (a cardiologist) now just tells me to keep on doing what I’m doing. For him, it’s no more lectures – just smiles, and when the test results come back, a congratulatory phone call. For my doctor, my office visit is one of the “high points” of his day, he’s told me. 

Tuesday, March 12, 2019

Retrospective #24: But What About Cholesterol?

What about cholesterol? What about dietary cholesterol? Again, quoting from WAPF’s Sally Fallon and Mary Enig, PhD, authors in 2000 of “The Skinny on Fats: “Here, too, the public has been misinformed. Our blood vessels can become damaged in a number of ways—through irritations caused by free radicals or viruses, or because they are structurally weak—and when this happens, the body's natural healing substance steps in to repair the damage. That substance is cholesterol. Cholesterol is a high-molecular-weight alcohol that is manufactured in the liver and in most human cells. Like saturated fats, the cholesterol we make and consume plays many vital roles:
  • Along with saturated fats, cholesterol in the cell membrane gives our cells necessary stiffness and stability. When the diet contains an excess of polyunsaturated fatty acids, these replace saturated fatty acids in the cell membrane, so that the cell walls actually become flabby. When this happens, cholesterol from the blood is "driven" into the tissues to give them structural integrity. This is why serum cholesterol levels may go down temporarily when we replace saturated fats with polyunsaturated oils in the diet.46
  • Cholesterol acts as a precursor to vital corticosteroids, hormones that help us deal with stress and protect the body against heart disease and cancer; and to the sex hormones like androgen, testosterone, estrogen and progesterone.
  • Cholesterol is a precursor to vitamin D, a very important fat-soluble vitamin needed for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function.
  • The bile salts are made from cholesterol. Bile is vital for digestion and assimilation of fats in the diet.
  • Recent research shows that cholesterol acts as an antioxidant.47 This is the likely explanation for the fact that cholesterol levels go up with age. As an antioxidant, cholesterol protects us against free radical damage that leads to heart disease and cancer.
  • Cholesterol is needed for proper function of serotonin receptors in the brain.48 Serotonin is the body's natural "feel-good" chemical. Low cholesterol levels have been linked to aggressive and violent behavior, depression and suicidal tendencies.
  • Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system.
  • Dietary cholesterol plays an important role in maintaining the health of the intestinal wall.49 This is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal disorders.
Cholesterol is not the cause of heart disease but rather a potent antioxidant weapon against free radicals in the blood, and a repair substance that helps heal arterial damage (although arterial plaques themselves contain very little cholesterol.) However, like fats, cholesterol may be damaged by exposure to heat and oxygen. This damaged or oxidized cholesterol seems to promote injury to the arterial cells as well as a buildup of plaque in the arteries.50
Damaged cholesterol is found in powdered eggs, in powdered milk (added to reduced-fat milks to give them body) and in meats and fats that have been heated to high temperatures in frying and other high-temperature processes. High serum cholesterol levels often indicate that the body needs cholesterol to protect itself from high levels of altered, free-radical-containing fats. Just as a large police force is needed in a place where crime occurs frequently, so cholesterol is needed in a poorly nourished body to protect the individual from a tendency to heart disease and cancer. Blaming coronary heart disease on cholesterol is like blaming the police for murder and theft in a high crime area.” End of long quote. Note: all the footnotes are in the Weston A. Price article, “The Skinny on Fats.”
To add insult to injury, remember that our own liver and cells make cholesterol to “make up” for all those good foods (eggs, butter, cream, marbled beef, shrimp, liver, etc.) that we avoid eating to follow doctor’s orders. It has too. Our body needs cholesterol to do the things described above, and it works holistically to get what it needs. It’s a good thing too. Imagine if the human race were dependent for survival on the vagaries of a government’s public health policies. I’ll take autonomic homeostatic regulation over the Dietary Guidelines for Americans any day.

Monday, March 11, 2019

Retrospective #23: The Benefits of Saturated Fats

Benefits of Saturated Fats? Admitting to such a belief is surely heretical, so I do not expect my reader to commit such apostasy “on faith.” But, purely as an observer of another’s fall from grace, you may want to read further to see how this idea developed and is supported by science. If this sounds like a classic battle of orthodoxy vs. the enlightened, you’re right. You certainly won’t hear it spoken by any of the usual sources of information in our modern society: Government, Agri-Business, Big Pharma, the medical and public health establishments, and the Mass Media. Who but the small, grass-fed beef or pastured egg purveyor might benefit, besides YOU?
Mary Enig, PhD, (1931-2014), was a Director Emeritus of the Weston A. Price Foundation (WAPF). Together with Sally Fallon, President and Founder of WAPF, they wrote in 2000, “The Skinny on Fats.” This is still a really “must read” for anyone interested in eating in a healthy way and living a long life. Do yourself a favor and Google it.
Because it is more technical than I am qualified to write about, and cites many sources as references, I quote from it directly here. Find the 8 references cited from “The Skinny on Fats” at the Foundation’s website.
“The much-maligned saturated fats—which Americans are trying to avoid—are not the cause of our modern diseases. In fact, they play many important roles in the body chemistry:
  • Saturated fatty acids constitute at least 50% of the cell membranes. They are what give our cells necessary stiffness and integrity.
  • They play a vital role in the health of our bones. For calcium to be effectively incorporated into the skeletal structure, at least 50% of the dietary fats should be saturated.38
  • They lower Lp(a), a substance in the blood that indicates proneness to heart disease.39 They protect the liver from alcohol and other toxins, such as Tylenol.40
  • They enhance the immune system.41
  • They are needed for the proper utilization of essential fatty acids.
    Elongated omega-3 fatty acids are better retained in the tissues when the diet is rich in saturated fats.
  • Saturated 18-carbon stearic acid and 16-carbon palmitic acid are the preferred foods for the heart, which is why the fat around the heart muscle is highly saturated.43 The heart draws on this reserve of fat in times of stress.
  • Short-and medium-chain saturated fatty acids have important antimicrobial properties. They protect us against harmful microorganisms in the digestive tract.
The scientific evidence, honestly evaluated, does not support the assertion that "artery-clogging" saturated fats cause heart disease.44 Actually, evaluation of the fat in artery clogs reveals that only about 26% is saturated. The rest is unsaturated, of which more than half is polyunsaturated.45(end of quote from “The Skinny on Fats”)
Among the most vilified of animal foods high in saturated fats is butter. As previously noted, it is now enjoying a comeback, while margarine, made from partially hydrogenated vegetable oil (trans fat), has suffered a decline.
In 2000, before her more than 20-year campaign to bring trans fats to the public’s attention had reached full fruition (she had testified on it at the 1977 McGovern Commission), Dr. Enig wrote (again, in “The Skinny on Fats”):
“The Diet Dictocrats have succeeded in convincing Americans that butter is dangerous, when in fact it is a valued component of many traditional diets and a source of…fat-soluble vitamins. These include true vitamin A or retinol, vitamin D, vitamin K and vitamin E as well as all their naturally occurring cofactors needed to obtain maximum effect. Butter is America's best source of these important nutrients. In fact, vitamin A is more easily absorbed and utilized from butter than from other sources.61 Fortunately, these fat-soluble vitamins are relatively stable and survive the pasteurization process.”
But what about cholesterol and heart disease? Well, if you’re still asking these questions, I recommend you go back and read this Retrospective series from the beginning. Or, if you’re just a little skeptical, stay tuned; the next article will be “What About Dietary Cholesterol?” and then the next, “Understanding Your Lipid Panel.” The apostasy goes on and on unabated, for your reading pleasure. This is just #23 in a series of 500 heretical essays on Healthy Eating.

Sunday, March 10, 2019

Type 2 Nutrition #476: Martin/Hopkins, “a better LDL calculation method”

Last year I noticed that Quest Laboratories had changed their method of calculating low-density lipoprotein (LDL-C) on my lab report. For more than 40 years the method used was the Friedewald formula (LDL-C = TC – HDL – TG/5), where TG/5 (TG<400mg/dl) was a surrogate for VLDL cholesterol. The method Quest uses now is the Martin/Hopkins method. Quest says that this “novel” method is “more accurate than the usual method.”
Of course, the most accurate method to measure LDL-C is a DIRECT measurement, not a calculation. Dr. Michael Eades explains this on his website and I discuss it here. It requires another test – a special test which is expensive and generally not done unless you request it and your doctor and insurer agree.
I’m writing about this change because, based on what Dr. Eades wrote, and from my own affirming data, I assumed that Quest changed to the new method because the new method reported a lower LDL-C. To my surprise, while doing some research recently, I discovered that the new method actually shows a higher LDL-C.  I found the story here in MEDPAGE TODAY, under Cardiology > Dyslipidemia. The sub-title of the article is, “Friedewald lowballed lipids; Martin/Hopkins was on par with lab reference” [for patients with stable CVD].
“According to an analysis of the FOURIER trial, the median Martin/Hopkins LDL cholesterol level was 2mg/dl below the reference standard of preparative ultracentrifugation – a statistically similar result, whereas the Friedewald method underestimated LDL cholesterol by 4mg/dl (P<0.001)” (all emphases added by me). So, relative to Friedewald, Martin/Hopkins produced an LDL-C that was 2mg/dl higher.
“While 22.9% of Martin/Hopkins LDL cholesterol values were at least 5mg/dl different from reference and 2.6% were off by more than 10mg/dl, these proportions were 40.1% and 13.3% with Friedewald estimation.” NB: “The difference between methods was more pronounced when triglyceride levels exceeded 150mg/dl.”
While the MEDPAGE TODAY article did not give the whole Martin/Hopkins formula, it did reveal that “the Martin/Hopkins method ‘uses the same standard lipid measurements of total and HDL (high-density lipoprotein) cholesterol and triglycerides as the Friedewald equation does, but it uses a personalized rather than a fixed conversion factor in calculating LDL cholesterol levels,’ Martin and colleagues noted.”
A “personalized conversion factor”? If Quest’s use of a personal conversion factor usually results in an LDL-C higher (even if only 2 mg/dl), I find it intriguing that on the three lab reports I’ve had since Quest switched to the Martin/Hopkins method, my personal LDL-C values have all dropped below where they were before. This is why I presumed, based on what Dr. Eades had said about a DIRECT measurement, that my own values would probably be lower, not higher, using the new method as it was intended.
For the 3 tests before the switch from Friedewald to Martin/Hopkins, my LDL-C values were 101, 114 and 100mg/dl. Then, using Martin/Hopkins, the Quest reports for my last 3 labs were 87, 79 and 83mg/dl. Of course, my labs were for different samples, but I have not changed my Way of Eating. Why are my LDLs lower?
Chol/HDL ratio
LDL (calc.)
Triglycerides (TG)
 * calculated by Martin/Hopkins method   ** first TG > 100mg/dl in 12 years
The JAMA article explains: Martin/Hopkins uses statistics for 3 stratifications of TGs from 100 to 399mg/dl, which resulted in higher LDLs. My lower LDLs are because my 3 most recent TGs have all been in the mid-50s.