Sunday, March 31, 2019

Retrospective #54: Loren Cordain, Robb Wolf and Kurt Harris

What do these three guys have in common? If you answered Paleolithic nutrition, only Kurt Harris, MD would disagree. Harris’s interest in nutrition was piqued after he read science writer Gary Taubes’s “Good Calories – Bad Calories,” (“The Diet Delusion” in the UK). At first, he called his blog PaNu for Paleolithic Nutrition. He subsequently changed the name to Archevore, deleting the reference to Paleo. Before he disappeared into the ether 5 or 6 years ago, he said his thinking continued to evolve. His website used to say that his thinking “is not derived from a single science or field of inquiry, but draws first on medical sciences like biochemistry and endocrinology, and only then looks back with history and paleoanthropology.” I liked that. I miss Kurt Harris’s presence in the blogosphere.
In 2012 other differences between Harris and the other two is that Dr. Harris hadn’t written a book. Cordain has a PhD in exercise physiology, and Wolf has a BS in Biochemistry, a popular podcast on Paleolithic nutrition and exercise, and is a power lifting champ and weightlifting coach. He worked with Cordain in his biochemistry lab and describes Cordain as his mentor. Cordain’s book, “The Paleo Diet” (2002) was a best seller. Before writing this column, I had read the 2011 revised edition. I had also read Wolf’s book, “The Paleo Solution,” published in 2010.
Both books preach essentially the basic Paleo prescription: no grains, no dairy, no added sugars, no legumes and very little salt. Eat only lean meat, non-starchy fruits and vegetables (for vitamins, phytochemicals and fiber) and mostly monounsaturated and some polyunsaturated fats.  Both diets cut you some slack in different ways. To induce you to try it, I think, Cordain gives you a day or two “off diet” a week. Wolf says “just try it for a month” to see and feel the difference. Cordain allows a little honey; Wolf says, barring autoimmune problems, “it’s tough to build much of a case against grass-fed butter.” Both authors advocate lots of exercise.
Cordain’s “The Paleo Diet” is a useful introduction to the paleo way of eating, as are many online sources. It is designed for someone who doesn’t want to get “into the weeds” of the science, and asks the reader to trust in the author’s academic research credentials and lab staff. He assumes you won’t eat much organ meat, so he substitutes plant protein for the nutrients you would otherwise miss. He advises that you only eat “lean meat” and fats mostly from monounsaturated and polyunsaturated sources, the latter for the essential Omega 6 and Omega 3 fatty acids. In the revised edition he says he has “softened his stance on the saturated fat issue,” allowing that stearic acid, from grass-fed beef, is “healthful,” unlike palmitic acid “which dominates the fat of feedlot cattle.”
Wolf’s book, “The Paleo Solution,” starts off with a primer in Paleo biochemistry for the non-geek. His book also has a lot more energy and is more fun to read. It seems to be geared to a younger demographic. Interestingly, Cordain’s book makes many references to “fad low-carb diets,” while Wolf’s target is vegans. Being a long-term Type 2 diabetic and low-carber myself, and acutely aware of the vegan menace in public health policy making in Washington, I take Wolf’s side on this issue. It is interesting that both authors seem to need an antagonist.
Cordain’s book has an index but no footnotes. The bibliography only adds gravitas (and pages) but isn’t divided by chapter, so there is no way to dig deeper into any of the claims made. It includes brief menu and recipe sections.
Wolf’s book has no index and no footnotes, but the bibliography is divided by chapter. His menus incorporate some recipes. Both books are simply commercial tracts, with their primary purpose appearing to be sales revenue.
My favorite of these three, though, is easily the little-known Dr. Harris. His approach is so sublime. He said on his website, “An Archevore is someone who eats based on essential principles, and also someone who hungers for essential principles. Take your pick.” And, “After hearing Gary Taubes on the radio, I had an epiphany and ever since I've been exploring the field of nutrition through the lenses of medicine and evolutionary biology.” And, “I have had a lifelong interest in science and medicine as culture, and believe all claims to scientific authority should be subject to thoughtful skepticism.” How can you not like this guy? His intellectual curiosity is the driver; the scientific method his “mechanism”; his vision pure. How could a guy like this sell his soul to a book publisher?

Retrospective #53: On the Digestion and Absorption of Food

Food digestion physiology varies between individuals and with the composition and size of a meal. A primer on what is most common and universal will be useful to understanding the various processes and their effect on our biological systems. This digest (note the pun), from Wikipedia, should provide some useful information.
Digestion, the hormonal process, has three phases. The cephalic phase begins when receptors in the head are stimulated by the thought, sight or smell of food, triggering various enzymatic and hormonal activities. The gastric phase starts with distension, acidity, and the presence of amino acids and peptides in the stomach. The intestinal phase is initiated by distension, acidity, and osmolarity of digestive products in the intestine, as we’ll explain.
Digestion, the mechanical and chemical process, begins with chewing. Chewing breaks food down to smaller units that are in turn broken down by enzymes to the smallest units, permitting them to be absorbed into the blood, mostly through the wall of the small intestine. Saliva containing mucus and the enzyme amylase is secreted from salivary glands located in the mouth. Mucus moistens the food and amylase partially digests polysaccharides (starches) into a disaccharide called maltose. About 30% of starch is broken down in the mouth (optimum pH: 6.8).
In addition, papillae on the surface of the tongue secrete a small amount of the enzyme lingual lipase which begins the process of breaking down certain fats from triglycerides into diglycerides. Long chain triglycerides cannot be absorbed unless completely broken down to monoglycerides, so the process starts in the mouth and continues in the stomach. As much as 30% of fat is broken down in 1 to 20 minutes by lingual lipase, according to Wikipedia.
Food then passes through the pharynx and descends the esophagus to the stomach, a sac that stores, mixes and processes food into a milky solution called chyme. Glands lining the stomach secrete hydrochloric acid, which is necessary for protein digestion. The stomach’s high acidity (optimum pH 1.8) inhibits breakdown of carbohydrates within it. However, a small amount of the enzyme lipase is secreted to continue the digestion of fats.
So far, although the breakdown of food particles by enzymatic and mechanical action is continuing apace, virtually no absorption of nutrients into the bloodstream has occurred. The exceptions are water, some simple sugars, and other small molecules like alcohol that are absorbed in the stomach, entering the circulatory system directly.
The final stages of digestion and most of the nutrient absorption occur in the next portion of the tract: the small intestine. The small intestine is divided into three segments – duodenum, jejunum and ileum. The duodenum in turn is connected to the hepato-pancreatic duct which connects to the liver and to the gall bladder and pancreas, providing digestive enzymes and an alkaline fluid (pH 8.5) to neutralize acid emptied from the stomach.
In the duodenum, dipeptides from partially broken-down protein from the stomach are broken down to amino acids by these enzymes. Other enzymes break down the disaccharides (maltose, lactose and sucrose) into the monosaccharides glucose, fructose and galactose.  The major portion of fat digestion, also happens here.
Absorption of nutrients occurs mostly in the jejunum and ileum. Amino acids (from protein) and the monosaccharides (glucose, fructose and galactose, all from carbohydrates) are water soluble and enter the blood directly through the small intestine wall. However, the products of fat digestion, fatty acids and glycerol, are not water soluble and therefore enter the circulation through the lymph system by a process called passive diffusion.
Passive diffusion requires no energy input from the body because it is driven by concentration. The small intestine is full of nutrients and the blood is not, so they cross over. This process is also called osmosis. Monosaccharides (“sugars”) and amino acids from protein, are transported across the membrane barrier by a process called “facilitated diffusion,” meaning they need a little help because they occur against a concentration gradient.
Finally, gastric emptying –the rate that food leaves the stomach to enter the small intestine – is tightly controlled. Liquids are emptied more quickly than solids; then carbohydrates are emptied, followed by protein, fat and fiber.

Retrospective #52: Thermic Effects of Food

Thermogenesis is the process of heat production in organisms, and heat is a form of expended energy. The unit of measurement is a calorie. Human metabolism is comprised of three components of energy expenditure: 1) the energy expended by the basal metabolic rate (to keep the resting organism alive), 2) the energy expended through exercise (motion), and 3) the energy expended due to the “cost” of processing food for use and storage. This last component is known as the thermic effect of food.  
It is estimated that the thermic effect of food is about 10% of the caloric intake of any given meal though, according to Wikipedia, “the effect varies substantially for different food components.” Of the three macronutrients, fat has minimal thermic effect. Carbohydrates – especially simple sugars and carbs in highly processed, manufactured foods – are very easy to process and have very little thermic effect. Proteins – and whole foods and complex carbohydrates to a lesser extent – are harder to process and have a larger thermic effect. The ratio of protein to carb energy expenditure is between 2:1 and 3:1, depending on how “simple” the carb is.
So, total daily energy expenditure includes a resting metabolic rate component (60-70% of total), the physical activity component (15-30% of total), and the thermic-effect-of-food component (~10%). While 10% is a small percentage, if the energy expended to digest, absorb and eliminate protein is two or more times the amount required for carbs and fat, replacing carbs with protein in an isocaloric diet would nevertheless increase the metabolic rate and help burn more calories, including stored fat. And if the difference in the “burn rate” was even greater for simple sugars and processed carbs, made easier to digest by manufacturing, that would account to a degree for why our metabolisms burn less on today’s modern processed-food diets.
Thus, we can naturally increase our metabolic rate by 1) increasing the amount of protein in our diet and 2) replace simple sugars and processed-foods in the diet with whole foods, that is, unprocessed, complex carbohydrates. Note that 2) above assumes that you don’t already have Insulin Resistance (IR), Pre-diabetes, or frank Type 2 diabetes, or are obese. It you do (are), you should severely restrict/limit carbs in the diet anyway, whether whole or processed.
The typical American diet currently gets about 15% of calories from protein. The Standard American Diet (SAD for short), espoused by the USDA/HHS and promoted on food packages in the Nutrition Facts Panel, is 10% protein. (On a 2,000kcal diet, 10% = 200kcal = 50g/d of protein. My Very Low Carb diet is about 20% protein by calorie.
Barr SB and Wright JC examined the issue in, “Postprandial energy expenditure in whole-food and processed-food meals: implications for daily energy expenditure,” published online July 2010 in The Journal of Food and Nutrition Research. An abstract on PubMed explains:Empirical evidence has shown that rising obesity rates closely parallel the increased consumption of processed foods…in the USA. Differences in postprandial thermogenic responses to a whole-food meal vs. a processed food meal may be a key factor in explaining obesity trends…” Their conclusion: “Ingestion of the particular processed food meal tested in this study decreases postprandial energy expenditure by nearly 50% compared with the isoenergetic whole food meal. This reduction in daily energy expenditure has potential implications for diets comprised heavily of processed foods and their associations with obesity.”
Wow! 50% is a big difference in thermic effect. And, in the meals they were comparing, “either ‘whole’ or ‘processed’ cheese sandwiches (multi-grain bread and cheddar cheese) were deemed ‘whole,’ while white bread and processed cheese product were considered ‘processed.’” Imagine if they had chosen a real whole food instead of ‘multigrain bread’ which is a far, far cry from a real whole food. And what if it had been a protein food instead?
The authors explained, “A more strict whole food would be one devoid of any processing, such as a specific fruit, vegetable, or meat. However, we sought to compare two meals that were familiar to the Western diet, and could be easily interchangeable.” And while the much higher thermic effect of protein is probably too small to have a noticeable effect on weight in the short term, over a period of months or years this difference would be significant.

Type 2 Nutrition #479: “If you’re over 65 and have diabetes…”

“If you’re over 65 and have diabetes, you should have a DEXCOM,” a guy in a white coat exhorts the viewer in a TV ad. Have you ever thought about a Continuous Glucose Monitor (CGM)? You’re supposed to assume the huckster is a doctor, not an actor shilling for the maker of this CGM. You’re also supposed to believe that his spiel is guided by “best medical practice.” But is using a CGM “best medical practice”? In an ideal world?
Just a day earlier I had read that the American College of Physicians (ACP) concluded that “home monitoring of blood glucose does not benefit blood glucose control.” In this case the ACP was denigrating the finger-stick home monitoring that I do every morning. How could they, with such conclusiveness, dis this practice, with no conditions or no exceptions? I know home monitoring has helped me a lot with my blood glucose control.
The Dexcom CGM TV ad also lacks nuance. The huckster does say “every 65yr old diabetic should have a CGM.” Unfortunately, Medicare (and supplemental) insurance will only cover the cost of a CGM and its ongoing supplies, for some diabetics. Coverage is qualified and severely limited. It is only “for diabetics who use insulin to control their blood glucose,” and, more specifically, ONLY for diabetics who take insulin with every meal.” The small print at the bottom of the screen reads “patients must meet coverage criteria.”
CGM’s are attached to your body and connected via a small skin prick which monitors your interstitial fluid every 5 minutes 24/7. The DEXCOM CGM sends downloadable readings and/or audible alarms to your phone or your caregiver’s phone. So, contrary to what the ACP said, CGMs are certainly a type of “home monitoring of blood glucose” that DOES benefit blood glucose self-management (BGSM). Quid erat demonstratum (QED).
So, as much as I would like to have a CGM to monitor and help me control my blood glucose, I am very happy that now CGMs are covered for type 1 diabetics and insulin-dependent type 2s who inject mealtime insulin. Of course, I would argue that there SHOULD and WOULD be NO insulin dependent type 2s if diet rather than pharmacology was considered “best medical practice” -- by the medical establishment or just by the patient!
Insulin is a dangerous drug, especially in the hands of a patient who injects it multiple times a day every day and who has to know a great deal about carbohydrates and the insulinogenic properties of some proteinsand estimate portion size and other variables. It’s complicated and risky. That’s why 1) doctors prefer to err by under dosing, with consequent higher blood sugars and A1c’s and 2) patients sometimes under dose insulin, because overdosing on insulin can (and sometimes does) lead to hypos (hypoglycemia), coma and death!
The irony is that once a type 2 patient has learned so much about carbs and insulinogenic proteins, they could just as easily eat low carb, even VERY low carb, and dispense altogether with the need to inject insulin!
But what about the finger stick? How does it benefit me? With a daily Fasting Blood Glucose (FBG), I am reminded that I control my type 2 diabetes by diet. If I ever cheat, my FBG will invariably be in the prediabetic range (100-125mg/dl) the next day. If not, it could be anywhere from 65 to 99mg/dl, depending on how many days in a row I was “good.” My FBG is also an indicator of what my A1c will be at my next doctor’s visit.
Years ago, when I was still learning about which foods elevated my blood glucose, testing before a meal and 1-hour after taught me about my insulin resistance. Everyone’s different, depending on where you are on your journey. Thus, it was a useful aide to me in the learning process for self-management of my type 2 diabetes.
For most type 2s that I know, or for “pre-diabetics” or folks who are just overweight and in cahoots with their doctor about their metabolic state (“denial is not a river”), BGSM is a way for patients to take responsibility for their health. But if that’s not you, your doctor will be happy to track your A1c and say nothing (except maybe “lose weight”) until you are diagnosed. Then, as Tom Hanks was told by his doctor, he’ll say, “Congratulations, you've graduated,” and he’ll write you a prescription. What else can he do?

Saturday, March 30, 2019

Retrospective #43: Paula Deen, Lessons Learned?

In early 2012 syndicated journalist Mike Luckovich REALLY “nailed” American TV personality and cooking show host Paula Deen with one of his brilliant 2-panel cartoons. In the first panel she says, “I got diabetes from the unhealthy recipes I peddle. Now I’m spokesperson for a diabetes drug…” In this panel she is surrounded by boxes and bags labeled ‘lard,’ ‘butter,’ ‘high fat grease,’ ‘salted sugar,’ and ‘buttered sodium.’ In the second panel she says, “…plus there’s my new book….,” which she’s holding. The title is, “Have Your Cake and Eat It Too.”
The cartoon is both hilarious and infuriating. It’s hilarious because hypocrisy is always a good target and ridicule the best weapon. It’s infuriating because Luckovich’s understanding of nutrition is completely, totally wrong. It’s doubly infuriating because Luckovich doesn’t know it is wrong; however, for ridicule to resonate with the reader – the average American – both he and they have to have the same misunderstanding of the message. And they do.
She has released a video on her web site addressing her diabetes, but she is inexplicably silent about which foods were responsible. One has to wonder if she even knows, if she has not obtained the best advice, or if it is just not financially advantageous for her to advocate a Way of Eating that is not supported by the packaged food industry.
I hate to be cynical, and I dislike piling on, even if I’m last on this pile, but Paula Deen is missing a big opportunity to really do some good, plus the chance to control her blood sugar without expensive medications and side effects.
First of all, fat didn’t make Paula Deen fat, so those blurbs labeled ‘lard’, ‘butter,’ and ‘high fat grease’ are simply wrong. The truth is simple sugars and refined carbohydrates, principally flour, make us fat. The body is designed to use glucose from sugars and refined carbs for energy before it uses fat.  So, if you are burning carbohydrates for energy, any fat you eat that isn’t needed for energy gets stored. That’s the way the body, from a paleolithic and neolithic perspective, saves energy for use after failed hunts, crop failures, and even during the occasional famine.
We didn’t always have a year-round food supply. Berries and other fruits were seasonal and not nearly as sweet as modern hybrids. My maternal grandparents, who were farmers, kept a root cellar. They also canned and pickled vegetables and ‘put up’ fruit preserves to eat during the non-growing season. It was just a survival thing.
Paula Deen’s fat build-up resulted from insulin resistance in the cells to which too much glucose (from sugars and refined carbs) was being transported by insulin. Eventually the pancreas burns out and its beta cells die. At this point, 80% of all T2’s are obese.  It’s good for everyone not to over work their pancreas, even if they are slender.
I’ve never seen the Paula Deen show -- only the video I mentioned – but she is getting a bad rap. Luckovich is only playing to the popular perception that fat makes you fat and diabetic. The truth is fat makes you fat only if you eat it with lots of ‘sugars’ (both simple sugars and refined carbohydrates). And it’s the sugar and refined carbs (flour) that over work the pancreas (making you diabetic) and the liver converting carbs to fat via de novo lipogenesis.
Some people have criticized Paula Deen for withholding news of her condition for a couple of years until she could get a drug company endorsement and book deal lined up. Others, among them “yours truly,” criticize her for not using her celebrity status and fan base to educate the public on what caused her to develop Type 2 diabetes.
The federal government (HHS/USDA) still recommends the Standard American Diet (ironically SAD), which is 60% carbohydrates (300g/d), 10% protein (50g/d), and 30% fat (+/-67g/d) on a 2000 calorie a day, woman’s diet plan. For men, it’s the same percentages: 375g/d carbs, 62.5g/d protein and +/- 83g/d fat.  That’s way too many carbs.
Try cutting carbs back to 150 or 100 grams of carbohydrate a day, 30% or 20% (vs. 300g or 60%) of a 2,000-calorie diet. Many people aim lower for 50 grams a day, and some go Very Low Carb (VLC) at 20 or 30 grams a day. Type 2 diabetics (and pre-diabetics) should try to eat in the VLC range for optimum blood sugar control and easy weight loss. When you eat carbohydrates at that level, all you ‘Paulas’ out there, you can eat butter and cream for energy, feel good and look great. Plus, you will save lots of money on food and medicine, and avoid the side effects.

Wednesday, March 27, 2019

Retrospective #50: Free Radicals and Oxidative Stress

In Retrospective #46, we posited that oxidative stress was one of the three prime contributors to cardiovascular disease, along with inflammation and imbalances in blood sugar and insulin. What is oxidative stress and what causes it? Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to neutralize them. A delicate balance is required. Too many reactive oxidizing species or too few (or ineffective) anti-oxidant defenses produce oxidative stress. And oxidative stress can lead to atherogenesis.
Free Radicals are one of the most common ROS. They have an unpaired electron that makes them highly reactive chemically, but also generally short-lived. long-lived free radicals can be dangerous too, depending on their stability. According to Wikipedia, “Excessive amounts of these free radicals can lead to cell injury and death, which may contribute to many diseases such as cancer, stroke, myocardial infarction and diabetes. Many forms of cancer are thought to be the result of reactions between free radicals and DNA, potentially resulting in mutations that can adversely affect the cell cycle and potentially lead to malignancy.”
Some of the symptoms of aging such as atherosclerosis are also attributed to free-radical induced oxidation of many chemicals in the body. Free radicals contribute to alcohol-induced liver damage, perhaps more than alcohol itself. Radicals in cigarette smoke are implicated in the process that promotes the development of emphysema.
Free radicals play an important role in a number of biological processes, and “some of these are necessary for life, such as the intracellular killing of bacteria by… macrophages,” according to Wikipedia. See Retrospective #48. So, because some free radicals are necessary for life, the body produces a number of enzymes to minimize free radical-induced damage and to repair damage that does occur. In addition, antioxidants play a key role in these defense mechanisms. Research is underway to determine the relative importance and interactions between antioxidants. Meanwhile, antioxidant supplements to prevent disease are controversial; real food sources are probably the best.
Antioxidants are classified into two broad divisions: water soluble or fat soluble. These compounds may be synthesized in the body or obtained from the diet or through supplementation. Some are mostly present within cells while others, such as uric acid, are more evenly distributed. In fact, human blood has a high concentration of water-soluble uric acid. Antioxidants are found in vegetables, fruits, grains, eggs, meat, legumes, and nuts. Certain herbs and spices are particularly high in antioxidants.
·         Vitamin C (ascorbic acid): Bell pepper, parsley, broccoli, Brussels sprouts, cauliflower and kale.
·         Vitamin E (tocopherols, tocotrienols): green leafy vegetables, almonds, asparagus, papaya.
·         Polyphenolic antioxidants (flavonoids): tea, coffee, fruit, olive oil, chocolate, red wine, herbs and spices.    
·         Carotenoids (lycopene, carotenes, lutein): sweet potatoes, spinach, tomatoes, and chili peppers.
In general, processed foods contain fewer antioxidants than fresh and uncooked foods, since generally the preparation process exposes the food to oxygen.
Wikipedia: “The paradox in metabolism is that, while the vast majority of complex life on earth requires oxygen for its existence, oxygen is a highly reactive molecule that damages living organisms by producing reactive oxygen species (ROS). Consequently, organisms contain a complex network of antioxidant metabolites and enzymes that work together to prevent oxidative damage to cellular components such as DNA, proteins and lipids. 
Oxidant systems either prevent these reactive species from being formed, or remove them before they can damage vital components of the cell. However, reactive oxygen species also have useful cellular functions. Thus, the function of antioxidant systems is not to remove oxidants entirely, but instead to keep them at an optimum level.” The oxidative challenge is to maintain proper cellular homeostasis -- a balance between reactive oxygen production and consumption. Diet and lifestyle play a large role in this complex system… and you are in charge.

Retrospective #49: Dietary Causes of Inflammation

Do you have syphilis? Or snort cocaine, or smoke tobacco, or have a bacterial infection or periodontal disease that causes an overproduction of cholesterol to accumulate in your arteries? If you answered “no” to all of the above, the cause of chronic inflammation, and thus of atherosclerotic plaque in your arteries, is likely to be dietary.
The relationship between dietary fat and atherosclerosis, however, is contentious. The USDA’s current “MyPlate” and their Dietary Guidelines for Americans, promote a low-fat diet, based largely on belief that fat in the diet is atherogenic. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. Especially singled out are saturated fats, dietary cholesterol and trans fats.  Trans fats are one of the few consensus points in nutrition as everyone thinks these are very bad for your health. But could all of these authorities be wrong about the role of saturated fats and dietary cholesterol?
In a word, “yes.” There is growing unanimity that monounsaturated fats, such as are found in olive oil and avocado, are healthy. But polyunsaturated fats, such as are manufactured by unnaturally processing seed crops (called euphemistically “vegetable” oils, are coming under increasing scrutiny. Soy bean oil and corn oil are the most widely used fats, accounting for over 90% of food oils used in the U.S. The latest (2015) Dietary Guidelines for Americans (DGA) still strongly and doggedly encourages their use and defends their safety.
Interestingly, though, the DGA’s recommended limits on dietary cholesterol of 300mg/dl, and 30% total fat of total calories, in place from inception (1980) up to 2015, has been lifted. The proscription on consuming saturated fat, however, remains. The government want Americans to “replace saturated fats with unsaturated fats.”
Polyunsaturated fats are particularly unstable. Referencing Wikipedia, they become damaged or oxidized very easily. In one study when oxidized or rancid fats were fed to lab rats, they developed atherosclerosis. In another, rabbits fed atherogenic diets containing various seed and grain oils showed the largest increase in “oxidative susceptibility of LDL.” In a study involving rabbits fed heated soybean oil, “grossly induced atherosclerosis and marked liver damage were histological and clinically demonstrated,” according to Wikipedia.
More from Wikipedia: Rancid fats and oils taste and smell very bad even in small amounts and people avoid eating them. But, in the United States, “vegetable” oils used in cooking are refined, bleached, deodorized and degummed. The resultant oils are colorless, odorless, tasteless, and have a longer shelf life than their unrefined counterparts. This extensive processing makes fully oxidized, rancid oils much more elusive to detection via human senses.
To properly protect polyunsaturated fats (all “vegetable” oils) from oxidation, it is best to keep them cool and in a dark, oxygen free environment. Keep them in the cupboard, not on the counter. And buy monounsaturated oils that are sold in dark glass bottles, not clear plastic ones. Finally, don’t overheat or use any of them repeatedly, such as in deep fat frying. And keep your Omega-3 fish oil capsules and Flax Oil (high in Omega-3s) in the refrigerator.
So, if atherosclerosis is defined by Wikipedia as “a chronic inflammatory response in the walls of arteries, promoted by LDL…without adequate removal of fats and cholesterol…by…HDL,” then we should be concerned about the quality and quantity of LDL in our arteries – lest it become oxidized LDL. Likewise, we should be concerned if our circulating HDL in not high enough to transport any oxidized-LDL back to the liver as it is supposed to do.
Why do the two bad conditions (high LDL and low HDL) co-exist in so many of us today? It’s our diet! To avoid oxidized LDL, we should eat far fewer polyunsaturated fats (PUFAs), especially ones that are partially hydrogenated or hydrogenated (as in margarine and many store-bought baked goods), oxidized, or heated (as in deep fat frying).
We can also take supplementary Omega-3s to help us regain a better Omega 6/Omega 3 balance (Retrospective #22. And, we can raise our HDL so they can do their job. For that, see Retrospective #34, “Foods that Raise HDL.”
The oxidized-LDL hypothesis as the cause heart disease, of inflammation and of atherosclerosis, posits that, “Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals and become toxic to the cells.” Read Retrospective #48, “Inflammation and Atherosclerosis,” to refresh. Free radicals cause the oxidative stress that “triggers a cascade of immune responses which over time can produce the characteristic “atheroma” nodule in the artery wall that is the start of atherosclerosis.”
“Free Radicals and Oxidative Stress” is the subject of the next Retrospective, #50.                           

Retrospective #48: Inflammation and Atherosclerosis

Wikipedia begins, “Atherosclerosis…is a condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, caused by the accumulation of macrophage white blood cells and promoted by low-density lipoproteins (LDL) -- plasma proteins that carry cholesterol and triglycerides -- without adequate removal of fats and cholesterol from the macrophages by…high-density lipoproteins (HDL).” (all italics added). 
Atherosclerosis is a chronic disease that remains asymptomatic for decades. Atherosclerotic lesions, or plaques, cause narrowing of the artery and, if unstable, can rupture and induce a thrombus (blood clot, attached or motile). A thrombus, in place or more likely downstream, can cause an occlusion of the lumen of the artery, stopping blood flow, resulting in the death of tissues fed by the artery. This catastrophic event is called infarction. Thrombosis in the coronary artery is a myocardial infarction (heart attack). Stroke is often caused by a clot in the carotid artery.
These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. What’s “new” in the understanding of atherosclerosis, however, is an appreciation of the role of inflammation in atherosclerosis. The 2002 abstract of a paper, “Inflammation and Atherosclerosis,” begins, “Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response.” The full paper was published in Circulation (2002; 105:1135-1143), the Journal of the American Heart Association.
The main cause of atherosclerosis is yet unknown, but a considerable body of experimental evidence points to oxidized LDL. This hypothesis posits that the inflammatory processes in the artery wall are initiated in response to retained low-density lipoprotein (LDL) molecules. The LDL molecule is globular shaped with a hollow core whose purpose is to carry cholesterol throughout the body. Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals, and become toxic to the cells. The damage caused by the oxidized LDL molecules triggers a cascade of immune responses which over time can produce a fatty nodule in the eroded artery wall.
The body’s immune system responds to the damage to the artery wall by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. These white blood cells are not able to process the oxidized-LDL, and ultimately grow, then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. According to the theory, this triggers more white blood cells, continuing the cycle. The primary documented driver of this process is therefore oxidized-LDL particles within the artery wall.
According to Wiki, various anatomic, physiological and behavioral risk factors for atherosclerosis are known. They can be divided into the categories modifiable or not modifiable. The points labeled ‘+’ in the list below form the components of Metabolic Syndrome, first described in Retrospective #9 below and discussed in multiple columns.
Modifiable Risk Factors
·         +Diabetes or Impaired Glucose Tolerance (IGT)
·         +Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats and cholesterol, such as)
o   High LDL (bad if elevated and small/dense particles) and/or High VLDL
o   Low HDL (protective if large/fluffy particles and high enough)
o   An LDL:HDL ratio great than 3:1
·         +Hypertension, on its own increasing risk by 60%
·         Elevated serum C-Reactive Protein (hsCRP) concentrations
·         Vitamin B6 deficiency
·         Tobacco smoking, increases risk by 200% after several pack years
·         Periodontal disease
Non-modifiable Risk Factors include advanced age, male sex, having close relatives who have some complication of atherosclerosis (e.g. coronary heart disease or stroke), and genetic abnormality, e.g. familial hypercholesterolemia.
Other lesser or uncertain risk factors for atherosclerosis includes obesity +, a sedentary lifestyle, hypercoagulability, post-menopausal estrogen deficiency, high intake of saturated fat (may raise total and LDL cholesterol), intake of trans fats (may raise total and LDL cholesterol while lowering HDL), high carbohydrate intake, elevated triglycerides +, high homocysteine, uric acid, or fibrinogen or lipoprotein(a) concentrations, chronic systemic inflammation, as reflected by upper-normal WBC concentrations, elevated hs-CRP or serum insulin levels +, stress or symptoms of clinical depression, hyperthyroidism, short sleep duration and Chlamydia pneumoniae infection. 

Retrospective #47: Testing for Heart Disease Risk

“Key tests can reveal problems with a person’s blood sugar and insulin, inflammation level, level of folic acid, clotting factors, hormones and other bodily systems that affect your risk of cardiovascular disease,” says Mark Hyman, MD, the Lennox, MA, practitioner and author, on an old May 2010 blog post.  This last-of-three columns on that post will discuss some of these tests and zero in on these prime markers for cardiovascular disease.
“There’s no doubt about it,” Dr. Hyman says. “Inflammation is a key contributor to heart disease. A major study done at Harvard found that people with high levels of a marker called C-Reactive Protein (hs-CRP) had higher risks of heart disease than people with high cholesterol. Normal cholesterol levels were NOT protective to those with high CRP. The risks were greatest for those with high levels of both CRP and cholesterol.”
“Another predisposing factor to heart disease, Dr. Hyman says, is insulin resistance or metabolic syndrome, which leads to an imbalance in the blood sugar and high levels of insulin. This may affect as many as half of Americans over age 65. Many younger people also have this condition, which is sometimes called pre-diabetes.”
“Although modern medicine sometimes loses sight of the interconnectedness of all our bodily systems, blood sugar imbalances like these impact your cholesterol levels too. They will cause your good cholesterol [HDL] to go down, while your triglycerides rise, which further increases inflammation and oxidative stress. All of these fluctuations contribute to blood thickening, clotting, and other malfunctions – leading to cardiovascular disease,” he says.
“What’s more, elevated levels of a substance called homocysteine (related to our body’s levels of folic acid and vitamins B6 and B12) appear to correlate to cardiovascular illness. Where problematic levels occur, they can be easily addressed by adequate folic acid intake, along with vitamins B6 and B12.” My own internist, who is also a board-certified cardiologist, put me on a supplement called Homocysteine Modulators (Solgar), as well as CoQ10.
“Heart disease is not only about cholesterol. It is important to look at many factors that contribute to overall risk.” Dr. Hyman notes, “It seems that insulin and blood sugar imbalances and inflammation are proving to be more of a risk than cholesterol.” If you want to test your risk, Dr Hyman says, ask your doctor to perform the following tests:
·         Cardio C-Reactive Protein (hs-CRP): There can be many causes of inflammation in the body, but this marker of inflammation is essential to understand in the context of overall risk. Your CRP should be <1.0.
·         Standard Lipid Panel: Total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides. Pay particular attention to your HDL and triglycerides and the TC/HDL and TG/HDL ratios and work to improve them.  Pay less attention to lowering Total Cholesterol by lowering LDL, an outcome shown to be of dubious value alone. Your doctor can’t write a script for raising HDL and lowering triglycerides. You have to do it yourself by the food choices you make at each and every meal.
·         VAP cholesterol test: directly measures LDL (vs. calculated as in the standard lipid test above), also VLDL, LP(a), and LDL particle size and characteristics (small dense vs. large fluffy).
·         Hemoglobin (Hb) A1c: This measures your average blood sugar over the last 6 weeks to 3 months. Anything over 5.5% is high. Dr. Richard K. Bernstein, the glucose self-testing guru and leading diabetes expert, considers 5.7% to be full-blown diabetes. Alas, the ADA now considers 5.7% to be pre-diabetes and 6.5% to be type 2 diabetes. Studies show that CVD risk doubles from an A1c of 5.5% to 6.0%.
·         Glucose Insulin Tolerance Test (OGTT + Insulin): Measurements of fasting and 1 and 2 hr. levels of glucose AND insulin helps identify pre-diabetes and high levels of insulin. Most doctors just check blood sugar and NOT insulin, the first thing to go up. By the time your blood sugar goes up, “the train has left the station.”
·         Homocysteine: Your homocysteine measures your folate status and should be between 6 and 8.
·         Fibrinogen: Looks at clotting factors in the blood. It should be less than 300.
And, most importantly, know your test results. Take charge of your health. It’s your life. Make the most of it.

Retrospective #40: “Safe Starches.” Safe for Whom?

From my perspective, having been a diagnosed Type 2 diabetic for 33 years, there are no safe starches. My metabolism was ruined 40 or 50 years ago when certain of my genes expressed themselves in response to my excessive use of certain foods, presumably too many highly processed carbohydrates and simple sugars.
When I learned about 17 years ago (as I write this in 2019) that I could manage my disease by changing the way I eat, I was ecstatic. I was no longer doomed to be the victim of “a progressive disease” with a worsening prognosis. I got my life back, so long as I stuck to my new way of eating. I quickly was able to give up almost all the diabetes drugs I had been on for 16 years, I lost a lot of weight (170 pounds), and my lab tests showed my doctor that my health had greatly improved. So, I turned my attention to maintaining my redemption and spreading the word.
Starches are long chains of glucose molecules. 100% glucose molecules. The chains are long but easily broken down by an enzyme that is secreted in the mouth and is also present in the small intestine where most digestion occurs. But many simple glucose compounds are broken down to single glucose molecules before they reach the stomach.
If you think this is a column about the Glycemic Index, you are wrong. If you think it is about “simple sugars and refined carbohydrates,” vs. “complex carbohydrates,” you are wrong. Those are comparisons that you might make if you thought you had an understanding that the former spiked blood sugar and the latter raised it more slowly. This is true, as far as it goes, but if you’re a Type 2 diabetic or Prediabetic, or a little Insulin Resistant (overweight?), it is irrelevant. When digested, they are all glucose “under the curve,” and they all get in your blood after you eat.
In addition, the phrase “complex carbohydrate” is falsely believed to mean any starch that is long chain vs. a simple “sugar,” i.e. a mono or disaccharide, as in cane sugar. Wrong! Bread, for example, is a starch but not a “complex carbohydrate.” Its main ingredient is flour, a highly refined carbohydrate, easily broken down. In fact, white bread has a glycemic index of 100! It is the ultimate refined carbohydrate. And all other breads, all made from highly refined flour, are not far behind. Besides, after water the next ingredient in all store-bought breads is sugar!
So, what is a “safe starch,” and for whom are they safe? For those who can eat them, they are generally whole foods. Paul Jaminet, PhD, in the book “Perfect Health Diet” (, lists sweet potatoes, potatoes, plantains, and taro. Kurt Harris, MD, creator of the now defunct Archevore blog, adds yams and bananas.
Both Jaminet and Harris include white rice. Harris says, “Except for white rice, these are all whole food starch sources with good mineral and micronutrient content that have been eaten in good health for thousands of years in many environments by genetically diverse populations. Many of these plants have spread far from their biomes of origin and serve as staples for populations who have adopted them with success for several thousand years.” “White rice is kind of a special case. It lacks the nutrients of root vegetables and starchy fruits like plantain and banana, but is good in reasonable quantities, as it is a very benign grain that is easy to digest and gluten free.”
So, who can eat “safe starches”? Researchers examined diets for many indigenous populations in the world who have not developed the Diseases of Civilization (Metabolic Syndrome, Type 2 diabetes, CHD and CVD, stroke, many cancers, and Alzheimer’s). They found that certain carbohydrates, what they are calling “safe starches,” can be eaten, without vegetable oils, in reasonable amounts (10% to 30% of total calories) by people whose metabolic function has not been compromised by Insulin Resistance. These “safe-starches” people (those who can eat them) are most likely people who are not already metabolically unhealthy or overweight as a consequence of their Insulin Resistance. To be clear, if you are already overweight, you probably have Insulin Resistance, or if you have high blood pressure, or if you have high cholesterol (dyslipidemia), you cannot safely eat these ‘safe starches.
So, there you are. If you’ve followed the low-fat, high-carb “Dietary Guidelines,” and you’re not overweight or not otherwise metabolically unhealthy (now just 11% of the population), you can eat “safe starches” guilt-free and to your heart’s (LOL) content. But don’t forget to put lots of butter, sour cream and bacon on those baked potatoes.

Tuesday, March 26, 2019

Retrospective #46: How to Treat Heart Disease Risk

If lowering LDL and therefore Total Cholesterol [by taking a statin] is not the great panacea that we thought [See Retrospective #45 below],” Dr. Mark Hyman asks, “then how does one treat heart disease risk?” “How do we get the right kind of cholesterol?” he asked in an old post on his website.  How do we get high HDL, low LDL and low triglycerides, and have cholesterol particles that are large and fluffy rather than small and dense, which is the type that actually causes heart disease and plaque to build up?”
Dr. Hyman continues, “We know what causes the damaging small cholesterol particles.  And it’s not fat in the diet. It is sugar. Sugar in any form or refined carbohydrates (white food) that drives the good cholesterol down, causes triglycerides to go up, creates small damaging cholesterol particles, and causes metabolic syndrome or pre-diabetes. That is the true cause of most heart attacks, NOT LDL CHOLESTEROL.” (emphasis added by me)
“One of the reasons we don’t hear about this is because there is no good drug to raise HDL,” Dr. Hyman says. (See Retrospective #34, “Foods that Raise HDL”) “Statin drugs lower LDL – and billions are spent advertising them, even though they are the wrong treatment. If you are like most of the patients I see in my practice,” he says, “you’re convinced that cholesterol is the evil that causes heart disease. You may hope that if you monitor your cholesterol levels and avoid the foods that are purported to raise cholesterol, you’ll be safe from America’s number-one killer. If only it were so simple,” he laments.
According to Dr. Hyman (and, increasingly, many other cutting-edge practitioners), the three prime contributors to cardiovascular disease are: 1) inflammation, 2) imbalances in blood sugar and insulin, and 3) oxidative stress.  “To control these key biological functions and keep them in balance, you need to look at your overall health as well as your genetic predispositions, as these underlie the types of disease you’re likely to develop. It is the interaction of your genes, lifestyle, and environment that determines your risks and the outcome of your life,” Dr. Hyman says.
“This is the science of nutrigenomics, or how food acts as information to stall or totally prevent some predisposed disease risks by turning on the right gene messages with our diet and lifestyle choices. That means some of the factors that unbalance bodily health are under your control, or could be. These include nutritional status, stress levels and activity levels.” Nutritional status means the foods you choose to eat. They are under your control.
To demonstrate the effect of diet on nutritional status, I offer my own test results (n = 1) as an example. Before I started eating Very Low Carb 10 years ago, my average HDL over the previous 22 years was 43mg/dl. The desired range for men is 40mg/dl and for women 50mg/dl. My average HDL now is 78mg/dl. My most recent (when this was originally in 2012) was 92mg/dl. An old link (no longer working) from The American Journal of Cardiology, posted in Newsmax Health, suggests a correlation between high HDL and longevity in men.
Before I started eating Very Low Carb, my triglyceride average of 21 previous tests was 137. The desired range for both men and women is <150mg/dl. My triglyceride average is 54. My most recent (again, in 2012) was 32mg/dl.
The ratio of triglycerides to HDL is “…the strongest predictor of a heart attack.” See Retrospective #27. My ratio of triglycerides to HDL is now 0.35 (ideal range is < 1.0). My ratio of Total Cholesterol to HDL is 2.3 (209/92). Desired range is < 5.0. My doctor never asks me what I eat any more. He just says, “just keep on doing what you’re doing.”
As for inflammation, the most statistically significant marker for overall heart disease risk is the high sensitivity C-Reactive Protein (hs-CRP) blood test. Your C-Reactive Protein level should be less than 1.0. At the time I started low-carbing, mine was 5.8. My most recent was 0.8 (August 2017). With such a low Chronic Systemic Inflammation score, and my continued Way of Eating, my doctor says he can’t “medically justify” ordering the test more often.

Retrospective #45: Do You Need to Lower Your Cholesterol?

“We have all been told that ‘high cholesterol’ is bad and that lowering it is good,” Mark Hyman, MD, posted on his website back in 2010. This belief is almost universal. And, a sure-fire way to lower Total Cholesterol and the “bad LDL” (calculated) cholesterol is to take a statin drug:  Crestor, Lipitor, Zocor or their generic equivalents.
“But on what scientific evidence is this advice based?” and “What does the evidence really show?” Dr. Hyman asks. Many health professionals have asked similar questions, but back in 2010 Dr. Hyman offered a comprehensive Summary of Findings in the medical literature that question the rationale and justification for prescribing statins:
·         If you lower bad cholesterol (LDL) but have a low HDL (good cholesterol), there is no benefit to statins.
·         If you lower bad cholesterol (LDL) but don’t reduce inflammation (marked by a test called C-Reactive Protein or hsCRP), there is no benefit to statins.
·         If you are a healthy woman with high cholesterol, there is no proof that taking stains reduces your risk of heart attack or death.
·         If you are a man or a woman over 69 years old with high cholesterol, there is no proof that taking statins reduces your risk of heart attack or death.
·         Aggressive cholesterol treatment with two medications (Zocor and Zetia) lowered cholesterol much more than one drug alone but led to more plaque build-up in the arteries and no fewer heart attacks.
·         75% of people who have heart attacks have normal cholesterol
·         Older patients with lower cholesterol (<180) have higher risks of death than those with higher cholesterol.
·         Countries with higher average cholesterol than Americans such as the Swiss or Spanish have less heart disease.
·         Recent evidence shows it is likely statins’ ability to lower inflammation that accounts for the benefits of statins, not their ability to lower cholesterol.
“So, for whom do the statin drugs work anyway?” Dr. Hyman asks. “They work for people who have already had heart attacks to prevent more heart attacks or death. And they work slightly for middle-aged men who have many risk factors for heart disease like high blood pressure, obesity or diabetes. And that data also shows that treatment really only works if you have heart disease already. In those who don’t have…heart disease, there is no benefit.”
“So why did the 2004 National Cholesterol Education Program (NCEP) guidelines expand the previous guidelines to recommend that more people take statins (from 13 million to 40 million) and that people who don’t have heart disease should take them to prevent heart disease? Could it have been that 8 of the 9 experts on the panel who developed these guidelines had financial ties to the drug industry?” he asks rhetorically. “Thirty-four other non-industry experts sent a petition to protest the recommendations to the National Institutes of Health (NIH) saying the evidence was weak.” Dr. Hyman’s summed it up neatly: “It was like having a fox guard the chicken coop.”
Yet, at a cost of over $20 billion a year [in 2012, approaching 1 trillion by 2020] 75% of all statin prescriptions are for exactly this type of unproven primary prevention. “If these medications were without side effects, then you may be able to justify the risk – but they cause muscle damage, sexual dysfunction, liver and nerve damage and other problems in 10-15% of patients who take them. Certainly not a free ride,” says Dr. Hyman.
William Castelli, MD, a Director of the famous Framingham Study said, “In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active.”
And George Mann, ScD, MD, former Co-Director of The Framingham Study, said, “The diet-heart [lipid] hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons of price, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises [AHA], food companies and even governmental agencies. The public is being deceived by the greatest health scam of the [last+current] century.”
And heart surgeon Michael DeBakey, said, “An analysis of cholesterol values in 1,700 patients with atherosclerotic disease revealed no correlation between serum cholesterol…and the nature and extent of atherosclerotic disease.”
So, if lowering cholesterol is not a great idea, how does one treat heart disease risk? See the next Retrospective.