Thursday, February 27, 2014

The Nutrition Debate #187: Chronic Systemic Inflammation and C-reactive protein (hsCRP)


This is a primer for the layman on the narrowly defined subject of “Chronic Systemic Inflammation.” Chronic means “persistent, long-standing, long term,” in contrast, “acute” means “with a rapid onset and/or a short course.” Systemic means “throughout the body,” as in when you have a fever. Inflammation is the bodys response to an “injury.” I put injury in quotes because, while we understand the outward manifestation of the bodys “acute” inflammatory response to stubbing a toe (pain, swelling, etc.), we are often unaware of the presence and dire consequences of “chronic, systemic inflammation.” It is a continuing “injury” that is often undetected, and the consequences can be very serious.

First, to be clear, our bodys response to an acute injury, which we perceive as pain and swelling, is actually a good thing. It means the bodys immune system has swung into high gear to defend itself against the “injury.” The processes are too technical to describe in detail but suffice it to say they involve a temporary mobilization of “hormone-like” proteins such as cytokines and macrophages. But enough of that; my own eyes glaze over when I write about those little buggers. The point is: when the body has completed a repair to the injury, the inflammation goes away and everything returns to normal.

Chronic systemic inflammation is a whole other thing and is mostly unrecognized. So, why should we care? Dr. Art Ayers, a PhD biomedical researcher with a special interest in inflammation and disease, puts it this way: “Inflammation is the foundation for cancer and degenerative/autoimmune diseases. Small changes in diet and exercise, e.g. omega-3 oils, vitamin D, low starch, and maintaining muscle mass, can dramatically alter predisposition to disease and aging, and minimize the negative impact of genetic risks. His blog, “Cooling Inflammation,” is on my personal Blogger “reading list.”

Im not sure I agree with his characterization of the changes in diet and lifestyle being “small”, but I do agree that they can make a big difference. One of the most common and inexpensive markers of chronic systemic inflammation is the high-sensitivity C-reactive protein (hs CRP) blood test. When I started eating Very Low Carb in September 2002, my doctor didn’t test my CRP (and it had never been tested since the time I first began keeping copies of lab reports in 1974.) Results in the range of 3.1 to 10mg/L are considered “Higher Relative Cardiovascular Risk;” 1.0 to 3.0 “Average Relative Cardiovascular Risk;” and <1.0 “Lower Relative Cardiovascular Risk.” Here are my hs CRP scores for the last 11 years:

3/03
10/03
12/06
4/09
4/10
7/10
4/11
8/12
11/12
4/13
10/13
1/14
6.4
5.8
2.5
1.8
1.5
0.7
1.5
<0.3
0.1
1.3
2.9
1.2

Note that my then doctor, a cardiologist/internist, tested my CRP twice in the first year, both times with a “Higher Risk” (6.4 & 5.8mg/L) result. I guess he wasnt surprised with that result (See Note 2 below), or maybe he didn’t have a pill to prescribe to lower it. Anyway, he didn’t test me again for 3 years and by this time my CRP-based risk had dropped to “Average” (2.5mg/L). The next test, 3 years later, it had dropped further to 1.8mg/L. After that, he tested my hs CRP once or twice a year. I guess my doctor had noticed the kind of “big difference” that Dr. Ayers mentions on his blog. The next 6 tests results were all lower yet, three of them <1.0 (0.7, <0.3 and 0.1). Then my doctor died, and I had to find a new doctor.

Now I have to ask for a high sensitivity CRP test. The first was 2.9mg/L (“Average” according to the AHA/CDC guidelines), so my new doctor said nothing. But I was concerned with the spike, so this winter in Florida I saw another doctor and asked him to help me monitor and control my Chronic Systemic Inflammation. He agreed and ordered a series of tests from the Cleveland Heart Lab. My “PLAC” test (Lp-PLA2) was “in-range” (192ng/mL) or “low risk;” however, my hs CRP was 1.2mg/L (out of range), or “moderate risk.” Interesting, I thought. It had dropped from 2.9 to 1.2 but the risk went from “Average” (in range) to “Moderate” (out of range). Well, I dont disagree. I want my hs CRP to be <1.0, and I am working to make it so.

How do I do that? Well, there are two ways you can find out. You can read my two previous blog posts, “Your Diet is Very Restrictive” here and “Your Diet is Very Restrictive Part 2” here, or you can read the 3 related posts on Dr. Ayerss “Cooling Inflammation” here. Actually, you should do both. Dr. Ayers, of course, speaks with a lot more authority than I (to put it mildly), but he also comes at the issue from a totally different perspective: a healthy gut biota. I learned a lot from reading his rejoinders to a recent Dr. Oz broadcast, and from his “Anti-Inflammatory Diet and Lifestyle.” I think you will too.

Note: A common cause of Chronic Systemic Inflammation is periodontitis, an inflammatory disease affecting the tissues that surround and support the teeth. Periodontitis is caused by microorganisms on the tooth's surfaces, along with an overly aggressive immune response by pro-inflammatory cytokines, lymphocytes & macrophages against these microorganisms.

Note 2: The Google heading “Inflammation” includes the following: “Chronic inflammation is widely observed in obesity.”[31] The obese commonly have many elevated markers of inflammation, including: CRP (C-reactive protein)[34][35]”; “Waist circumference correlates significantly with systemic inflammatory response,[37]” and “C-reactive protein (CRP) is generated at a higher level in obese people. Mild elevation in CRP increases risk of heart attacks, strokes…and high blood pressure.”
Read up; there’s more to come on this topic.

Saturday, February 22, 2014

The Nutrition Debate #186: “Your Diet is Very Restrictive” Part 2


I realized after writing over 1,000 words for the last column, I had told only half the story. Yes, my diet is “very restrictive,” including in several additional major ways I didn’t mention: 1) I eschew (as much as possible) all vegetable and seed oils, especially polyunsaturated soy bean oil, corn oil, Canola, sunflower and cottonseed oil, etc.; and 2) I avoid practically all grains, especially wheat, barley and rye (the primary gluten grains), and everything made from them. That means I eat very little fried food and virtually nothing that has been made with flour, including most gravies. And I know I feel better for it.

Instead, I eat monounsaturated oils (olive oil, and occasionally half an avocado with vinaigrette dressing) and saturated fats (especially coconut oil and MCT oil in homemade mayo). I select fatty cuts of meat (beef and pork) and fatty cold water fish. I eat chicken with the skin on, sardines in olive oil, and fish oil (2 grams a day for their essential Omega 3s (DHA & EPA). I also eat lots of eggs (18/week) from pastured hens. Forget about dietary cholesterol! I wish I could say I ate beef from grass-fed, grass-finished beef and even butter from grass fed cows, but alas, I cannot. Marriage, they say, is a compromise. I also eat offal (organ meats) once a week, but I have to prepare them myself (on Sunday mornings).

Is this a challenge? Sure, at times, especially when dining out or entertaining at home. In restaurants the workaround I have developed is often to order from the appetizer menu. Sometimes I will order a salad and an appetizer, or two appetizers. That way, I avoid the proverbial starch that seems to accompany most main dishes. Of course, almost every kitchen will gladly give a double portion of vegetables instead of a vegetable and a starch, but I don’t want a double of anything. It’s too much food. Small meals, remember? Also, when you order from the appetizer menu, you don’t get a bread basket. That makes it easier too. If my wife orders an entrée, and the bread is placed between us, I move it to her side of the table.

At home, the workaround for all the “forbidden goodies” in the house is not to open the freezer door (where my wife’s ice cream stash is), or the cabinets where chips and crackers are stored. Out-of-sight/out-of-mind really works for me. My (our?) eyes are powerful “appetite” (hormone) stimulators, seriously. I bet there’ve been more than a few scientific papers written on how visual stimulation excites the brain (think sex, guys) and prepares the salivary glands, etc. I think I’ve read more than a few Stephan Guyenet (Whole Health Source) and J. Stanton (gnolls.org) columns about this.

So, these two additional ways in which what I eat are “very restrictive” is actually only one. That’s because all grains are carbohydrates and would have been “verboten” anyway. This carbohydrate aspect applies to the overweight and obese population, as well as all the diagnosed pre-diabetics and type 2 diabetics; but does it apply to the other 30% of us (“…the rest of us who don’t even know we’re pre-diabetic”)? Maybe not, in a strict sense. I would, if I could, still eat rice and starchy tubers (potatoes, yams, etc), but alas, I cannot tolerate carbohydrates. You, if you are overweight or obese (especially omental, or pre-diabetic or diabetic, would do well to avoid them too, because you too are insulin resistant.

But the shift in the balance of saturated to polyunsaturated fats over the last 50-100 years is wholly unrelated to carbohydrates. Their contribution to chronic inflammation is an area of great interest in the independent scientific community (as contrasted with the corrupt science in agribusiness/academic/government sponsored science cabal). Of particular interest in the very heavy shift in the Omega 6 (linoleic acid) to Omega 3 (linolenic acid) balance in our diet from roughly 1: 1 to as much as 30:1 over this time period. That’s why it is important to seriously curtail the consumption of vegetable and seed oils (linoleic acid) and increase the Omega 3s from fish oil. But you can’t “fix” this problem with fish oil alone; you have to cut back sharply on the polyunsaturated vegetable and seed oils you eat, starting with fried foods.

It is important to eliminate fried foods because oils, already damaged in manufacturing by pressure, heat and chemicals, are then reheated (often repeatedly) to high temperatures (boiling!) in the fryer. These oils are also easily damaged by exposure to daylight and quickly become rancid. Saturated fats do not. So, cook with butter, coconut oil and lard, not vegetable oils! And use olive oil as a salad dressing or a drizzle to add flavor and richness, and you will eat well indeed.

As Dwight Lundell, MD, quoted in #185 a few days ago in Jimmy Moore’s good book, Cholesterol Clarity (pg 35), said, “The population will become split between the smart and the dumb. The smart ones will begin taking their health into their own hands because they’re already seeing that what we are doing now is not working.” Moore then commented as follows:

“I am a huge proponent of people taking responsibility for their own health. We are all unique individuals with different needs and yet we are treated like lemmings by the medical profession when it comes to our health. I get why so many people abdicate personal responsibility with their health; it’s so much easier to just do what we’re told. But that approach clearly doesn’t work: Science changes all the time, and medical and nutrition specialists simply can’t keep up. How can they possible have all the answers? There’s no way around it. If you want to be healthy, it’s up to you to make it happen! Educate yourself, and then act on what you learn. You must be the final arbiter of your own health.”
So, what are you waiting for? Want to be healthy? Take charge and change what you eat. You will see a world of difference.

Wednesday, February 19, 2014

The Nutrition Debate #185: “Your Diet is Very Restrictive!”


A Facebook friend recently noticed my blog on nutrition and that I posted it to Facebook (when I remember to). He then said, “Your diet is very restrictive.” I objected! Of course, I was being defensive. My diet is “very restrictive” in the general sense, especially to someone who eats a diet “without restriction” and who appears to be able to “get away with it.” And that appears to apply to a fairly large segment of the population. It includes everyone who is of “normal” weight and/or who is not a diagnosed pre-diabetic or type 2 diabetic. And that’s probably still almost half of us.

Lest these ones who appear to be healthy take comfort from this, I am reminded of a quote from Dr. Dwight C. Lundell, MD, author of The Cure for Heart Disease and The Great Cholesterol Lie, on pg. 36 of Cholesterol Clarity by Jimmy Moore with Eric C. Westman, MD: “Our diet is not working because 70% of us are overweight and obese, we have 29 million diabetics and 75 million pre-diabetics, and the rest of us don’t even know we’re pre-diabetic”(my emphasis). Lundell continues, “People are realizing that what we are doing is not working, and they are looking for other ways around this. That’s where do-it-yourself healthcare and self-monitoring will become the norm.”

And do-it-yourself healthcare begins with diet. See The Nutrition Debate #173, “Anyone can be a doctor....” So, if you fall into the 70%, even if just by virtue of being a little overweight, it is your diet that you should address to “fix” your health. And if you are among the 30% “who don’t even know (you’re) pre-diabetic,” then it is your diet that you need to address to “fix” that. If I haven’t made myself clear yet: Everyone needs to look at their diet and change it. But how? That’s the question. The most reliable way, as Dr. Lundell says, is “self-monitoring.

The best markers are blood glucose (fasting and, importantly, hg A1c), HDL cholesterol, triglycerides, LDL particle size and type, and chronic, systemic inflammation (hs C-reactive protein or CRP). Forget Total Cholesterol and LDL cholesterol. Of course, you’ll need to see a doctor to get these lab tests (except blood glucose), but, if you are in the 70%, or he/she suspects that you are, most of these tests will be ordered anyway. Ask for a copy of your lab test, and learn your markers.

So, how do you fix these markers? By changing your diet. I am not talking about eating less and exercising more. A growing consensus is emerging that the dietary advice we are getting from our government and our healthcare providers is what is causing the 70% already afflicted and the 30% who are not, yet, as well, i.e., “the rest of us (who) don’t even know we’re pre-diabetic.” Of course, I knew I was a type 2 diabetic when I changed my diet 12 years ago (in 2002). I had been since 1986. And I changed my diet, at my cardiologist doctor’s suggestion, to Atkins Induction (20g of carbohydrate a day) and lost 60 pounds in 9 months (without hunger). I later switched to Bernstein's Diet for diabetics and lost 110 pounds more.

But the big change from eating Very Low Carb (VLC) was in my diabetes health and my lipid chemistry (cholesterol tests). Immediately, from day 1 on VLC, I started getting hypos (low blood sugar symptoms: sweating, light-headedness), so the doctor eliminated first one of the oral diabetes meds I took. A day or so later, he cut the other two in half, and a few days later, in half again. Eventually I eliminated a 2nd med, and today I take just a minimum dose of Metformin. Of course, my hg A1c’s dropped dramatically to a level in the mid 5s. Note: a doctor examining me today would say I was “non-diabetic.”

Even more amazing were the changes in my lipid chemistry. Over the course of time my HDL more than doubled (from an average of 39 to an average of 81). My latest HDL-C was 90. And my triglycerides declined by almost 2/3rds from 137 average to 49 average. My latest TG was 34. Total Cholesterol remained about the same and my LDL inched up slightly but now they are Pattern A (of the large, fluffy buoyant type). The latest test results were TC = 207 and LDL-C = 110.

I’m now working on getting my chronic, systemic inflammation marker (hs CRP) down to below 1.0, the ideal target. My latest test result was 1.2, but it has been as low as 0.3 and even 0.1, so I have a ways to go. So, how do I do it? By eating a restrictive diet, obviously. I’m not perfect. I cheat all the time. But I have a paradigm that I strive to follow, and I do follow it, for the most part. But you’ve gotta have a life (hopefully, a long and healthy one). So, what are my guidelines/goals? My target macronutrient ratios: 75% fat; 20% protein; 5% carbohydrate. Two or 3 small meals a day, spaced at least 5 hours apart; no eating less than 3 hours before bedtime; no snacks, except sometimes a small snack an hour or so before dinner.

Breakfast: 3 fried eggs, 1 strip of bacon, and a large cup of coffee with stevia extract and half and half; Lunch (when I eat it): 1 can of sardines in olive oil. Sometimes I add a tsp. of coconut oil. Dinner: a small portion of protein and a large vegetable serving (with butter added or roasted in olive oil). I also take a bunch of supplements, but that’s another story.

My cheats: a square (or two) of 85% cocoa dark chocolate a couple times a week; a glass (or two) of red wine a couple times a week; one or two Perfect Rob Roys - up with a twist - and a garlic crouton (or two) with a Caesar Salad in a restaurant. (I always “forget” to say “hold the croutons.”) I drink artificially sweetened ice tea or diet tonic with lunch/dinner or with a pre-dinner snack. Water would be better, but as I said, I’m not perfect. Anyway, this is what I strive to eat, most of the time.

Saturday, February 15, 2014

The Nutrition Debate #184: “VLC = Not So Much Thinking”


My editor made this comment in the margin of one of my columns recently, and it occurred to me she had made (as usual) a really cogent observation. The full comment was, “I suppose that making people think about food choices is the key, but VLC = not so much thinking. That’s a real plus for me.” It’s all the more interesting since neither she nor her husband is diabetic; but besides being a great editor/collaborator, she really knows about healthy eating and good nutrition.

Of course, “making people think about food choices IS the key” to healthy eating whether you’re diabetic (or pre-diabetic) or not. I am coming increasingly to think it is also the way everyone should eat…in part because it is the way we all used to eat. We were healthier as a population before the advent of manufactured and processed foods. That’s a fact.

But I also know that what turns many people off about VLC is the prospect of numbers and counting carbohydrates. If it’s not counting calories, it’s counting carbs and fat and protein. I admit, I used to do it compulsively (which is my nature), but it’s not necessary. That’s my editor’s point. And the point of many other experts in VLC who recognize and accept that many people have an aversion to obsessing over numbers. Well, it’s not necessary to do that. (Am I repeating myself?) All you have to do to adopt this Way of Eating is to understand the basic principles and then adhere to them.  Not much thinking.

Strict adherence is a daunting prospect to some, but with an open mind (and strict adherence) you will quickly learn that hunger will not be a driver of non-adherence. You will not be hungry if you adhere strictly to the basic principles. It’s that simple. It may take a few days (maybe a little longer for some), but your hunger will disappear. Your hormones will take over. They will detect that since you’re not eating carbs, there must be none available. (Your hormones don’t know about your stash.) Hormones operate entirely within the milieu intérieur – inside the body. Admittedly, my eyes at times betray me when they see food, but that’s another biological imperative that we can to control with our will (and a little trickery), if we’re not hungry. Our body has many drivers/actuators of survival, hormones being just one. Sight and smell are others.

Your hormones are acutely attuned to what you put in your mouth for energy. If you only eat a few carbs, your body uses those, with protein and fat first, and then it will use your body’s stored carbs (glycogen) for energy, then the fat you ate (that usually accompanies protein). And then, if you don’t eat too much fat and protein, it will use your body fat for energy. Voila! Bingo! You’re losing body fat and all you had to do was eat VLC. (Note: if you don’t eat some protein 2 or 3 times a day, your body will use your muscle for energy too, so be sure to eat a small amount of protein 2 or 3 times a day.

So, “not so much thinking” works, so long as you know what a carbohydrate food is and which foods have more and which have fewer. There is a learning curve to that, but it doesn’t require so much thinking. It just requires strict adherence. I started on Atkins Induction and stayed on it for 9 months, losing 60 pounds. Notice I didn’t mention that Atkins Induction is 20 net grams of carbohydrate a day. You don’t need to know that. You just need to strictly eat just what Atkins Induction says you can eat. They (and many other sites) have lots of helpful lists of foods you can eat, and what foods you can’t eat.

And if you want to succeed, please don’t give yourself a “holiday” or day off. I don’t mean, nor do I expect, that you won’t cheat. I do.  I just mean don’t plan to do it. (You won’t feel deprived, especially if you’re not hungry, and you have more energy, and you feel better, and you’re losing weight and your lab tests keep improving. Just don’t think that you can succeed if you only do this VLC 5 or 6 days a week. It won’t work. You can’t fool your body. It’ll think you found your stash, and everything is now hunky dory. It will stop burning your body fat and start saving it, and banking more, for the next “famine.” It’s doesn’t know we now live in a world of plenty, a veritable cornucopia of abundant and readily available food.

And the trigger for this new “hunky dory” hormonal message will be that silly Reese’s Cup you picked up on the checkout line. “Eye candy.” It will trigger a glucose and then an insulin response, which means it will shut down your fat burning metabolism and restart the glucose burning metabolism that causes the pancreas to secrete and pump insulin to carry the sugar energy (glucose) to your cells. I repeat: Fat. Burning. Stops. And your body, thinking the cornucopia is flowing again, will ask for more “sugar.” Your hormones will send you hunger, “feed me” signals, relentlessly craving more “sugar.”

Of course, the simplest, easiest and quickest sugars to digest are the liquid ones, and then the ones that have already been pre-digested by processing. And these are the very ones that have been damaged in the manufacturing process. So, as my editor/collaborator says, “making people think about food choices” is what we need to do. Please tell us how we are doing.
As I write this (in January), The Nutrition Debate has just passed the 50,000 page views mark, with 40,000 of those in the last year. We’d like to know what you like about this blog and what you don’t. What would you like me to write about going forward? And what would you like me to write about less? Do you open and read the hyperlinks provided? Who are your favorite writers/bloggers? Do you read this column in Google Translate? Did you know it is available in 77 languages? And finally, are you a type 2 diabetic, or prediabetic, or just someone interested in healthy eating and the nutrition debate?

Wednesday, February 12, 2014

The Nutrition Debate #183: My New Doctor and Me


I had an appointment recently with a “new” doctor – new to me, that is. He’s an established physician in a large group that is part of a larger consortium of groups. He practices “Family Medicine,” which means he’s a generalist, essentially a General Practitioner or GP with an added 3-year ­­­residency in Family Medicine and Board Certification, which gives him hospital privileges.

I met my new doctor in a bar. He was having broiled salmon, and I was having a drink (while my wife shopped). I recall that I initiated the conversation by commenting on his side dish, or possibly the bread. I don’t recall. Anyway, he told me he was a physician, and he mentioned the group name, and I told ­­­­­­­him I had just been “fired” (for being rude) to an endocrinologist in that same group. His response was to tell me to call his office the next day and make an appointment with him, so I did.

The appointment didn’t go well. I told him I had been off my Very Low Carb eating plan off almost 2 months, had gained more than a few pounds, and expected my A1C was going to be up from 5.7% to +/- 6.0%. My goal was to get it back to 5.6% or below again, and he said, “That would be ‘non-diabetic.’” He added that if I lost 40 pounds, “You would be non-diabetic.” I told him that a few years ago I was 50 pounds lighter than I am now and, “believe me, I was still diabetic.”

I then mentioned that when I am “on” my program, I eat between 10 and 15 grams of carbohydrate a day. He responded with a tone and air of certitude, “Twenty grams of carbohydrate a meal is what you should eat.” This really set me off. My new doctor knew everything there was to know about me and my insulin resistance and my carbohydrate intolerance, without even taking a history. I’ve been a type 2 diabetic for 28 years, the last 12 of which I have managed to get off virtually all my oral meds and keep (for the most part) good glucose control by diet alone, and now he was telling me how to manage my diabetes his way. I know. I know. He was just following clinical guidelines, as set down by the ADA, etc. etc.

That’s when somehow the subject of statins came up. I told him I would refuse a statin if he ordered it, and I told him why. I mentioned my latest (at the time) lipid panel (TC: 217; LDL: 122: HDL: 85; TG: 49; TC/HDL ratio: 2.6). I said I considered that stellar. He replied that the National Cholesterol Education Program (NCEP-4) Guidelines recommend a TC < 200 and an LDL < 100 (which is true), even though the new ACC/AHA guidelines no longer set LDL targets in absolute numbers. I called the NCEP guidelines pure BS and said the gurus and guidelines that I follow are very happy with a TC between 200 and 220.

Actually, I recalled later that one of my favorite resources, Paul and Shou-Ching Jaminet’s “Perfect Health Diet” says (page 366), “The ideal serum lipid profile – the one that produces the best health and minimum mortality – looks like this:

·         Total Cholesterol level between 200 and 260 milligrams per deciliter

·         LDL Cholesterol level above 100 milligrams per deciliter

·         HDL Cholesterol level above 60 milligrams per deciliter

·         Triglyceride level around50 to 60 milligrams per deciliter

At this point, I thought it was appropriate to emphasize my exceptional HDL (85) and TG (49) numbers and that my LDL (122) was Pattern “A.” My doctor’s response was (I can’t believe this!): “Define ‘Pattern A.” I replied, “large, buoyant, fluffy, rather than small dense, the better to avoid oxidized, small dense LDL particles getting stuck in the eroded endothelial layer of my arteries, if I had such erosions, which my low hs C-Reactive Protein (CRP) scores suggest I do not. I showed him my history of CRPs and he did admit it was “impressive.” They had plummeted from a high of 6.4 when I started very low carbing in late 2002 to a low of 0.1 last year, but have begun to creep up again. He agreed to help me look into that.

But then he said something that shook my faith that my new doctor and I were going to work things out. He said, “The latest science is that all LDL are alike. They all get stuck. I asked him to give me a citation in the medical literature for that. I said I read a lot of medical journals and scientific papers – probably more than he did. He didn’t like that, and replied I did not. How can he know? Anyway, when I asked him later for the “LDL are all alike” citation, he said, “Give it up.” Okay, I said.

What I gleaned from this appointment is that Family Medicine MDs are trained to diagnose and treat, primarily with pharmacotherapy, incipient type 2 diabetes. They’ve learned by rote what is “diabetic” and what is “non-diabetic.” They’ve learned that a “pre-diabetic” can “reverse” the progression to full-blown type 2 diabetes (and improve blood pressure) by losing weight. They know what Insulin Resistance is and that insulin sensitivity can be increased by severe carbohydrate restriction (and exercise) and “non-diabetic” A1Cs achieved. But that does not reverse IR or carbohydrate intolerance.  

After he ordered some tests we shook hands and the phlebotomist came in to draw blood. I gave him my card, and he said he would take a look at my blog. Maybe he’s reading this. I have a follow-up appointment in a few weeks, so I’ll find out.

Saturday, February 8, 2014

The Nutrition Debate #182: Avoiding “incident type 2 diabetes”


What do I mean by “incident type 2 diabetes”? The medical definition refers to the diagnosis and first intervention for the medical condition diabetes mellitus. For my purposes here (as I’ll relate later) “incident diabetes” is defined as two successive glucose readings of ≥126mg/dl or an A1C≥6.5% or treatment with a hypoglycemic medication such as Metformin. Using Metformin as a defining criterion may seem overly broad to some, but it was used in this important study in 2003 linking type 2 diabetes to CVD and CHD. Let me also remind everybody that the American Diabetes Association standard for diagnosing type 2 diabetes has changed substantially over the years and continues to be very controversial.

Until 1997, when it was changed to 126, the criterion for diagnosing type 2 was a fasting reading of 140mg/dl. In 2009, the inexpensive A1C test, which measures sugar on the surface of red blood cells over their 2-3 month lifetime, became the new standard, and the diagnosis point was lowered from 7.0% to 6.5%. The A1C blood test simulates the continuous level of glucose circulating in our blood, including the “excursions” (spikes) in postprandial blood sugar levels (after meals and snacks). This “averaging” methodology is a more accurate measure of insulin resistance (IR), especially when “challenged” by a carbohydrate load. IR is the underlying mechanism responsible for high blood sugar, and you can read a very good explanation of it in this About.com article. Shortcut: Easiest at-home test to determine IR – your waist to hip ratio.

A1Cs are also controversial. Most clinicians still follow the guidance of the American Diabetes Association and strive, thru “lifestyle intervention” and pharmacotherapy, to maintain a patient’s A1C at 7.0mg/dl, but that translates to an estimated Average Glucose (eAG) of 154mg/dl (determined with this calculator http://www.phlaunt.com/diabetes/20898027.php) and assures that the disease, and the pharmacotherapy, will be progressive. In other words, the onset of complications and co-morbidities, like cardiovascular disease, kidney disease, neuropathy and retinopathy , are inevitable. In clinical practice most practitioners are complicit. I don’t suggest overt self-interest, but the “trail of breadcrumbs” tells a cautionary tale.

Quest Diagnostics lab reports state the current A1C “reference intervals,” as published annually in Diabetes Care, the Journal of the American Diabetes Association, are a guide to the diagnosis of incident type 2 diabetes. They are:

< 5.7%           Decreased risk of diabetes

5.7-6.0%       Increased risk of diabetes (most prediabetics become diabetic within 10 years)

6.1-6.4%       Higher risk of diabetes

≥6.5%            Consistent with diabetes

A plain speaking translation of this very lax ADA testing standard for “incident type 2 diabetes” is : ≥6.5% = You’ve got Type 2 Diabetes, period; 6.1-6.4% = You’re Pre-Diabetic; 5.7-6.0% = You’ve got “impaired glucose tolerance” (IGT); and <5.7% but closing on it = you’ve got “impaired fasting glucose” (IFG). In all instances, you are Insulin Resistant (which means you are Carbohydrate Intolerant); you’ve lost and continue to lose beta cell function including the ability to make insulin. This “Natural History of Type 2 Diabetes,” explaining beta cell function and Pre-Diabetes, is described in “The Nutrition Debate #99” here. It is based on Dr. Ralph A DeFronzo’s presentation in his Banting Award Lecture at the ADA’s 2008 convention.

In the full published paper in the ADA Journal Diabetes, Dr. DeFronzo says, “In summary, our findings (4042) demonstrate that, at the stage of IGT, individuals have lost over 80% of their β-cell function, while the results of Butler et al. (47) suggest that subjects with “pre-diabetes” have lost approximately half of their β-cell volume. In the next section, “Pre-Diabetes,” he adds, “The clinical implications of these findings for the treatment of type 2 diabetes are that the physician must intervene early, at the stage of IGT or IFG, with interventions that target pathogenic mechanisms known to promote β-cell failure.
As a physician/researcher, Dr. DeFronzo cannot be faulted for advocating that “the physician must intervene early, at the stage of IGT or IFG, with interventions that target pathogenic mechanisms known to promote β-cell failure.” That’s the doc’s job! But how about the patient? The intervention that best targets the mechanism that kills beta cells is dietary. Eating carbs forces the pancreas to work. As you reduce carbohydrates, you spare your pancreas. It’s that simple, folks.

Wednesday, February 5, 2014

The Nutrition Debate #181: The New AHA/ACC Statin Guidelines and Type 2 Diabetes


In The Nutrition Debate #180, here, the 3rd category for individuals who should be on a statin, according to the recommendations of the new American Heart Association/American College of Cardiology cholesterol guidelines, is:

“Those with diabetes aged 40 to 75 years with LDL between 70-189mg/dL and without existing heart disease.”

That includes me! I’m 72 years old and my most recent LDL cholesterol (calc.) was 110. Never mind that my HDL was 90 and my triglycerides (TG) 34. My total cholesterol (TC) was 207. Do the math: The actual formula actual is LDL = TC-HDL-TG/5. In addition, by the way, my NON-HDL was 117 and my Chol/HDL ratio was 2.3!

(I wonder, by the way, what happens when I turn 76? With the new Medicare budget cuts, do they (the medical establishment and new insurance guidelines) just turn me out to pasture? Have I lived, in their collective judgment, a useful but long enough life? Without treatment, would I just be left to slowly dissipate…and then die of “natural causes?” I ask this question because category #3, “those with diabetes,” is the only category with age guidelines for statin treatment.

So, my issue with this #3 category (besides the age question) is with the unqualified phrase “those with diabetes.” Even Ann Peters, MD, writing about “How do New Statin Guidelines Affect Diabetes Care?” for Medscape Medical News here, had to “ponder these guidelines” that “lump people with type 1 and type 2 together.” “I don’t think that type 1 and type 2 diabetes share similar features, at least not similar features with respect to the metabolic syndrome in all patients.” She treads lightly here, but I get her point. The clinician in practice needs to consider their individual patients. Bravo, Dr. Peters!

Dr. Peters describes herself “as one of the authors of the new diabetes position statement on the treatment of hyperglycemia” and “a diabetes specialist.” So, as a fixture of the establishment, she comes home to the AHA/ACC fold:

“So I think I will still monitor lipid panels. Perhaps not for absolute numbers, but to see that a patient is responding to therapy -- maybe as a marker for the fact that my patients are taking their therapy, and also to reinforce patients with some of the benefit from the treatments and lifestyle changes they have made, which I think can still be had along with the use of statin therapy in these high-risk individuals.”

“High risk individuals”? That’s how ALL diabetics are categorized by these new statin guidelines. That includes not only type 1s, as Dr. Peters mentions and then carves out an exception for in her piece, but ALL type 2s as well, regardless of “the benefits of the treatments and  lifestyle changes they have made.” Of course, by “treatments” Dr. Peters is referring to “my patients (who) are taking their therapy,” by which she means drugs. And by “lifestyle changes” Dr. Peters is referring to “diet and exercise,” although certainly not the low-carb, high-fat Way of Eating that is followed by this type 2 diabetic.

The medical establishment’s justification for this all-inclusive position with respect to diabetics is that, as Dr. Peters explains, “…regardless, (all) patients with diabetes are considered to be at high risk.” Thus, “Depending on their 10-year risk for an event, whether or not it’s greater than 7.5%, they are put on either a moderate-intensity statin regimen or the high-intensity statin regimen. But they are all put on statins if they are between the ages of 40 and 75.” After that they can eat all the fudge they want. Why not! Type 2 diabetes is “progressive” for all who are “treated” by medical association standards and insurance guidelines. So, with standard nursing home care, where they will be given basal and mealtime insulin, even if their glucose control is less than perfect, and allowed to die of some other cause, such as heart disease or dementia.

In contrast, patients who have well-controlled type 2 diabetes, by eating a Very Low Carb diet, will have very good A1c’s, with stable blood glucose all day long, low blood pressure, low systemic inflammation, and great lipids including high HDL and low triglycerides, all without “taking their therapy”…since medical treatment for hyperglycemia will be unnecessary and unwarranted. But this doesn’t occur to Dr. Peters because her clinical practice as a diabetes specialist is for people who need a diabetes specialist. If you treat yourself by the dietary choices you make, you will not need to see her, or her ilk.
You will not, however, be spared the likelihood of this altogether unappealing nursing home outcome if you follow the AHA/ACC Lifestyle Modifications that accompany the new AHA/ACC Cholesterol Guidelines. The Lifestyle Modifications recommended are the same-old, same-old: “Consume a dietary pattern that emphasizes intake of vegetables, fruit and whole grains; includes low-fat dairy products, poultry, fish, legumes, non-tropical vegetable oils and nuts, and limits intake of sweets, sugar-sweetened beverages and red meats, ” with special emphasis on lowering saturated fat and sodium intake. And “to achieve this pattern by following plans such as the DASH dietary pattern, the USDA Food Pattern, or the AHA diet. And to exercise more, 3 to 4 sessions per week, lasting on average 30-40 minutes per session. As if to “throw a bone” to the type 2’s, they do allow that you could “adapt this dietary pattern to…nutrition therapy for other medical conditions (including diabetes mellitus).” They must have read the new ADA dietary guidelines described in The Nutrition Debate #155.

Saturday, February 1, 2014

The Nutrition Debate #180: The AHA/ACC Cholesterol Guidelines


Last November, the American Heart Association and the American College of Cardiology (AHA/ACC) issued a new set of cholesterol guidelines that is proving to be as disruptive and discombobulating as the Affordable Care Act (Obamacare). In fact, it is so much so that Medscape Cardiology issued this Special Report titled, “CV Risk Calculator and Guidelines Controversy.” It has six separate links to “News” and six more to “Experts Weigh In.” That’s too much information for here.

So, succinctly put, what are the new cholesterol guidelines and what’s the stir all about?

The main recommendations are that individuals who fall into any of the following four categories should be on a statin:

1.       Those with existing heart disease.

2.       Those with LDL levels above 190mg/dL

3.       Those with diabetes aged 40 to 75 years with LDL between 70-189mg/dL and without existing heart disease.

4.       Those without heart disease or diabetes, with an LDL between 70-189mg/dL and as estimated 10-year heart attack risk of above 7.5%.

The above bullets and the following analysis were provided by Ronesh Sinha, MD, at his South Asian Health Solution site:

“When comparing the old guidelines to this one, the first 3 categories are essentially unchanged. Most doctors would put heart disease patients, diabetics and those with LDLs above 190 mg/dl on statins. There are some advantages to the newer guidelines:

·         The focus of therapy is on statins, which are the default drug of choice. This is a good thing for those who truly need statins and should hopefully avoid cumulative toxicity from multiple drugs.

·         The concept of treating to a specific LDL target number has been eliminated. This is good since it should reduce unnecessary high dose statin therapy to reach low targets which have not been proven to reduce heart attack risk.

·         These guidelines do a better job of highlighting statin adverse side effects which will hopefully make clinicians think twice before pulling the statin trigger.

·         Greater overall emphasis on heart attack risk rather than a focus on the LDL number which makes more sense.”

But it is Dr. Sinha’s (and many others) major criticism of the guidelines is “The 4th category where individuals who have no risk factors other than a 10-year heart attack risk above 7.5%. This is significantly lower than the prior cutoff of 20% and will result in many more people taking statin medication.” Many more? That’s actually an understatement, in my opinion. I saw an interview of a healthy individual the other day on TV in which the doctor said to the 38-year old male, “In 2 years [when the patient achieved the threshold age of 40] you’ll be on a statin.” So, I decided to test the risk calculator myself.

The “risk factors” that are the sole basis of the 10-year heart attack risk are as follows: Sex, Age, Race, Total Cholesterol, HDL-Cholesterol, Systolic Blood Pressure, Treatment for High Blood Pressure, Diabetes, and Smoker. I plugged in my data and came up with a 10-year risk of atherosclerotic cardiovascular disease (ASCVD) is 28.1%, using the new calculator. Wow!

Then, I decided to see what I could do to lower my risk.  Age, sex, race were not things I could change. Neither could I improve my systolic blood pressure (110) or my diabetes (yes), treatment for hypertension (yes) or smoking status (no). And my HDL (85) was already outstanding. So, for me, that left only Total Cholesterol (TC). And since LDL-cholesterol is a calculated value (by the Friedewald formula), it is reduced (by a statin or otherwise) in direct proportion to TC. So, I decided to ‘prescribe’ a statin for myself to lower my TC (217) and thus LDL cholesterol by 50mg/dL to 167mg/dL, easily achieved on a statin. That would lower my LDL from 122 to 72, aligned to the “old” goal of 70. Result, my 10-year risk of ASCVD was reduced from 28.1% to 25.3%. The reduction was disappointing, to say the least. Hmmm…

What would happen if I lowered my age by 15 years to 57 (keeping the 217 TC)? The 10-year risk: 8.0%, just above the 7.5% cutoff. So, following these new guidelines literally (which I know no cardiologist would do, right?), I would be a candidate for a statin. No way, Jose, but I hope you see where I’m going. Dr. Sinha sums it up nicely in his “closer look” commentary:

What’s missing? How about triglycerides, weight or waist circumference, prediabetic blood sugars, and physical activity levels? I have many patients, especially those of Indian and Asian background, who have high triglycerides, abdominal obesity and prediabetic blood sugars, but don’t smoke and have normal blood pressures. They have a condition called metabolic syndrome, caused by insulin resistance, which accounts for a huge burden of global heart disease and this calculator misses it in most cases. In fact, I’ve plugged in the “before” numbers for some of my heart attack patients and this magical calculator spit out a <1% risk of heart disease. Yes, a 60-year-old smoker with high blood pressure will register a high risk score, but you don’t need a medical degree or a risk calculator to figure that out.” What about cardiovascular fitness? Why do my 60+ year old lean, aerobically fit patients who eat a healthy diet continue to score as higher risk than my 40-year-old sedentary, obese, computer engineers who eat an unhealthy diet? I’ve already detected plaque and premature arthritis in these patients in their 30s and 40s, so in today’s high-tech world “age,” a key variable for the risk calculator, is much less critical than lifestyle and fitness levels.” Well said, doctor. Would that other clinicians did the same!
Next, I’ll take a “closer look” at the 3rd category above, which seems to me to have escaped scrutiny in all the hullabaloo.