Sunday, June 26, 2016

Type 2 Diabetes, a Dietary Disease #334: A Unifying Hypothesis of Chronic Disease: Part 1

I don’t remember how I landed on South African blogger Marika Sboros’s site, FOODMED.NET; but I love it, and I have signed up for regular delivery. Her blog’s subtitle is “Let food be your medicine,” so you can readily see my affinity. I first read a post in the “Managing Your Blood Sugar” series titled NOAKES: "IT'S THE FATTY LIVER DISEASE, STUPID' PART 2, tagged “LCHF.” Interestingly, Marika explains, LCHF in her lexicon means “Low Carb Healthy Fats.” I like it. It’s time to take on the PUFAs!
The author of this particular post is world-renowned scientist and University of Cape Town Professor Emeritus Dr. Tim Noakes. Noakes introduces his subject via the misunderstood term “risk factors” as taken from epidemiology and “observational” or “associational” studies. He delves briefly into “hazard ratios” (HRs), relative and absolute risk, and related subjects to show how data is commonly manipulated and abused.
“This is intellectually absurd,” Noakes says. “How can everything be a risk factor for everything else?” he asks. He answers, “The answer can be found in the ignored work of Dr. Gerald Reaven, Emeritus Professor of Medicine at Stanford University.” “Reaven has spent the past 60 years studying the condition that intellectually he now owns, insulin resistance.”
Reaven’s interest in insulin resistance was piqued by the distinction between Type 1 and Type 2 diabetes. Type 1 is characterized by the total absence of endogenous insulin; Type 2, insulin resistant diabetes, by “abnormally high amounts [of insulin] because the target cells on which the insulin normally acts are resistant to its action; hence the condition of insulin resistance or carbohydrate intolerance. Persons with insulin resistance have blood insulin concentrations that are elevated most of the time, a condition known as hyperinsulinemia.”
Noakes says, “Reaven’s great contribution has been to show this persistent hyperinsulinemia in insulin resistance, whether or not associated with T2DM, produces a collection of grave secondary consequences.”
“But Reaven’s greatest (and bravest) intellectual contribution is to suggest that insulin resistance and hyperinsulinemia are the necessary biological precursors definitely for four and perhaps for all six of the most prevalent chronic conditions of our day: 1) Obesity; 2) Arterial disease (local: heart attack or stroke; disseminated: T2DM; 3) High blood pressure; 4) Non-Alcoholic Fatty Live Disease (NAFLD); Cancer; and Dementia (Alzheimer’s Disease, also known as Type 3 Diabetes).”
Reaven gave the  keynote Banting lecture at the 1988 American Diabetes Association annual meeting. His talk explained the underlying factor for a constellation of abnormalities: glucose intolerancehyperinsulinemia, hypercholesterolemiahypertriglyceridemia, and hypertension.  He named it “Syndrome X; it was also given the moniker Reaven’s syndrome. Today it is simply called Metabolic Syndrome.
“The key finding from Reaven’s work,” Noakes says, “is that these conditions are not separate – they are different expressions of the same underlying condition. Thus a patient should not be labeled as having high blood pressure or heart disease or diabetes or NAFLD (or perhaps even cancer or dementia).”
“Instead,” Noakes continues, “the patient should be diagnosed with the underlying condition – insulin resistance – with the realization that the high blood pressure, the obesity, the diabetes, the NAFLD, or the heart attack or the stroke are simply markers, symptoms if you will, of the basic condition.”
“And that basic condition,” Noakes concludes, “is insulin resistance which, simply put, is the inability of the body to tolerate more than an absolute minimum amount of carbohydrates eaten each day. “
Thus we have it: Reaven’s unifying hypothesis of chronic disease: “One disease, one cause, many symptoms.” Tune in next week for a glimpse at the profound implications of this fundamental advance in medical science.

Sunday, June 19, 2016

Type 2 Diabetes, a Dietary Disease #333: NAFLD, Supplements, Fructose and PUFAs

A friend recently asked me to look over a list of supplements suggested as “interventions” for a diagnosis of NAFLD (Non-alcoholic fatty liver disease). I’ve been helping her with concerns about appropriate prophylaxes for other health issues – Insulin Resistance (IR) and Alzheimer’s Disease (AD) – so she sent me a link from Life Extension (LE), a supplement seller recommended by her doctor. I agreed to look it over and get back to her.
Life Extension’s “suggestions” include eight (8) supplements, all but one of which – a drug, metformin – they sell. All “have been shown to boost liver health and help manage NAFLD,” and “prevent progression to the more deadly NASH, which is a precursor of liver failure.” Pretty scary stuff! How many of these supplements should I buy? Then, at the bottom of the page, I saw that the tab on the link my friend sent was pg. 2. I clicked on pg. 1.
“Roughly one-third of the American population suffers from nonalcoholic fatty liver disease or NAFLD. NAFLD can go undetected for years and may eventually progress to inflammation and scarring of the liver (cirrhosis) and, in some cases, full-blown liver failure. A formerly rare condition, its rapid emergence has been linked to skyrocketing rates of metabolic syndrome and diabesity, the term many experts use for co-occurring diabetes and obesity.
My friend is not obese, but her IR and abnormal lipid profile puts her squarely in the Metabolic Syndrome “X.”
 “While poor dietary choices are often to blame, cutting-edge research suggests that hidden genetic factors may also play a role, and some people do not metabolize polyunsaturated fats properly, resulting in fatty deposits in the liver.”
Life Extension’s “fix,” of course, is predictable: They offer to sell you some supplements.
“As mainstream medicine continues to struggle in the search for drugs to manage this widespread condition, emerging scientific evidence has shed light on effective natural interventions that may halt or even reverse its progress.”
But wait, these “interventions” are just surrogates for drugs, and the best “treatment” for a condition that was caused by poor dietary choices and polyunsaturated fats is to make good dietary choices and eat healthy fats.
While you can’t change your genes, you can change the way they “express” themselves, even after being exposed to a barrage of the poor dietary choices advocated by our government going on 50 years now!
And, Life Extension has identified the likely causes of NAFLD: poor dietary choices and polyunsaturated fats.
What are those “poor dietary choices”? Life Extension hones in on the main one, a simple sugar, fructose. Fructose is half of every (cane) sugar molecule, and it is shunted directly to the liver to be metabolized. If the liver is already full of stored carbs (glycogen), it makes, via de novo lipogenesis, new fat molecules in the liver.
“Of course, what we eat is as important as the calories it contains. One of the major bad actors in today’s world is fructose, found in high quantities in high-fructose corn syrup. Fructose promotes formation of new fat molecules in the liver, blocks breakdown of existing fats, stimulates free radical production, and promotes insulin resistance. Increasing numbers of studies are linking increased fructose consumption with NAFLD, and even with its deadlier consequence, NASH. Patients with NAFLD consume 2-3 times as much fructose as do control patients, even corrected for body weight.”
The other dietary choice LE cites as a probable cause of NAFLD is “polyunsaturated fats,” or PUFAs, found in highly processed vegetable oils (canola, corn and soy bean oil, among many others). These are unnatural food oils that did not exist before technology was developed to extract them. I have written about the harm PUFAs do many times, but Life Extension’s citation was refreshing to see because liquid fats are still recommended to us to by the Dietary Guidelines for Americans (2015-2020)!
A small amount of PUFAs are “essential,” meaning the body can’t make them; however, the ratio of the “essential” ones (Omega 6s and Omega 3s) is important. Historically this has been 2:1 to 4:1. With the proliferation of “industrial” food oils over the last half century, and the USDA’s advocacy of them (and Cargill’s and ADM’s production and marketing of them), the ratio for most Americans is now 20:1 to 30:1.
You can’t fix this ratio by just supplementing the denominator with fish oil. You need to cut back dramatically on the numerator: on all fried foods and processed foods, like commercial baked goods, containing PUFA’s.
Replace PUFAs with monounsaturated fats (e.g., from olive oil and avocados) and saturated fats, such as coconut oil and grass-fed butter, lamb and beef, full-fat dairy and wild-caught fin and shellfish. All Real Foods!

Sunday, June 12, 2016

Type 2 Diabetes, a Dietary Disease #332: “Pre-Diabetic” or un-diagnosed Type 2?

I recently talked for an hour or so to a friend who knows that I know a lot about Type 2 Diabetes. He sought me out to ask me what he should do. I asked him, “What is your situation?” Here’s what he told me:
His fasting blood sugars (FBG), he said, are consistently running in the 140s. That’s 140mg/dl. I told him that was “out of control.” I asked him what his postprandials were. He didn’t know “postprandial” so I said your blood sugar 1 or 2 hours after starting breakfast. He said he didn’t know. He didn’t do postprandials.
I asked him what his latest A1c was. He replied 6.9. That’s 6.9%, but he said it was almost 2 years ago. I asked him if his doctor had told him that he was diabetic. He said “No,” and I said, “Well, you are!” The American College of Endocrinologists define Type 2 Diabetes as an A1c of ≥6.5%, and the American Diabetes Association as ≥7.0%, but that definition is part of the problem. Some clinicians today regard an A1c of ≥5.7% as full-blown Type 2 diabetes.
I asked my friend if he was currently taking any medications to control his blood sugar. He said, “Yes.” He was taking two 500 mg tablets of metformin twice a day, plus glyburide (a sulfonylurea). He didn’t remember how much, and I don’t remember how often he takes it, because this set me off on a rant.
He said, “What should I do?” I didn’t hesitate to tell him: “You’ve got to change what you eat, I mean seriously change what you eat.” “What do you have for breakfast,” I asked? “Oatmeal,” he said, “with milk and a little sugar.” “Switch to eggs,” I said, “any way (fried, scrambled, poached).” “How many”, he asked? “One, two or three; add a strip of bacon if you like,” I said, “but no juice, cereal, bread or jelly. Only heavy cream and artificial sweetener in your coffee, if you must.” I told him he wouldn’t be hungry. He wouldn’t need a mid-morning snack. (He had mentioned he ate an apple in mid-morning “’cause he was starving.” I just rolled my eyes in horror.)
I also told my friend that he had to get off the SU. But the effect could be that his A1c will go up unless he instead replaces it with a drug that acts in a different way, sparing the pancreas. There are now several more modern classes of drugs, both oral and injectable (not insulin). Many clinicians would even argue reasonably that a temporary course of exogenous insulin would perhaps be the best course of treatment in his case to get his blood sugar under “good control.” But I would argue that the best course of “treatment,” and the only one that addresses the cause of Type 2 Diabetes (which is Insulin Resistance), is to radically change what you eat, NOW.
My own experience supports this course of action. In 2002 I weighed 375 pounds and I was maxed out on metformin and a sulfonylurea and starting a DPP-4 inhibitor (Avandia). In retrospect, I was on my way to injecting insulin. My doctor wanted me to lose weight, of course, so he “prescribed” a radical change of diet, a Very Low Carb diet called Atkins Induction. The surprising result was that on the 1st day of strict compliance I got a hypo (a low blood sugar). The doc ordered me to stop the Avandia. The next day, another hypo, and he told me to cut the metformin and the glyburide (the SU) in half. A few days later I had to cut them in half again. Still later I cut out the SU altogether. Eventually, I transitioned to Dr. Richard K Bernstein’s 6-12-12 program for diabetics.
After a few years or eating this entirely different way, I had lost 170 pounds, my blood pressure was 110/70 (on the same meds), my HDL-C more than doubled and my triglycerides dropped by 2/3rds. And all I did was change what I ate.

Sunday, June 5, 2016

Type 2 Diabetes, a Dietary Disease #331: Dear Max: Don’t Eat Oatmeal for Breakfast!

(Note: This is a Universal Fill-in Form. Just change the name of the person and the carb food as appropriate.)
I know you’re busy, Max, but…your health is at stake, so pay attention: You’re Pre-Diabetic, and in all likelihood, you’re will become a full-blown Type 2, unless you change what you eat. Type 2 Diabetes is a Dietary Disease.
Doctors treat Type 2 Diabetes by treating one symptom, high blood sugar. They give you vapid advice (lip service, really) to undertake “lifestyle changes” like “eat less and exercise more,” to lose weight! Then, for your high blood sugar, they treat it (you) with meds. They follow up by monitoring your blood sugars at intervals to see that they are “well controlled” (by Diabetic Association standards), and, when they are not, they add meds.
Their response, to treat you with more meds (too little, too late, and all wrong!), will only result in wearing out your pancreas, the organ that makes insulin. In the end (literally), you are likely to have to inject insulin. You will eventually die from one of the micro or macrovascular complications of the disease.
Doctors should advise you to treat the cause of your Type 2 Diabetes, which is Insulin Resistance (IR). If they advise you with respect to diet, the advice you get is likely to be just plain wrong. If you follow it, you will do so at your personal risk. They are also treating your disease to much too lax a standard. They will regard your blood sugars as “well controlled” at a level where they are doing you harm. To repeat, if you don’t change what you eat, your Type 2 Diabetes will progress, with increased risk for all the attendant complications.
Insulin Resistance means that insulin receptors in your cells are refusing to take up the glucose that is being transported in your blood by the carrier insulin. Glucose is the fuel that your body makes from digesting carbs, (and to a lesser extent from excess protein returned to the liver). Result: your blood sugar rises. Solution: eat fewer – many fewer, carbs. Did you know, there is no (zero) nutritional requirement for carbs? And your IR means you are becoming, or have become, Carbohydrate Intolerant. Insulin Resistance = Carbohydrate Intolerance.
Your body needs some glucose (not carbs).  Some glucose is so essential to the body that the body has multiple ways to make it from protein and fat. And your body does need both protein and fat, and that is what you have to eat if you want to treat the cause of your Pre-Diabetes. Takeaway: Eat mostly fat and protein.
Hunger is the principal (but not the only) biological driver of eating. It is both intrinsic and autonomic. Your conscious will pales by comparison. You are a slave to your hunger – especially if you are carb dependent. If you eat carbs at every meal, and between meals eat carbohydrate snacks, your body will come to biologically expect that since carbs are abundant, you can depend on them as an easy and quick source of energy. In today’s world, carbs are abundant, and ubiquitous. And they are a quick and easy and cheap source of energy 24/7/365.
Biologically, when your body becomes dependent on carbs, it blocks access to an alternate and totally complete source of fuel that everyone has: stored body fat. Stored body fat is packed full of energy: 9 calories per gram vs. 4 for carbs and protein. But, your body can’t access that dense stored energy source because added insulin, accompanying the glucose still circulating in your blood, sends a signal to the brain that you don’t need to use your body fat to maintain the body’s steady energy state (homeostasis). The fact is, as a Pre-Diabetic, because of your Insulin Resistance, both your plasma glucose and your plasma insulin are continually elevated.

Translation: when the carbs you last ate are quickly digested, your body tells you that you are hungry again! You crave carbs. It tells you to eat more.
SOLUTION: After an overnight fast, just eat protein and fat (with ‘zero’ carbs) for breakfast. That means: no juice, no cereal, no bread, no jelly. You will feel full. After a few days, your body adjusts its internal metabolism and you will never be hungry again in the morning, mid-morning or even at lunch. If you continue with protein and fat for lunch, you will not be hungry again until the cocktail hour. And if you eat a small supper of mostly protein and fat, with a serving of low-carb veggies, you will not need to eat again until breakfast (or lunch). Repeat this every day and before long your fasting blood sugars will drop back into the “normal” range, and after a few months, your A1c’s will too. And your doctor will be happy because you lost weight. He or she will also likely reduce or eliminate your meds! And all you did was change what you ate!