The Nutrition Debate #103: Your Mileage May Vary (YMMV)

Your Mileage May Vary is an expression that I didn’t put much stock in when I first read it six years ago on a Low Carb Forum for diabetics (Dr. Bernstein’s, here). I was a neophyte in the self-management of my Type 2 diabetes, even though I had been a Type 2 for 16 years. Like most of us, I suppose, I left my health care in the hands of my physician. So, in those early days of self-management – if I thought about it at all, I thought that we Type 2s were all pretty much alike.

What prompts me to write this is a recent personal experience (n = 1) with blood sugar control. My most recent HbA1_c (as I write this) is 5.6. It’s been better and, of course, a lot worse. I have been eating a restricted-calorie Very Low Carb (<15g net) ketogenic diet for several months now to lose weight, and I have lost 25 pounds. Recently, five consecutive daily fasting blood glucose readings averaged 90mg/dl, with a tight range of 88 to 92). Then, at a small dinner party in our home, I ‘blinked’ (transgressed) for the first time in more than 3 months: I had less than a cup of risotto (with Osso Bucco and broccoli rabe) and a few sweets (2 cookies and 2 homemade double-bouillon-cube sized petit fours). My body hadn’t had this much starch and sugar in a long time, and it was not prepared for it. It probably never will be again. My fasting blood glucose the next morning, 12 hours later, was 120mg/dl. A day (24 hours) later, it was 117. The next day 114, the next 123, and so on. I had fallen off the ketogenic cliff. How many days will it take now to “recover” BS control?

That’s where YMMV comes in. It depends on your medical history (both the type and degree of metabolic dysfunction and when and how you and/or your doctor responded to the discovery that you were pre-diabetic or a full-blown Type 2. I was diagnosed a Type 2 in 1986, 27 years ago. The first thing my doctor did, besides advising me to lose weight on a ‘healthy’ balanced diet, was prescribe a sulfonylurea, a class of oral anti-diabetes medication (OAD med) that causes the pancreas to increase insulin secretion. At the time, a sulfonylurea was the first-line OAD med prescribed in the U. S. for type 2s. (Metformin was already in use in Europe but would not be approved in the U.S. for another 10 years after my diagnosis). When semi-starvation (restricted-calorie “balanced”) diets didn’t work, and I continued to eat carbs, the dosage was increased until I ‘maxed-out’ on this med after a few years. Years later, when Metformin was approved for use in the U. S., I eventually maxed out on that as well and I was started on a 3^rd class of meds. My blood sugar continued to elude control (on a “balanced” diet), and my Type 2 disease inexorably progressed.

 My Type 2 diabetes didn’t stop its progression until I changed my diet. Then it began to reverse to the point of being undetectable as long as I “eat right.” After starting to eat Very Low Carb (VLC), my blood sugars crashed, I started getting “hypos” (dangerously low blood sugars), and I was immediately forced to take fewer and fewer OAD meds. Still, it was almost five years before I completely titrated off the sulfonylurea. So, I took the sulfonylurea at some dosage level for about 21 of the last 27 years. Now, based on what we know today, what does that likely say about my remaining β-cell function? Well, I’m not a doctor, so I’ll turn to what one of my favorite diabetes specialists has been saying for years.

Ralph A. DeFronzo, M.D., in his Banting-award lecture at the 2008 Annual Meeting of the American Diabetes Association in San Francisco said, “By the time that the diagnosis of Diabetes is made, the patient has lost over 80% of his/her β-cell function…” I most recently told you this in The Nutrition Debate # 99, “Natural History of Type 2 Diabetes” linked here. He also said in the first paragraph of the full-text article published by the ADA on the NIH website here, “Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1_c and a progressive loss of β-cell function.”

So, where does this leave me? Or you? Insert your own n = 1 experience, and compare the extent YMMV conforms or varies with mine. I assume that when I was diagnosed, I had lost “over 80%” of my β-cell function. After being diagnosed, I continued eating lots of carbs for another 16 years (until I started VLCing in 2002), which means my pancreas still needed to produce lots of insulin (secreted in my β-cells). The sulfonylurea that I continued to take for another 5 years, albeit at a much lower dosage on VLC to avoid hypos, continued to push my pancreas to do that. The goal was to try to control my blood sugar with medications. My doctor (and I) were relatively happy, but at what cost? My pancreas is now shot. It is burned out. I cannot tolerate eating carbohydrates without losing blood sugar control, and you know what that means. (See #98, “The ‘Dreaded Complications’ of Type 2 Diabetes,” here)

So, as we saw in #99, a disease that starts with insulin resistance progresses to pancreatic β-cell burnout as it responds to that resistance. That is inexorable if you don’t dramatically change your diet, and will accelerate if you continue to take a sulfonylurea to pump-up your β-cell production. That is the “course of action” of the disease. That course will be invariable if 1) you don’t change your diet and 2) you don’t stop taking a sulfonylurea. You must do both to protect and preserve what pancreatic β-cell function you have left before it’s too late. If you choose to do 1) and 2) when you are at an early stage of this disease, YMMV from mine. If you don’t, like me, you may become totally carbohydrate intolerant.

The Nutrition Debate #102: Denial is not…

Denial is not a river in Egypt. You’ve probably heard that joke before. It may be said by a close friend/counselor, or even an enlightened physician, to not so gently make a point about the need to confront a matter. It avoids treating it as a mere “peccadillo,” the consequences of which are small and relatively unimportant. In fact, it could be said to affect a change that may be life altering. It was that way for me once. I remember it well.

While floating down a “lazy river” at a resort in Puerta Vallarta, Mexico, I began a conversation with another “floater.” I turned the conversation to my interest in nutrition for Type 2 diabetics and told my “new friend” what I had accomplished a few years before by a Low Carb Way of Eating (WOE). I followed Atkins induction. I then described how I had drifted away from that WOE for a number of years. It turns out my “friend” was one of those enlightened physicians (a Canadian) who then bluntly said to me, “You’re in denial.” Boy was I shocked!

He was right, of course. It’s easy to delude oneself. We do it all the time, every day, in many ways. It’s called rationalization, a process of reasoning, or suspension of reason that allows us to do something that we know is a “bad” option. The process is invidious. It sneaks up on us when we are unprepared. It happens in unexpected or unplanned circumstances. That is, if we are not practiced in dealing with it and if we lack total commitment.

That passing acquaintance had a lasting impact on my life. I returned to my previous WOE (after returning home, of course) and I lost another 100 pounds. I did that by eating VERY Low Carb and as a consequence was able to completely eliminate the 5mg of Micronase, a sulfonylurea drug that I was then still taking. And my blood pressure dropped further to 110/70 (on the same meds).  Sulfonylurea drugs are “the worst,” but until the mid-‘90s (when Metformin was finally allowed in the U. S.) they were the only anti-diabetes oral medications permitted here. Europe had been using Metformin for years, and today Met has been transformed here into the first line of defense (after “lifestyle modifications”) for pre-diabetics and diagnosed Type 2s.

One of Metformin’s mechanisms of action is to make our insulin resistant cells more insulin sensitive so that less insulin is needed. The sulfonylurea drugs are harmful because they force an already seriously compromised pancreas to secrete more insulin to deal with elevated blood glucose from the carbs we eat. By “seriously compromised” I mean that most of the beta cells which are formed in the Islets of Langerhans of the pancreas and produce insulin, have already been destroyed by the time a Type 2 diabetic is diagnosed. That shocking assessment is, sadly, true, and you need all you can get; they may figure something out later!

“Beta Cells in Diabetes, a website created by The Endocrine Society, describes a presentation by Dr. Ralph A. DeFronzo thus: “This article represents Dr. Ralph DeFronzo’s Banting award lecture, which he delivered as the 2008 recipient of the American Diabetes Association’s most prestigious scientific award (the Banting Medal for Scientific Achievement). It is noteworthy because in it he identifies that beta cell failure begins earlier and is more severe than previously thought. Based on this finding, he argues the need for early and aggressive treatment to preserve remaining beta cell function and to limit further disease progression.”

Dr. DeFronzo’s very technical paper, later published by the ADA, is available for free with full text and figures on PubMed here. Early in it, under the sub-heading “Prediabetes”, Dr. DeFronzo said, “In summary, individuals with IGT [impaired glucose tolerance] are maximally or near- maximally insulin resistant, they have lost 80% of their β-cell function, and they have an approximate 10% incidence of diabetic retinopathy. By both pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have type 2 diabetes.”

The sulfonylurea drugs accelerate the destruction of pancreatic beta cells. That’s why they have (thankfully!) fallen into disfavor. They pump the pancreas dry and are one of the reasons why Type 2 diabetes is described in the medical lexicon as a “progressive disease.” It’s the medical treatment that (in part) drives the progressivity. Of course, the other equally egregious reason is that the medical establishment does not advocate modifying the diet to restrict dietary carbohydrates to cope with a disease that is defined by carbohydrate intolerance.

Denial is a touchy subject. It is touchy because it is a very personal thing. (It can also be an institutional thing.) Addressing it requires the ability to look at oneself in an objective way. That confrontation can be pretty messy if our lives are complicated. We all have family and friends who care about us but who do not know about the advances in understanding the optimal way to treat people whose damaged metabolisms cannot tolerate dietary carbohydrates. It is, to the extent possible or practicable, to not eat carbohydrates. That course of treatment works for everybody who has insulin resistance, is pre-diabetic, or is diagnosed with Type 2 diabetes. It is also a great way for anybody to lose weight. Take an honest look at your own life, and ask yourself if you are in denial. If so, are you ready to change, now?

The Nutrition Debate #101: Why I’m Never Hungry

I have had a raised consciousness about food and feeding since I began writing this blog. And one of the things I have observed is when I “feel” hungry. Of course, hunger is not an emotion; it is a physiological signal that has been sent and received that motivates us to (look for and) eat food. (The “look for” is a reference to our ancestral behavior as “hunters and gatherers” which is still hard wired into our genes.) The signals travel from our stomach, where the hormone ghrelin senses it is empty, via the vegus nerve to the hypothalamus in the center of the brain. That is the central place there where hunger signals are interpreted and controlled. It’s from there that the signal is emitted. And we act. We eat.

This “empty stomach” syndrome works like clockwork in the disregulated metabolism that so many of us have developed. It is very familiar to those who eat a Westernized diet and especially the Standard American Diet (SAD, ironically) recommended by our government. According to the Nutrition Facts Panel, that diet is 60% carbohydrate, 10% protein and 30% fat. If you don’t believe that, do the math yourself. That’s 300g (1,200kcal) of carbohydrate, 50g (200kcal) of protein, and 66.6g (600kcal) of fat. That’s 2,000kcal total. Of course, the government wants you to cut down on solid (animal) fat, but not corn or soy bean oil, so what are you supposed to do? Your choice: increase carbs or protein. And if you eschew animal products, to avoid saturated fat and cholesterol, as Big Brother would have you do, what can you eat? Eat more carbs, of course. Big Agri Business at your service!

But I digress. To feed the disregulated metabolism our contemporary lifestyle offers us an endless supply of packaged, preprocessed, and easily digested “food” to choose from, most of which are carbs. We eat them, we digest them quickly, get quick energy, and then as they quickly empty from the stomach, we get the “hungry again” signal. That’s why carb eaters and especially carb addicts are always hungry. That’s why many diets recommend between meal snacks, or even 5 or 6 “small meals” a day. If you have done these diets, you know it is because you are hungry. Now you know why.

So, why am I not hungry, as I often used to wonder? Well, what are the possibilities? 1: I’m old (I’m 71). We’re all told that as we get older, we lose our appetite, and we eat less. Some of us actually lose weight “naturally.” I love the study that made the observation there are fewer fat people among the aged population; therefore, they concluded we must lose weight as we age because we’ve lost our appetite. Perhaps that is true, but how about this possibility? There are fewer fat people among the aged population because all the fat people are dead!  There are plenty of long term studies that show that fat people are more likely to die of many diseases. And all-cause mortality is definitely a lot higher among the overweight and obese population. This was the primary motivation for me to lose weight more than 10 years ago.

Possibility2: I have advanced cancer. Well, I can’t rule that out, but I am not wasting away. I have to work hard to lose weight. I eat a restricted calorie diet that is very low carb. In fact, most of the time I think I am in a mild ketogenic state. That allows my body to burn fat instead of “sugar” (carbs, either ingested or stored) for energy. The fat is also either ingested or stored. Stored energy, my body fat, is my targeted source of fuel. That’s why I need to eat a restricted calorie diet. I need to be in negative calorie balance to lose weight. I am doing this without exercise and without hunger. For one thing, I’m “allergic” to exercise. It also would make me hungry, as in “work up an appetite.”

Not being hungry is my subject here, not exercise, so the question is, why am I not hungry? Possibility 3: I am not hungry at breakfast because my body has been in a mild ketogenic state, allowing for digestion, for maybe 10 of the 14 hours since I last had a meal or ate anything. That means I didn’t raid the fridge before or after dinner, or eat a bed-time snack, as I used to do. When I am in ketosis, my body is happily burning fat for energy – hopefully my body fat. It doesn’t need ‘sugar’ (glucose) for fuel, so it doesn’t signal that I need a “carb fix.” This is a natural state. It is called ketosis.

Then I eat a breakfast with 6 carbs “tops.” It is just fried eggs, bacon and a cup of coffee with half & half & Splenda – a small ketogenic meal. After that small meal I can easily go all day without hunger because I am still in ketosis. But, because I don’t want my body to break down muscle tissue for energy, I eat a very small lunch of zero carbs, just protein and fat: a can of sardines and a beverage. Another small ketogenic meal, and I stay in ketosis. Then, an hour or so before supper, I sometimes sit down to watch the news and snack on radishes with salt and a “schmeer” of ghee. Butter works as well, but I like my ghee. The idea is to eat just a little fat to satiate and thus short circuit any tendency to eat too much at dinner.

I always used to eat too much at dinner. I think it was a cultural thing. For most Americans, dinner is the “big” meal of the day, and cultural habits require a conscious effort to break. Dinner has always been a big problem for me. My wife put too much on my plate (Sorry, Honey), and I always ate it all. (I can’t blame her for that!) We learned as kids not to leave food on the plate. (Blame it on our parents instead.) Now, with my wife’s help (Thanks, Honey!) I am eating a small supper, and I am passing up 2nds (even with really “palatable” food, as it always is). We have a vast choice of menu options: fatty meats, poultry, and seafood (fish and crustaceans), plus a low-carb vegetable roasted in olive oil or finished with lots of butter. In other words, another small ketogenic meal. This makes losing weight easy. And that’s why I’m never hungry.

The Nutrition Debate #100: Liquid Calories

What’s wrong with taking nourishment in liquid form? It’s certainly convenient, and if you make your own “smoothie” or some nutrient-dense concoction in a juicer or blender, you are assured of a “healthy” beverage of your own composition and making, right? Well, “yes” up to a point, but “no” for a host of other, very good reasons. Let me enumerate.

1)  The calories we drink go quickly “down the hatch,” no chewing required. Chewing is the first mechanical step in digestion. It takes energy (see The Nutrition Debate #52: “The Thermic Effect of Food” here) and time, not just the time spent chewing but also the time needed for enzymes in the mouth, stomach and small intestine to process chewed solid food into chyme and then further break it down to where it can be absorbed. If they have already been “liquefied,” these physiological functions are “side-stepped.” Liquid calories are absorbed more quickly and easily. In fact, in The Nutrition Debate #53, “On the Digestion and Absorption of Food” here, we explain 1) how some liquids are absorbed directly through the stomach wall and 2) how the priority of gastric emptying for those that are not is: liquids first and much more quickly than solids, then carbs, then protein, and then fat and fiber.

 2)  “The mechanisms controlling hunger and thirst are completely different,” wrote food writer and nutritionist Katherine Tallmadge in the Washington Post in this December 2004 piece. “Physiologically, your thirst is quenched once your blood and cell volume are increased by water. This sends signals to your brain that you are no longer thirsty. In contrast, hunger is regulated in your stomach and intestines. When you’re eating, nerves in the stomach wall detect that the stomach is stretching and send satiety signals to the brain. The intestines also release nerve regulators and hormones. At the same time, the level of the hunger hormone (called ghrelin), which is released by the stomach when it’s empty, is suppressed. All this helps you feel full.” Ghrelin doesn’t work as well with liquids as it does with solid foods. “Our bodies don’t detect the calories in these liquids foods the same way as when we eat solid foods,” Tallmadge said.

3)  Liquid calories add up in a way that can be surprising. The liquid calories in smoothies, juice drinks, sodas and even specialty coffees are stealthy. “A White Chocolate Mocha totals 410 calories (whole milk, no whip) or 510 calories with whip. In my world, 510 calories is an entire meal,” says Elaine Magee on WebMD. Tallmadge, in her Washington Post article, concurs: “When you consider that an appropriately sized meal is anywhere from 400 to 700 calories, and one 44 ounce Super Big Gulp is 800 calories, you understand the scope of the problem. A 16-ounce Starbucks blended coffee Frappuccino is 470 calories. A single mixed drink can set you back 300 calories. One glass of wine contains at least 100 calories. Double or triple these numbers at any given party, tack on the calories in your meals, and you can understand how weight gain is inevitable,” she adds. Tallmadge also notes, “Most caloric drinks consumed before or during a meal are not satiating and have little effect on how much you eat in one sitting or over the course of several meals.”

The good news, Tallmadge notes, is that “since liquid calories don’t contribute to feelings of satiety, cutting back on them doesn’t make people feel deprived; most find the change is an easy one to make.” So, what changes should be considered? The Harvard School of Public Health pondered this question and put together a Beverage Guidance Panel. Here are their recommendations from the March 2006 issue of the American Journal of Clinical Nutrition. Drink:

 

1) Water: Quelle surprise! But pure H₂O does provide “everything the body needs – to restore fluids lost through metabolism, breathing, sweating, and the removal of waste. It’s the perfect beverage for quenching thirst and rehydrating your system” according to the group. Wish that we could end this list here! We used to, come to think of it.

 

2) Tea and Coffee: “Drunk plain, they are calorie-free beverages brimming with antioxidants, flavonoids, and other biologically active substances that may be food for health.” They especially recommended the strong green tea varieties served in Japan. However, the addition of cream, sugar, whipped cream and flavorings makes it “closer to a dessert.”

 

3) Low-fat and skim milk and soy beverages: Here’s where the Harvard School of Public Health/Beverage Guidance Panel and I part company. I avoid the carbs in milk and only take heavy cream (sometimes half & half). I am not afraid of saturated fat – in fact, I choose to eat it. I also avoid soy products altogether: soy bean oil, soy milk and soy sauce, etc.

 

4) Noncalorically Sweetened Beverages: This category includes the “so-called diet sodas and other diet drinks that are sweetened with calorie-free artificial sweeteners. They include stevia in this category too, and the liquid sugar alcohols.

 

5)  Caloric Beverages with Some Nutrients: This group includes “fruit juice, whole milk, sports drinks, vitamin-enhanced waters, and alcoholic beverages. The inclusion of all these beverages on this list in the number 5 (penultimate) position says it all for me. This list includes 100% fruit juice, which a blogger famously called a “liquid candy bar” a while ago.

 

6) Calorically Sweetened Beverages: These “least recommended” include drinks sweetened with either sugar or high-fructose corn syrup (HFCS). The two are basically the same. This group also includes noncarbonated soft drinks, fruit drinks, lemonade, and other “ades.” They’re just sugar calories with virtually no other nutrients and should be shunned.

The Nutrition Debate #99: “Natural History of Type 2 Diabetes”

“Natural History of Type 2 Diabetes” is the heading of the first section of a scientific paper by Ralph A. DeFronzo, M. D. The full text can be found on the PubMed site here. It was also the basis of his Banting award lecture at the 2008 annual meeting of the American Diabetes Association in San Francisco. This paper caught my attention for the statement (cited in The Nutrition Debate #86 here) in which Dr. DeFronzo says in the section under Prediabetes, “In summary, individuals with IGT [impaired glucose tolerance] are maximally or near-maximally insulin resistant, they have lost 80% of their β-cell function, and they have an approximate 10% incidence of diabetic retinopathy. By both pathophysiological and clinical standpoints, these pre-diabetic individuals with IGT should be considered to have Type 2 diabetes” (emphasis mine).

Dr. DeFronzo is using the medical phrase “natural history” to describe the progression of a disease from incidence to full-blown diagnosis. In this blog I will comment on quotes from this “history” section of Dr. DeFronzo’s paper to explain this progression and attempt to simplify the language to make it more user-friendly for the lay reader. I think his expert exposition of the stages of development of Type 2 diabetes is so important that it is worth the slog. Dr. DeFronzo’s point is that we need a “new paradigm” of early intervention: “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 [impaired glucose tolerance] or IFG [impaired fasting glucose].The main thrust of his presentation is that we need a “new paradigm”  where “the physician must intervene early.” In writing this blog primarily for “patients” and other individuals who may have IGT or IFG, it is my hope that they will see the need to “intervene early” as well. It is much easier to control blood sugar if you have some remaining beta cell function. 

DeFronzo begins, “Individuals destined to develop Type 2 diabetes inherit a set of genes from their parents that make their tissues resistant to insulin.”(I don’t think the gene set is definitively known yet, but it surely will be soon.)  “In liver, the insulin resistance is manifested by an overproduction of glucose during the basal state despite the presence of fasting hyperinsulinemia and an impaired suppression of hepatic glucose production in response to insulin, as occurs following a meal.” (The liver overproduces glucose when we are in the fasting state despite low blood insulin levels. That is why physicians now usually prescribe Metformin first to both suppress this glucose production -- called gluconeogenesis – and improve insulin sensitivity.)

“In muscle, the insulin resistance is manifest(ed) by impaired glucose uptake following ingestion of a carbohydrate meal and results in postprandial hyperglycemia.” (Interesting. It’s the muscles.) “Although the origins of the insulin resistance can be traced to their genetic background, the epidemic of diabetes that has enveloped westernized countries is related to the epidemic of obesity and physical inactivity. Both obesity and decreased physical activity are insulin resistant states and, when added to the genetic burden of insulin resistance, place a major stress on the pancreatic β-cells to augment their secretion of insulin to offset the defect in insulin action.” (So, insulin production increases to deal with the combination of elevated levels of circulating glucose and our impaired insulin action due to insulin resistance.)

“As long as the β-cells are able to augment their secretion of insulin sufficiently to offset the insulin resistance, glucose tolerance remains normal.” (So, we have two faulty mechanisms at work here yet our blood glucose levels in response to both fed and fasting states are still normal.) “However, with time the β-cells begin to fail and initially the postprandial plasma glucose levels and subsequently the fasting plasma glucose concentration begins to rise, leading to the onset of overt diabetes.” (Note that postprandial blood sugars rise first, then later fasting blood glucose.) That is the reason that the HbA_1c test is rapidly replacing the fasting blood glucose test. The HbA_1c test measures the average of all blood glucose values over a 3-month period and thus captures the elevated postprandial values in the average, whereas obviously the fasting blood glucose test does not. Ask your doctor to do an HbA_1c test! An A1c over 5.5 indicates an increased risk for heart disease. In the U.S., if you have indications of Metabolic Syndrome, your insurance should pay for 4 tests per year.)

“Collectively, the insulin resistance in muscle and liver and β-cell failure have been referred to as the triumvirate. (This is again a reference to part of the title of Dr. DeFronzo’s presentation.) “The resultant hyperglycemia [elevated blood glucose] and poor metabolic control may cause further decline in insulin sensitivity, but it is the progressive β-cell failure that determines the rate of disease progression.”

Dr. DeFronzo’s paper then continues to describe his own research into the β-cell failure rate in detail but let this suffice: “Although the plasma insulin response to the development of insulin resistance typically is increased during the natural history of Type 2 diabetes, this does not mean that the β-cell is functioning normally. To the contrary, recent studies from our group have demonstrated that the onset of β-cell failure occurs much earlier and is more severe than previously appreciated.” That frightening statement is in pretty plain English. I don’t think it requires any interpretation on my part.

The Nutrition Debate #98: The “Dreaded Complications” (of Type 2 Diabetes)

With the meteoric rise in the incidence of Type 2 Diabetes and obesity (“diabesity”, in the contemporary parlance), and their associated public health implications, the “dreaded complications” of the pandemic should now be front-and-center in the news. They do deserve our attention, and I’m not sure whether I am just blocking them out of my consciousness or that in fact they are not being widely aired.  Of course, they are pretty scary, and fear is a good motivator, but that is not the purpose of this post. I just want to put the facts “out there” so it cannot be said that I have swept the chronic complication of Type 2 diabetes “under the rug.”

Let’s begin with this truthful but hopeful note from the American Diabetes Association: “Diabetes increases your risk for many serious health problems. The good news? With the correct treatment and recommended lifestyle changes, many people with diabetes are able to prevent or delay the onset of complications.” I think this last sentence is actually a gross understatement. Given the current treatment protocols recommended by the ADA, however, I am not surprised that their hopefulness is so qualified. I would go much further, as regular readers here know. I say that a Type 2 who follows a Very Low Carbohydrate diet can avoid the complications altogether. However, if you do not control your blood sugar by diet or other means, the NIH’s Medline Plus site tells us this: “If you have diabetes, your blood sugar levels are too high. Over time, this can cause problems with other body functions, such as your kidneys, nerves, feet, and eyes. Having diabetes can also put you at a higher risk for heart disease and bone and joint disorders. Other long-term complications of diabetes include skin problems, digestive problems, sexual dysfunction, and problems with your teeth and gums.”

To give the reader a sense of scale, the order of magnitude of the leading risks of complications of chronic Type 2 diabetes are described in this Wikipedia entry:  “In the developed world, diabetes is the most significant cause of adult blindness in the non-elderly and the leading cause of non-traumatic amputation in adults, and diabetic nephropathy is the main illness requiring renal dialysis in the United States” (emphases all mine). The medical terms for these chronic complications are diabetic retinopathy, diabetic neuropathy, and diabetic nephropathy. All of these complications are directly associated with Type 2 diabetes, and they are all the result of damage to the small blood vessels. This damage leads to a microangiopathy which can also damage the heart. The result is diabetic cardiomyopathy, a diastolic dysfunction that eventually leads to heart failure, according to Wikipedia.

Another complication of chronically elevated blood glucose is macrovascular disease, which leads to cardiovascular disease (CVD). Wiki lists the following examples: Coronary artery disease (CAD), leading to angina or myocardial infarction (“heart attack”); diabetic myonecrosis (”muscle wasting”); peripheral vascular disease, which contributes to intermittent claudication (exertion –related leg and foot pain) as well as diabetic foot; and stroke (mainly the ischemic type).

In addition, Diabetic encephalopathy, the increased cognitive decline and risk of dementia – including Alzheimer’s disease – is observed in and associated with chronically elevated blood sugar, i. e. inadequately controlled Type 2 diabetes. And these are just some of the risks! But I said I wasn’t going to scare the living bejesus out of you, so let’s end on an up note.

 An abstract presented at a poster session of the ADA meeting in Philadelphia in June 2012 is apt. It reported a Swedish observational study of 12,359 patients with poorly controlled Type 2 diabetes. None of the patients had any cardiovascular or coronary heart disease at baseline. The patients averaged 62 years of age with mean disease duration of 9 years. The average baseline HbA_1c was 7.8% and their mean body mass index was 30. Their mean blood pressure was 140/78. 62% were taking antihypertensive (blood pressure) meds and 46% were on lipid-lowering (cholesterol) drugs.

After 5 years, the study’s investigators separated the patients into 2 groups: those whose HbA_1c decreased by at least 1% over the 5 years (6,841) and those whose HbA_1c remained stable or increased  (5,518). At the study’s conclusion the mean HbA_1c was 7% in the improved-control group (-0.8%) and 8.4% in the poorly controlled group (+0.7%), they reported.

By then, 12% of the well-controlled group and 20% of the poorly controlled group had developed coronary heart disease (CHD). Cardiovascular disease (CVD) was present in 17% of those in the well-controlled group and 30% of the poorly controlled group. And all-cause mortality was 15% among the group with no improvement in HbA_1c and 10% in the group with improved HbA_1c. Thus, after adjusting for baseline risk factors and treatment changes during the study period, they concluded that “patients who had suboptimal glycemic control and reduced their HbA_1c value by slightly less that 1% were 50% less likely to die within 5 years than were patients whose HbA_1c did not improve…” A study team presented similar results at the annual meeting of the European Association for the Study of Diabetes (EASD) in Sept 2012, as reported here.

So, with improvement in HbA_1c of less than 1% (7.8 to 7.0%) and an average blood glucose level of 154, there is still a 50% benefit. I wonder what the benefit would be for a 2% or even a 2.5% improvement in A1c? Would the increased risk of cardiovascular disease, coronary heart disease, and all-cause mortality be eliminated completely? It’s something you might want to think about.

The Nutrition Debate #97: Fructose in Foods

There is a dangerous misconception that fructose, commonly thought of as fruit sugar, is present primarily in fruit. And since fruit is generally thought of as a “healthy” food, since it is natural and has fiber, pectin, micronutrients and phytochemicals, all of whose mysteries we have yet to unwrap, we consider them beneficial.  And besides, the bottom line is: all fruit, especially the modern, hybridized varieties, contains “natural sugar” and therefore are okay to eat in moderation. Besides, who can eat a dozen apples? All true enough, except: watch out for apple sauce and apple juice. You can easily overdose on the liquefied sugars (and fructose), in these processed food products.

But fructose, the “natural fruit sugar,” is not just found in fruit. It is present naturally in many other whole foods. It is 49% to 82% of the sugar in sweeteners, both natural and manufactured, 40% to 67% of the sugar in fruits, and from 38% to 55% of the sugars in some vegetables.  It is 50% of the content of granulated sugar, made either from sugar cane or sugar beets. And it is 55% of the liquid form of high fructose corn syrup (HFCS) used to sweeten soft drinks in the U.S. HFCS is used for a variety of reasons in solid food including “mouth feel.” In a loaf of bread, it is brushed on to brown the surface and to get a few whole grains to stick to it. HFCS used in baked goods and many more products is 42% fructose.

The recent ruckus over high fructose cane sugar is having some effect, though. On a recent inspection of bread loaves in my local supermarket, a number of the “better” brands (e.g. Arnold and Pepperidge Farm) now advertize that they have “No HFCS.” The Cane Sugar Refiners Association has fired back that there is really very little difference between sucrose (sugar, as in cane sugar) and HFCS, made from corn, and I’m afraid I have to agree with them. The difference between 55% fructose and 50% fructose is small, and they are both equally bad! Check out the ingredients listed on any loaf of bread. In the order of prevalence: Flour, water, sugar, unless it is flour, water, molasses or flour water, honey. The store brand is usually still: flour, water, HFCS, because HFCS is cheaper than sucrose (cane sugar) due to subsidies.

So, what’s all the fuss about fructose? Take a look at some earlier columns of mine, particularly #29, “Fructose, Formerly Known as Fruit Sugar,” #30, “Is Fructose a Liver Toxin?” and also #28, “Sugar in the Diet,” and #31, “Carbohydrates and Sugar.” Dr. Kurt Harris’s Archevore program (#19) is one of my favorites. His mantra is to avoid the three Neolithic Agents of Disease: Wheat, excess fructose and excess Omega 6s. Check it out at here.

Since this column is, “Fructose in Foods,” I have created, from USDA and Wiki sources, a table of common “foods,” including fruits, vegetables and sweeteners (including natural, refined and manufactured). Note the percent fructose.

Sugars in Foods	Sucrose	Free	Free	Other	Total	Total	Fructose/
as % of total sugars	50%F/50%G	Fructose	Glucose	Sugars	Fructose	Glucose	glucose ratio
Sweeteners
HFCS55 (beverages)	0%	55%	41%	4%	57%	43%	1.34
HFCS42 (solid foods)	0%	42%	53%	5%	44%	56%	0.79
Granulated sugar	100%	0%	0%	0%	50%	50%	1.00
beet sugar	100%	0%	0%	0%	50%	50%	1.00
brown sugar	97%	1%	1%	1%	50%	50%	1.00
maple syrup	96%	1%	3%	0	49%	51%	0.96
honey	1%	53%	46%	0	53%	47%	1.14
molasses	54%	24%	22%	0	51%	49%	1.03
agave nectar	0%	82%	18%	0	82%	18%	4.47
Fruits
apple	20%	57%	23%	0	67%	33%	2.01
apricot	64%	10%	26%	0	42%	58%	0.72
banana	20%	40%	41%	0	50%	50%	0.98
dried fig	0%	48%	52%	0	48%	52%	0.92
grapes	1%	52%	46%	0	53%	47%	1.12
peach	58%	18%	24%	0	47%	53%	0.89
pear	8%	63%	29%	0	67%	33%	2.06
pineapple	61%	21%	17%	0	52%	48%	1.09
plum	16%	32%	52%	0	40%	60%	0.66
water melon	20%	55%	26%	0	64%	36%	1.81
Vegetables
red beet	97%	1%	1%	0	50%	50%	1.00
carrot	75%	13%	13%	0	50%	50%	1.00
popcorn	69%	16%	16%	0	50%	50%	1.00
sweet corn	15%	31%	55%	0	38%	62%	0.61
sweet red pepper	0%	55%	45%	0	55%	45%	1.21
sweet onion	14%	40%	46%	0	47%	53%	0.89
sweet potato	60%	17%	24%	0	46%	54%	0.87

 

When this table is then sorted by total percent fructose, from highest to lowest, the results are an eye-popper:

Sugars in Foods	Sucrose	Free	Free	Other	Total	Total	Fructose/
as % of total sugars	50%F/50%G	Fructose	Glucose	Sugars	Fructose	Glucose	glucose ratio
agave nectar	0%	82%	18%	0	82%	18%	4.47
pear	8%	63%	29%	0	67%	33%	2.06
apple	20%	57%	23%	0	67%	33%	2.01
water melon	20%	55%	26%	0.06	64%	36%	1.81
HFCS55 (beverages)	0%	55%	41%	4%	57%	43%	1.34
sweet red pepper	0%	55%	45%	0	55%	45%	1.21
honey	1%	53%	46%	4.54	53%	47%	1.14
grapes	1%	52%	46%	0	53%	47%	1.12
pineapple	61%	21%	17%	0	52%	48%	1.09
molasses	54%	24%	22%	0	51%	49%	1.03
Granulated sugar	100%	0%	0%	0%	50%	50%	1.00
beet sugar	100%	0%	0%	0%	50%	50%	1.00
brown sugar	97%	1%	1%	1%	50%	50%	1.00
red beet	97%	1%	1%	0	50%	50%	1.00
carrot	75%	13%	13%	0	50%	50%	1.00
popcorn	69%	16%	16%	0	50%	50%	1.00
banana	20%	40%	41%	0	50%	50%	0.98
maple syrup	96%	1%	3%	0	49%	51%	0.96
dried fig	0%	48%	52%	0	48%	52%	0.92
sweet onion	14%	40%	46%	0	47%	53%	0.89
peach	58%	18%	24%	0	47%	53%	0.89
sweet potato	60%	17%	24%	0	46%	54%	0.87
HFCS42 (solid foods)	0%	42%	53%	5%	44%	56%	0.79
apricot	64%	10%	26%	0	42%	58%	0.72
plum	16%	32%	52%	0	40%	60%	0.66
sweet corn	15%	31%	55%	0	38%	62%	0.61

Did it ever occur to you that the sugars in pears and apples were so high in fructose – the highest, in fact: two thirds fructose! And look at agave nectar. It is hands-down the absolute worst! And how about those high fructose veggies: red bell pepper, red beets and carrots, all at or above 50% fructose as a percent of sugars, with sweet onions and sweet potatoes not far behind. Only sweet corn is low in fructose, but correspondingly high in glucose.

And did you ever imagine that honey and maple syrup were so high in fructose? They’re not even fruit! So, fructose is not just the fruit sugar in fruit. I guess we can be glad that the USDA last June (2012) declined the request to rename HFCS as Corn Sugar. The Sugar Association sure was. They commended the government for their action. It would make it sound too much like Cane Sugar. But wait a minute, isn’t that what they are saying? That HFCS (ersatz “Corn Sugar”) is processed by the body exactly the same as cane sugar? Of course it is, and once again, I’d have to agree with them.