Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people.

I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.

Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:

Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people.

Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.)

Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher.

Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars.

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.

Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.

I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.

This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.

32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:

Increased LDL cholesterol (calculated) by 7.6%

Increased Apoprotein B (a measure of the number of LDL particles) by 24%

Increased small dense LDL by 41%

Increased oxidized LDL by 12.6%

In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.)

This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.

Marion sat in my office, sobbing.

It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips.

"I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"

Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)

This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread.

Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:

14 lbs weight loss in 14 days

Increased mental clarity, reduced moodiness, deeper sleep

70% reductions in small LDL

More than 300 mg/dl reductions in triglycerides

Relief from chronic scalp rash

I could go on.

All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains."

70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet.

You won't know until you try.

Here's the prototypical male with lipoprotein(a):

Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.

Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

When it comes to the Internet and Nascar, speed is good: The faster the better.

But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better.

Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss.

Strategies that can slow gastric emptying include:

--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%.

--Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl.

--Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties.

--Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates.

Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse.

However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)

Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)

Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L (193/1810 = 10.6% of total)

Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L (729/1113 = 65.4% of total)

Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles

For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

In the Cureality program, we embrace information and strategies that empower you in health without drugs, without hospitals, without procedures. We convert your doctor from director of healthcare to your assistant in health. He or she is there when you need help, but you largely direct your own health future.

How did we gain the know-how, information, tools, even chutzpah to take on such an ambitious project?

It started around 10 years ago with the awkwardly named Track Your Plaque program. In fact, some of the current followers of the Cureality program are former Track Your Plaque members, having learned of the wonderful list of strategies that can be adopted to gain better control over, even reverse, coronary atherosclerotic plaque and risk for heart attack. They also learned that something special happens when you engage with other people with similar interests, all sharing ideas, insights, and resources to get the self-directed health job done. Over time, what started out as simply a source of better information for coronary health evolved into a self-directed coronary disease management program. We never set out to create something as wildly ambitious as a do-it-yourself-at-home coronary disease risk management program, but that is how it inadvertently turned out.

How we went from Information Provider to Health Empowerment Program

So we never intended to take on something so seemingly impossible as managing coronary risk on your own. But, because we armed people with such empowering, profound insights into better ways to manage their heart disease risk beyond “don’t smoke, cut saturated fat, be active, and take a statin drug”—the typical advice offered by doctors—they returned after an interaction with their doctors disappointed: doctors often declared such strategies unnecessary, or the doctor didn’t understand them—even when there were clear-cut clinical data already available to support their use. In other words, the patients—everyday people, not experts—knew more than their doctors.

This flip-flop in the balance of knowledge made for some very interesting stories, like “Harold” (not his real name) who, having survived a heart attack and received a stent, was told by his doctor to cut his fat intake, eat more whole grains, exercise, take aspirin and a beta blocker drug, and reduce his cholesterol values with a statin drug. Upon learning all the additional information from the Track Your Plaque program, Harold returned to his doctor and asked “I’m not so ready to just go along with this idea of ‘reducing cholesterol’ to address heart disease risk. Because my goal is to gain as much control over coronary disease as possible, maybe even reverse it, I’d like to address some additional issues that I believe may be important. I’d like to have my advanced lipoproteins drawn to measure the proportion of small LDL particles I have, whether I have lipoprotein(a), an omega-3 fatty acid index and 25-hydroxy vitamin D level, and a thyroid assessment. Oh, and I believe I should also have an assessment of my inflammation status, perhaps a c-reactive protein and phospholipase A2, and my blood sugar status measured with a fasting glucose, insulin, and hemoglobin A1c.” Harold’s doctor was dumbfounded and speechless. Rather than reveal his ignorance, his doctor advised Harold that none of that was necessary, sending him on his way and telling him that he was fine.

But this left Harold with a sour taste in his mouth, having engaged in many online discussions with people who had followed conventional advice that resulted in more heart attack, more heart procedures—the conventional answers simply did not work. He also discussed his situation with people who had successfully obtained the additional information he sought, added it to their program and enjoyed dramatically improved health, including freedom from more heart attacks, heart symptoms, and heart procedures, as well as improved overall health. So Harold found an easy way to obtain the testing on his own. Within a couple of weeks, he returned to his online community and shared all his information. Within moments, he was provided useful discussion to help him understand the values, all leading to changes in nutrition, nutritional supplement choices, how and where to get the simple tools necessary, such as iodine and vitamin D supplements. He even entered his data, choosing which values he was willing to share with others, which remained private, allowing him to compare his own follow-up values several months later. Engaged in this process, self-directed but collaborative, he witnessed marked transformations in his health. Not only did he never again—over several years—ever re-develop heart symptoms nor require any more trips back to the cath lab, he lost weight, reversed a pre-diabetic sugar profile, improved his cholesterol values without drugs, got rid of the acid reflux symptoms he endured for many years, dropped his blood pressure to normal, enjoyed better mood, energy, and sleep. Slender, healthier, all accomplished without his doctor.

Harold returned to his doctor for a routine follow-up. Slender, energetic, without complaints, on no drugs except the aspirin for his stent, the basic laboratory assessment his doctor ordered in front of him, his doctor admitted,” Well, I don’t know how you’re doing it, but these values look like a 20-year old substituted his blood for yours. They’re unbelievable. What drugs are you taking to do this?” “No drugs,” Harold replied, “I’m following a program to reverse heart disease, but it means doing some things that are different from conventional solutions.” His doctor closed their meeting with the signature response of doctors nationwide: “Well, I don’t understand what you are doing, but just keep doing it.”

Yes, Harold knew more about how to control heart disease than his doctor, more than his cardiologist. The cardiologist knew how to insert a stent or defibrillator. But deliver information that empowered Harold in all aspects of health from head to toe, while also dramatically reducing, perhaps eliminating, his coronary disease risk? As you now know, that is not what conventional healthcare does, nor is it interested in doing so, as it would relinquish control and threaten to cut off this hugely profitable revenue stream that drives “healthcare.”

Having managed to inadvertently create a self-directed coronary risk management program with such spectacular results and in probably one of the most difficult areas of all—heart disease—it became clear that a similar approach could be even more easily applied to many other areas of health, such as weight loss, bone health, cholesterol and blood pressure issues, diabetes and pre-diabetes, hormonal health, autoimmune conditions, and others. You can do it when empowered by safe, effective information, and supported by a community of sharing and collaboration. We don’t fire our doctors; they are there when we need them when, for instance, we get injured or catch pneumonia, or as an occasional resource. But doctors should no longer be able to get away with neglect, misinformation, or blindly directing you to the next revenue-generating procedure because you are empowered by the information and support you receive in Cureality.

As we get more effective in delivering this information and new tools to you, just imagine what we can accomplish in this new age of information and self-empowerment. The future for us is bright with ambitions for better interactive tools with Cureality expert staff, better ways to crowd source health answers, provide more engaging community conversation, all while the health insights that help accomplish our self-directed health goals get better and better. Each person that joins Cureality helps make this service more effective because your wisdom, insights, and experience are added to the collective knowledge. We are more powerful together than we are as individuals.

If you are already a Cureality Member, please add your comments and questions to the growing conversation. If you are not a Member, consider joining our discussions, as each new voice gets us closer and closer to better answers to take back control over health.

You just THINK you're low-carb

The LDL-Fructose Disconnect

I told you bread was bad

"I dream about bread"

Prototypical Lipoprotein(a)

Gastric emptying: When slower is better

Genetic vs. lifestyle small LDL

Carbohydrate sins of the past

Saturated fat and large LDL

Is glycemic index irrelevant?

How did Cureality get its start?

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