ld 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.
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:
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.
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.
