Words To Strike Fear In Your Heart -

Glycation and Apoprotein B.  You just don't want to go there.  Reposted in its entirety:
"The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability"depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque."

http://heartscanblog.blogspot.com/2010/03/ldl-glycation.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+blogspot%2Ftpzx+%28The+Heart+Scan+Blog%29

Evidence Of High Intensity Benefit

In the CrossFit world, intensity is defined by the work performed and the take it takes to complete that work.  IOW, if you move a specified weight a specified distance as fast as you can, you are producing a measure of work that may be calculated as horsepower (or any other measure of power).  The more horsepower generated in a workout, the better, with the caveat that variety in modalities (weights, running, gymnastics) and workout duration (some short, some long, most 10-15 minutes) will be necessary to become fit (in the CrossFit sense of fit; which is fit for the unknown and unknowable). 

This study shows some correlation of CF's premise that high intensity is beneficial to health.  Other correlates of high intensity workouts include better faster lipid profiles, better bone density, and the reversibility of anaerobic work - that is to say, working in the anaerobic/glycolitic energy pathway will sustain and contribute to work in the aerobic/oxidative energy pathway, but the reverse is not true (with the exception of those who are so de-conditioned they cannot perform anerobic work).

http://www.brightsurf.com/news/headlines/39799/Study_reveals_how_blood_flow_force_prevents_clogged_arteries.html

How To Be Able To Fast

This is a magnificent description by Dr. Davis about why most overweight folk cannot fast, how they could change their diets so that they can fast, and why they (and we) should do so. Note also the impact of wheat on the process.

Speaking from experience, this is one of my favorite aspects of carb restriction. If you wake and either cannot or don't want to eat, it is not a big deal. Your protein and fat fueled body makes plenty of ketones to fuel your brain, and your metabolism will liberate as much body fat as needed to fuel the rest of you.
http://heartscanblog.blogspot.com/2010/04/what-to-eat-diet-is-defined-by-small.html

Two Sides of the Diabetes Issue - Which Is More Convincing To You?

http://comfort-eaters-diet.blogspot.com/2010/02/diabetes-discussion.html

"Expert" to Richard Bernstein:
"I struggle to understand why you are publishing information recommending low-or no-carb meals for people with diabetes.  As someone who has taken insulin for 29 years, I would expect you most of all to understand the relationship between carbohydrate and insulin.  I have to fight this confusion with my patients on a regular basis.  Do you not agree that people with type 1 diabetes who take insulin are at high risk of hypoglycemia and ketoacidosis when they deplete carbohydrate from their meals?  What happened to the knowledge that carbohydrate is our body's primary fuel source as well as B vitamins and fiber?  I truly wish that we would stop confusing our diabetes population by giving them so much conflicting information.  Many of my patients are advised to avoid carbohydrate to promote "weight loss" by most of our primary care and family practitioner physicians.  Unfortunately, many of them are also on long acting insulin or sulfonylureas.  These patients will be causing hypoglycemia and possible ketosis by following their physicians advise.  My request to you is to stop publishing articles that contain controversial, unproven, and possibly harmful advice.  Let's give people clear, concise, proven, and recommended guidelines from health organizations with credibility, shall we?  Signed Diane, LDN, RD, CDE. P.S. I thought we all knew by now that diets don't work."

The blog author responds:  "The idea here seems to be that diabetics have got to eat lots of carbs because of all the insulin they are pumping into themselves.  It's a bit like saying 'keep taking the poison so that you can keep overdosing on antidote.'"
Here's Richard's reply:
"I was present in the late 1940s when the American Diabetes Association (ADA) first recommended a high-carbohydrate diet.  At that time, it was believed that the long-term complications of diabetes were due to the high cholesterol levels so common to people with diabetes.  It was assumed that this was a consequence of dietary fat and that by dramatically reducing fat and substituting large amounts of carbohydrate, these complications would be avoided.  There never were, and still have never been, any studies supporting this hypothesis.  So if anything is "un-proven," it is the ADA hypothesis.

Except for a brief change of mind in 1975-76, it wasn't until the Diabetes Control and Complications Trial terminated that the ADA acknowledged that the real culprit might be high blood sugars.  More recently, studies comparing high- and low-carbohydrate diets have finally been performed and show that low-carbohydrate diets reduce both blood sugars (HbA1c) and conventional cardiac risk factors.

A number of these studies were actually published in ADA research journals such as Diabetes Care.
In spite of this, probably because of a rigid adherence to tradition, the ADA continued to raise carbohydrate guidelines and even now recommends the use of rapid-acting carbohydrate such table sugar, bread, potatoes, pasta, etc..

The new but unproven ADA hypothesis is that people with diabetes can keep blood sugars normal by covering large amounts of carbohydrate with "industrial" doses of insulin.  This never worked for me (I've had diabetes for 58 years) or for my thousands of patients.  The reasons for this include the following:
1) We can never know the exact carbohydrate content of a meal. In the United States, labeling laws permit an error of +/- 20 percent of the carbohydrate content of a serving.  For a typical ADA meal containing 150 grams of carbohydrate, he uncertainty is +/- 30 grams. One gram of carbohydrate will typically raise the blood sugar of a type 1 person by 5 mg/dl for a net uncertainty of +/- 150 mg/dl.
Carbohydrate estimates in books are even more uncertain.
2) John P. Bantle, MD, professor of medicine, division of diabetes, endocrinology and metabolism at the
University of Minnesota Medical School, demonstrated that for a given individual from day to day, the uncertainty of insulin absorption from typical ADA megadoses varies from +/-29 percent to +/- 39 percent.  He further showed that the timing of action of these large doses is likewise highly variable.
Thus, it is the high-carbohydrate diets covered by megadoses of insulin that increase the likelihood of hypoglycemia.

In the 20 plus years that I have been in practice, only five of my patients have had severe hypoglycemia causing loss of consciousness.  Two of these people were eating excessive amounts of carbohydrate and three made major mistakes such as taking the wrong type of insulin.  I'm sure this is a far cry from the incidence of severe hypoglycmia among patients of high carbohydrate practitioners.

The ADA's designation of high blood sugar - an A1C of 7% (corresponding to an average blood glucose of 170 mg/dl) when non-diabetics whom I have tested show about 4.2-4.8% - attests to its lack of interest in blood-sugar normalization.   This may further explain the ADA failure to give up on its high-carbohydrate diet.  This likelihood is also supported by ADA opposition to blood glucose self monitoring (BGSM) for 14 years - from 1969 when I first demonstrated it to their president until 1983 when pressure from patients became overwhelming.

To this day, the ADA opposes BGSM for the 90 percent of people with diabetes who don't take insulin. As a result, Medicare will not pay for BGSM for this 90 percent.  Doesn't this suggest that all of us with diabetes have an "orphan" disease without strong organized support for our well being?"

Taubes About Saturated Fat

"The question hinges on whether saturated fat raises cholesterol and causes heart disease. One way or the other this trial is a test of that hypothesis. It’s arguably the best such trial ever done and the most rigorous. To me that’s always been the story. If saturated fat is bad for us, then these trials should demonstrate it. They imply the opposite.

Why does the A.H.A. continue to insist that saturated fat should be avoided, if these trials repeatedly show that high saturated fat diets lead to better cholesterol profiles than low-saturated fat diets? And how many of these trials have to be done before the National Institutes of Health or some other august institution in this business re-assesses this question? After all, the reason the food guide pyramid suggests we eat things like butter and lard and meats sparingly (and puts them high up in the pyramid) is that they contain saturated fat. This is also the reason that the A.H.A. wants to lower even further what’s considered the safe limit for saturated fats in the diet."

http://tierneylab.blogs.nytimes.com/2008/07/21/good-news-on-saturated-fat/?pagemode=print

Consensus - Science - Never Shall They Meet

"It may seem bizarre that a surgeon general could go so wrong. After all, wasn’t it his job to express the scientific consensus? But that was the problem. Dr. Koop was expressing the consensus. He, like the architects of the federal “food pyramid” telling Americans what to eat, went wrong by listening to everyone else. He was caught in what social scientists call a cascade.

We like to think that people improve their judgment by putting their minds together, and sometimes they do. The studio audience at “Who Wants to Be a Millionaire” usually votes for the right answer. But suppose, instead of the audience members voting silently in unison, they voted out loud one after another. And suppose the first person gets it wrong.

If the second person isn’t sure of the answer, he’s liable to go along with the first person’s guess. By then, even if the third person suspects another answer is right, she’s more liable to go along just because she assumes the first two together know more than she does. Thus begins an “informational cascade” as one person after another assumes that the rest can’t all be wrong.

Because of this effect, groups are surprisingly prone to reach mistaken conclusions even when most of the people started out knowing better, according to the economists Sushil Bikhchandani, David Hirshleifer and Ivo Welch. If, say, 60 percent of a group’s members have been given information pointing them to the right answer (while the rest have information pointing to the wrong answer), there is still about a one-in-three chance that the group will cascade to a mistaken consensus."

http://www.nytimes.com/2007/10/09/science/09tier.html?_r=1&sq=John%20Tierney%20Findings%20Gary%20Taubes&st=cse&scp=1&pagewanted=print

"With skeptical scientists ostracized, the public debate and research agenda became dominated by the fat-is-bad school. Later the National Institutes of Health would hold a “consensus conference” that concluded there was “no doubt” that low-fat diets “will afford significant protection against coronary heart disease” for every American over the age of 2. The American Cancer Society and the surgeon general recommended a low-fat diet to prevent cancer.

But when the theories were tested in clinical trials, the evidence kept turning up negative. As Mr. Taubes notes, the most rigorous meta-analysis of the clinical trials of low-fat diets, published in 2001 by the Cochrane Collaboration, concluded that they had no significant effect on mortality.

Mr. Taubes argues that the low-fat recommendations, besides being unjustified, may well have harmed Americans by encouraging them to switch to carbohydrates, which he believes cause obesity and disease. He acknowledges that that hypothesis is unproved, and that the low-carb diet fad could turn out to be another mistaken cascade. The problem, he says, is that the low-carb hypothesis hasn’t been seriously studied because it couldn’t be reconciled with the low-fat dogma."

BFO - Some Folk Have More Athletic Genes Than Others

http://www.msnbc.msn.com/id/35242442/ns/health-fitness/?ns=health-fitness
"They initially identified, using a novel approach, a set of 29 genes that seemed to predict a person's ability to improve their VO2 max. Then, they examined the individual DNA sequence of those genes, looking for differences in the genetic code. They found a total of 11 DNA differences, or markers, which appeared to be predictive of a person's ability to get fitter.  But these markers don't tell the whole story. Remember, heredity is only thought to account for 50 percent of a person's capacity to improve their fitness. Of this 50 percent, the newly identified genes can only explain about 23 percent of the variation in an individual's ability to be trained to improve VO2 max.  "With this we can identify, with a reasonable degree of precision, who is a low responder [to exercise], an average responder, or a high responder," Bouchard said. "We can begin to rank order people for their ability to be trained before they are trained.""

While it is a BFO (blinding flash of the obvious) that genetics dictates athleticism in large measure, I think this is a hint of the future of fitness.  If you could identify an athlete's athletic potential - for say strength, sprint speed, VO2 max, agility, coordination, etc - you could then evaluate in an entirely new way how various training modalities affected their development towards their maximum potential.  Imagine when we can identify exactly what programming would get one athlete or another to their 90% point with the least training and the least time.  Imagine what it would be like to know how fast you are getting to that 90% point as an athlete - and then could choose how much time to invest to get that last 10%, or not to chase it.