Wednesday, February 24, 2010

You Can Learn a Lot From a Rat's Eicosanoids

This is a fantastic post on an interesting rat chow study - read the whole thing but if you don't have time, here's the conclusion:

"So there you have it folks: direct evidence that insulin resistance, leptin resistance, high blood pressure and fatty liver are mediated by excessive inflammatory eicosanoid signaling. I wrote about something similar before when I reviewed a paper showing that fish oil reverses many of the consequences of a high-vegetable oil, high-sugar diet in rats. I also reviewed two papers showing that in pigs and rats, a high omega-6:3 ratio promotes inflammation (mediated by COX-2) and lipid peroxidation in the heart. Are you going to quench the fire by taking drugs, or by reducing your intake of omega-6 and ensuring an adequate intake of omega-3? 

*Of course, they didn't mention the sucrose in the methods section. I had to go digging around for the diet's composition. This is typical of papers on "high-fat diets". They load them up with sugar, and blame everything on the fat. This kind of shenanigans wouldn't fly in a self-respecting field, but it's typical of nutrition-health papers.

**Rats gain fat mass when fed a high-fat diet (even if it's not loaded with sugar), although when the fat is butter or coconut oil, they gain less than if it's vegetable oil. But humans don't gain weight on a high-fat diet (i.e. low-carb diet); to the contrary. What's the difference? It may have to do with the fact that rats eat more calories when they have ad libitum access to high-fat food, while humans don't. In fact, most low-carbohydrate diet trials indicate that participants spontaneously reduce their caloric intake when eating high-fat food."

This is a fantastic post for understanding that no study says only what its author says that the study says.  It is the perfect illustration of a 'peer review.'

Tuesday, February 23, 2010

HSB Gem on Fructose
"A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects.  The study is published in its entirety here.  Compared to glucose, fructose induced:
1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)
2) 13.9% increase in LDL cholesterol but doubled Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).
3) 44.9% increase in small LDL, compared to 13.3% with glucose.
4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC),fructose increased postprandial triglycerides 99.2%.
The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.
Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.
Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).
Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.
 When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says."

Taubes points out in "Good Calories Bad Calories" that part of the negative impact of fructose is that processing it ties up the liver.  That means the impact of high blood sugar and subsequent high insulin levels is exacerbated, and therefore insulin resistance is enhanced.  Fructose added to a high carb diet is a 'one-two' punch to your metabolism, speeding you on your way to insulin resistance, obesity and metabolic derangement.

Monday, February 22, 2010

Hijacking Science to Save Us From Ourselves,8599,1884864,00.html

This a good example of hijacked science.

The facts - people with high blood pressure benefit from reductions in salt intake.  If you don't have HBP, there's no evidence to show a BP benefit from reduced salt intake nor an increase in BP from eating too much salt.

These public health models are nice, but they can only make sense as a basis for experimentation.  To actually use them as a basis to restrict consumer choices or industry offerings would be madness.  Of course, that would not stop the 'true believers' from taking that course ...

Sunday, February 21, 2010

Amyloid - An Introduction

Gary Taubes highlights this condition as one of the outcomes of chronically high blood sugar levels.  BLUF:  High sugar levels result it gummy proteins that reduce your body's flexibility, in both interior and external tissues.  THink of how problematic that would be for your arteries, for example.

How to avoid amyloid issues?  Carb restriction.  It frees up your body's 'housekeeping' cells to hunt down and remove the amyloid plaques.

Friday, February 19, 2010

More From "Your Unstoppable Heart"

"Those pamphlets adorning your doctor's waiting room may portray LDL as a kind of lone gunman taking a bead on your heart, but they hide a basic fact of science: "Bad cholesterol" is at best a poor shorthand for four major types of independently behaving LDL, each with its own implications for heart disease. We ignore the distinctions at our peril.

Some of these forms of LDL are relatively safe and some are dangerous, and treating them all as one and the same -- the way we do every time we pay our clinic for a three-part lipid panel that simplistically says "LDL: 125" -- is telling us little about the LDL cholesterol that matters, all the while sending health costs through the roof. We may be medicating many people who have no clear need for medication, using drugs that don't target the right particles, and replacing foods that are benign with foods that are anything but.

So in the heart-disease world, we've been stalking the devil we know instead of the devils we don't know. But we need to get to know them if we hope to dodge the number one killer of men.

LDL COMES IN FOUR BASIC FORMS: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high insaturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night.

But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles -- it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.

Dr. Krauss and collaborators from Harvard and Malmo, Sweden, have helped identify what influences the difference. Working with blood samples from 4,600 healthy Swedish men and women, they used ion mobility analysis to count 11 forms of cholesterol subparticles for each person, and then ran the data through a complex statistical sorting program. After looking for relationships correlating with the 8 percent of people who went on to develop cardiovascular disease, they found three scenarios that predicted it, from the most powerful predictor to the least:

1. High levels of smaller and medium LDL combined with low HDL (a dreaded diabetes-linked syndrome Dr. Krauss had previously called atherogenic lipoprotein phenotype, or pattern B)

2. Low HDL levels

3. High total LDL levels

According to Dr. Krauss, the three risk factors appear to represent three separate processes that put your cardiovascular health at risk. For men, the first two scenarios are more predictive of heart disease, but the third -- high total LDL -- was only marginally predictive of heart disease in men. Nowhere to be seen, of course, is the "total cholesterol" number doctors have been bashing us over the head with for decades. Turns out that number is not as useful a predictor for individuals. "LDL cholesterol is used as a marker for heart-disease risk," Dr. Krauss explains. "It's not a perfect marker, and the particle story is part of the reason for that."

In other words, when you tease apart the subsets of LDL that are preferentially involved in heart disease, total LDL is a less reliable bio-marker. It's like the sniffles that could signal allergies, or the onset of swine flu, or nothing at all. This ambiguity works both ways. Just because you have less of the symptom (statin users take note) doesn't mean you'll have less of the disease. A drop in your total LDL cholesterol might mean nothing at all. A higher LDL cholesterol reading, for that matter, could simply mean you are a healthy person who has learned how to build an amazing sauce out of wine, garlic, shallots, butter, and heavy cream."

Thursday, February 18, 2010

Diabetes Linked to Cognitive Decline

"Diabetes can take a toll on the body, taxing the heart, circulation, the kidneys and even the eyes. Now it's becoming clear that the disease may affect the brain as well, contributing to a decline in mental functioning.

Studies have shown that diabetes may speed up aging-related deficits in mental function and lead to a twofold increase in the risk of dementia. Some researchers have speculated that diabetes could even boost the risk of developing Alzheimer's disease. Roger Dixon, a psychologist at the University of Alberta in Canada, wanted to learn whether this was true and set out to study exactly how uncontrolled blood sugar affected the brain.
Dixon and his colleagues studied 41 adults with diabetes and 424 healthy adults between the ages of 53 and 90, and reported their findings in the journal Neuropsychology. After testing the participants on memory, recall, verbal fluency, executive functions involving critical thinking and the speed of their mental faculties, researchers found the most significant deficits in diabetes patients on tasks of executive function and speed. These problems showed up in the youngest patients as well as the older ones, and once the cognitive symptoms appeared, they did not seem to worsen or change over time. Although Dixon's study failed to add new information on the question of diabetes and Alzheimer's disease, other experts view these results as useful fodder in the growing field of diabetes research.
"This study in general supports what we understand," says Dr. Alan Jacobson, chief of psychiatric services at the Joslin Diabetes Center in Boston. "It's another study adding to our recognition that Type 2 diabetes portends some type of problem in terms of cognitive function."
Earlier this week, another group of researchers, from Columbia University, reported in the journal Annals of Neurology that spikes in blood-glucose levels affect a region of the brain that forms memories and can lead to faster memory decline in people with diabetes.
Exactly how diabetes is associated with cognitive deficits isn't clear, but there is evidence suggesting that certain areas of the diabetic brain — such as the amygdala, which processes emotions, and the hippocampus, which is related to memory — are smaller than normal, a difference that may affect learning and recall of information. Early studies have even suggested that these physical differences may also predict Alzheimer's disease. While Dixon's study did not find a difference between the diabetes patients and controls on memory skills, Jacobson says the connection between the two diseases is an area of intense research.
As more people develop Type 2 diabetes in adulthood — diabetes has been diagnosed in 20% of American adults, and the vast majority have Type 2 — "more and more people are going to show significant cognitive problems," says Jacobson. "This whole area of research is going to be one of considerable importance in coming years." And studies like this one remind us that conditions like diabetes have wide-ranging effects throughout the body — and that we have only begun to pick apart some of these network connections."

Read more:,8599,1869815,00.html#ixzz0eimOiUmG

Low-Carb Diet Reduces Inflammation And Blood Saturated Fat In Metabolic Syndrome
"Lead researcher Jeff S. Volek, PhD, RD, associate professor of kinesiology at the University of Connecticut, describes the study as "adding to the evolving picture of improvement in general health beyond simple weight loss in keeping blood glucose and insulin under control." The work is part of a larger study (currently under review) showing numerous improvements in blood lipids. The current work concludes that "lowering total and saturated fat only had a small effect on circulating inflammatory markers whereas reducing carbohydrate led to considerably greater reductions in a number of pro-inflammatory cytokines, chemokines, and adhesion molecules. These data implicate dietary carbohydrate rather than fat as a more significant nutritional factor contributing to inflammatory processes."

This could have been written by The Zone's Dr. Barry Sears - and actually was only not in association with this study.  At the least, this sort of work confirms that the low carb approach hit on many, many elements of good health - fasting lipid profile, fat loss, inflammation, and blood sugar management.

Wednesday, February 17, 2010

Tuesday, February 16, 2010

"You say anyone can eat saturated fat?"

Here's Dr. Davis' no nonsense explanation of why some folks might do well to avoid a lot of saturated fat:
"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."

Follow Up on Diet Questions from this Month

The following is another good post on interval/high intensity training vice long slow distance running by Mike Boyle. There's little argument about this info - interval running at high intensity provides far more fitness gained, and even fat burned, for the amount of time spent and does so with decreased oxidative stress, fewer foot falls, and while building muscle (whereas long slow distance training consumes muscle).
However, one should not look to running, walking or any exercise for weight loss. The evidence that exercise is useful for body composition management is slim to none - as highlighted here .

"In the September/October 2006 issue of the ACSM's Health and Fitness Journal Dr. David Swain wrote an article called Moderate or Vigorous Intensity Exercise: What Should we Prescribe?
In the article Dr. Swain states that "running burns twice as many calories as walking".
Great news for those who want to lose bodyfat. This is actually a huge difference, particularly when you do the math.
Swain states that a 136 pound person walking will burn 50 calories per mile and, proportionally more as the persons weight increases. In other words a 163 lb person would weigh twenty percent more and as a result burn twenty percent more calories. This means that expenditure goes from 50 to 60 calories, also a twenty percent increase.
Swain goes on to state that running burns twice as many calories at 7 miles per hour as walking at 4 miles per hour.
This means a runner would burn 100 calories in roughly eight and one half minutes or about 11 calories a minute.
The walker at 4 miles per hour would burn 50 calories in
15 minutes ( the time it would take to walk a mile at 4 MPH).
That's less then 4 calories per minute of exercise. That's nearly three times as many calories per minute....As I have said in my fat loss articles and on my fat loss DVD, the facts clearly support higher intensity exercise for fat loss. The nice thing is that science continues to do research that supports the value of high intensity exercise. The fact is, it's not should you exercise harder, it's can you. The key is to work as hard as your health and body allows."

Monday, February 15, 2010

Willet on Trans Fats, Carbs and Protein

"Q:Will eating a calorie of fat make you fatter than eating a calorie of carbohydrate?
A: From many kinds of studies conducted over years, we are quite confident now that a calorie from fat will cause a similar amount of weight gain as a calorie from carbohydrate. There are some interesting questions about whether eating carbohydrate calories versus fat calories will make you eat more calories, but based on what you put into your mouth, it's pretty clear that the source of the calories is really not important."

Read more:,8599,1822118,00.html?iid=sphere-inline-sidebar#ixzz0eihgeowd

"We've now looked at over 250,000 men and women for up to 30 years, and we [also] haven't seen that the percentage of calories from fat or from carbohydrates in your diet makes any difference in relation to heart attacks, various cancers or stroke. Having said that, the type of fat is very important, and so is the type of carbohydrate. So we find that trans fats, again, are particularly harmful with regard to type 2 diabetes and heart disease. On the other hand, unsaturated fats are actually beneficial in terms of reducing the risk of heart disease and type 2 diabetes. It's the same with carbohydrates. The total amount is not important. But high intake of refined starch and sugar is related to a higher risk of heart disease and diabetes, whereas high-fiber whole-grain carbohydrates are related to a lower risk. That's not too surprising, as we know that high intakes of sugar and refined starch have an adverse effect on blood glucose levels."

It would be unusual to see one so close to the conventional wisdom say anything more than the above - but essentially everyone agrees on the negative aspects of transfats.  Sadly, it was phobia of saturated fats - proven more and more unfounded by the day - that made the transfats a common part of diets.

If you can eat those whole grains and control your hunger and blood sugars - more power to you.

Get An A in LDL Profiling

".... into the 1990s as Dr. Krauss began to test whether changes in diet could change a person's LDL profile from good to bad, or from pattern A to pattern B. Using data from the Framingham Heart Study -- the longest-running study of its kind -- health organizations had begun to roll out the message of "good" and "bad" cholesterol, a message that in turn created the concept of good fats and bad fats. But during experiments, Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, "saturated fat intake results in an increase of larger LDL rather than smaller LDL particles," as he wrote in an American Journal of Clinical Nutrition review he co authored in 2006. A diet heavy in full-fat cheese and butter -- but not overloaded in calories -- triggered the relatively harmless health profile described as pattern A. (Having demonstrated the benign consequences for cholesterol from consuming dairy fat, he is currently conducting studies to find out if the same holds true for diets high in saturated fat from beef.)

Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducingsaturated fat in a way that increases carbohydrates in a diet can shift a person's LDL profile from safe to dangerous. That's pretty much what happens whenever some well-meaning person with "high LDL" starts eating "low-fat" frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls."

Sunday, February 14, 2010

LDL, HDL and the Boogeyman

"The researchers whose names are listed at the top of this paper are all affiliated with prestigious institutions.  I am quite sure that there is not a single one of them who is unfamiliar with the work over the last 15 years or so of Ronald Krauss, the researcher who made the discovery of the differences between LDL particle sizes. (The same Krauss, by the way, who published the paper about the meta-analysis of saturated fat and heart disease much in the blogosphere currently.) Krauss and his team showed that large, fluffy LDL particles aren’t particularly harmful whereas the small, dense LDL particles are the ones that cause the problems.  He also discovered that increasing carbohydrate in the diet caused LDL to shift to a smaller, denser pattern while decreasing carb and adding fat made LDL change to the larger, fluffier non-problematic kind.  (You can read a nice review of LDL particle size in this article published in the popular press.)
If you reduce carbs and add fat to the diet, not only does your HDL go up, but your LDL makes a particle size change for the better.  However, when you increase carbs and reduce fat, your HDL goes down and your LDL goes down too, but it changes for the worse. So even though the high-carb, low-fat diet decreases LDL, it doesn’t decrease risk – it increases it because even though LDL is lower, it is made up of a dangerous particle size,which negates any possible value of the fall in LDL.  All of these researchers know this."

In other words, with restricted carb intake, you get larger, benign LDL particles, and higher HDL numbers, lower triglyceride numbers, increase your insulin sensitivity, AND will likely lose weight.  You can do this following the Paleo Diet, Atkins Diet, Neanderthin, The Zone, The Protein Power Diet, and probably South Beach, too.  Oh by the way, you'll also sleep better than when on a high carb/low fat diet, your athletic performance will improve, you'll avoid the most likely causes of cancer and the other diseases of the west, you will rarely feel hungry, and your steady blood sugars will keep your brain humming at full tilt all day long.  Post meal crashes will become a thing of the past.
What's the downside of a high fat, restricted carb (50-75g/day of mostly vegetables with some fruit and little starch), moderate protein diet?
I'm not aware of a single downside, unless you can't get over the beer, cake, candy and grains.

It's Not the LDL That Gets You

High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study.

Lipid and lipoprotein values, including fasting triglycerides and high density lipoproteins (HDL), low density lipoproteins (LDL) and total cholesterol levels, were obtained on 2,815 men and women aged 49 to 82 years chiefly between 1969 and 1971 at Framingham. In the approximately four years following the characterization of lipids, coronary heart disease developed in 79 of the 1,025 men and 63 of the 1,445 women free of coronary heart diseases. At these older ages the major potent lipid risk factor was HDL cholesterol, which had an inverse association with the incidence of coronary heart disease (p less than 0.001) in either men or women. This lipid was associated with each major manifestation of coronary heart disease. These associations were equally significant even when other lipids and other standard risk factors for coronary heart disease were taken into consideration. A weaker association with the incidence of coronary heart disease (p less than 0.05) was observed for LDL cholesterol. Triglycerides were associated with the incidence of coronary heart disease only in women and then only when the level of other lipids was not taken into account. At these ages total cholesterol was not associated with the risk of coronary heart disease.

Monday, February 8, 2010

Exercise and Weight Loss, II,8599,1914857,00.html
"In general, for weight loss, exercise is pretty useless," says Eric Ravussin, chair in diabetes and metabolism at Louisiana State University and a prominent exercise researcher. Many recent studies have found that exercise isn't as important in helping people lose weight as you hear so regularly in gym advertisements or on shows like The Biggest Loser - or, for that matter, from magazines like this one.
The basic problem is that while it's true that exercise burns calories and that you must burn calories to lose weight, exercise has another effect: it can stimulate hunger. That causes us to eat more, which in turn can negate the weight-loss benefits we just accrued. Exercise, in other words, isn't necessarily helping us lose weight. It may even be making it harder."
Read more:,8599,1914857,00.html#ixzz0dNeohhnA

Exercise works for the Biggest Loser because the result they need is max weight loss right now; long term weight loss revolves around completely different issues, never mind the fact that the exercise volume displayed on BL is not sustainable for a life time.

Friday, February 5, 2010

The Cure for Cancer is ... Fat?!?,8599,1662484,00.html
Control cancer with fat?

Here's how it might work, and a bit about an ongoing test.

I think it will work!

Meta Analysis Considering Impact of Fat on CVD
This is the abstract of the article I referenced from Whole Health Source.  Short and to the point.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease1,2,3,4,5
Patty W Siri-Tarino, Qi Sun, Frank B Hu and Ronald M Krauss
1 From the Children's Hospital Oakland Research Institute Oakland CA (PWS-TRMK)the Departments of Nutrition (QSFBH)Epidemiology (FBH) Harvard School of Public Health Boston MA.
2 PWS-T and QS contributed equally to this work.
3 The contents of this article are solely the responsibility of the authors and do not necessarily represent the official view of the National Center for Research Resources ( or the National Institutes of Health.
4 Supported by the National Dairy Council (PWS-T and RMK) and made possible by grant UL1 RR024131-01 from the National Center for Research Resources, a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research (PWS-T and RMK). QS was supported by a Postdoctoral Fellowship from Unilever Corporate Research. FBH was supported by NIH grant HL60712.
5 Address correspondence to RM Krauss, Children's Hospital Oakland Research Institute, 5700 Martin Luther King Junior Way, Oakland, CA 94609. E-mail:

Background: A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.
Objective: The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.
Design: Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.
Results: During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.
Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

Thursday, February 4, 2010

Getting Technical on Sat Fat (warning - have to give up an email address to get this link)

This is a three part article from two wicked smart ladies.  Sally Fallon is President of the Weston A. Price Foundation, and wonderfully articulates the findings of Dr. Price's priceless book.  Dr. Enig, PHD and all, brings the biochemistry aspect into the discussion.  Between the two of them, you can get your learning on about why you want to eat a big batch of saturated fat in your healthy diet.

Even the Mass Media Catching On to Saturated Fat
"If Atkins means eating lots of meat, eggs and cheese, won't all that saturated fat wreck your cholesterol levels and put you on the road to heart disease?  Well, no. There's no good evidence of that. And there's plenty of evidence that the opposite is true--that eating more saturated fat lowers the risk for heart disease. That's what a recent Harvard University study found: People who had the highest saturated fat intake also had the least plaque buildup on their artery walls. The American Journal of Clinical Nutrition described the findings as an "American Paradox."  In the Stanford University study that made recent headlines, women on the "fatty" Atkins diet ended up with the healthiest cholesterol levels and the best blood pressure readings, compared to those on other diets, notably the famous Ornish low-fat diet."
The paradox here, if there is one, is how so many smart people - doctors, nutritionists, health researchers - could have gotton it so wrong with regards to fat, cholesterol and heart disease.  In fact, the mounting evidence is that for the last 30 years, they've been giving the opposite of the right advice. 
One note - with regard to women and the last sentence above - no one really knows what a good or bad level of cholesterol is.  The studies show different results for different age groups of women.  One thing is certain - there's absolutely no evidence that high cholesterol is unhealthy for any age women.  If anything, the reverse is true and especially for older women. 

Wednesday, February 3, 2010

Be A Fat Head

If you have not seen this film, I highly recommend it.

Aside from being an education wrapped into a very entertaining format, it skewers many of my favorite targets.  It also introduces you to several SMEs, who have mountains of free information on the web, as well as published writing. 

Did I mention it is also funny?  If you are converted to the low carb approach but have friends or family who are afraid of fat, get them in front of this movie - available on Amazon for under $20.

More on the Stanford Low Carb Study by Gardner
"If you listened to the radio or caught the TV news shows recently, you know what the big news was for overweight Americans: Low-carb diets work, and they're healthy.  "  "But the 12-month study by Stanford University, published today in the Journal of the American Medical Association, is the strongest evidence so far that carbohydrates, not fat, are the main culprit in America's struggle to slim down and to lower risk of heart disease.  And that's the big takeaway from this study--that eating the fat of an Atkins diet doesn't increase heart-disease risk, it reduces it."

Read on and enjoy.  You can see the study's author speak (youTube) about this study following the link here:

Tuesday, February 2, 2010

Saturated Fat IS THE GOOD FAT!

"For decades, Americans have been told that saturated fat clogs arteries and causes heart disease. But there's just one problem: No one's ever proved it.  Suppose you were forced to live on a diet of red meat and whole milk. A diet that, all told, was at least 60 percent fat -- about half of it saturated. If your first thoughts are of statins and stents, you may want to consider the curious case of the Masai, a nomadic tribe in Kenya and Tanzania. 
In the 1960s, a Vanderbilt University scientist named George Mann, M.D., found that Masai men consumed this very diet (supplemented with blood from the cattle they herded). Yet these nomads, who were also very lean, had some of the lowest levels of cholesterol ever measured and were virtually free of heart disease.
Scientists, confused by the finding, argued that the tribe must have certain genetic protections against developing high cholesterol. But when British researchers monitored a group of Masai men who moved to Nairobi and began consuming a more modern diet, they discovered that the men's cholesterol subsequently skyrocketed.
Similar observations were made of the Samburu -- another Kenyan tribe -- as well as the Fulani of Nigeria. While the findings from these cultures seem to contradict the fact that eating saturated fat leads to heart disease, it may surprise you to know that this "fact" isn't a fact at all. It is, more accurately, a hypothesis from the 1950s that's never been proved."

Take the link and read on, it's awesome to find information this useful and interesting in the mass media.

The info regarding the Masai highlights a pattern seen frequently - traditional diets yeild healthy, fit humans, who, when subsequently are exposed to the Western diet, become sick like Westerners.  Thus, the Paleo model of nutrition for health.

Nice Bird Dog from Whole Health Source

This is really interesting.  Here's a respected researcher who's pursued proof that saturated fats are the cause of human illness, who recently recognized there's no proof to support that conjecture. 

I recommend WHS blog very highly.  Muck like Dr. Mike Eades' blog, one can learn almost as much from the comments as from the author's posts.

Monday, February 1, 2010

The Good, The Bad, the Ugly
The good in this article starts with stating that being slender does not mean one is healthy. Eating poor quality, or too much, food is a recipe for poor health regardless of your waist size. This is a nice bit of writing, and useful info to boot: "The findings of the Mayo study, which was published in November in the European Heart Journal, suggest that reducing heart risk requires increasing the percentage of lean muscle mass at the expense of body fat. That underscores the importance of exercise in maintaining cardiovascular health-including weight lifting and other resistance training, which helps build lean body mass. Eating a healthy diet is important in reducing body fat, too, but Dr. Lopez-Jimenez observes that if you only restrict calories, you risk losing an equal amount of body fat and lean muscle tissue and thus you could end up weighing less without significantly reducing the percentage of body fat."
Here's another bit of really good info: "But Dr. Eckel and other medical experts caution that the findings need to be validated with additional research. Big epidemiological studies such as the Mayo report are useful for spotting important trends and raising hypotheses for further inquiry. But they are not necessarily reliable for prescribing specific remedies for individual patients." This quote should be in every article about observational studies. It would help many folk sort through the confusion of conflicting conclusions that are inevitable with so many published reports about observational studies.
Summary of the good: exercise is important for health and fitness, and specific types are more important than others. I also like the fact that they say, even if they don't say it clearly enough, that caloric restriction (aka starvation diets) are not the best means to healthy weight loss, as they cost you lean mass in the short term (and in the long term, lead to weight gain, usually with increased body fat).
The bad in this study is it still refers to BMI as a meaningful measure of individual health. Any individual with a rigorious strength program and a moderate body fat level will exceed the BMI standards BECAUSE they are healthy! This number may hold significance for a population, but is beyond stupid to use as a measure of individual health. At least the writer documents this fact: "A BMI of 30 or higher indicates obesity, while people in the range from 25 to 29.9 are considered overweight. The overweight category in particular has generated controversy because many people who exercise regularly and are considered fit have BMIs above 25." So why didn't the WSJ stop there before printing this bit of tripe: "BMI, or body mass index, is a key indicator of healthy weight."
The ugly is that they missed the key conclusion, there for the taking, for anyone with knowledge of these topics: The real cue that one is ill and at greater risk for contracting the diseases of civilization is HAVING metabolic syndrome. Excess body fat is a symptom of eating poor quality food, and indicates you may soon have metabolic syndrome, but isn't the key variable. "High body fat among normal-weight men and women was associated with a nearly four-fold increase in the risk for metabolic syndrome-a cluster of abnormalities including elevated blood sugar and blood pressure. This syndrome is common among people who are obese and is an increasingly important precursor to diabetes and cardiovascular disease." That language is far too general.
To boil it all down - if you restrict carbohydrate intake and control metabolic syndrome, your health improves as do the markers of good health. If you eat too much carbohydrate but lose weight by compulsive exercise or chronic calorie restriction (great example of this in Taubes' "Good Calories Bad Calories" discussion of the treatment of President Eisenhower); or reduce your blood pressure with meds; or reduce your LDLs with statins; you are still sick - and are just masking symptoms with medicine.  Better to use meds if you need them, but in my logic, I will never 'need' meds until after I've pursued remedy via a restricted carbohydrate (50-100 grams per day) dietary alternative.