It's Not True Because He Said It

...but I think it's true nonetheless, and the evidence to support the idea that cholesterol intake or blood levels "causes" heart disease is paper thin.

"Despite the fact that 25% of the population takes expensive statin medications and despite the fact we have reduced the fat content of our diets, more Americans will die this year of heart disease than ever before. 

"Statistics from the American Heart Association show that 75 million Americans currently suffer from heart disease, 20 million have diabetes and 57 million have pre-diabetes. These disorders are affecting younger and younger people in greater numbers every year. 

"Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped. 

"Inflammation is not complicated -- it is quite simply your body's natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process,a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial."
http://www.sott.net/article/242516-Heart-Surgeon-Speaks-Out-On-What-Really-Causes-Heart-Disease 

Sorry for the double re-post doc, but this is very well said!

Attia: Predicting Cardiac Risk

Doctors typically measure the following in a standard cholesterol test:

• LDL-C – the concentration of LDL (“bad”) cholesterol in your blood
• HDL-C – the concentration of HDL (“good”) cholesterol in your blood
• TG – the level of triglycerides (“bad”) in your blood

Combining HDL-C and TG into a ratio (i.e., TG/HDL-C) is probably the single best predictor of cardiac risk you can derive from a standard cholesterol test.  The lower the ratio, the lower your chances of having an “adverse cardiac event,” as the medical community describes it (e.g., a heart attack). Despite what doctors tell you, LDL-C is pretty much useless for predicting your risk of heart disease. In fact, it’s not even part of the risk assessment for metabolic syndrome, which everyone agrees is the central link to heart disease (and virtually all other chronic diseases we’re afflicted with).

http://eatingacademy.com/how-low-carb-diet-reduced-my-risk-of-heart-disease

This guy's site is just a goldmine for detailed but digestible information, I highly recommend it.  Unlike me, he's willing to include photos and drawings with his posts which can be very helpful.  Like me, he's a student of the "carbohydrate hypothesis" as advocated by Gary Taubes most recently/commonly.  

This weekend, I gave my fourth presentation of a three hour brief I call "That Stuff Will Kill You".  The brief describes why a neolithic diet is toxic, how the paleolithic model might be useful to understand the pathology of the neolithic diet, and how one might best attempt to implement a diet based on the Paleolithic model.  I'm always amazed when folks stay for the 3rd hour, but also very gratified when they do.  I'm also very grateful to the audiences since each time I present, I become aware of how I might change the material to improve the impact on the audience.  

One thing I'm well aware of and grateful for - a big part of the reason these sessions are well received is that they are attended by CrossFitters.  As a group, it's difficult to imagine folks that are more eager to learn.

Variation Is Evidence Of Weak Science

Mercola:
When I eliminated all my grains and starchy vegetables, I actually experienced some negative effects. My energy levels declined considerably, and my cholesterol, which is normally about 150, rose to over 200. 
*Fascinating!  Dr. Mercola thinks a cholesterol of 150 is good, and a cholesterol of 200 is bad, as expressed above - but what is that information based on?  He never clarifies, but he should.  One could just as easily say a 150 is worse than a 200 based on the correlations with mortality - but neither number is significant in my view.  They are but correlates.

It appears I was suffering a glucose deficiency and this can trigger lipoprotein abnormalities. It also seemed to worsen my kidney function. So, while carbohydrate restriction is a miracle move for most people, like most good things in life, you can overdo it.
*The questions is - how long did he try the low carb?  Some people of course take a longer time than others to adapt to running on low carb.  On the other hand, he was never obese, so it may have been the case that he simply doesn't need to go very low in carb intake.
This information really underscores how important glucose is as a nutrient, and some people can't manufacture glucose from protein as well as others, so they need SOME starches in their diet or else they will suffer from metabolic stress.
*There has to be some truth in this - ectomorphs, those who tend towards length and leanness, are clearly not "fat loving" in physiology.  It would be easy to believe that the "skinny" like Dr. M just don't run as well on fat as those of other somatotypes.
About half of your proteins have glucose attached to them, and if they don't have glucose, they simply don't work well, if at all. Your body needs glucose both as a substrate and as a fuel in order for these proteins to work well. If you drop below 200 calories of glucose per day, you might notice some negative consequences in the way you feel and even in some of your blood work, as I did.
*200kcal/day obviously is about 50g/day.  I would count that as very low carb.  50-100g/day works well for me.
My experience now shows me that I need to have some source of non-vegetable carbs. I still seek to avoid nearly all grains, except for rice and potatoes. I typically limit my total carbohydrate calories to about 25 percent of total daily intake, and my protein to about 15 percent, with the additional 60 percent coming from healthful fats like butter, egg yolks, avocados, coconut oil, nuts and animal fat.
*Impressive!  Most people will do well on this type of diet.  But you have to try it and see how you look feel and perform - after allowing time for fat adaptation - to see what level of carb consumption allows you to maintain glycemic control (as evidenced by body composition, especially abdominal circumference, and how you feel).
http://articles.mercola.com/sites/articles/archive/2012/01/23/wheat-or-rice-as-safe-starch.aspx?e_cid=20120123_DNL_art_1

The more I learn about cholesterol, the more convinced I am that it is the proverbial key under the lightpost - folks are looking at it because it can be seen, but there's not much reason to think it matters.  It is at best a correlate with heart disease and stroke (aka vascular disease), but not a cause.

But, you might say, if high cholesterol is a correlate of vascular disease, and cholesterol makes up a significant component of atherosclerotic plaques, isn't is rational to think there's a causal relationship?  Yes, it is a rational thing to think, but after years and years of trying, no one has yet proved the causal relationship.  I was a low brow solution to think that cholesterol, like grease, was killing folks by sticking to arteries like grease in a pipe.  "Really?"  Yes, they really wanted to think of human arteries as if they were static like a grease filled pipe.   "Pull the other one."

Get Your Sulphur On

Fascinating concept:

"The macrophages in the plaque take up LDL, the small dense LDL particles that have been damaged by sugar... The liver cannot take them back because the receptor can't receive them, because they are gummed with sugar basically. So they're stuck floating in your body... Those macrophages in the plaque do a heroic job in taking that gummed up LDL out of the blood circulation, carefully extracting the cholesterol from it to save it – the cholesterol is important – and then exporting the cholesterol into HDL – HDL A1 in particular... That's the good guy, HDL.

The platelets in the plaque take in HDL A1 cholesterol and they won't take anything else... They take in sulfate, and they produce cholesterol sulfate in the plaque.

The sulfate actually comes from homocysteine. Elevated homocysteine is another risk factor for heart disease. Homocysteine is a source of sulfate. It also involves hemoglobin. You have to consume energy to produce a sulfate from homocysteine, and the red blood cells actually supply the ATP to the plaque.

So everything is there and the intent is to produce cholesterol sulfate and it's done in the arteries feeding the heart, becauseit's the heart that needs the cholesterol sulfate. If [cholesterol sulfate is not produced]... you end up with heart failure."

So, in a nutshell, high LDL appears to be a sign of cholesterol sulfate deficiency—it's your body's way of trying to maintain the correct balance by taking damaged LDL and turning it into plaque, within which the blood platelets produce the cholesterol sulfate your heart and brain needs for optimal function... What this also means is that when you artificially lower your cholesterol with a statin drug, which effectively reduces that plaque but doesn't address the root problem, your body is not able to compensate any longer, and as a result of lack of cholesterol sulfate you may end up with heart failure.

http://articles.mercola.com/sites/articles/archive/2011/09/17/stephanie-seneff-on-sulfur.aspx?e_cid=20110917_DNL_art_1

Reproductive Function Indicates Health

While many of the specifics in this article are throwaways, the concept is a BFO - when you find that a function as significant to life as reproduction has been damaged, you know that is a systemic issue.  It unlikely on its face that a man that cannot engage in reproductive functions is NOT healthy. 

http://thechart.blogs.cnn.com/2011/08/17/erectile-dysfunction-the-leading-indicator-of-heart-disease-in-men/

Of the behaviors that correlate with ED, number one on the list is smoking.  I always found it ironic that image makers in the media found a way to associate to the masses the idea that smoking was "sexy." 

Of course, just as diabetes - uncontrolled blood sugars - is the gateway to every other disease of civilization, it is also thus for ED. 

Here's a model for you, proposed by CrossFit's founder, Greg Glassman (kindly forgive the male only perspective):  Suppose you are 80 years old, you have hyper tension, "high cholesterol", eat nothing but processed red meat, and in the past week have:

-impregnated your wife

-beaten up a mugger

-dragged a harvested deer 400 meters to your truck

-written a paper on advanced mathematics

Are you healthy?  Are you fit? 

What if you have "good" cholesterol numbers from a statin, good blood pressure numbers from a medication, and your gout is "well controlled" by the latest gout medication, but you don't feel like doing much, never lift anything heavy "to protect your back", and cannot successfully engage the ladies without the blue pill ... is that person "healthy"? 

The point?  Just as "stupid is as stupid does", healthy is as healthy does.  We look to numbers like cholesterol and blood pressure to evaluate health, but the real evaluation is in the living, the doing, the good experiences, and the actualization of what our bodies were built for.  Manipulating correlates of health does not make one "healthy."  What allows the health, that was built into your genetics via millions of years of ruthless "life in the paleolithic fast lane", to be expressed is fueling yourself with those things which do not compromise normal function, and demanding enough from your body through physical activity that the body retains the capacity to act when needed, and how needed. 

I'm all for having access to medications for those who won't take care of themselves, or for those who need them short term to facilitate "recovery".  I think it is foolish and short sighted, however, to say "health care" is the process of extending life via continuous, chronic medication without exploring simple dietary strategies that eliminate the needs for the medications.  And yet - governments the world over are bankrupting themselves doing just that. 

Brody Statins Reverso World

Mike Eades Summary of Brody's Story, from an article he cites.


Key points?  She is a long term advocate of the high carb, low fat, low cholesterol diet and widely viewed as an authority.  I'll let Mike take it from there:

She has been bopping along for most of her 65 years slowly following her own idiotic nutritional advice. And, I’m sure, feeling very full of herself for being so very, very good. She goes in for a routine check up and discovers – GASP! – that her cholesterol is slightly elevated. It was 222 mg/dL with a high normal being 200 mg/dL. Never mind that her HDL is nicely positioned at 69 mg/dL or that her triglycerides are pretty low at 99 mg/dL, she freaks out over her total cholesterol (a meaningless reading) and her minimally elevated LDL levels (134 mg/dL). 

Translation from Eades-ese:  she finds her fasting lipid panel is good but not GREAT.  Since her entire diet is designed to give her a GREAT fasting lipids panel, she's quite upset.

Eades:  Now if she were a reader of this blog – or even of the pertinent medical literature – she would know that a low triglyceride level and a high HDL level means that her LDL is of the large particle variety that is not only not dangerous, but actually beneficial.

What do you reckon she’s gonna do?  You’re right. She’s gonna go whole hog on a low-fat diet. She’s going to cut out the cheese; she’s going to take some over-the-counter plant stanol cholesterol-lowering supplements; she’s going to lose some weight.

And she does it all. But when she returns for a recheck in three months her cholesterol has gone up even more. It is 236 mg/dL and her LDL is 159.

Now she’s in big time gotta-get-serious-about-this mode. Gotta get the fat down, gotta cut the red meat, gotta go for the low-fat ice cream, gotta ratchet up the fiber, gotta, gotta, gotta…

She goes back in three months later for another blood test and AAAAAARRRRRRGGGGGGHHHHHHHH. Her total cholesterol is at 248 and her LDL is 171.

She is now in blind panic mode. What can she do? 

Ultimately, she takes statin drugs to treat not her health, but her fasting lipid profile NUMBERS.  There's no research to indicate she's can reduce her risk of disease with statins, nor is there for any woman under any circumstance.  The only proven beneficiaries in all cause mortality for statins are men, under age 65, with a prior cardiac event.  As Mike Eades puts it:

...women over the age of 65 (she is 65) who have high cholesterol live longer than those who have normal to low cholesterol. And she missed the studies that show that both men and women over the age of 65 who take statins have an increased incidence of cancer.

Much like the case of Clarence Bass, the low fat is best conjecture leads to wretched conclusions and poor decision making which negatively impacts these folks' lives despite their passion and dedication to their own health and wellness.  The low fat conjecture as a model for health is like trying to drive through Detroit with a map of Memphis.  You can't get to where you want to be using that map except by accident.

There are many lessons to be learned besides the apparent folly of "statinating," or  the now dis-proved conjecture that low fat protects from heart disease.  One is that there is no proof about what we humans ought to eat, and one should always be scanning for more complete answers.  

But the biggest lesson to learn is that if you want a better fasting lipids profile, carbs are what you must limit.  Carb restriction will give you a smaller abdomen, lower triglycerides, higher HDLs, lower blood pressure, and a better glucose number.  What you lose in a "perfect" LDL number you gain in better LDL particle type.  The irony that smart people became convinced that reducing fat and cholesterol intake would result in a better fasting lipids profile can't possibly be lost on you if you read the rest of Mike Eades' post.  Perhaps it'll be another torpedo in the side of the Bismarkian low fat conjecture.

Wolf Eats Grains, Part 2

Excerpts from Robb's post follow, link below:
"Grains are mostly starchy carbohydrate, and starchy carbohydrate, when consumed in any amount, causes the release of a significant dose of insulin. The starch in grains can be subdivided into two basic forms, amylose and amylopectin.
Amylose is a long chain of glucose molecules and amylopectin is a highly branched, interwoven structure also comprised of glucose molecules. Think of amylose as a rope and amylopectin as a dust bunny. Grains are made up of differing amounts of amylose and amylopectin, and this variation accounts for differences in the glycemic index of various grains. Starches are digested by the enzymes salivary amylase and pancreatic amylase. Amylase acts on the last glucose molecule in the polymer, whether it is amylose (rope) or amylopectin (dust bunny). I think it's pretty clear that the rope has far fewer locations for the amylase to attack in the digestion process than the dust bunny does. The more locations for the enzyme to attack, the faster the digestion, the quicker the rise in blood glucose levels, and typically the larger the insulin release. Any type of processing (cooking, milling) breaks up both the varieties of starch molecules, thus facilitating digestion. Easier digestion means a greater insulin response. The making of pizza crust fractures the starch grains in such a way that the body produces more insulin in response to pizza crust than raw glucose! No one knows why, but the processing inherent in most grain products can increase the insulin response far above what would otherwise be expected."
"One of the fallacies that is still spewed forth by the likes of the ADA is that slow-releasing carbs (beans, whole grains) causes a flat insulin response and consequently do notpose a problem. This is true only if one is consuming grains as condiments, as in a tablespoon here and there. Eat them a cup at a time, and not only does blood glucose level rise dramatically, but it stays elevated for a long time. Research is pretty conclusive that the insulin spike is more detrimental than the lower level chronically elevated insulin, but the end results are the same: Syndrome X, AKA the Metabolic Syndrome.
______________________________________________________________________
"You always need multiple names for things in science and medicine to ensure that as few people as possible have an idea of what is going on."
______________________________________________________________________
Grains, both processed and unprocessed, are a major player in metabolic derangement in that they are almost entirely carbohydrate and they are typically consumed in large quantities."
"The signs and symptoms of Syndrome X include high triglycerides, low HDL cholesterol, high blood pressure, high risk of stroke and heart attack… and a bunch of other stuff. Professor Loren Cordain wrote a paper that sheds some light on some of that "other stuff" Called "Syndrome X: Just the Tip of the Hyperinsulinemia Iceberg". That other stuff runs the gamut from cancer to myopia, but many diseases that have been associated with Syndrome X and hyperinsulinemia are slowly being put under the umbrella of Chronic Inflammation."
"Inflammation has many factors, including antioxidant and essential fatty acid status, but one of the key contributors to the condition we call inflammation is insulin level. Here is a detailed look at what happens with elevated insulin levels (Scroll down to insulin dysregulation). The insulin and inflammation topic is absolutely huge and far beyond the scope of this article or publication for that matter. The main point is grains pack a potent impact with regards to insulin response and that can lead to a variety of problems."
"Grains are essentially a reproductive structure and contain not only a dense energy source for the developing embryo, but also a number of control mechanisms that prevent both predation and abnormal germination. Sequestering away key nutrients like calcium, zinc and magnesium prevents abnormal germination. One of the main antinutrients is a chemical called Phytic acid of which there are several varieties, all going by the general term "phytates". Now the phytates are powerful chelators; that is they bind to metal ions very tightly. This is postulated to be the main reason why cultures that consume large portions of their diets as grains and/or legumes tend to be shorter than their westernized transplants. The Okinawan vs. Japanese story is clearly illustrative of this. Okinawans have historically been significantly taller than their Japanese counterparts. The diets of the two groups differed in that the Okinawans consumed more protein and most of their carbohydrates in the form of highly nutritious tubers and only a modicum of rice. Japanese Americans show a markedly different phenotypic expression than their rice and tofu-eating ancestors."
___________________________________________________________________________
"It is interesting to note that phytates are used in some alternative medicine circles as an anti-cancer agent. Apparently phytates exert some influence on the growth of tissues by removing metal ions such as calcium, magnesium and zinc that are important for growth. This seems like a nice closed system: feed people grains, let them get cancer from the elevated insulin levels then use grain extracts (phytates) to try to treat their condition."
___________________________________________________________________________
"This antinutrient concept is found in all eggs including those of birds and reptiles. Avidin binds to biotin, which is an important growth factor for bacteria. Hide away the biotin and it's hard for the egg to spoil. These antinutrients are so powerful that avidin has even been genetically engineered into some grains… to extend their storage. Avidin is destroyed with cooking but phytates are not. Bon appetite!
Another sub category of irritants/toxicants includes items such as gluten. Gluten is a protein found in wheat and other grains. It is also categorized under a huge family of molecules called lectins. Many of these lectins actually damage or destroy the gastrointestinal tract.
In the small intestine we have structures called microvilli that interact with the food in our intestines.  Microvilli are covered with enzymes that help to digest and transport food particles into the blood stream or lymph. Certain proteins such as gluten found in wheat, rye and barley cause a severe autoimmune reaction in some individuals, which is called Celiac Sprue. Celiac is a full-blown autoimmune reaction in which the microvilli of the intestines are destroyed. This condition makes it nearly impossible to absorb fats, minerals and many vitamins.
Not everyone shows a full blown celiac response; however, irritation is present with virtually all grain consumption. This lower level irritation has been broadly labeled as "leaky gut syndrome" and is emerging as a primary player in all autoimmune disorders. The theory is that once the gut lining is damaged, large food particles are able to make their way into the blood stream. Once there, the immune system mounts an attack against the foreign, undigested food particles. These particles may have elements that are similar in structure to body proteins and thus antibodies are produced that have affinity for one's own tissues. The seed of autoimmunity has then been sown (nice grain cliché, no?). This is something that has been kicked around for many, many years, but some other very interesting disease processes have been uncovered, like schizophrenia and congestive heart failure, which appear to owe their existence, at least in part, to leaky gut.

_____________________________________________________________________________
"Nay Sayers (read also: The Ignorant) frequently make the point that not everyone gets celiac. That is true, but across all species tested, grains cause gut irritation. Check PubMed."
_____________________________________________________________________________

"It is worth mentioning that dairy is a potent cross reactor for celiacs. It is fairly easy to assay dairy and get high concentrations of grain lectins. It has also been noted that grass-fed dairy shows little or no cross reactivity in celiacs. I'm going to look at some of the other deleterious effects of grain consumption for animals later, but this is obviously a source of grains that most people would not have considered.
"Just to completely beat this into the ground, let's look at quinoa. Quinoa is similar to a grain in its carbohydrate content and layout as a reproductive structure, but quinoa is botanically a fruit, and if you remember your botany, is a dicotyledon, whereas wheat, obviously a grain, is a monocotyledon. Relevance? They differ phylogenetically at the class level. To put that in perspective, mammals are a class, as are fish, as are reptiles. This is a huge difference and denotes ages since a common ancestor. Despite that fact, quinoa still has a protein fraction that can cause problems with celiacs. What I take from this is nature found a similar answer to reproductive strategies with quinoa and grains, and not surprisingly, quinoa presents similar potential problems.
"Grains also have a highly addictive nature beyond the carbohydrate content. They contain opiate-like substances that can be very problematic. Not surprisingly, these opioid constituents can be concentrated in dairy. Makes one look at pizza in a new and frightening way.
"Grains are not just bad for humans; they give livestock some serious problems as well, ranging from creating heat and acid resistant forms of E. Coli to completely altering the fatty acid and nutrient content of meat. Grass-fed meat should contain significant amounts of n-3 fatty acids, alpha lipoic acid, CLA, Vitamin E and loads of carotenoids. Grain fed meat is the protein version of cardboard.
"Grains obviously play a major dietary role for many people, but I hope this exploration helps to clarify why they may not be a wise choice for optimized health."
http://crossfitflood.typepad.com/nutrition/2009/03/damn-dirty-grains.html

WHS - Pertinent on Saturated Fat

"If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not at all the case. The Masai traditionally get almost 2/3 of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man? Junk food.

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. I think fructose (which makes up 50% of sucrose-- or table sugar-- and 55% of high-fructose corn syrup) is a more logical explanation for the high serum cholesterol and LDL of modern affluent societies, particularly considering the results of this study.

The inevitable conclusion is that if saturated fat influences total cholesterol or LDL concentration at all, the effect is modest and is dwarfed by other factors." http://wholehealthsource.blogspot.com/search/label/Tokelau

Red Meat Study - Some of the Issues

"The study was a meta-analysis, which combines the results of several studies looking at the same issue. Like others of its kind, the study "is limited in terms of scientific value," Dr. Eckel said. None of the studies in the analysis, for example, was a randomized controlled clinical trial, just one factor affecting the strength of the findings. The report is helpful in raising issues for further study, but "it doesn't answer any questions," he said.
http://online.wsj.com/article/SB10001424052748704314904575250570943835414.html
==These are great points and should be taken to heart as regards all study results.  If the study is not an intervention trial, it cannot be used to establish causality, but it may be useful to form or refine a conjecture/hypothesis for further study.

"The American Meat Institute Foundation took issue with the findings [regarding processed meat products], saying they conflict with national dietary guidelines. "The body of evidence clearly demonstrates that processed meat is a healthy part of a balanced diet," James H. Hodges, president, said in a statement. He said the study didn't "achieve the standard threshold that would generate concern" and that "it is no reason for dietary changes." "
==Mr. Hodges is correct in this case - this study is no reason for dietary change. 

Current U.S. dietary guidelines call for limiting saturated fats-the kind found in red meats and dairy products such as milk, cheese and butter-to less than 10% of calories consumed each day-while keeping overall fat consumption to under 30% of calories. A big reason is that saturated fats are associated with higher levels of cholesterol in the blood. Dr. Eckel said that "is still a reasonable recommendation."
==The thing to keep in mind when hearing this bit of drivel - that saturated fat intake raises cholesterol levels -  is that it's true but irrelevant, as Taubes covers in delicious detail in "Good Calories Bad Calories."  Saturated fat intake raises both HDL and LDL, and almost always improves the total cholesterol to HDL ratio that is a far more significant (if imperfect) predictor of CVD.  Saturated fat, as we've covered many times, has a significant health benefit, and virtually no negative health impact (except for a few folks who are sat fat sensitive).

"The report is the second meta-analysis in recent weeks to question just how much of a culprit saturated fats are when it comes to cardiovascular risk. In March, a meta-analysis (involving 21 different studies) by a team headed by Ronald Krauss at Children's Hospital Oakland Research Institute, Oakland, Calif., found that intake of saturated fat wasn't linked to a statistically-significant increased risk of heart disease, stroke or cardiovascular disease."
==More on that study here:  http://fireofthegodsfitness.blogspot.com/2010/02/meta-analysis-considering-impact-of-fat.html

"That's not necessarily a license to unleash your inner carnivore. Calorie control as well as a diet rich in fruits and vegetables, fish, whole grains and nuts remain the mainstay of heart-healthy eating, he said."
==They have to advocate something - but be advised they do not have anything like scientific certainty for much of what they advocate.  Eat fruit and vegetables if you like them, nuts are great, fish is great, but don't let them convince you they KNOW (I think they have their head in the sand if they think grains, whole or otherwise, are a significant part of a healthy diet).  They are making a guess.  You are perfectly capable of sorting through the issues and coming to your own conclusions, testing and experimenting with what works for you.  The recommended prescription remains the same - "Eat meat and vegetables, nuts and seeds, some fruit, little starch and no sugar." 

More Taubes - Saturated Fat and Science of Diet

Taubes quoted in Tierney's blog, discussing saturated fat, cholesterol, and the science of diet:

"all the relevant diet trials done in the last decade — randomized controlled trials comparing Atkins-like low-carb diets to AHA low-fat, calorie-restricted diets — of which there are now more than half a dozen, have observed the same result., In each one, LDL on the two diets was a virtual wash and cholesterol profiles (total/HDL) showed greater improvement on the Atkins diet. When the trial looked at blood pressure, that improved significantly on the higher fat, lower carb diet. In this Israeli study, they looked at markers of inflammation — same story.

What we have to keep in mind here is that nutrition is a science (or at least should be) and science is about generating hypotheses, making predictions from our hypotheses, and then seeing if they hold true. The relevant hypothesis here — i.e., what we’ve believed for the past 30-odd years — is that saturated fat causes heart disease by elevating either total cholesterol or LDL cholesterol, specifically. So our prediction is that the diet with the higher saturated fat content will have a relatively deleterious effect on cholesterol. We do the test; we repeat it a half dozen times in different populations. Each time it fails to confirm our prediction. So maybe the hypothesis is wrong. That seems like a reasonable conclusion. No one is proving anything here — as some of your respondents like to decry — we’re just looking at the evidence and trying to decide which hypotheses it supports and which it tends to refute.

The knee-jerk response — as exemplified by quite a few respondents — is to assume that sometime in the not-too-distant past, maybe the 1960s or 1970s, before this low-fat dogma set in, such trials, or far better trials, were done and found the opposite — that the higher the saturated fat in the diet, the lower the cholesterol and the better the cholesterol profile. Or the higher the saturated fat, the greater the mortality. But that’s simply not the case, as I point out in my book. In fact, I’ve been criticized (by Gina Kolata, among others) for going on and on in the book about all the different studies. But I did so precisely because I didn’t want to be accused of cherry picking the data. (I was anyway, but that’s just the nature of this business.) When Ancel Keys, for instance, reported in the 1950s reported that saturated fats raised total cholesterol, which they did in his studies, he based it on comparisons of butter fat to polyunsaturated oils in studies that lasted only two to nine weeks. (He also reported, curiously enough, that the saturated fats had no significant effect on LDL.)

These latest trials just happen to be the best data we have on the long-term effects of saturated fat in the diet, and the best data we have says that more saturated fat is better than less. It may be true that if we lowered saturated fat further — say to 7 % of all calories as the American Heart Association is now recommending — or total fat down to 10 percent, as Dean Ornish argues, or raised saturated fat to 20 percent of calories, as Keys did, that we’d see a different result, but that’s just another hypothesis. The trials haven’t been done to test it. It’s also hard to imagine why a small decrease in saturated fat would be deleterious, but a larger decrease would be beneficial.

It’s also true that I don’t think that LDL is a particularly meaningful predictor of heart disease risk, and I think total cholesterol is meaningless (based on the evidence that I recount in the book). But the point is that the AHA and the National Cholesterol Education Program and the authorities at the National Heart, Lung and Blood Institute do think LDL is meaningful, and that’s the basis by which they have always recommended low-saturated-fat diets. They also think that total cholesterol/HDL is the single best predictor of heart disease risk, so by their assessment, more saturated fat is better than less. I think the best predictors of risk regarding cholesterol profiles are HDL and the size and density of the LDL particles themselves, and maybe measurements of a protein known as ApoB (the protein component of the LDL particle itself) — and the existing diet trials in those cases also suggest that saturated fats are at worst harmless and perhaps even beneficial.

Last point, the funding. It’s true that the study was financed by the Atkins Foundation, but to assume that the researchers went out and falsified their findings or twisted their observations to satisfy the source of funding is naive. Regrettably, the only institutions that will finance clinical trials, for the most part, are those that stand to gain from the results. That’s why the pharmaceutical industry finances drug trials. It would be nice if the government financed all these trials, but they don’t. So it’s up to the Atkins Foundation and any other organizations that might hold similar beliefs. In this case, the Atkins-funded diet trial observed the exact same results as similar NIH-funded diet trials.

Worth noting here is that the NIH has also spent $5 million recently for a large (300+ subjects, two-year-long) Atkins vs. AHA low-fat diet trial. This is a larger and longer version of a pilot trial that observed results similar to the Israeli trial. To my knowledge, it’s the largest diet/weight trial the NIH has ever funded. The principal investigator was Gary Foster of Temple University, currently the president of the Obesity Society, which is to obesity these days what the American Heart Association is to heart disease. In February of 2007, Dr. Foster told me the researchers had “completed the final 2 year assessments on most but not all” of their subjects. This week he told me that a paper on the results is “in the peer review process” and that “journal policies prevent me from saying more than that.” It would be nice to see those results, and we can only hope they’ll be published soon."

http://tierneylab.blogs.nytimes.com/2008/07/24/the-fat-fight-goes-on/

Deadly Quartet

http://archinte.ama-assn.org/cgi/content/abstract/149/7/1514
Does obesity cause hypertension, hypertriglyceridemia, glucose intolerance, and hyperinsulinemia?

Or does hyperinsulinemia cause the rest?  If you control the hyperinsulinemia, you affect the others, suggesting a causal relationship.

How do you control hyperinsulinemia?  Carb restriction.  Eat meat and vegetables, nuts and seeds, some fruit little starch and no sugar.

Dr. Cordain Revises Stance on Sat Fat

BLUF:  "The bottom line is that we do not recommend cutting down saturated fatty acid intake but rather decrease high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy."


Nice bit that follows describing the mechanisms driving formation of atherosclerotic plaques (note: the LDL that oxidizes most easily is the small, dense LDL; the levels of these LDLs are driven higher by high carb consumption):
"Moreover, some studies have suggested that there’s not enough scientific data to support the view that increased total or LDL cholesterol is an independent risk factor for CVD, but rather oxidized LDL. Plaque production is mediated by oxidized LDL but not LDL. Oxidized LDL can produce shedding of the inner layer of the artery namely glycocalix. Then oxidized LDL infiltrates in the intima of the artery. Oxidized LDL is eaten by macrophagues, a process known as phagocytosis, and therefore macrophagues are transformed into foam cells which produce the fibrous cap.

Once the fibrous cap has been produced we need to break it down in order to produce an ischemic event. Lectins and low-grade chronic inflammation are involved in the activation of matrix metalloproteinases which break down the fibrous cap.

In summary, high total cholesterol or LDL levels do not increase CVD risk but rather oxidized LDL. To produce oxidized LDL we need the factors mentioned above. Hence, consumption of saturated fatty acids is not an issue if we control several other factors such as those mentioned before.

Dr. Cordain wrote a book chapter where he shows that saturated fat consumption in ancient hunter-gatherer populations were usually above recommended 10% (American Heart Association) of energy from saturated fats yet non atherogenic."

The bottom line is that we do not recommend cutting down saturated fatty acid intake but rather decrease high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy."

http://thepaleodiet.blogspot.com/2010/03/paleo-diet-q-saturated-fat.html

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

Review - The Great Cholesterol Con

http://www.proteinpower.com/drmike/statins/646/
BLUF:  Dr. Mike Eades reviewing another MD's book giving the lie to the diet/heart hypothesis.

"I read Dr. Malcolm Kendrik’s book The Great Cholesterol Con in the UK-published edition several months ago... the UK publisher did a sorry job on what is a truly wonderful book. Dr. Kendrick’s writing style is accessible, humorous and to the point. He slashes and burns the diet/cholesterol/heart hypothesis in easy-to-understand terms and with great verve. I didn’t really find much in the first part of the book that I disagreed with except for one little throw away sentence about prions causing mad cow disease. I’m one of those folks who just don’t buy that entire premise, so Dr. Kendrick’s referring to it as established medical fact was a little jarring. Other than that one false note, I was completely engrossed in the book. As anyone who reads this blog knows, Dr. Kendrick was preaching to the choir with me, but the choir certainly enjoyed it. I’m going to excerpt a fairly long section for a couple of reasons, one of which is totally self serving. First, I want you to get the feel for Dr. Kendrick’s writing style, and second, I’ve been wanting to write a section on this blog about ad-hoc hypotheses for a while so that I could link back to it and not have to explain the term each time I write about it. Dr. Kendrick has done it perfectly, so I’ll simply link back to this post and let him do all the work. Here is Dr. Kendrick on the ad-hoc hypothesis:

"But there is no evidence that any of these three factors [he’s just been talking about how people claim that garlic, red wine, and lightly cooked vegetables are protective against heart disease] are actually protective.
"NONE. By evidence, I mean a randomized, controlled clinical study. Not epidemiology, meta-analysis, discussions with French wine producers or green-leaf tea growers, or a trawl through the Fortean Times. In reality, the only reason that these three factors appeared was to protect the diet-heart hypothesis. They are what Karl Popper would call ‘ad-hoc hypotheses,’ which are devices that scientists use to explain away apparent contradictions to much-loved hypotheses. Ad-hoc hypotheses work along the following lines. You find a population with a low-saturated-fat intake (and a few other classical risk factors for heart disease) – yet, annoyingly, they still have a very high rate of heart disease. One such population would be Emigrant Asian Indians in the UK. The ad-hoc hypothesis used to explain away their very high rate of heart disease is as follows. Emigrant Asian Indians are genetically predisposed to develop diabetes, which then leads to heart disease. Alakazoom! The paradox disappears. On the other hand, if you find a population with a high-saturated-fat intake, and a low rate of heart disease, e.g. the Inuit, you can always find something they do that explains why they are protected. In their case it was the high consumption of Omega 3 fatty acids from fish. Yes, indeedy, this is where that particular substance first found fame, and hasn’t it done well since? This particular game has no end. In 1981, a paper was published in Atherosclerosis (a crackling good read), outlining 246 factors that had been identified in various studies as having an influence in heart disease. Some were protective, some causal, some were both at the same time. If this exercise were done today I can guarantee you would find well over a thousand different factors implicated in some way. Recently, just to take one example, someone suggested that the much lower rate of heart disease in south-west France, compared to north-east France, was because the saturated fat they ate was different. In the south-west they ate more pork fat and less beef fat. So now it is no longer simply saturated fat that is deadly, it is the precise type of saturated fat, in precise proportions. Just how finely can one hypothesis be sliced before it becomes thin air? What this highlights, to me at least, is one simple fact. Once someone decided that saturated fat causes heart disease, then NOTHING will change their minds. There is no evidence that cannot be dismissed in one way or another. And there is also no end to the development of new ad-hoc hypotheses. You can just keep plucking them out of the air endlessly – no proof required. Genetic predisposition is one of the most commonly used ‘explain-all’ ad-hoc hypotheses, and it is a particular bug-bear of mine. Someone I knew quite well had a heart attack recently, aged 36. He was very fit, almost to international level at cycling. He was also extremely thin. His resting pulse was 50 a minute, his blood pressure was 120/70 (bang on normal). His total cholesterol level was 3.0 mmol/l, which is very low [116 mg/dL, very low indeed]. He was vegetarian and a non-smoker. I know what you’re thinking: he deserved it. Steady, he’s a nice bloke, actually, if a bit worthy. Now, you can go through all the risk factors tables produced by the American Heart Association, the European Society of Cardiology and the British Heart Foundation – and any other cardiology society you care to mention. According to the lot of them, he had no risk factors. Therefore, he should not have had a heart attack. However, it did emerge that his father had a heart attack aged 50. A-ha! He was genetically susceptible, then! Phew, there’s your answer. I beg to differ: if you think about this in any depth, it is a completely idiotic statement to make. If someone is genetically susceptible to heart disease, that susceptibility must operate through some identifiable mechanism. Or does a big finger suddenly appear from the sky and go: ‘Pow! Heart attack time, bad luck.’ Genetically susceptible people don’t need high LDL levels or high blood pressure. They don’t need to smoke or eat a high-fat diet. They don’t need to be overweight or have diabetes – or anything, actually. They are felled by a mysterious genetic force, operating in a way that no one can detect. Other people are killed by risk factors. But such factors count for nothing if you are genetically susceptible. I have one word to say to this – and it’s a word I’ve used before in a similar context. Balls."
 The entire book is written in this engaging style and I found myself laughing out loud often. In fact as I was reading late one night I woke MD from a sound sleep with my laughter. The book is that funny in places. Funny, but accurate in its laying waste to the idea that fat in general and saturated fat in particular have anything to do with heart disease. Dr. Kendrick has pretty much the same take as I do on the statin issue. He has a chapter detailing all the hoopla the drug companies put out and the reality, which is that statins work only for a very few people. He even mentions our old friend Dr. John Reckless. The latter part of the book is an elaboration of what Dr. Kendrick believes is the driving force behind heart disease: stress. I hadn’t given stress a whole lot of thought until I read this book. Now I am reconsidering it as a major risk factor and working it in to my own ideas of what causes so much heart disease. I really can’t recommend this book strongly enough."

Still Love to Run Long?

BLUF (Bottom Line Up Front):  Another reason why long slow distance running should not be considered 'healthy', and another reason to keep the bulk of your training short and intense.  If you want to be able to go long, without burning up hours and your health training that way, I recommend this approach:  http://www.crossfitendurance.com/.

http://www.paleonu.com/panu-weblog/2010/3/21/still-not-born-to-run.html
"My three hypotheses all remain viable:
Weak form: Chronic Steady state aerobic training* (CSSAT) does nothing to prevent or reverse atherosclerosis.
Mild Form: Some effects of CSSAT may be beneficial or neutral, but they are overridden by the inflammation promoting effects of the diets favored by those who train this way.
Strong Form: CSSAT itself promotes the inflammatory state via cortisol, cytokines, inadequate recovery, etc."

Even Slate Is Onto It?

"The foundation for the "fat is bad" mantra comes from the following logic: Since saturated fat is known to increase blood levels of "bad" LDL cholesterol, and people with high LDL cholesterol are more likely to develop heart disease, saturated fat must increase heart disease risk. If A equals B and B equals C, then A must equal C.
Well, no. With this extrapolation, scientists and policymakers made a grave miscalculation: They assumed that all LDL cholesterol is the same and that all of it is bad. A spate of recent research is now overturning this fallacy and raising major questions about the wisdom of avoiding fat, especially considering that the food Americans have been replacing fat with—processed carbohydrates—could be far worse for heart health."
"In a 2000 study in the American Journal of Clinical Nutrition,Harvard researchers compared the food intakes of 75,521 women with their health over the course of a decade and found that the quintile of women who ate food with the highest glycemic load—a measure that incorporates portion size—had twice the risk of developing heart disease than the quintile who ate food with the lowest glycemic load. A 2008 meta-analysis of 37 studies reported a significant association between intake of high glycemic index foods and increased risk of type 2 diabetes, heart disease, gallbladder disease, and breast cancer."
"In a 2008 study published in Nutrition Research, researchers reported that subjects who followed high-fat, low-carb diets for eight weeks experienced a 46 percent drop in blood concentrations of small LDL particles, while those who followed a high-carb, low-fat diet experienced a 36 percent spike in them. What's more, processed carbohydrates lower "good" HDL cholesterol, whereas saturated fat increases it."
"Research published by Peter Havel, a professor of nutrition at the University of California-Davis, suggests that compared with glucose, fructose incites less of an insulin response, which ultimately results in lower circulating levels of the appetite-suppressing hormone leptin and higher levels of the appetite-boosting hormone ghrelin—so fructose may make you hungrier.
"It could also put you at greater risk of heart disease and diabetes. When overweight people supplemented their diets with drinks sweetened either with fructose or with glucose for 10 weeks, fructose drinkers ended up with higher concentrations of small LDL particles in their blood after they ate. They also experienced, on average, a 20 percent drop in insulin sensitivity—low insulin sensitivity is a risk factor for type 2 diabetes—over the course of the experiment compared with the glucose drinkers."

http://www.slate.com/id/2248754

Tubs of Taubes

This is the summary of Gary Taubes brilliant book, "Good Calories Bad Calories."
Would you be kind enough to review, and post your thoughts to comments below? I am working on a series of articles about this book, and it would be very helpful for me to know what thoughts and questions and observations my audience has in reviewing this summary. Thanks for your help!

1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire hormonal ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.
3. Sugars -sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.
4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
7. Fattening and obesity are caused by an imbalance- a disequilibrium – in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.
8. Insulin is the primary regulator of fat storage. When insulin levels are elevated - either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.
9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.
10. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.

Lukewarm Low Carb Endorsement

http://www.time.com/time/magazine/article/0,9171,1558294,00.html?loomia_si=t0:a16:g2:r1:c0.15245:b24314702&xid=Loomia

"Pass the avocado! Scientists from the Harvard School of Public Health last week announced the results of a pioneering 20-year-long study, which showed that low-carb diets--typically high in fats and proteins--don't necessarily raise the risk of coronary heart disease. The study, which tracked the health of more than 82,000 women, showed that cutting back on white bread and pasta--as advocated by the South Beach diet--doesn't boost chances of a heart attack. "The diet is healthy," says study co-author Frank Hu.

Of course, there's healthy, and there's even healthier. The researchers do not think the study should be interpreted as a license to go hyper-Atkins and eat as much meat as you want. "You should pay attention to healthy fats and proteins rather than just load your plate with bacon," Hu says. In fact, he and his team did find benefits to eating less meat--subjects who ate low-carb diets that took their fats and proteins from sources like vegetables and nuts cut the risk of developing heart disease 30%. --C.S."

Read more: http://www.time.com/time/magazine/article/0,9171,1558294,00.html?loomia_si=t0:a16:g2:r1:c0.15245:b24314702&xid=Loomia#ixzz0eigxOd4K

Interesting results.  Would be interesting to dig into the study to piece together what the authors meant by the final para, and which if any inconsistencies could be found.  The fact that they were looking means they likely believed the 'animal bad plant good' dogma to begin with.  How did that affect their analysis?

Sat Fat Summary of the Issues

http://articles.mercola.com/sites/articles/archive/2010/02/25/saturated-fat-is-not-the-cause-of-heart-disease.aspx
This is a great summary of the issues, but of course, not completely accurate. For one thing, the study he cites was a survey of a collection of observational studies, which of course cannot prove causation one way or the other (see this post on the actual study:  http://fireofthegodsfitness.blogspot.com/2010/02/meta-analysis-considering-impact-of-fat.html).
My biggest gripe with the doc's post is he pumps REAL food, but then includes whole grains which are only REAL food if you happen to be a bird!  Dump the wheat and you lose nothing you need, and many things you don't need.

Lies, Damned Lies, and LDL Stats

The LDL-Fructose Disconnect from the Heart Scan Blog:
" 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."