The Wheat Belly Diet

The cardiologist-created Wheat Belly Diet is built on the premise that wheat, not sweets, is making you fat. Here's how a wheat-free diet may help you lose weight.

By Beth W. Orenstein          Medically reviewed by Lindsey Marcellin, MD, MPH

Forget your beer belly — William Davis, MD, a preventive cardiologist in Milwaukee, Wisc., says your wheat belly is the real health hazard. Davis’ prescription for a whittled middle is simple: Cut all wheat from your diet. Better yet, Davis argues in his book, Wheat Belly: Lose the Wheat, Lose the Weight, and Find Your Path Back to Health, that eating wheat-free will both prevent and reverse health problems such as acne, cataracts, diabetes, heart disease, and arthritis.

The Wheat Belly Diet suggests we get back to eating more like our ancestors who existed solely on foods found in nature, not those grown for production or manufactured for sale. In that way, the diet is similar to another popular diet, the Paleo or hunter-gatherer diet, says Joan Salge Blake, MS, RD, a Boston nutritionist, author of Nutrition & You: Core Concepts for Good Health, and a spokeswoman for the American Dietetic Association. Here’s how to find out if going wheat-free is right for you.

The Wheat Belly Diet: What Is It?

Your menu choices on this eating plan include natural foods such as eggs, nuts, vegetables, fish, poultry, and other meats. You can use herbs and spices freely and healthy oils, such as olive and walnut, liberally. Eat fruit occasionally — just one or two pieces a week — because the naturally occurring fructose in fruit is a simple carbohydrate. As part of this diet, you’re required to eliminate all fast food, processed snacks, and junk foods, and drink lots of water.

The Wheat Belly Diet is in fact gluten-free, but Davis doesn’t advocate eating packaged gluten-free foods. His reasoning: These products often simply substitute brown rice, potato starch, rice starch, tapioca starch, or cornstarch for wheat flour, and those substitutes can raise your blood sugar or glucose higher than wheat.

The Wheat Belly Diet: How Does It Work?

Cut wheat from your diet, and you’ll eat about 400 fewer calories a day than you normally would, Davis says. This calorie deficit alone is almost enough to add up to a pound of weight loss per week. “Anything that is going to cut calories is going to work because losing weight is a numbers game,” Blake says. “Eat fewer calories than you burn, and you’ll lose weight. Likewise, eat more than you burn, and you’ll gain weight.”Another reason the diet works, Davis says, is that wheat contains a unique protein, gliadin, which stimulates your appetite— so when you eat wheat, your body just wants more wheat. Eliminate wheat and your appetite diminishes on its own. Wheat also causes blood sugar spikes, and elevated blood-sugar levels can cause your body to store calories as fat. Lower your blood sugar by eliminating wheat, and it can contribute to weight loss.

The Wheat Belly Diet: Sample Menu

Breakfast: Plain yogurt with berries and almonds
Lunch: Grilled chicken breast with salsa, 1/2 cup brown rice, steamed vegetables sprinkled with extra-virgin olive oil
Dinner: Baked eggplant topped with mozzarella cheese and tomato sauce, mixed green salad spritzed with extra-virgin olive oil
Snacks: Black-bean dip and raw vegetables

The Wheat Belly Diet: Pros

• If you adhere strictly to the diet, you will lose weight. Over three to six months, you can lose 25 to 30 pounds depending on your age, gender, and physical activity, Davis says.
• The diet is simple. There’s no need to count calories, limit portions, or calculate fat grams. All you have to do is eliminate foods that contain wheat.
• The diet is rich in vegetables, which are full of vitamins and fiber. Eating a diet rich in fruits and vegetables can help lower cholesterol, stabilize blood sugar, and reduce the inflammation that can cause conditions from acne to arthritis.

The Wheat Belly Diet: Cons

• The diet is restrictive, and it may be hard to maintain for the long-term, especially if foods such as bread, cookies, and pasta are among your favorites. “Losing weight doesn’t have to be this challenging,” Blake says. “Do you really need to go to this extreme?”
• Wheat is in a huge number of packaged foods. You have to read food labels carefully because it can be hidden in everything from chewing gum to granola as an emulsifier or leavening agent.
• When you remove all wheat from your diet, if you “cheat” and eat a slice of whole-wheat toast or half a bagel, the wheat could cause digestive problems, such as stomach cramps and gas.
• You could be missing out on some important nutrients. “Whenever you limit whole types of foods, you have to make sure you’re eating healthfully,” Blake says. “This isn’t a well-balanced diet. You should sit down with a registered dietitian to be sure you’re meeting all your nutrient needs if you choose this diet.”
• Although you can lose weight with this diet, it will be lost from all over your body, not just your “wheat belly” or love handles, Blake says. Weight loss doesn’t work that way — you don’t lose from a specific area.

The Wheat Belly Diet: Short-Term and Long-Term Effects

The foods you can eat on the Wheat Belly Diet are healthy, and you should lose weight rapidly if you stick to the plan. Weight loss can affect more than just your appearance: Study after study has shown it can boost heart health, reduce pain, improve your energy levels, and more. For example, someone who is prediabetic and loses just 15 pounds can reduce the risk for diabetes over three years by 58 percent, Blake says.

Because the diet is so new, not much is known about the long-term effects, Blake says, but serious health consequences are not anticipated. Overall, Blake remains skeptical.

“There’s nothing wrong with wheat,” she says.“It isn’t wheat that’s causing you to gain weight; it’s the calories you’re eating. Just eat more fruits and vegetables as part of a balanced diet, and you can cut calories and lose weight while still occasionally eating foods that contain wheat.”

Last Updated: 02/23/2012

http://www.everydayhealth.com/diet-and-nutrition/the-wheat-belly-diet.aspx

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Statins for 8-Year-Old Children

The American Academy of Pediatrics recently announced new recommendations for giving cholesterol-lowering drugs to children as young as eight years old. They also recommend giving low-fat milk to infants as young as one year old.

The New York Times published several articles on this, first announcing the recommendation the day the academy made it, then describing the backlash of saner doctors and other members of the public against it, and finally editorializing that while they were first "appalled" at the recommendation, after reading the report they were more dismayed at the state of our children's health.

Concerning this frightful state of children's health, the Times reported the following:

"We are in an epidemic," said Dr. Jatinder Bhatia, a member of the academy's nutrition committee who is a professor and chief of neonatology at the Medical College of Georgia in Augusta. "The risk of giving statins at a lower age is less than the benefit you're going to get out of it."

Dr. Bhatia said that although there was not "a whole lot" of data on pediatric use of cholesterol-lowering drugs, recent research showed that the drugs were generally safe for children.

An epidemic of what? High cholesterol? Not according to the academy's report, which states that cholesterol levels in children declined between 1966 and 1994 and stayed the same between 1994 and 2000.

No, we are in an epidemic of obesity. As the Times reported:

But proponents say there is growing evidence that the first signs of heart disease show up in childhood, and with 30 percent of the nation's children overweight or obese, many doctors fear that a rash of early heart attacks and diabetes is on the horizon as these children grow up.


Is there any evidence that statins lead to weight loss? If there is, I am not aware of it.

The point is immaterial, because the academy doesn't claim to have any evidence for its position in the first place. For example, its report states the following:

Also, data supporting a particular level of childhood cholesterol that predicts risk of adult CVD do not exist, which makes the prospect of a firm evidence-based recommendation for cholesterol screening for children elusive.

And further down:

It is difficult to develop an evidence-based approach for the specific age at which pharmacologic treatment should be implemented. . . . It is not known whether there is an age at which development of the atherosclerotic process is accelerated.

In other words, they don't know what level of cholesterol is risky and at what age it starts posing a risk, but they will nevertheless assume that there is some level that does start to pose a risk at some age and they will thus have to make a guess just what that level and what that age is.

The report discusses evidence that the "metabolic syndrome" and the "recent epidemic of childhood obesity" are tied to the risk of diabetes and heart disease and evidence that even modest weight loss at a level of five to seven percent is sufficient to prevent diabetes. Yet somehow instead of making a recommendation about how to more effectively lose weight the authors derive from this data a much less logical but much more profitable conclusion that 8-year-olds should be put on statins.


As to the recommendation to feed infants low-fat milk, the Times reported the following:

The academy also now recommends giving children low-fat milk after 12 months if a doctor is concerned about future weight problems. Although children need fat for brain development, the group says that because children often consume so much fat, low-fat milk is now appropriate.

This is rather remarkable, because the academy attributed the drop in childhood cholesterol levels to the successes of the anti-fat, anti-cholesterol campaign that began in the 1950s. But now children no longer need milkfat because they are getting plenty of fat. Well which is it? Are they getting more fat now or less fat?

Of course milkfat is also a source of choline, along with liver and egg yolks, which is essential to brain development.


But even this misses the point. Cholesterol is essential to brain development!

One of the first articles I added to my section on the functions of cholesterol was an article entitled "Learning, Your Memory, and Cholesterol." It discusses the evidence uncovered eight years ago that cholesterol is the limiting factor for the formation of synapses, which are the connections between neurons that allow learning and memory to take place.

Lowering brain levels of cholesterol can be detrimental at any age beacause of this, but the consequences for children -- whose brains are still developing at a much more rapid rate -- could be much more dire.


No doubt, most researchers and medical doctors mean well and are honestly trying to help our children. But surely someone in these drug companies must know that cholesterol is necessary for brain development, and that cholesterol-lowering drugs reduce mental performance in adults. Surely they must know that if we raise our next generation of children on statins during the critical periods of brain development, we may raise a whole generation with compromised intelligence.

And if that's the case, are they trying to dumb us down? Sometimes it seems like that's the case.

Article written by Chris Masterjohn
http://www.cholesterol-and-health.com/Statins-For-Children.html

Chris Masterjohn, has a blog blog called “The Daily Lipid”. He writes about fats, cholesterol and health. Chris is pursuing a Ph.D. in Molecular and Cell Biology and is a knowledgeable contemporary writer about cardiovascular health.

Statins for Pregnant Women???

Statin manufacturers, the sycophantic researchers they pay, and the shameless hucksters who sell them are always up to no good, but their recent attempts to market them to pregnant women are simply horrifying.

According to a recent news article published in Mail online, researchers from liverpool believe that taking statins during pregnancy might help women avoid caesarean sections by promoting more robust uterine contraction. They hope to begin human trials in three to five years.


Somehow, the author of this article failed to react with the shock and horror appropriate to the situation -- which should be the same shock and horror with which we would react to the suggestion that pregnant women should take thalidomide to avoid morning sickness.


Back in 2004, a report in the New England Journal of Medicine showed that the use of statins in the first trimester of pregnancy was associated with birth defects, especially severe central nervous system defects and limb deformities. In fact, 20 out of 52 women exposed to statins gave birth to offspring with such defects, which represents a birth defect rate of 38 percent, nearly 20 times the background rate of birth defects!


Even before this report was published, researchers already knew that statins caused birth defects in animal experiments, and the FDA already required the drugs to carry a label warning pregnant women to stay away from them. The article linked to above stated the following:

"FDA took this action because it was recognized that fetal cholesterol synthesis was essential for development, and because animals given statins during pregnancy had offspring with a variety of birth defects," [one of the study's authors] said.

Less than a year later, Merck and Johnson & Johnson jointly asked the FDA for permission to market an over-the-counter statin. One of the concerns about the proposal was the risk to pregnant women. USA Today reported:

The FDA classifies Mevacor and other statins as pregnancy category X, which means they are not supposed to be taken by pregnant women. Not only have category X drugs been linked to fetal abnormalities in animal or human studies, but the FDA also has declared that the benefits of taking them do not outweigh potential risks.

According to the same article, Merck made a disturbing admission:

"Of course, there will be women who take it off-label," acknowledges Merck executive Edwin Hemwall, referring to the use of non-prescription Mevacor by women under 55.

And what could prompt women to use statins during pregnancy against recommendations? Certainly a news article declaring that statins might prevent the need for caesarean sections and their associated complications could prompt some women to do so.


So what ground-breaking research made these Liverpool researchers so confident that taking drugs associated with twenty times the normal rate of major birth defects during pregnancy might be a good idea that they put out a press release declaring this confidence to the public before any trials were even under way?


Well, according to the article:

Tests have already shown that raising levels of cholesterol interferes with womb tissue's ability to contract.

Really. Raising levels of cholesterol. You might wonder how they accomplished that. Did they use cholesterol-raising drugs? I don't know of any drugs that do that. Did they use egg yolks, or the dreaded dietary villain -- gasp -- saturated fats?


No, the story is quite different.


The apparent basis for this ridiculous statin cheerleading is a 2004 study published by researchers from the University of Liverpool in the American Journal of Physiology -- Cell Physiology entitled "Increased cholesterol decreases uterine activity: functional effects of cholesterol alteration in pregnant rat myometrium."


Rather than feeding anything to pregnant women or pregnant rats, the researchers took pregnant rats and killed them. So the first thing we can say is that statins might help you deliver a baby if your doctor kills you first.


Then they extracted the uterine tissue and either extracted cholesterol from it with a chemical solvent called methyl beta-cyclodextrin, or enriched it either with cholesterol mixed with this solvent or with LDL (which they didn't measure for oxidation prior to use). Then they added drugs to induce contraction under either cholesterol-depleted or cholesterol-enriched conditions, and found that contraction was greater under cholesterol-depleted conditions.


So now we know that -- wait, what is it we know?


Well, quite clearly, we don't know anything that we can have any confidence has any physiological relevance at all. That is, except the fact that statins cause birth defects in animals, and they increase the rate of birth defects in humans by nearly twenty times, primarily by causing severe defects of the central nervous system and limb deformities.


To add to that, we also know that the vast majority of humans conceived with Smith-Lemli-Opitz Syndrome (SLOS), a genetic inability to synthesize enough cholesterol, die of spontaneous abortion in the first 16 weeks of gestation. Those who live long enough to be born suffer from mental retardation, autism, facial and skeletal malformations, visual dysfunctions and failure to thrive.


Statins for pregnant women? I don't think so.

Article written by Chris Masterjohn
http://www.cholesterol-and-health.com/Statins-For-Pregnant-Women.html

Chris Masterjohn, has a blog blog called “The Daily Lipid”.  He writes about fats, cholesterol and health. Chris is pursuing a Ph.D. in Molecular and Cell Biology and is a knowledgeable contemporary writer about cardiovascular health.

The most important thing you probably don’t know about cholesterol

Following article by CHRIS KRESSER http://chriskresser.com/the-most-important-thing-you-probably-dont-know-about-cholesterol

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Summary:

• The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
• Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
• Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
• Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
• The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.

Not all cholesterol is created equal

By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.

But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”
Words to live by.

The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.
But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.

In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.

You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).

Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.

It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.
The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.

In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.
On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.
Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.
Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.

I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.

Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol

Here’s where the story gets even more interesting. And tragic.
Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.

It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.
Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.
In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.
Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.
Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.
Here’s what the authors said about their results:

The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.

Translation: following the advice of the American Heart Association is hazardous to your health.

Eating cholesterol reduces small LDL

The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.

Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.

If you’re confused right now I certainly don’t blame you.
Let’s review what we’ve been told for more than 50 years:

1. Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
2. Reducing intake or saturated fat and cholesterol protects us against heart disease.

Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:

1. Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
2. Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.

Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”

In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.
I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.
We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.
Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?
Really?
Sometimes it seems like everything is backwards.

How to reduce small LDL

Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.

Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.

As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.

In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.

Testing your small LDL level

I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.
If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.
However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.

First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.

The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.

Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.
If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:

1. LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
2. The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.

Tagged as: carbohydrates, cholesterol, dense, fat, hdl, ldl, low-c, low-fat, myths_truths, small

A Headline You Will Never See: 60 Year Old Man Dies of Cholesterol

Cholesterol scam: Disinformation slowly unraveling among health professionals

Learn more: http://www.naturalnews.com/035033_cholesterol_disinformation_fats.html#ixzz1n7iFu2ir

(NaturalNews) The idea of cholesterol creating cardiac problems has caused obsessive cholesterol count blood testing for decades. Another outcome of this scare was obsessively avoiding fat, especially saturated fats.

The food industry responded with low and no fat foods from milk to cottage cheese and more. Processed foods promoted their low or no fat contents as though they were the healthiest foods in the freezer.

Healthy fats such as coconut oil and palm oil were spurned and replaced by very unhealthy trans-fat, processed and heated cooking oils. Relatively healthy whole butters were replaced by plastic margarines.

However, this myth of cholesterol dangers lurking in saturated fats waiting to clog your arteries and cause you to die of cardiac arrest is beginning to unravel.

Unraveling the myth of cholesterol

A meta-analysis of properly performed previous studies on heart health and saturated fats concluded there was no association between cardiac issues and saturated fats. This was published in the American Journal of Clinical Nutrition (AJCN) on January 13th, 2010. (1)

Meta-analysis is a statistical method of proving or disproving varied epidemiological studies within a set topic. The AJCN meta-analysis covered studies involving 350,000 subjects who were followed for 5 to 23 years.

The trend set by the saturated fat high cholesterol disinformation a few decades ago has resulted in many Americans eating less fat and showing lower blood cholesterol levels. Yet, heart disease rates have continued to rise along with diabetes, pre-diabetes and obesity. (1)

Dr. William Davis explains in his article "A Headline You Will Never See: 60 Year Old Man Dies of Cholesterol" that cholesterol doesn't kill "any more than a bad paint job on your car could cause a fatal car accident." (1)

He explains the cause of most heart attacks and coronary problems is atherosclerotic plaque in the coronary arteries, which can build up and rupture or clog the arteries. He goes on to describe other factors that can cause plaque ruptures, including inflammatory pneumonia.

Though there can be some cholesterol in the plaque, cholesterol itself is waxy and pliable. Cholesterol is important for brain cells, nerves and other cellular structural components. Calcium deposits (calcification) in artery interiors are much worse components of plaque. It belongs in your bones and not in your arteries. Vitamin K2 helps transport calcium out of your blood and into your bones.

Dr. Davis recommends avoiding cholesterol panels for heart health concerns and opting for a measure of coronary atherosclerotic plaque.

The scam continues despite overwhelming contradictory evidence

Despite more and more published journals and doctors proving coronary heart disease (CHD) is not caused by high saturated fat diets and cholesterol, the myth persists. Many peoplewith low cholesterol have died of CHD while in their 40s, while many with high cholesterol never have CHD issues.

Several studies of heart attack cadavers have also revealed the disinformation of cholesterol dangers. Yet the common advice from cardiologists upon seeing high cholesterol is to get an angiogram,adiagnostic testwhichis expensive and not so safe. Then there are those pricey drugs meantto lower cholesterol while wreaking havoc on overall health. (2)

Cholesterol is vital for many functions. For example, it helps convert sunlight into vitamin D3. If you're not getting enough with your food, the liver is forced to manufacture it. Low cholesterol has been linked to higher stroke risks.

Oxidized cholesterol from hydrogenated and refined polyunsaturated cooking oils and margarine can lead to complications that result in CHD. This comes not only directly from the oils themselves, but indirectly from the oxidation process those oils initiate. (3)

These toxic oils and butter substitutes were created to replace thewholesome saturated fats that should be consumed.

Sources for this article include:

(1) http://www.sott.net

(2) http://www.opednews.com

(3) http://www.treelight.com/health/healing/Cholesterol.html

About the author:
Paul Fassa is dedicated to warning others about the current corruption of food and medicine and guiding others toward a direction for better health with no restrictions on health freedom. You can visit his blog at http://healthmaven.blogspot.com


Learn more: http://www.naturalnews.com/035033_cholesterol_disinformation_fats.html#ixzz1n7i8Tdlx

Read the article here > http://www.naturalnews.com/035033_cholesterol_disinformation_fats.html

Cholesterol and Statins: Who’s the Hero? Who’s the Villain?

Read the full article HERE. This is only an exerpt.
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Cancer

It is not easily shown that statins increase risk to cancer, because it takes considerable time for cholesterol to become depleted in the tissues as the supply line to replenish worn out cholesterol is reduced, and then more time for this depletion to lead to cancer due to genetic mutations. However, low cholesterol is a risk marker for cancer [15], and, despite the fact that statin trials are usually too short to reveal the trend towards increased cancer risk, several statin trials have resulted in observable differences between treatment and control groups, with treatment groups faring worse. In the first two trials on simvastatin, non-melanoma skin cancer was more prevalent in the treatment group, a result that becomes statistically significant if the data from the two trials are combined. In the CARE trial, which involved exclusively women, 12 women in the treatment group developed breast cancer, as against only one in the control group, a result that was highly significant (p = 0.002). Two other trials, both PROSPER and SEAS, also showed statistically significant increases in cancer incidence in the treatment group compared to the control group.

The story, in my view, for how statins increase your risk to cancer, involves a number of players and some complexity regarding mechanism. But it’s a very logical step-by-step progression, taking place steadily over an extended period of time. To understand the story, you first have to know something about vitamin B12 (cobalamin), a key player in the story. Vitamin B12 catalyzes a great number of reactions that require methionine, an essential sulfur-containing amino acid, as substrate, extracting the methyl group from methionine and adding it to some other molecule. One of the key molecules that benefits from such reactions is DNA. Methylation of DNA protects it from damage due to exposure to carcinogens or oxidation or radiation.

Methionine can also be degraded via a different pathway, and it’s an either-or situation here. This alternative fate results in the production of homocysteine, which later becomes substrate for the synthesis of sulfate. So, logically, if sulfate is in short supply, then methionine would get side-tracked down the homocysteine pathway, and less of the DNA would get methylated. Eventually, this would manifest as an increased risk to cancer.

Why might sulfate supply be deficient? This is something I have already discussed in previous blog posts, and one way it could happen is if the cells in the epidermis didn’t have enough cholesterol. This is because they need cholesterol in order to produce cholesterol sulfate, upon exposure to sunlight. The cholesterol sulfate is then shipped out via the blood stream to all the tissues, which eagerly take it up to resupply themselves with both cholesterol and sulfate.

The cells in the skin can synthesize their own cholesterol, but statin therapy would interfere with this process. As a result, they would not be able to spare cholesterol to ship out. What happens first is that, due to cholesterol deficiency in their membranes, they start leaking potassium at an excess rate, and an energy burn they can’t afford ensues, to pump the potassium back in. This becomes untenable, so calcium is brought in to replace some of the potassium as a positively charged electrolyte. Being a much bigger molecule, calcium doesn’t leak out nearly so easily. Its presence has a dramatic effect, however, on the eNOS molecules that had been responsible for synthesizing sulfate. They detach from the cell membrane and start making nitric oxide (−→ nitrate) instead. Unfortunately, this also results in some nasty side products like peroxynitrite and superoxide, which are potent oxidizing agents.

One of the first molecules that gets oxidized is cobalamin [1]. This drives the cobalt atom in cobalamin to a +3 charge, which inactivates the molecule, meaning that it will no longer support the methylation of the vulnerable DNA, thus increasing the risk to cancer. This is interesting from a biological standpoint, because it means that the methionine will naturally shift towards producing sulfate, a good idea since the skin is no longer going to be able to keep up with the supply.

One of the other molecules whose synthesis is catalyzed by cobalalmin is coenzyme Q10, probably the most important antioxidant in the mitochondria. The mitochondria are the chambers where sugars and fats are oxidized to produce ATP, the energy currency of the cell. Mitochondria are the organelles in the cell that suffer the greatest exposure to oxidizing agents, because oxidative metabolism takes place there. They contain their own separate mitochondrial DNA, now highly vunerable to attack.

To add insult onto injury, statins also interfere with the synthesis of coenzyme Q10, so this potent antioxidant is now in very short supply in the mitochondria of any cell in the skin that has been hit hard by a statin drug. The cells in the skin are now poised to develop cancer: they’ve got an extra burden of oxidizing agents, an increased vulnerability in their DNA to susceptibility to damage due to the demethylation process, and a decrease in the agents that would mop up extra free radicals. It’s not at all surprising that skin cancer is where the increased risk to cancer with statin therapy was first noted.

Another cancer which I suspect is increasing in incidence directly due to statin therapy is prostate cancer, which is the most common cancer by far in men. A very interesting recently noted observation is that prostate cancer tumors actually are producers of cholesterol sulfate! [3]. It has been suggested that this feature might be useful as a more reliable indicator of prostate cancer than the PSA test. I suspect in fact that this is a positive role they play, to try to correct a severe deficiency in this vital molecule, as cholesterol sulfate plays an essential role in fertilization [6]. Unlike women, men normally remain fertile throughout life, but not if cholesterol sulfate is insufficient. I would predict that surgery to remove a prostate tumor, beyond rendering a man infertile, will lead to an increase in various medical problems related to cholesterol sulfate deficiency.

From:  http://cindy-on-health.blogspot.com/2011/12/cholesterol-and-statins-whos-hero-whos.html

See also: http://stephanie-on-health.blogspot.com/

The author Stephanie is a research scientist at MIT.

Statin Drugs Raise the Risk for Diabetes in Postmenopausal Women by 48%

Statin Drugs Raise the Risk for Diabetes in Postmenopausal Women by 48%

Older women using Statin Drugs like Lipitor may be at a 48% higher risk for becoming Type 2 Diabetics. This result was published in the Archives of Internal Medicine and reported by Medpage Today, January 9, 2012. The study didn’t specifically prove that statins cause Diabetes but rather proved that either the use of statins causes Diabetes or that statin use is somehow related to the incidence of Diabetes. Future studies will be needed to prove any cause/effect relationships.
This is yet another “shot across the bow” at the statin drug industry which has convinced many Americans that they have to take statins for their cardiovascular health. I stopped taking Lipitor months ago because I deemed the risk much greater than the benefit – and my physician went along with it because of my weight loss with a low carb diet. To acquaint you with the dark side of statins and why many are doing as I have, watch the following video by Dr. Diamond. He covers statins starting at 33:45 into the clip. His presentation is backed up by data and references from the University of South Florida.

In terms of the 48% higher risk figure, it is important to realize that this is called a Hazard Risk and is a ratio of a ratio, masking some important issues. You need to consider a simpler perspective of the data to meaningfully assess what this means. I don’t have the exact figures, but based on the published study data, the likelihood of all the women in the study becoming Diabetic was around 6.7%. The women on statins were (based on the study results) found to have a 48% higher risk of becoming diabetic. The rough estimate of the likelihood of women on statins to become diabetic was therefore 148% of 6.7%, or 9.9%. From this simpler perspective the numbers aren’t so frightening. In other words, for these women, going on a statin increased the likelihood of Diabetes by 3.2%, from 6.7% to 9.9%. It is still, however, a finding that is not good news for patients on statins.
Getting back to the new statin study: Yunsheng Ma, MD, PhD, of the University of Massachusetts School of Medicine, was intrigued by prior research that suggested a link between statins and Diabetes and established an estimate of a 9% higher risk of Diabetes for statin users. Based on this, Dr. Ma and his colleagues decided to investigate further with an analysis of the data from a large study called the Women’s Health Initiative. After that analysis, in short, they found a much higher risk for Diabetes, for postmenopausal women on statins.
The Women’s Health Initiative provided data on 153,840 women with an average age of 63, who didn’t have Diabetes when they entered the study in 1993. About 7% of the women were on statins at the beginning of the study. Analysis of the women on statins compared to women not on statins yielded a 48% greater risk of the onset of Type 2 Diabetes during the study, which was last analyzed in 2005. This result was obtained after analysis adjustments were made to make sure that issues like age, race, and weight weren’t contributing factors. The 48% higher risk was seen for all types of statins (for example Lipitor, Crestor, Zocor, and Mevacor).
Since the study didn’t conclusively find that statins cause Diabetes, the researchers were clear in recommending that patients consult with their doctors on this issue before changing their medications. They did suggest, however, that since there is a higher risk of Diabetes with statin users, patients should strongly consider lifestyle change (such as weight loss and exercise) to improve their health rather than think that they can, “without risk”, just take the easy approach with statins.
Some interesting things are going on with the TV News coverage. Yesterday NBC reported on the study mentioned here, using the 48% increased risk factor (Hazard Risk). On the Today Show today, however, NBC reported on the same story but chose to report the numbers from the “simpler perspective” with no mention of the Hazard Factor 48% number. They reported that the likelihood of women becoming Diabetic was 10% for women who were on statins but only 6.4% for women who weren’t. That doesn’t look so frightening does it? I wonder if the change from the Hazard Risk to the less frightening simple perspective had anything to do with the minute-long Lipitor commercial that NBC aired during the show!
It’s ironic that the supporters of statin drugs may have pulled the same trick (but in reverse) when they put together the original clinical study analysis that got us onto statins in the first place. See the video above from Dr. Diamond at around 37:30 into the clip. The detailed analysis results indicated that reducing cholesterol lowered the likelihood of death by Coronary Heart Disease from 2% to 1.6% (only 0.4%) – not very exciting. The statin supporters however proclaimed that it was a 24% reduction in risk (Hazard Risk)!
This post is featured on the Modern Paleo Blog.
From: http://cravingsugar.net/statin-drug-study-reveals-48-increased-risk-diabetes-women-lipitor.php

Letter to your doctor about taking statins.

If your doctor is pushing you to take a statin drug to lower your LDL Cholesterol you might consider printing out this letter and presenting it to him to point out some of the concerns about this treatment and that you would be open to his response to those concerns.
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Patient’s Details:

Dear Doctor   ____________________ 

I wish to raise the following concerns with you regarding your advice that I should lower my cholesterol with the use of statins or other medications.

Large scale studies have shown that cholesterol levels follow a normal distribution having a range of values from around 2.7 mmol/l (105 mg/dL) to 8.8 mmol/l (343 mg/dL). This same normal distribution is seen in people who do have heart disease and people who do not have heart disease [1].

I am concerned about the definition of ‘high’ cholesterol, since most adults naturally have a cholesterol level that is above the suggested target.  Furthermore, records show that cholesterol levels in industrialised countries are decreasing, not increasing [2]. What is being suggested as ‘high’ is in fact just normal in many cases. 

I am also concerned by the fact that most people who have a heart attack have an average cholesterol level, not a high cholesterol level: this has been found during studies completed on people in the UK, Australia, New Zealand and America [3]  [4]  [5].

Studies have also raised questions about so called ‘bad’ cholesterol. A study published in the American Heart Journal looked at cholesterol levels for people who have been admitted to hospital in America with coronary artery disease (CAD). The study included 136,905 people.The average LDL level for this group of people was 2.7 mmol/l (105 mg/dL) [6].Which was actually lower than the average level for the general population: the average for the general population was 3.2 mmol/l (125 mg/dL) [7].

If people with CAD have lower LDL levels than the general population, then where is the evidence that higher LDL levels cause heart disease?

The conclusion of a BBC Radio 4 program in the UK was that 99% of people who take statins for primary prevention do not benefit from them. This was admitted by the UK governments chief advisor on heart disease (Professor Boyle) [8].

Any benefit associated with statins is routinely shown as a relative percentage reduction and this is misleading for patients. To illustrate this point we could look at the Lipid Lowering Arm of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-LLA) [9].

Within the group of people who were given the statin, 1.9% of them had a heart attack or died of heart disease, versus 3% of people in the placebo group. The statin reduced the risk by just 1.1%. Unfortunately the authors of the report described the results as a 36% relative risk reduction.

There is evidence that high cholesterol in elderly people is associated with a longer life. This was the conclusion of a study completed by a team of researchers at Yale University School of Medicine [10]. Researchers in the Netherlands also found that in the case of the elderly, life expectancy increases when cholesterol levels are higher. Those with higher cholesterol levels appeared to be better protected from cancer and infection [11].

I am also concerned that adverse effects from statins have been under-reported. The procedures used during clinical trials, such as the run-in period, may mean that the trial participants are not representative of the general population.

‘Stopped Our Statins’ is a forum for people who have experienced significant adverse effects from the use of statins. The most commonly reported adverse effects on this forum include:

Gout, Numbness / Tingling of the Hands/Feet, Muscle ~ Weakness, Cramps, Spasm, Stiffness, Insomnia, Loss of Libido, Impotence, Heart Palpitations, Heart Arrhythmias, Depression, Short Term Memory Loss, Long Term Memory Loss, Transient Global Amnesia, Neck and Shoulder Pain, Fatigue, Migraine, Headaches, Chest Pain, Digestive Disorders, Trouble Walking (Shuffling), Trouble Walking (Balance), Hand Tremors, Speech - Trouble finding the right word, Slurred Speech, Dizziness, Sciatica Pain.

Although this data is not part of a clinical trial it does provide testament to the wide range of adverse effects experienced in the real world with real people.  

Before I make the decision whether or not to lower my cholesterol through medication, I would be very grateful if you could provide a response to the points raised above.

Thank you very much for your consideration.

Yours sincerely,

 References:

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[1] Smith, J 2009 $29 Billion Reasons to Lie about Cholesterol: Making Profit by Turning Healthy   People into Patients Troubador Publishing, Leicester

[2] Blood Cholesterol Chapter 10 of the British Heart Foundation Coronary Heart Disease Statistics. July 2007

[3] Durrington, P Dyslipidaemia Lancet 2003; 362:717-731

[4] Tonkin, AM et al. Effects of Pravastatin in 3260 Patients with Unstable Angina: Results from the LIPID Study Lancet 2000; 355:1871-1875

[5] Rubins, HB et al. Distribution of Lipids in 8,500 Men with Coronary Artery Disease American Journal of Cardiology 1995; 75:1202-1205

[6] Sachdeva, A et al Lipid Levels in Patients Hospitalized with Coronary Artery Disease: An analysis of 136,905 Hospitalizations in Get with the Guidelines American Heart Journal 2009; 157:111-117

[7] Carroll, MD et al Trends in Serum Lipids and Lipoproteins of Adults, 1960-2002 Journal of the American Medical Association 2005; 294:1773-1781

[8] BBC Radio 4 Program “The Investigator” April 3, 2008 20:00hrs GMT

[9] Sever, PS et al. Prevention of Coronary and Stroke Events with Atorvastatin in Hypertensive Patients who have Average or Lower-Than-Average Cholesterol Concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA): A Multicentre Randomised Controlled Trial Lancet 2003; 361:1149-1158

[10] Krumholz, H et al. “Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause Mortality in Persons Older Than 70 Years” Journal of the American Medical Association 1994; 272:1335-1340

[11] Weverling-Rijnsburger, AW et al. “Total Cholesterol and Risk of Mortality in the Oldest Old” Lancet 1997; 350:1119-1123

Wheat and Heart Disease (Ch 10)

"So it's not really about cholesterol. It's about the particles that cause atherosclerosis. Today you and I are able to directly quantify and characterize lipoproteins, relagating cholesterol to join frontal lobotomies in the outdated medical practice garbage dump in the sky."

Wheat Belly - William Davis, MD  (p 148)
www.rodalebooks.com

60-Year Old Man Dies of High Cholesterol

60-year old man dies of high cholesterol

from Heart Scan Blog by Dr. William Davis

Never saw a headline like this? Neither have I. That’s because it doesn’t happen.

Cholesterol doesn’t harm, maim, or kill. It is simply used as a crude–very crude–marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a “dipstick,” for lipoproteins in the blood to those who don’t understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It’s not about cholesterol; it’s about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL’s relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It’s bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don’t get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.