The Cholesterol Myths - Ravnskov

Did you know. . . 

        

. . . that cholesterol is not a deadly poison, but a substance vital to the cells of all mammals? 

               

. . . that your body produces three to four times more cholesterol than you eat? 

                

. . . that this production increases when you eat only small amounts of cholesterol and decreases when you eat large amounts? 

                

. . . that the  “prudent” diet, low in saturated fat and cholesterol, cannot lower your cholesterol more than a small percentage? 

                

. . . that the only effective way to lower cholesterol is with drugs? 

                

. . . that the cholesterol-lowering drugs are dangerous to your health and may shorten your life?

                 

. . . that the cholesterol-lowering drugs, called statins, do lower heart-disease mortality a little, but this is because of effects other than cholesterol lowering? Unfortunately, they also stimulate cancer. 

                

…that you may become aggressive or suicidal if you lower your cholesterol too much? 

                

…that polyunsaturated fatty acids, those which are claimed to prevent heart attacks, stimulate infections and cancer in rats? 

                

…that if you eat too much polyunsaturated oil you will age faster than normal? You will see this on the outside as wrinkled skin. You can’t see the effects of premature aging on the inside of your body, but you will certainly feel them. 

                

…that people whose blood cholesterol is low  become just as atherosclerotic as people whose cholesterol is high? 

        

…that more than thirty studies of more than 150,000 individuals have shown that people who have had a heart attack haven’t eaten more saturated fat or less polyunsaturated oil than other people? 

                

…that old people with high cholesterol live longer than old people with low cholesterol? 

                

…that high cholesterol protects against infections? 

                

…that many of these facts have been presented in scientific journals and books for decades but proponents of the diet-heart hypothesis never tell them to the public? 

                

…that the diet-heart idea and the cholesterol campaign create immense prosperity for researchers, doctors, drug producers and the food industry?

"Dr. Ravnskovs contention is that the diet-heart idea is built on sand. He leads us through the history of the concept in an interesting and readable way. His writing clearly demonstrates the enormous depth and range of his reading on this subject. Step by step he examines the evidence for the diet-heart idea, and step by step he shows us how that evidence may be flawed and contradicted by other research that is rarely acknowledged and quoted."

 ~ Michael Gurr, PhD

Terrific response to Uffe Ravnskov's offer to view “The Cholesterol Myths” at  http://www.ravnskov.nu/CM 
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Read the complete article here.

Red Meat and trimethylamine N-oxide - Kresser

Red Meat and TMAO: Cause for Concern, or Another Red Herring?

By Chris Kresser on April 10, 2013 

 

 

I’m sure many of you have seen reports on a recent study published in the journal Nature suggesting a possible mechanism linking red meat consumption to heart disease. The day after one such report was published in the New York Times, I received numerous emails and numerous Facebook and Twitter messages from concerned red meat enthusiasts. This is understandable, but rest assured it’s not yet time to switch over to soy burgers.

 

The researchers in this study published a paper a while back proposing that a chemical called TMAO (trimethylamine N-oxide) increases the risk of heart disease. In this study, they hypothesized that eating red meat may increase levels of TMAO in the bloodstream, which would intern ramp up your chances of having a heart attack. Sounds plausible, right?

 

There’s another hypothesis that also seemed plausible for why red meat increases the risk of heart disease (if we even accept that, which I do not; more on this in a moment). It’s called the “diet-heart hypothesis”, and you’re all very well aware of it whether you know it by name or not. It holds that eating cholesterol and saturated fat increase cholesterol levels in the blood, and high cholesterol levels in the blood cause heart disease. This theory became so widely accepted that few people even question it anymore. The problem is it’s simply not true. Recent research has shown that dietary saturated fat and cholesterol are not associated with heart disease after all, and even if they were, high cholesterol levels in the blood are not the culprit. I’ve written about this extensively in the past, and I will be starting a brand new series with updated information this month.

 

The mistaken blame of saturated fat and cholesterol as drivers of heart disease led to a decades-long campaign to encourage low-fat, high-carbohydrate diets. Unfortunately, the effects of this campaign were not harmless. Not only did it unnecessarily deprive people of nutrient-dense, nourishing (and delicious!) foods like meat, butter and eggs, it may have indirectly contributed to the epidemics of obesity, heart disease and diabetes. Studies have shown that when people replace saturated fat with carbohydrates, the risk of heart disease doesn’t go down—it goes up. (1) This is not because of the carbohydrates, per se, but because 85% of the grain consumed in the U.S. is in the highly refined form. (2)

 

The diet-heart hypothesis should be a cautionary tale that prevents us from jumping to rash conclusions based on limited evidence. Alas, the almost complete lack of criticism or scrutiny in the popular media reports on this study indicate that caution has been thrown to the wind. Let’s now examine three reasons why I’m not yet ready to take the conclusions of this study (i.e. red meat causes heart disease via TMAO) at face value.

Epidemiological evidence is inconsistent

If red meat consumption elevates TMAO, and elevated TMAO increases the risk of heart disease, we’d expect to see higher rates of heart disease in people that eat more red meat. The epidemiological evidence examining this question is mixed. A large meta-analysis published in Circulation by Micha et al. covering over 1.2 million participants found that consumption of fresh, unprocessed red meat is not associated with increased risk of coronary heart disease (CHD), stroke or diabetes. (3) On the other hand, a smaller prospective study including about 121,000 participants from the Nurses Health Study and Health Professionals Follow-up Study did find an association between red meat consumption (both fresh and processed) and total mortality, cardiovascular disease (CVD) and cancer. (4)

 

If eating meat increases heart disease risk we might expect lower rates in vegans and vegetarians. Early studies suggested this was true, but later, better-controlled studies suggest it’s not. The early studies were poorly designed and subject to confounding factors (i.e. vegetarians tend to be more health conscious on average than general population, so there could be other factors explaining their longevity, such as more exercise, less smoking, etc.). Newer, higher quality studies that have attempted to control for these confounding factors haven’t found any survival advantage in vegetarians. For example, one study compared the mortality of people who shopped in health food stores (both vegetarians and omnivores) to people in the general population. They found that both vegetarians and omnivores in the health food store group lived longer than people in the general population. (5) This suggests, of course, that eating meat in the context of a healthy diet does not have the same effect as eating meat in the context of an unhealthy diet. (Hold this thought: we’ll be coming back to it shortly.) A very large study performed in the U.K. in 2003 including over 65,000 subjects corroborated these results: no difference in mortality was observed between vegetarians and omnivores. (6)

 

Taken together, these data do not suggest a strong relationship between red meat and heart disease. It’s also crucial to remember that epidemiological evidence does not prove causality. Even if red meat intake is associated with a higher risk of CVD (or any other health problem), such studies don’t tell us that red meat is causing the problem. If you’re new to this concept, I suggest reading these excellent articles by Denise Minger and Chris Masterjohn.

The “healthy user bias” strikes again

The healthy user bias is the scientific way of explaining the phenomenon I described above, where people that engage in one behavior that is perceived as healthy (whether it is or not) are more likely to engage in other behaviors that are healthy. (7, 8) Of course the flip-side is also true: those that engage in behaviors perceived to be unhealthy are more likely to engage in other unhealthy behaviors. The healthy user bias is one of the main reasons it’s so difficult to infer causality from epidemiological relationships. For example, say a study shows that eating processed meats like bacon and hot dogs increases your risk of heart disease. (9) Let’s also say, as the healthy user bias predicts, that those who eat more bacon and hot dogs also eat a lot more refined flour (hot dog and hamburger buns), sugar and industrial seed oils, and a lot less fresh fruits, vegetables and soluble fiber. They also drink and smoke more, exercise less and generally do not take care of themselves very well. How do we know, then, that it’s the processed meat that is increasing the risk of heart disease rather than these other things—or perhaps some combination of these other things and the processed meat? The answer is, we don’t. Good studies attempt to control for some of these confounding factors, but inevitably some will not be controlled for. And one of the most important potential confounding factors that is never controlled for is the gut microbiome.

 

Numerous studies, which I’ve written about on this blog and spoken about on my podcast, suggest that the balance of bacteria in our gut may be one of the most important factors—if not the most important—that determines our overall health. Gut dysbiosis (an imbalance between healthy and unhealthy bacteria in the gut) and small intestine bacterial overgrowth (SIBO, a condition involving an inappropriate overgrowth of bacteria in the gut) have been linked to health problems as diverse as skin disease, depression, anxiety, autoimmunity, and hair loss.

 

The study we’re discussing here found that those who eat red meat produce TMAO, whereas vegans and vegetarians who hadn’t eaten meat for at least a year do not. The researchers claimed that this means eating red meat must alter the gut flora in a way that predisposes toward TMAO production. However, there’s another explanation that I believe is much more plausible: the red meat eaters are engaging in unhealthy behaviors that have led to dysbiosis and/or SIBO. This could include eating fewer fruits and vegetables and less soluble fiber, and more processed and refined flour, sugar and seed oils. All of these behaviors have been shown to be more common in the “average” red meat eater, and all of them have been associated with undesirable changes in the gut microbiota. (10, 11, 12) In other words, the problem isn’t the red meat, it’s the gut bacteria. This is supported by the finding in the study that the red meat eaters did not produce TMAO after a course of antibiotics. It is also supported by data indicating that a breakdown in the intestinal barrier, which occurs in dysbiosis and SIBO, may increase heart disease risk by elevating the number of circulating LDL particles in the bloodstream. (13) I will be covering this (i.e. the connection between LDL particles and heart disease) in my updated series on heart disease.

 

In the last section I presented evidence suggesting that eating meat in the context of a healthy diet does not have the same effect as eating it in the context of an unhealthy diet. This study is likely yet another example. In order to know whether red meat is really to blame for changes in the gut flora that increase TMAO production, we’d have to do another study with two groups: one that follows a Paleo diet rich with fruits, vegetables and soluble fiber, as well as red meat; and another vegan/vegetarian diet with equivalent amounts of plant matter and no meat. If the Paleo diet followers still had higher levels of TMAO, this hypothesis would be a lot stronger.

The jury is still out on TMAO

The evidence linking TMAO production to eating red meat, and serum TMAO levels to heart disease, is not as cut-and-dry as the study authors suggest. For example:

• The Nature paper on TMAO contained data from two studies: an epidemiological study on humans, and a clinical study on mice. The human study compares a single vegan that they managed to convince to eat a steak to a single “representative” meat-eater. A single person in each group is not an adequate sample size, and is hardly convincing given the wide variation in the response to carnitine (see next bullet) among meat-eaters.

• The mouse study used a carnitine supplement. While it is well established that free carnitine increases TMAO production, previous studies have not shown that carnitine-rich foods like red meat increase TMAO. In fact, in one 1999 study, out of 46 different foods tested, including red meat, only one food elevated TMAO levels in the participants: seafood (see graph to right, from Chris Masterjohn’s article referenced below). This makes perfect sense since trimethylamine occurs naturally in seafood. Does this mean we should cut back on fish and shellfish because they’re going to give us a heart attack?(15)

Another obvious question we should ask is whether there are alternative explanations for why we see elevated TMAO levels in meat or seafood eaters (if indeed we do see them in a wide sample of meat eaters, which at least one earlier study didn’t support)? According to a 2011 article by Chris Masterjohn touching on TMAO in a different context: (16)

Elevated TMAO could reflect dietary trimethylamine or TMAO from seafood, but it could also reflect impaired excretion into the urine, or enhanced conversion of trimethylamine to TMAO in the liver.

The enzyme Fmo3 carries out this conversion, mainly in the liver, as reviewed here. There are a number of genetic variants affecting the activity of this enzyme, some of which appear only in certain ethnicities, and the enzyme also processes a number of drugs used to treat psychoses, infections, arthritis, gastro-esophageal reflux disease (GERD), ulcers, and breast cancer. Iron or salt overload may also increase the activity of the enzyme. TMAO could, then, be a marker for ethnicity, drug exposure, genetically determined drug efficacy, or other conditions.

As you can see, it’s overly simplistic to suggest that eating red meat causes elevated TMAO; there are many other factors at work.

But even if Paleo meat eaters have higher TMAO levels than vegans and vegetarians, we still don’t have evidence proving a causal relationship between TMAO and CVD. Once again, the supposed link between cholesterol and saturated fat and heart disease should serve as a reminder not to jump to hasty conclusions that unnecessarily deprive people of nutrient-dense, healthy foods. It is virtually impossible to control for all of the possible confounding factors, and the study we’re discussing in this article only further highlights this problem.

Conclusions

I’d like to end with an observation from the discussion section of the TMAO paper. The authors state:

Numerous studies have suggested a decrease in atherosclerotic disease risk in vegan and vegetarian individuals compared to omnivores; reduced levels of dietary cholesterol and saturated fat have been suggested as the mechanism explaining this decreased risk. Notably, a recent 4.8-year randomized dietary study showed a 30% reduction in cardiovascular events in subjects consuming a Mediterranean diet (with specific avoidance of red meat) compared to subjects consuming a control diet.

This might sound like damning evidence against red meat. However, when you look at Table One in Mediterranean Diet trial, you’ll find that the Mediterranean diet allowed more red meat than the control diet (a low-fat diet)! The Mediterranean Diet allowed for “one serving or less of red or processed meat per day“, whereas the low-fat diet only permitted “one serving or less of red or processed meat per week“. (You can see this for yourself. Click here to access the PDF version of the study, then scroll down to Table One.) Clearly this paper does not support the authors’ conclusion that red meat increases the risk of heart disease.

They also claim that vegan and vegetarian diets reduce the risk of atherosclerotic disease compared to omnivorous diets; but the studies they reference fail to adequately control for the “healthy user bias”.

The study I mentioned in the beginning of this article compared heart disease risk amongst omnivores and vegetarians that shop at health food stores (which is a big step toward reducing healthy user bias), and did not find a difference in deaths from heart disease, stroke or all causes.
If you read the media reports and full-text of this study, you might have noticed something interesting. The study itself, and even most of the media article about it, quite simply and without much fanfare stated that saturated fat and cholesterol have little to do with the supposed increase in heart disease observed with red meat consumption. Hold the press! Shouldn’t THAT be front-page news?!? Apparently not. Of course, they’re only willing to admit this publicly in the context of an article where they’re proposing yet another mechanism for how red meat will kill you.

Finally, the most remarkable and sad part of this for me is seeing just how deep most people’s fear and distrust of red meat is, even if they’ve been following a Paleo diet for a long time. The day after the TMAO study was published, I woke up to no fewer than 20 emails and the same number of Facebook messages and Tweets from people expressing concern that their choice to eat red meat might be killing them. It really is a testament to the power of brainwashing. Most of us grew up with the idea that red meat is harmful, and it’s perhaps not so easy to leave that behind—even when you think you have.

Chris Masterjohn is working on a detailed analysis of the data from this paper, which should be ready soon. I believe we may be seeing more “red meat is bad because of TMAO” studies in the near future, so as always, when you see a media report on such a study, take it with a heavy grain of salt (which, by the way, doesn’t cause high blood pressure in most people!).
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Read the complete article here.
Also read more here.

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Sent Wednesday, November 23, 2011

Diet Heart News, volume 1, number 8

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Since the early 1950s, mainstream researchers have been seeking the cause of atherosclerosis and heart disease spearheaded early on by University of Minnesota professor and American Heart Association board member Ancel Keys. The result - the 50 year old Diet Heart or Cholesterol Hypothesis: If you eat too much food containing cholesterol and/or saturated fat, the level of cholesterol in your blood will rise. The excess cholesterol will be deposited in artery walls, causing them to thicken and narrow. In time, this will block blood supply to the heart or brain causing a heart attack or stroke. According to this still unproven but enduring hypothesis, high blood cholesterol is caused by an atherogenic diet high in cholesterol and saturated fat - found mainly in animal products such as red meat, whole milk, eggs, butter - and the tropical saturates coconut and palm. In this scenario, high blood cholesterol is the main cause of atherosclerosis and heart disease. The medical and nutrition communities and various government agencies have been behind Diet Heart ever since. If animal fat and high blood cholesterol are the chief villains, then cholesterol-lowering diets and cholesterol-lowering drugs would appear to be wise choices. But 50 years later - after a lengthy test of time - the incidence of heart disease has not gone down as promised, and researchers like science writer Gary Taubes have uncovered a great deal of their evidence that is unsupportable, contradictory, and hopelessly wrong. A look at the recent five year UCLA/AHA Study The UCLA research team used an American Heart Association database that included 541 hospitals across the country. The database provided detailed information on 136,905 patients hospitalized for cardiovascular disease whose lipid levels upon hospital admission were documented. The results after five years: 75 percent of patients hospitalized for a heart attack had LDL cholesterol below 130 mg/dl - in the so called safe range. Even more astounding, 50 percent of patients had LDL below 100 mg/dL - considered optimal. (21 percent of the patients were taking a statin cholesterol-lowering drug.) Now don't you think that the UCLA researchers would have concluded that there was no association between elevated LDL and risk of heart attacks? After all, this was a five year study of heart attacks suffered by 136,905 patients in an American Heart Association database that included records from 541 hospitals. Yes - this should have been the nail in the coffin for the Diet Heart or Cholesterol Hypothesis, but not according to study director Dr. Gregg C. Fanarow, Professor of Cardiovascular Medicine and Science, David Geffen School of Medicine, UCLA, who concluded: "Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk... " May not be low enough! Low cholesterol is already associated with depression and death by accidents, cancer and violence. According to the American Heart Association's journal Circulation, 1992; 86:3, the all cause death rate increases when total cholesterol drops below 180. Isn't there sufficient evidence now to conclude that elevated LDL and total cholesterol are not the cause of heart attacks and that the cholesterol hypothesis should be discarded along with official low fat diets and cholesterol-lowering drugs? Don't hold your breath! UK cardiologist Dr. Malcolm Kendrick: "I have come to realize that there is, literally, no evidence that can dent the cholesterol hypothesis... The effect of this study on the cardiovascular research community was....as you would expect...nothing at all, a deafening silence..." Dr. Fonarow disclosed that he has conducted research for GlaxoSmithKline and Pfizer and serves as a consultant and has received honorarium from the following drug companies: Abbott, AstraZeneca, GlaxoSmithKline, Merck, Pfizer and Schering Plough. Dr. H. Bryan Brewer, a physician-scientist at the National Heart, Lung and Blood Institute, failed to disclose his ties to AstraZeneca. Brewer had previously written a glowing report in a medical journal about Crestorwithout disclosing that he is a paid consultant and had presided over a company-sponsored symposium." He and the others forgot! Earlier in 2004, the doctors in the National Cholesterol Education Program (NCEP) who wrote the current cholesterol guidelines and, in effect, control cardiology, failed to disclose that six of the nine authors had direct financial ties to the makers of statin drugs, including: Pfizer's Lipitor, Bristol-Myers Squibb's Pravachol, Merck's Lovastatin, and AstraZeneca's Crestor. The new more stringent cholesterol-lowering guidelines boosted statinsales from $15 billion in 2004 to over $23 billion in 2005. And now the UCLA study provides more proof that lowering cholesterol with drugs or diet will not reduce cardiovascular disease or the risk of heart attack. But as Winston Churchill said: "Men occasionally stumble over the truth, but most of them pick themselves up and hurry off as if nothing had happened." [especially if there is money to be made]. ================================================================= Read the complete article here.

The Great Cholesterol Cover-Up STATIN NATION

Statin Nation - The Movie

For more preview clips, please click here
Film Synopsis:
We are told that cholesterol is a major cause of heart disease. At least 40 million people are currently taking cholesterol-lowering medications, known as statins, and millions more people are avoiding foods that contain saturated fat and cholesterol.

The basic idea is that dietary saturated fat raises cholesterol levels, and these two substances somehow clog-up our arteries, causing a heart attack. This idea is often referred to as the diet-heart hypothesis.

However, a numbers of doctors and researchers have been challenging this hypothesis for decades, and the latest heart disease statistics reveal some alarming facts. Such as:

● People with high cholesterol tend to live longer

● People with heart disease tend to have low levels of cholesterol

● Cholesterol-lowering of a population does not reduce the rate of heart disease

In addition, despite their widespread use, and description as “wonder drugs” statin medications do not extend life for the majority of people who take them.

Cholesterol-lowering has become a huge global industry, generating at least $29 billion each year. Have the facts about heart disease, cholesterol and cholesterol medications been distorted by pharmaceutical companies and food manufacturers keen to increase their profits?

If the focus on cholesterol has been a mistake, then the greatest cost is associated with the lost opportunity to tackle heart disease.

Producer/Director: Justin Smith
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Check it out here.

Statination: The Great Cholesterol Cover-Up

$tatination: The Great Cholesterol Cover-Up.


For more preview clips, please click here
Film Synopsis:

We are told that cholesterol is a major cause of heart disease. At least 40 million people are currently taking cholesterol-lowering medications, known as statins, and millions more people are avoiding foods that contain saturated fat and cholesterol.

The basic idea is that dietary saturated fat raises cholesterol levels, and these two substances somehow clog-up our arteries, causing a heart attack. This idea is often referred to as the diet-heart hypothesis.

However, a numbers of doctors and researchers have been challenging this hypothesis for decades, and the latest heart disease statistics reveal some alarming facts. Such as:

● People with high cholesterol tend to live longer
● People with heart disease tend to have low levels of cholesterol
● Cholesterol-lowering of a population does not reduce the rate of heart disease

In addition, despite their widespread use, and description as “wonder drugs” statin medications do not extend life for the majority of people who take them.

Cholesterol-lowering has become a huge global industry, generating at least $29 billion each year. Have the facts about heart disease, cholesterol and cholesterol medications been distorted by pharmaceutical companies and food manufacturers keen to increase their profits?

If the focus on cholesterol has been a mistake, then the greatest cost is associated with the lost opportunity to tackle heart disease.

Who is Justin Smith?
For 4 years, Justin was based at the BBC in West London as a personal trainer, sports massage therapist and nutrition coach.

In 2007, Justin set out to write a book about common nutritional myths. At this time, he was already aware of the issues surrounding cholesterol and planned to devote one chapter of his book to this subject. However, after looking into the subject in more detail, he was shocked to find just how much evidence, contrary to the diet-heart hypothesis, existed. The natural progression was to base his whole book on this subject.

Justin's book $29 Billion Reasons to Lie About Cholesterol was published in 2009, and the following year, he started the preliminary work on the documentary film Statin Nation.
Before his career as a health practitioner, Justin obtained a degree in engineering. He believes that this scientific background has provided him with the ability to evaluate published research and the conclusions that are drawn from it.

Justin was also a competitive cyclist for nine years.
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Read the full article here.

Why you should eat more (not less) cholesterol - Chri

Why you should eat more (not less) cholesterol

For decades now, the general American population has been neurotically avoiding cholesterol-rich foods for fear of developing heart disease, thanks to the promulgation of the unfortunate Diet-Heart hypothesis. (1)

Those of us that follow a paleo diet are well aware by now that dietary cholesterol does not significantly affect cholesterol levels in the blood or risk for heart disease, and that there is no reason to avoid whole foods with naturally high levels of cholesterol.

However, beyond just ‘not avoiding’ high cholesterol foods, there is a significant reason for us to make a special effort to include many high cholesterol foods in our diet.

The reason? The much under-appreciated B-vitamin called choline, found primarily in cholesterol-rich foods.

If you haven’t heard of choline, or don’t know much about this vital nutrient, you’re not alone. Choline has only been ‘officially’ recognized as an essential nutrient since 1998, when the Food and Nutrition Board of the Institute of Medicine established an Adequate Intake (AI) level of 425 mg per day for women and 550 mg per day for men. (2) Even though it has been deemed a nutrient vital for human health, only 10% of Americans are meeting the conservative AI levels established by the IOM.

If you eat a strict paleo diet, you may be closer to meeting your choline needs than the average American, but only if you are regularly including choline rich foods in your diet. The best whole food sources of dietary choline are egg yolks and liver, which are often avoided by many Americans due to unfounded fear of dietary fat and cholesterol. However, these high cholesterol foods are at the top the choline-rich foods list, followed (albeit distantly) by beef, cod, brussels sprouts, and broccoli. (3)

Why is choline such an important nutrient to consider in one’s diet?

Choline has a variety of functions in the body, including the synthesis of the neurotransmitter acetylcholine, cell-membrane signaling, lipid transport, and methylgroup metabolism. (4) In addition, it is an essential component of the many phospholipids that make up cell membranes, regulates several metabolic pathways, and aids detoxification in the body. During pregnancy, low choline intake is significantly associated with a higher risk of neural tube defects in the newborn.

Choline deficiency over time can have serious implications for our health. Symptoms of choline deficiency include fatigue, insomnia, poor kidney function, memory problems, and nerve-muscle imbalances. Extreme dietary deficiency of choline can result in liver dysfunction, cardiovascular disease, impaired growth, abnormalities in bone formation, lack of red blood cell formation, infertility, kidney failure, anemia, and high blood pressure. Incredibly, choline deficiency is the only nutrient deficiency shown to induce the development of spontaneous carcinoma. (5)

Chris Masterjohn has written extensively about choline deficiency and its relationship to fatty liver disease which affects as many as 100 million Americans and is often attributed to excess alcohol and sugar consumption by conventional practitioners. After a review of the literature, Masterjohn concludes that choline deficiency plays a role in virtually every type of diet-induced fatty liver model, and that adequate dietary choline is essential for proper liver function. He also suggests that high consumption of dietary fat, including saturated fats, increases the amount of choline required to prevent the accumulation of fat in the liver. (6)

This means that if you’re eating a higher fat diet, it is even more crucial that you include a variety of choline rich foods in your diet.

Another important factor to consider is that while humans are able to produce some level of endogenous choline, some people have a common gene variation that further increases the amount of choline they must consume to satisfy their body’s requirements. (7) These particular people are more susceptible to choline deficiency, and must be especially vigilant about including choline rich food in their diets.

As choline is so important, you may be wondering what the best food sources are in order to improve your intake. There are many natural, whole foods that are excellent sources of bioavailable choline, with the best sources being beef liver, poultry liver, and whole eggs. (8) These foods are not only high in choline, but are also very high in many different vitamins and minerals such as as vitamin A, arachidonic acid, DHA, and the B vitamins. (9)

We already know liver is an amazing superfood. Liver from pastured animals is a great source of trace elements such as copper, zinc and chromium, plus highly bioavailable folate and iron. (10)

Liver is also the most potent source of dietary choline that we know of.

For example, a three ounce serving of pan-fried beef liver has over 400 mg of choline in it, compared to less than 80 mg in the same amount of cooked ground beef. (11) While you don’t need to consume beef liver on a daily basis to reap the benefits of this superfood, it should be clear that including pastured liver and other organ meats as part of a nutritionally complete diet is one of the best ways to improve your health and prevent the many types of chronic disease caused by nutrient deficiencies.
If you’re not used to including lots of liver and whole eggs in your regular meal plan, give a few of the following recipes a try. It’s never too late to start incorporating more choline into your diet!

Liver recipes: get your choline!

• http://cavegirleats.com/2011/09/09/baked-liver-pate-yum-seriously-seriously
• http://balancedbites.com/2011/05/easy-recipe-chicken-liver-pate.html
• http://paleodietlifestyle.com/simple-and-delicious-liver-pate-recipes/
• http://www.foodnetwork.com/recipes/ina-garten/chopped-liver-recipe/index.html
• http://www.foodrenegade.com/egg-drop-soup/
• http://nomnompaleo.com/post/1983505174/easy-paleo-frittata
• http://www.theclothesmakethegirl.com/2011/01/17/dont-be-lily-livered-aromatic-chickenlivers/
• http://www.theclothesmakethegirl.com/2010/05/17/scotch-eggs-a-k-a-protein-pellets/
• http://www.primal-palate.com/2011/01/root-vegetable-hash-with-poached-egg.html

Read the complete article here.

The Diet Heart Hypothesis was just that - a Hypothesis.... a thought up scheme, never proven.

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Sunday, January 23, 2011 Here Comes Another $$$ Spinner

Seems there is talk in the food industry that the Fat is bad for you hypothesis is about to lie down and die! Can't say I am sorry, should have happened years ago - sorry Ancel Old Chap!

But why now you may ask...... what could possibly bring on such a huge about face? Couldn't possibly have anything to do with the fact that patents on some pharmaceuticals like Lipitor are or have already run out could it?

The Diet Heart Hypothesis was just that - a Hypothesis.... a thought up scheme, never proven. But because it was making so much money for the investors and companies involved, they fought long and hard to get everyman (grin) and his dog on board and popping their pills.

Now the pills will not make them so much money, they have to look for the next BIG blockbuster drug, with its own peculiar methodology and religion ... to drum up fervor and zeal, thereby making gazillions for the companies and their investors.

Watch out folks the fat is bad religion is about to have a HUGE about face! (please note italics are from the actual article)

However the very foundation of this hypothesis was shaken to the core at the AHA annual conference in Chicago in 2010. Amid great excitement, the pharmaceutical giant Merck revealed results of a preliminary safety study for a drug that could usher in a new age for treatment and prevention of heart disease: a cholesterol raising drug! In the safety study lasting 18 months with 1,600 participants, total cholesterol was raised 20% by the drug anacetrapib without any side effects. An efficacy trail of 30,000 participants with several cardiovascular end-points is scheduled to begin in 2011 and end in 2015 to verify if cholesterol raising can reduce actual incidence of heart disease. But the search for cholesterol raising drugs is not new. Most of the cholesterol lowering statin drugs have reached the limits of their heart protective capabilities (and are near the end of their patent lives). For several years drug companies have been quietly searching for the next blockbuster that will be more effective than statins. One class of candidates is cholesterol raising drugs.

Get ready to throw away your Lipitor folks, they will have a new drug to prescribe you in the near future. I can't wait to see how this unfolds, how they will explain away the untold damage they have done to humankind, by insisting we lower our cholesterol numbers, to unhealthy levels.

But haven't we been told over and over to lower our cholesterol, not increase it? Yes, but the cholesterol story has been repeatedly oversimplified. Total cholesterol is made up of 2 major components, good cholesterol (LDL) and bad cholesterol (HDL). So when your doctor tells you to lower your cholesterol, he really means lower your bad cholesterol – if you inadvertently lower your good cholesterol you could increase your risk of heart disease. The statin drugs selectively lower the bad cholesterol without lowering the good – and they work, reducing risk of heart attack by about 30%. The new class of drugs is designed to increase the good cholesterol, without increasing the bad. So in this case increasing cholesterol is a good thing. The scientific community is hoping that the upcoming Merck study will show a further reduction in risk of heart attack similar in magnitude to the statins – a real breakthrough.

As far as I am concerned, that statement above in red (coloured by me) is a barefaced lie, manufactured by the pharmaceutical industry to keep doctors pushing these drugs onto their patients!

Where does this leave the diet heart hypothesis, saturated fat and the simplified "lower your cholesterol" story? It leaves it in deep trouble. The advent of drugs that increase good cholesterol and thereby reduce risk of heart disease (yet to be proven), will force scientists to take another look at the effects of food ingredients on good cholesterol, not just the total and the bad. Applying this new approach could have a significant impact on national dietary recommendations that are designed to reduce risk of heart disease.

Ohhhh I can hardly wait to see the advertising campaign they work up for this new scheme. Hopefully they will turn the Food Pyramid upside down, while at the same time telling us that fats are good for us! I can dream can't I?

A large body of data showing the effect of food ingredients on both good and bad cholesterol has already been generated over the last 40 years. So far, the evaluation of this data has mostly focused on the bad cholesterol, while neglecting or even ignoring data for good cholesterol. But a review of the data for saturated fat gives a very unexpected result. The food component that increases good cholesterol the most is saturated fat! Yes, the same "artery clogging" saturated fat that has been demonized for decades. Although saturated fat still raises bad cholesterol, it appears that it raises good cholesterol by an equivalent amount and the effect of the bad cholesterol is mostly cancelled out. In this scenario saturated fat is expected to have little or no effect on risk of heart disease.

UFFE was right folks. Eat fat and live!

But good and bad cholesterol are components of blood, and not actual disease. What about direct evidence for the effect of saturated fat on incidence of heart disease? Early in 2010 a large human study measuring the link between intake of food components and heart disease was published. The study included over 340,000 people spanning 23 years. Here is what the authors said about saturated fat: "…there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD." Or in plain English - saturated fats have no effect on heart disease. Although this statement appears to fly in the face of everything we have been taught for decades, it corresponds exactly with powerful ability of saturated fat to increase good cholesterol. Neglect of the positive effect of saturated fat on good cholesterol has made it look worse that it really is.

A convincing body of evidence already exists that saturated fat is not as bad as once thought. Nevertheless public policy continues to demand further big reductions in saturated fat intake. The 2010 Dietary Guidelines Advisory Committee (DGAC) recommended reducing saturates by 5% of the diet. If this huge reduction was ever implemented, the US dairy and meat industries - the main dietary source of saturated fat - would be severely damaged, and all for nothing. Isn't it time to abandon the failed Diet Heart Hypothesis and focus our resources on issues that really make a difference to public health?

The Diet Heart Hypothesis is DEAD folks..... time we buried it and moved on.... be be very very careful, they will make a pill, another blockbuster drug to raise your HDL folks..... when all you need to do is reduce your carbohydrates, white breads, simple starches, junk foods etc, and go back to eating good health fats again.

I wonder how they will breed the fat back into the food chain? Could it be as simple as feeding cattle on grass, and stopping the hormones?

Above Article from: Food Processing.com
Also worth a read:
The Dirty Little Secret of the Diet-Heart Hypothesis
WHY THE CHOLESTEROL-HEART DISEASE THEORY IS WRONG  Dr. Malcolm Kendrick M.D.

Cholesterol: Friend Or Foe?

Natasha Campbell-McBride, MD, wrote an article with the title "Cholesterol: Friend Or Foe? " that appears here. Her last paragraph states:

"In conclusion, cholesterol is one of the most important substances in the body. We cannot live without it, let alone function well. The pernicious diet-heart hypothesis has vilified this essential substance. Unfortunately, this hypothesis has served many commercial and political interests far too well, so they ensure its long survival. However, the life of the diet-heart hypothesis is coming to an end as we become aware that cholesterol has been mistakenly blamed for the crime just because it was found at the scene."


Please avail yourself of the full article. You may find out some almost new information about cholesterol.



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Does Dietary Saturated Fat Increase Blood Cholesterol?

Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational Studiesfrom Whole Health Source by wholehealthsource@yahoo.com (Stephan)The diet-heart hypothesis states three things:


1. Dietary saturated fat increases blood cholesterol

2. Elevated blood cholesterol increases the risk of having a heart attack

3. Therefore, dietary saturated fat increases the risk of having a heart attack

To evaluate the second contention, investigators have examined the relationship between blood cholesterol and heart attack risk. Many studies including MRFIT have shown that the two are related (1):

The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.

Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These are the studies on which the diet-heart hypothesis was built.

But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks**?

I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between saturated fat intake and blood cholesterol, they haven't found one. Those findings have essentially been ignored, but let's have a look...

The Studies

It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.

The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method was much more thorough than in most observational studies today***. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They twisted the data every which way, but were never able to squeeze even a hint of an association out of it:

Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.

The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:

Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.

They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk****.

The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method*****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends little or no support to the hypothesis.

Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).

This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was mostly white rice in some areas. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and perhaps bordering on malnourishment.

In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold change in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's being trumped by other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat an impoverished diet that differs in many ways from the diets at the upper end of the range.

The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no hint of a relationship between saturated fat intake and blood cholesterol.

Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.

Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol. If it's a factor at all, it must be rather weak, which is consistent with what has been observed in multiple non-human species (13). I think it's likely that the diet-heart hypothesis rests in part on an over-interpretation of short-term controlled feeding studies. I'd like to see a more open discussion of this in the scientific literature. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a small long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.

The Diet-heart Hypothesis: Stuck at the Starting Gate

Animal Models of Atherosclerosis: LDL

* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.

** Besides the fact that it's a logical fallacy. Just because A causes B, and B causes C, does not mean A causes C.

*** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.

**** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.

***** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators made no effort to adjust for confounding variables.
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The above was copied from Whole Health Source

The Dirty Little Secret of the Diet-Heart Hypothesis

I constantly keep my eye out for 'Credible Evidence' related especially to my own health issues which you should be able to tell if you have read this or any of the posts on this blog, is coronary artery disease.

I have just discovered Stephan Guyenet's blog Whole Health Source. In particular a recent post titled "The Dirty Little Secret of the Diet-Heart Hypothesis" was especially interesting to me and is well presented. I recommend you read it.

I will certainly be digesting more of what Stephan posts on his blog.

The diet–heart hypothesis: a critique

An article under VIEWPOINT AND COMMENTARY in the Journal of the American College of Cardiology (JACC) titled "The diet–heart hypothesis: a critique" by Sylvan Lee Weinberg, MD, states the following in the final paragraph. Please read the complete article here.

"A balanced appraisal of the diet–heart hypothesis must recognize the unintended and unanticipated role that the LF-HCarb diet may well have played in the current epidemic of obesity, abnormal lipid patterns, type II diabetes, and the metabolic syndrome. Defense of the LF-HCarb diet, because it conforms to current traditional dietary recommendations, by appealing to the authority of its prestigious medical and institutional sponsors or by ignoring an increasingly critical medical literature, is no longer tenable. The categoric rejection of experience and an increasingly favorable medical literature, though still not conclusive, which suggests that the much-maligned LCarb-HP diet may have a favorable impact on obesity, lipid patterns, type II diabetes, and the metabolic syndrome, is also no longer tenable."