Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women

VA Mustad, TD Etherton, AD Cooper, AM Mastro, TA Pearson, SS Jonnalagadda and PM Kris-Etherton
Graduate Program in Nutrition, Pennsylvania State University, University Park, USA.

Studies with animal models suggest that saturated fatty acids raise low density lipoprotein (LDL)-cholesterol levels by reducing LDL receptor- mediated clearance. To examine this directly in humans, we studied the effects of lowering dietary saturated fat on LDL-receptor abundance in peripheral mononuclear cells which reflects hepatic LDL-receptor status. Healthy males and females (n = 25) participating in the DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activity) Study consumed three experimental diets in a randomized cross-over design. Diets provided 34% fat, 15% saturated fatty acids (Average American Diet); 29% fat, 9% saturated fatty acids (Step-One Diet); and 25% fat, 6% saturated fatty acids (Low SAT Diet). Peripheral mononuclear cells were isolated from blood samples collected after 6 and 8 wk. An ELISA was used to quantify LDL-receptor protein in total cell membranes. LDL- receptor abundance increased by 10.5% after the Low SAT Diet (P < 0.05). This was associated with an 11.8% decrease in serum LDL- cholesterol (P < 0.05). A linear inverse relationship was observed between the percentage change in LDL-cholesterol and the percentage change in LDL-receptor abundance (r = -0.59; P < 0.01). In addition, LDL-receptor abundance also was correlated inversely (P < 0.001) with serum levels of LDL-cholesterol (r = -0.747) and apoB (r = -0.593). In summary, reducing dietary saturated fat is associated with an increase in LDL-receptor abundance of magnitude similar to the decrease in serum LDL-cholesterol. Thus, an important mechanism by which reductions in dietary saturated fatty acids decrease LDL-cholesterol in humans is through an increase in LDL-receptor number.

http://www.jlr.org/cgi/content/abstract/38/3/459

The Cholesterol Controversy
By William Faloon
William Faloon
William Faloon

As we enter the year 2009, a heated debate continues about the role of cholesterol in the development of atherosclerosis and heart disease. Based on our analysis, both sides still have it wrong!

Almost comical is the role reversal this controversy has taken. When progressive individuals first proposed that high cholesterol increases heart attack risk, the medical establishment ridiculed the idea. The FDA went so far as to make it illegal for food companies to claim that diets low in saturated fat and cholesterol had any relationship to artery disease. (Note: High-saturated fat diets cause blood cholesterol to spike.)

The dispute raged for decades until the medical establishment (and the FDA) not only embraced the concept that high cholesterol causes heart attacks, but claimed this scientific area their exclusive domain.1-5 Many of today’s complementary medicine practitioners, who would have been early proponents of low-saturated fat diets, now question the association between cholesterol and vascular disease.

The fact that confusion still exists over this straightforward medical principle helps explain why atherosclerotic disease remains today’s leading preventable killer.
Early History of Cholesterol and Arterial Disease

If we travel back to 1913, we would learn of an impressive study showing that rabbits fed a high-cholesterol diet develop atherosclerotic lesions that closely resemble those seen in humans.6 This research was initially criticized because rabbits are plant eaters whose normal diets are not the same as humans. When dogs and rats are fed high-cholesterol diets, they do not develop artery disease. It was later discovered that dogs and rats efficiently convert cholesterol to bile acids that are excreted. When these excretion mechanisms are blocked, however, dogs and rats do develop atherosclerosis in response to cholesterol feeding.

The cholesterol theory gained a bit more credibility when atherosclerotic lesions were readily induced in guinea pigs,7,8 goats,9 hens, parrots,10 and even primates11 in response to cholesterol elevation.

Interestingly, the first hints that high cholesterol caused atherosclerosis in humans occurred back in 1889.2,12 A doctor reported a case of a child with a rare genetic disorder that caused massive overproduction of cholesterol. The child died suddenly at age 11. An autopsy revealed extensive atherosclerotic-like lesions in large arteries.
Early History of Cholesterol and Arterial Disease

It was not until 1939 that a publication in the Archives of Internal Medicine pulled together the evidence linking this rare genetic disorder (familial hyper-cholesterolemia) to coronary artery disease.2,13 It was argued back then, however, that the extraordinarily high cholesterol levels in those with this genetic defect could not be extrapolated to people with only moderate cholesterol elevations.

By 1955, the cholesterol-heart attack connection was attracting some respectability. A study was done that measured cholesterol blood levels in people from seven different countries. Citizens of Finland, who ate the most saturated fats, had an average cholesterol reading of over 260 (mg/dL). The Japanese, who consumed the least saturated fat, had average cholesterol readings of a little over 160. Over a 10-year period, the number of fatal heart attacks per 1,000 men was about 70 in Finland and a little less than 5 in Japan. Saturated fat made up 20% of the Finnish diet, but only 2.5% of the Japanese diet.2,14

These findings had a significant impact on the cholesterol debate, but the vast majority of physicians and the federal government still proclaimed that high cholesterol had nothing to do with heart attack risk.
Where Some Researchers Went Wrong

In trying to prove that diets high in saturated fats increase cholesterol levels and subsequent heart attack risk, scientists conducted studies that substituted omega-6-rich polyunsaturated fats (corn oil, safflower oil) in place of saturated fats (butter, lard, meat fats).15-17 While these studies showed reduced cholesterol levels and heart attack rates, the findings were not nearly as impressive as they could have been. This is because these kinds of polyunsaturated fats (corn oil, sunflower oil, safflower oil, etc.) rich in omega-6 fatty acids create inflammatory byproducts and induce LDL oxidation that damages arteries.

During this era of medical ignorance (the 1950s-1960s), the benefits of monounsaturated fats (such as those found in olive oil) and omega-3 fats (such as those found in cold-water fish, flaxseed, and walnut oils) in preventing heart attacks were not recognized. The best that doctors could provide in lieu of dangerous saturated fats was to substitute omega-6 polyunsaturated fats, which then created a dangerous proinflammatory state (due to an imbalance in omega-6 to omega-3 fats).18
The 1960s… More Lost Opportunities
Where Some Researchers Went Wrong

I’ll never forget going to my first funeral and seeing a 42-year-old neighbor lying in a coffin. He had died of a sudden heart attack, but no one talked about how unusual his early death was. That’s because men over age 40 were routinely dying of heart attacks in those days.

Heart attacks and strokes claimed astronomical numbers of lives in the Western world throughout most of the past century. During the early 1960s, for example, the number of acute fatal heart attacks in younger men was substantially higher than today.19-21 A lot of this had to do with cigarette smoking and the high-saturated fat diet that was a staple in most households.

By the early 1960s, however, the theory that one could reduce their heart attack risk by avoiding saturated fats had taken hold at least in the alternative medicine community. Even the American Heart Association went on record as early as 1961 with the following closely guarded statement:

“Those people who have had one or more atherosclerotic heart attacks or strokes may reduce the possibility of recurrences by such a change in diet.”2,22

Based on a wave of studies showing reductions in heart attack incidence in those who reduced their saturated fat intake, nutritionists and alternative doctors were finally espousing heart-healthy diets. The FDA responded by criminalizing the commercial dissemination of this information by the food industry. Heart attacks claimed about seven million American lives in the 1960s.20 The FDA’s suppression of the link between poor diet and heart attack risk kept funeral businesses thriving.
The Great Cholesterol Debates

In 1969, an American Heart Association spokesperson stated that those with excess cholesterol levels should be treated medically. This doctor went on to state, “in short, we have come ... to the point where we are probably preventing a disease that was considered to be an inevitable accompaniment of aging not very long ago.”26

The American Heart Association met with fierce criticism from prominent cardiologists who continued to proclaim there was no evidence that cholesterol reduction conferred protection against heart attacks. These attacks on the cholesterol theory of heart disease were published in the leading medical journals of the day.

Regrettably, it was not until 1984 that the medical establishment formally recognized the relationship between high cholesterol and heart attack incidence.27
The First Diet-Heart Cookbook
The First Diet-Heart Cookbook

Readers of Life Extension magazine may recall the name John Gofman, MD, PhD. This is the physicist turned medical doctor whose early work on radioactive isotopes resulted in him being recruited to work on The Manhattan Project to develop the first atomic bomb.

Dr. Gofman’s expertise on the biological effects of radiation caused him to later take a very controversial position. He meticulously documented how medical diagnostic X-rays are a cause of cancer and artery disease, something most in the medical establishment still refuse to accept.

In 1947, Dr. Gofman began research that would soon lead him to conclude that cholesterol is a cause of atherosclerosis.23,24 Dr. Gofman and his colleagues were the first to show that specific fractions of cholesterol such as LDL (low-density lipoprotein) are the most dangerous. Dr. Gofman was involved in the publication of possibly the first book in 1951 about how low-fat and low-cholesterol diets prevent heart disease.25

I am always amazed at individuals who are able to contribute so much. In Dr. Gofman’s case, he was instrumental in harnessing nuclear energy, warning of the dangers of low-level radiation, and then moved on to a completely different field to discover specific fractions of cholesterol that cause atherosclerosis.
Nathan Pritikin… An Early Hero of Mine

I will never forget as a teenager seeing a televised debate between Nathan Pritikin and a mainstream cardiologist. Pritikin explained how very low-fat diets could reverse coronary atherosclerosis, whereas the cardiologist ridiculed the notion.

I knew little about heart attacks back then, other than the fact that my family members and neighbors were having them on a regular basis. I also witnessed the poor diets these heart attack victims ate, which made Nathan Pritikin’s arguments all the more convincing to me.

What was so remarkable about Nathan Pritikin was that he had no medical training. In 1957, at age 40, Pritikin was diagnosed as having heart disease. Faced with a lifetime of ever-increasing disability, he pored over the scientific literature and formulated a diet and exercise program to treat his disease.28 After nine years of trial and error, he had cured himself.
Nathan Pritikin… An Early Hero of Mine

Long before the medical establishment acknowledged that something as simple as diet might be causing serious illnesses, Pritikin had created a scientifically sound program using food and exercise as medicine. This revolutionary departure from the flawed theories of the 1950s caused him to become a public enemy of the medical establishment. Nathan Pritikin’s healthy diet program did more than reverse heart disease. Patients who came to his clinic often saw their type 2 diabetes, arthritis, and hypertension disappear.29,30

Despite these clinical successes, Nathan Pritikin was ceaselessly attacked by doctors as being a charlatan. For much of the 1970s, Nathan Pritikin waged a public battle with government and private health agencies, as well as with the American Medical Association. The medical establishment doggedly refused to accept that what one ate had anything to do with their risk of heart disease.

Pritikin was so confident that he was reversing heart disease with healthy diets that he ordered his own body autopsied after his death. Almost 30 years after being diagnosed with irreversible coronary artery disease, the autopsy showed his arteries were akin to those of a young man and clear of any signs of heart disease.31

In 1987, two years after Nathan Pritikin’s death, the Journal of the American Medical Association announced a study that showed regression of atherosclerosis in the coronary arteries of humans who reduced their blood cholesterol by a similar degree as were accomplished at the Pritikin Longevity Centers.32 Numerous subsequent studies confirmed that Nathan Pritikin was scientifically correct…and the medical establishment’s position fatally flawed.33-36

Tens of millions of Americans needlessly perished because the role of cholesterol in causing heart disease was not recognized nearly as early as it should have been.
What is Cholesterol?
What is Cholesterol?

Cholesterol is a lipid (fat) that is chemically classified as a sterol. It provides critically important functions in the body such as building and maintaining cell membranes. Cholesterol also functions as a precursor to hormones like testosterone and fat-soluble vitamins.

While cholesterol is essential to life, the lipoprotein it is bound to plays a role in whether it injures or protects the arterial wall. Since cholesterol is insoluble in blood, it is transported in the circulatory system by lipoproteins.

LDL (low-density lipoprotein) transports cholesterol to the cells, whereas HDL (high-density lipoprotein) transports cholesterol away from the cells.

When one has excess LDL, too much cholesterol can be deposited into the arterial wall. Insufficient HDL, on the other hand, impairs cholesterol transport away from the arterial wall (for disposal in the liver). Too much LDL and/or not enough HDL can thus set the stage for atherosclerosis. These simple facts, however, explain only part of the problem.
Pomegranate Suppresses LDL Oxidation

LDL Atherosclerosis Risk Factor


Effect of Pomegranate61

LDL basal oxidative state


Reduced by 90%

LDL susceptibility to copper-induced oxidation


Reduced by 59%

Paraoxonase-1 (protects against LDL oxidation)


Improved by 83%

Total antioxidant status


Improved by 130%
Danger of Oxidized LDL

The over-promotion of “statin”drugs has resulted in today’s cardiologists focusing on getting their patients’ LDL and total cholesterol down as low as possible. Pharmaceutical company advertising has made it appear as if the only cause of atherosclerosis is excess LDL and cholesterol.
Danger of Oxidized LDL

Beginning in 1979, however, researchers made discoveries indicating that it is the oxidation of LDL that results in the most arterial damage.37-39 Thousands of studies now reveal how oxidized LDL contributes to the atherosclerotic process from start to finish.

There are doctors who argue that atherosclerosis is all about inflammation and response to endothelial injury and has nothing to do with LDL cholesterol. What these doctors overlook is the fact that oxidized LDL injures endothelial cells and causes inflammation!40-46

Oxidized LDL causes endothelial cells to secrete “adhesion molecules” that allow white blood cells to penetrate the inner lining of the artery (the endothelium). This is where initial fatty streaks and atherosclerotic plaques develop.47

Oxidized LDL turns on white blood cell gene expression that enables them to convert into foam cells, which results in continuous accumulation of oxidized LDL in the atherosclerotic plaque.48

Oxidized LDL initiates an inflammatory process by causing foam cells to secrete molecules that attract proinflammatory cells.47

Oxidized LDL enhances the process whereby immune cells, foam cells, smooth muscle cells, and endothelial cells degrade collagen, which leads to the rupture of the fibrous plaque.49

The endothelium requires nitric oxide to function properly. A hallmark characteristic of endothelial dysfunction is a lack of nitric oxide. Oxidized LDL impairs the endothelial cells’ ability to produce nitric oxide.50

As you may surmise by now, both absolute LDL level and LDL oxidation are involved in atherosclerotic processes and heart attack risk.
Coronary Risk Following Treatment with Statin Drugs According to Achieved LDL Levels

Achieved LDL Level (mg/dL of blood)


Under 54


54-71


72-94


Over 94

Lowest Risk


10%


30%


80%


Greater Risk


Greater Risk


Greater Risk

The data above is a tabulation of the results from patients who had already suffered a coronary event who were then prescribed either 80 mg of Lipitor® (atorvastatin) or 40 mg of Zocor® (simvastatin) per day.

These findings show that the achieved level of LDL was strongly predictive of recurring coronary events. These relative risks are adjusted for age, smoking status, diabetes, hypertension, and body mass index (BMI).64
Common Sense Approaches to Heart Attack Prevention

Financial bias, apathy, and scientific ignorance have resulted in most Americans failing to protect themselves against today’s leading crippler and killer… atherosclerosis.
Common Sense Approaches to Heart Attack Prevention

Some cardiologists erroneously believe that if all their patients took a statin drug and aspirin, coronary artery disease would disappear. Equally disturbing are doctors who claim that that aging people should not worry about their LDL levels.

For 29 years, we at Life Extension have emphasized that atherosclerosis has many underlying causes.51 Our findings have been validated in many subsequently published studies.52-54 At the end of this article, we have reprinted an updated version showing 17 daggers aimed at the heart, each dagger representing an independent risk factor for developing coronary artery disease. Fortunately, most Life Extension members are already taking nutrients, hormones, and sometimes drugs to protect against every one of these cardiac risk factors.

When it comes to inhibiting LDL oxidation, members should find comfort in knowing they have been taking supplements that have been confirmed to dramatically inhibit LDL oxidation. A number of studies document the ability of ubiquinol CoQ10 to protect against LDL oxidation better than lycopene, alpha tocopherol, and other lipid-soluble antioxidants.55-59 Some of these studies show that alpha tocopherol (vitamin E) can turn into an LDL pro-oxidant unless ubiquinol is also present.60 These studies help explain the inability of the alpha form of vitamin E by itself to significantly reduce heart attack rates in certain populations.
Keep Your LDL Levels Below 100
Relative risk for coronary heart disease based on level of low-density lipoprotein (LDL).62 As LDL rises, so does the risk of heart attack.

Perhaps no other nutrient has demonstrated better anti-LDL oxidation effects than pomegranate. In a clinical study, human subjects taking pomegranate showed a beneficial 35% reduction in carotid intima-media thickness accompanied by a 45% improvement in carotid blood flow. As evidenced by the chart above, pomegranate improved markers related to LDL oxidation by up to 130%!61

These kinds of impressive study results, showing how LDL oxidation can be suppressed, might tempt some people to ignore dangerously high LDL blood levels. We at Life Extension strongly advise against this. The chart below vividly shows the sharp increase in coronary artery disease risk as LDL concentrations increase in the blood.62
Keep Your LDL Levels Below 100

Atherosclerosis remains the leading cause of death in the Western world.63 Eastern populations who are switching to high-fat Western diets are seeing vascular disease rates spiral upwards. We cannot ignore almost 100 years of research showing that excess LDL-bound cholesterol is a coronary risk factor.

While there may someday be a definitive finding that something as simple as pomegranate provides complete protection against LDL oxidation, and therefore excess LDL itself, we don’t have these data confirmed today.

You have entrusted us to provide you with an accurate analysis of the available scientific literature to keep you alive in good health. We therefore reiterate our 29-year recommendation that healthy members keep their LDL levels below 100 mg/dL.

Very high-risk groups (e.g., smokers or those with diabetes, abdominal obesity, a recently sustained heart attack, low HDL, high triglycerides, or known coronary artery disease) should strive for a 70-75 mg/dL LDL target level. (Note: Those who drive LDL down to these very low levels should use blood tests to make sure they are not also suppressing critical hormones like testosterone and DHEA.)

The chart on top of this page clearly demonstrates that in people who have already suffered a coronary event, each progressive LDL elevation increases the risk of a second event. In this study, cardiac disease incidence was 80% greater in those with an LDL reading over 94 mg/dL compared with those whose LDL was under 54 mg/dL.64
See How Our Presidents Died in the Past Century

To better understand the epidemic of heart disease that existed during the era of the cholesterol debates, look no further than the medical histories of the presidents of the United States.

President Dwight Eisenhower suffered his first heart attack in 1955. That same year, Senator Lyndon Johnson suffered his first heart attack. Back in those days, recovery from a heart attack was a slow and arduous process.

Dwight Eisenhower smoked four packs a day of cigarettes until he quit in 1949. Combined with his high-saturated fat intake, he was at great cardiac risk. Here is what President Eisenhower ate the day of his first heart attack:77

*

Breakfast: sausage, bacon, mush, hotcakes
*

Lunch: hamburger with raw onion
*

Dinner: roast lamb

In 1957, President Eisenhower suffered a stroke. By the time of this death in 1969, Eisenhower had suffered at least seven heart attacks, along with multiple other diseases that can be related to the unhealthy nature of the typical American diet of his era.77

Three years later, former President Harry Truman died at age 88 from atherosclerotic coronary artery disease.

Lyndon Johnson was only 46 years old when he suffered his first coronary occlusion heart attack. He too had been a heavy smoker, but quit after his first heart attack. Shortly after leaving the presidency, Lyndon Johnson resumed cigarette smoking and continued eating foods that we know today damage arterial linings (the endothelium). Johnson developed severe angina pain that crippled him until he suffered his final heart attack in 1973 at age 65.78

So while the FDA and the medical establishment were ridiculing the notion that high-saturated fat diets caused artery disease, the most famous political leaders of the day were keeling over from heart attacks right before the public’s eyes.

Heart attack and/or stroke claimed the lives of most of the presidents in the past century including Theodore Roosevelt, William Taft, Woodrow Wilson, Calvin Coolidge, Franklin Roosevelt, and Richard Nixon.
Tying it all Together

In reviewing the history of dietary fats and heart disease risk, a number of interesting facts emerge. Nathan Pritikin put a lot of the pieces together when he mandated that virtually all dietary fat should be eliminated (less than 10% total calories from fat). This protected his followers against the atherogenic effects of both saturated fat and dangerous omega-6-rich polyunsaturated fat sources like corn, soybean, safflower, and sunflower oils. The problem is that adhering to Pritikin’s very strict diet is difficult for the vast majority of people.

Fortunately, we know today that following a low-saturated fat, Mediterranean-type diet with lots of natural polyphenol antioxidants provides huge cardioprotective benefits.65 We have also acquired the knowledge that specific fats (omega-3s and certain monounsaturated fats) are extremely beneficial in reducing vascular disease risk.66,67

As we report in this issue of Life Extension, a large number of studies continue to validate the ability of low-cost plant polyphenols to not only protect against LDL oxidation, but to also boost beneficial HDL and lower absolute LDL levels in the blood.68-76

It may thus be possible for many aging humans to achieve optimal blood lipid status using an integrative approach to support healthy cholesterol levels and reduce oxidant stress… without resorting to prescription drugs.
Natural Protection at the Lowest Prices
Natural Protection at the Lowest Prices

For 21 consecutive years, Life Extension members have taken advantage of the annual Super Sale to stock up on a large supply of their favorite nutrient formulations.

During this annual winter event, every Life Extension product is discounted so that members can obtain our most up-to-date formulas at the lowest prices of the year.

We recently upgraded our most popular products to provide even more life-protecting nutrients. Until February 2, 2009, members can obtain extra discounts on every one of these formulas during our once-a-year Super Sale.

For longer life,

For Longer Life

William Faloon
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http://search.lef.org/cgi-src-bin/MsmGo ... hiword=ldl

Dietary saturated and trans fatty acids and lipoprotein metabolism.

Mensink RP, Temme EH, Hornstra G.

Department of Human Biology, Limburg University, Maastricht, The Netherlands.

Earlier studies have shown that not all saturated fatty acids are equally hypercholesterolaemic: stearic acid (C18:0) and saturated fatty acids with less than 12 carbon atoms are thought not to raise serum cholesterol levels. This suggests that the cholesterol-raising effects of saturated fatty acids can be attributed to lauric acid (C12:0), myristic acid (C14:0) and palmitic acid (C16:0). These three saturated fatty acids also have different effects on serum total cholesterol levels. Results from recent controlled dietary experiments suggest that lauric acid raises serum total and low-density lipoprotein (LDL) cholesterol levels slightly less, and myristic acid more, as compared with palmitic acid. Myristic acid, however, also causes higher levels of high-density lipoprotein (HDL) cholesterol. Stearic acid has only a slight effect on serum LDL and HDL cholesterol levels as compared with oleic acid. Trans monounsaturated fatty acids, however, increase LDL and decrease HDL cholesterol levels. Precise effects on lipoproteins of short and medium chain triglycerides (C4:0-C10:0) have never been examined.

RoB wrote:It's the oxidation of LDL that is the problem, not the concentration of circulating LDL that matters with regards to atherosclerosis. Although I suppose if there's a reduced expression of LDL receptors then it's more likely to become stuck in the sub-endothelial space and become oxidized.

Either way I personally don't think it matters, if your diet isn't pro-inflammatory and you don't consume vast quantities of PUFA's them LDL is less likely to oxidized the inflammatory response isn't going to get out of control. Additionally just because atherosclerosis is happening doesn't mean you're going to have a coronary, if collagen synthesis matches degradation then the plaques won't burst.

Dtlv74 wrote:

RoB wrote:It's the oxidation of LDL that is the problem, not the concentration of circulating LDL that matters with regards to atherosclerosis. Although I suppose if there's a reduced expression of LDL receptors then it's more likely to become stuck in the sub-endothelial space and become oxidized.

Either way I personally don't think it matters, if your diet isn't pro-inflammatory and you don't consume vast quantities of PUFA's them LDL is less likely to oxidized the inflammatory response isn't going to get out of control. Additionally just because atherosclerosis is happening doesn't mean you're going to have a coronary, if collagen synthesis matches degradation then the plaques won't burst.

That makes sense RoB. In respect of non saturated fats, what do you think is a better way to achieve balance between omega3's and omega6's, assuiming a starting point that's a typical unbalanced diet with lots of omega6 but not much omega3 - a) to increase omega3 to improve the ratio, or b) to decrease omega6 to improve the ratio, or c) a combination of both?

Most people, including myself for a while, seem to choose option a and take lots of fish oil, but am beginning to think b or c are better options.

RoB wrote:

Dtlv74 wrote:

RoB wrote:It's the oxidation of LDL that is the problem, not the concentration of circulating LDL that matters with regards to atherosclerosis. Although I suppose if there's a reduced expression of LDL receptors then it's more likely to become stuck in the sub-endothelial space and become oxidized.

Either way I personally don't think it matters, if your diet isn't pro-inflammatory and you don't consume vast quantities of PUFA's them LDL is less likely to oxidized the inflammatory response isn't going to get out of control. Additionally just because atherosclerosis is happening doesn't mean you're going to have a coronary, if collagen synthesis matches degradation then the plaques won't burst.

That makes sense RoB. In respect of non saturated fats, what do you think is a better way to achieve balance between omega3's and omega6's, assuiming a starting point that's a typical unbalanced diet with lots of omega6 but not much omega3 - a) to increase omega3 to improve the ratio, or b) to decrease omega6 to improve the ratio, or c) a combination of both?

Most people, including myself for a while, seem to choose option a and take lots of fish oil, but am beginning to think b or c are better options.

Yes until very recently I've been having 10g of fish oil a day, but I've come to the conclusion that this just isn't particularly healthy. I feel that certainly the best option is a combination of B and C, trying to hit a ratio of 4:1 omega 6 to 3. I currently only have about 4g of fish oil a day and roughly 18-20g of total PUFA's. Whilst EFA's are certainly essential, they are only essential to a certain extent. The body just doesn't need the amount of PUFA's most people consume, and they are much better off being replaced by saturated and mono-unsaturated fat.

cleaver wrote:^^Avocado without doubt, then olive. I get almost all of my mono from them.

I find I need a fairly high o3 intake for optimum health. Although I evolved from coastal communities so fish would have been high on the Agenda. It is also worth remembering that in the 1800's that vitually the whole of Britain lived on Herring. So Britain would have had a much higher o3 intake as a whole.

TBH I feel that many of taday's health problems can be attributed to cheap vegetable oils deviod of any nutritional value other than cheap calories. Communties around the world where these oils are not used are in pretty good general health irrespective of their diets. But no research will ever come out and say this because it would mess with big business.

Alex wrote:To be honest I found online sources more money than supermarkets for most oils. I use Olivado Avocado Oil myself which can be had from Sainsbury for under £5 for 500ml.

Gothic_Muscle wrote:

cleaver wrote:^^Avocado without doubt, then olive. I get almost all of my mono from them.

I find I need a fairly high o3 intake for optimum health. Although I evolved from coastal communities so fish would have been high on the Agenda. It is also worth remembering that in the 1800's that vitually the whole of Britain lived on Herring. So Britain would have had a much higher o3 intake as a whole.

TBH I feel that many of taday's health problems can be attributed to cheap vegetable oils deviod of any nutritional value other than cheap calories. Communties around the world where these oils are not used are in pretty good general health irrespective of their diets. But no research will ever come out and say this because it would mess with big business.

Really?!?! Any particular reason you've gone for Avocado over EVOO?

Alex wrote:
Anyone know much about Rice Bran Oil?

Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.

Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS.

The Heart Research Institute, Sydney, Australia.

Comment in:

* J Am Coll Cardiol. 2007 May 1;49(17):1825-6.

OBJECTIVES: The purpose of this study was to investigate the influence of dietary fatty acids on the anti-inflammatory properties of high-density lipoproteins (HDL) and vascular function. BACKGROUND: The effect of dietary fatty acids on atherogenesis remains uncertain. METHODS: Fourteen adults consumed an isocaloric meal containing either a polyunsaturated or a saturated fat on 2 occasions. The effects of post-prandial HDL on endothelial cell expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined. Flow-mediated dilation (FMD) and microvascular reactivity were assessed before and 3 and 6 h after the meal.

RESULTS: Plasma triglycerides, insulin, and nonesterified fatty acids rose after the meals. The HDL collected 6 h after the saturated meal were less effective than HDL isolated from fasting plasma in terms of their ability to inhibit expression of ICAM-1 and VCAM-1, whereas HDL collected 6 h after the polyunsaturated meal had an inhibitory activity that was greater than that of HDL collected from fasting plasma (p < 0.004 and p = 0.01 for comparison of effect of meals on ICAM-1 and VCAM-1, respectively). Post-hyperemic microvascular flow significantly increased at 3 h after the polyunsaturated meal by 45 +/- 14% and by 21 +/- 11% after the saturated meal. The FMD decreased 3 h after the saturated meal by 2.2 +/- 0.9% (p< 0.05 compared with baseline) and by 0.9 +/- 1% after the polyunsaturated meal.

CONCLUSIONS: Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.

http://www.ncbi.nlm.nih.gov/pubmed/1690 ... t=Abstract" onclick="window.open(this.href);return false;

Pain wrote:It is important to note there are differential effects on insulin resistance in different parts of the body.

Dtlv74 wrote:The high fatters are really not going to want to hear this...

Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.

Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS.

The Heart Research Institute, Sydney, Australia.

Comment in:

* J Am Coll Cardiol. 2007 May 1;49(17):1825-6.

OBJECTIVES: The purpose of this study was to investigate the influence of dietary fatty acids on the anti-inflammatory properties of high-density lipoproteins (HDL) and vascular function. BACKGROUND: The effect of dietary fatty acids on atherogenesis remains uncertain. METHODS: Fourteen adults consumed an isocaloric meal containing either a polyunsaturated or a saturated fat on 2 occasions. The effects of post-prandial HDL on endothelial cell expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined. Flow-mediated dilation (FMD) and microvascular reactivity were assessed before and 3 and 6 h after the meal.

RESULTS: Plasma triglycerides, insulin, and nonesterified fatty acids rose after the meals. The HDL collected 6 h after the saturated meal were less effective than HDL isolated from fasting plasma in terms of their ability to inhibit expression of ICAM-1 and VCAM-1, whereas HDL collected 6 h after the polyunsaturated meal had an inhibitory activity that was greater than that of HDL collected from fasting plasma (p < 0.004 and p = 0.01 for comparison of effect of meals on ICAM-1 and VCAM-1, respectively). Post-hyperemic microvascular flow significantly increased at 3 h after the polyunsaturated meal by 45 +/- 14% and by 21 +/- 11% after the saturated meal. The FMD decreased 3 h after the saturated meal by 2.2 +/- 0.9% (p< 0.05 compared with baseline) and by 0.9 +/- 1% after the polyunsaturated meal.

CONCLUSIONS: Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.

http://www.ncbi.nlm.nih.gov/pubmed/1690 ... t=Abstract" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;