The Cholesterol Times, Issue #014 -- Oxidized Lipids Are the True Cause of Heart Disease
When it comes to LDL, size matters.
Or at least it may. Small, dense LDL is a risk factor for heart disease. But it's less about size and more about how you use it.
The theme of this newsletter is the role of oxidized LDL in causing heart disease. From the articles, reviews, and research blurbs below, you will see that we can conclude three main things about the causes of atherosclerosis:
The necessary initiating factor is the presence of oxidized lipids in the blood.
The necessary enabling factor is the lack of shear stress in areas where arteries curve and branch, making them permeable to large molecules — something that can be reduced and maybe abolished with lots of physical activity.
Other factors may aggravate or accelerate the process, but are probably not necessary for it to occur; other factors contribute to the rupture of established plaques alongside oxidized LDL, so its importance diminishes as the disease progresses.
It has little or nothing to do with the amount of LDL in the blood, but how fast you use that LDL is a critical factor. In fact, people with a genetic mutation that eliminates the enzyme that degrades the LDL receptor have an 88% reduced risk of heart disease!
If you don't use it, you lose it. The PUFA in the membrane oxidize, the coenzyme Q10 and fat-soluble vitamins oxidize, and the whole thing winds up in your arterial wall instead of in the cells that need those nutrients.
I hope you find this information as useful and as fascinating as I have. Enjoy!
-Chris Masterjohn
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In This Issue
Site Updates
Special Reports
Best of the 'Net
Research Watch
Mutation in Enzyme That Degrades LDL Receptor Virtually Abolishes Risk of Heart Disease
Curcumin Increases LDL Receptor and Suppresses Atherosclerosis
How to Link to This Newsletter
Copyright and Disclaimer
Search
Feedback
Site Updates
A Crash Course in Lipoproteins
LDL, HDL, so good so far. VLDL, IDL? Apo-what? Chylo-who? This brief article explains the basics of lipoproteins, what they are and how they function.
High Cholesterol and Heart Disease — Myth or Truth?
The cholesterol-fed rabbit developed atherosclerosis but the response-to-injury rabbit never did. Why? Atherosclerosis is a disease caused by degenerating lipids. The cholesterol skeptics ignore the evidence and the cholesterol warriors promote a diet that contributes to the problem. Read about the true cause of heart disease here.
All-New Review of Uffe Ravnskov's The Cholesterol Myths
An all-new critical review of Uffe Ravnskov's 2000 The Cholesterol Myths. Ravnksov's book is an important contribution to the debate about the role of cholesterol in heart disease, but Ravnskov ultimately leaves the reader with the idea that blood lipids have virtually nothing to do with heart disease, that existing animal models can teach us almost nothing about human heart disease, and that good scientists should never have given the cholesterol theory much weight because it was built entirely on a foundation of sand. In reality, blood lipids do matter, animal models are relevant, and though the cholesterol theory is a lopsided house, it is in fact built on a solid foundation of evidence that needs to be carefully looked at.
Colpo's The Great Cholesterol Con
Anthony Colpo's book, The Great Cholesterol Con: Why everything you've been told about cholesterol, diet, and heart disease is wrong! is the best cholesterol skeptic book out there. It is not without its flaws and double standards, but it should be part of anyone's library who is interested in the cholesterol controversy.
Kendrick's The Great Cholesterol Con
Read this book if you want a good laugh. It is filled with sarcastic humor, and reveals some of the most hilarious absurdities that pass for science in our day. But some of Kendrick's scientific errors and implausible speculations may just leave you scratching your head.
How International Bankers Gained Control of America
Did you know that the Federal Reserve is privately owned? That Thomas Jefferson said if we ever allowed private banks to control our currency, the large corporations that would rise around us would deprive us of our prosperity and we would wake up homeless on the continent our fathers conquered? Read the truth about the Fed in this review of the two-part DVD, The Money Masters. This will eventually be part of a new section of the site about the political side of health, especially the rapidly growing attack on small farming and nutritional supplements, as the food supply concentrates into fewer and fewer hands.
New Blog and RSS Feed
Have you been missing The Daily Lipid? Statins for pregnant women and children, bogus concerns about tilapia and lies about arachidonic acid, statins and UFOs, the dangerous overpopulation nutcases in the scientific establishment, not to mention updates to the site as soon as they are made. Subscribe to the RSS feed and you don't even have to visit the site to read them!
Cholesterol-And-Health.Com Special Reports
Thyroid Toxins: Double-Edged Swords of the Kingdom Plantae
One of the keys to preventing atherosclerosis is rapid clearance of LDL from the bloodstream into the cells that need the cholesterol, fats, and fat-soluble nutrients within it so that it does not sit around in the blood where it will oxidize over time.
Thyroid hormone is critical to maintaining robust function of the LDL receptor. But thyroid function can be inhibited by goitrogens in foods such as soy, millet, crucifers, and fruits and nuts in the Rosacea family. Confused about how cooking, fermenting, and other processing methods affect these chemicals? This 25-page report will answer all your questions. It contains six figures, one table and 66 references. It provides quantitative information about what proportion of the goitrogenic activity of cruciferous vegetables various cooking methods -- microwaving, steaming, boiling -- destroy. It explains that, contrary to popular belief, fermentation increases the goitrogenicity of crucifers. Traditional soaking and fermenting destroy the goitrogenicity of foods containing cyanogenic glycosides but increase the goitrogenicity of millet and soy. In fact, even cooking increases the goitrogenicity of millet. This is information you do not want to miss!
How Essential Are the Essential Fatty Acids?
Do you or anyone you know suffer from hair loss, skin problems, or infertility? These are signs of arachidonic acid deficiency. Do you want to build muscle? You may need arachidonic acid. Contrary to conventional belief, the only fatty acids for which there is substantial evidence of essentiality are arachidonic acid and DHA. EPA probably does not belong in the mammalian body at all. Plant oils are not essential. For most healthy adults, however, the essential fatty acid requirement is so low that it is negligible. For people with certain conditions of oxidative stress, or for growing children, pregnant and lactating women, and bodybuilders, small amounts of arachidonate and DHA should be obtained from egg yolks, butter, red meat fats, and occasional fish consumption. Cut through the misinformation and read the truth about essential fatty acids in this Special Report.
Best of the 'Net
Raw Milk: What the Scientific Literature Really Says
This fantastic report prepared by the Weston A. Price Foundation tells the truth about raw milk. Few scientific reports provide realy evidence tracing disease outbreaks to raw milk, and some even suggest substantial benefits. Much of the literature is biased, politicized, and sloppy. Ultimately, however, it all comes down to the consumer's freedom to choose.
Who Says Good Nutrition Means Animal Fats? Weston A. Price
The Washington Post gets it mostly right.
Milwaukee Man's Home Foreclosed Over Unpaid Parking Ticket
What is this world coming to?
Peaceful Protestors Considered "Suspected Terrorists"
Maryland state troopers infiltrated peaceful anti-war and anti-death penalty groups, spied on them, and enrolled some of their organizers in a "suspected terrorist" database. Despite their own documentation of the organizers' peaceful intentions, they reported them to seven government agencies. Under the PATRIOT Act, even American citizens lose their right to a jury trial if they are suspected terrorists. They can be detained indefinitely, secretly, and tried anywhere in the world by a secret military tribunal that requires 2/3 majority rather than unanimity to convict. Anyone who thinks the PATRIOT Act is for terrorists should familiarize themselves with history. Adolf Hitler convinced the German Parliament to democratically vote for his "Enabling Act" that suspended the constitution for the purpose of combatting terrorism — the Reichstag had supposedly been burned down by Communists, although most historians now believe the Nazis burned it down themselves as a "false flag" event to justify measures to combat terrorism. What followed was a slow and gradual loss of liberties and the eventual formation of a militarily expansionist police state that murdered 11 million people. If you don't see the beginnings of it here, I'm sorry but please open your eyes.
Can Skyscrapers Predict Economic Crashes?
Mark Thornton, developer of the "skyscraper index," says they can. When central banks inflate by printing money out of thin air, something that inevitably produces an economic crash, the first thing to happen is everyone lives beyond their means because they are living off wealth that does not exist. In the Money Masters review posted on my site, linked to above, I note how one historical consequence of such a boom was a project to drain the Red Sea and recover the gold that Pharao's Army lost when God drowned them as they were chasing after the Israelites. According to Mark Thornton, the modern world has seen a record-breaking skyscraper precede every major economic crash. If he's right, we're in for a big one.
Research Watch
Mutation in Enzyme that Degrades LDL Receptor Virtually Abolishes Risk of Heart Disease
This study is from 2006, but incredibly important. A mutation in the PCSK9 gene, which codes for an enzyme that degrades the LDL receptor, was found in 2.6 percent of African Americans. The mutation eliminates the functional enzyme, so the cells produce much more of the LDL receptor and bring LDL in from the blood much more quickly. The mutation is associated with an 88 percent decrease in the risk of heart disease!
Many researchers hail this study as further evidence that it is high LDL levels that cause heart disease. It is not, and this study does not show that — in fact, it flatly contradicts it.
9.7 percent of blacks who did not have the mutation suffered a coronary event, while only 1.2 percent of blacks with the mutation suffered a coronary event. Only 85 blacks had the mutation, so it was only one man who had a heart attack. He had very high blood pressure (186/85 mm Hg), was obese, and smoked. He had a family history of heart disease, despite the fact that the mutation must have ran in his family. He had an extremely low level of LDL, only 53 mg/dL, but died at the age of 68 within 24 hours of having a heart attack. Clearly low LDL is not sufficient to protect against heart disease.
As described in my article on the true cause of heart disease, animal experiments have shown that high blood pressure is not sufficient to cause atherosclerosis, but can contribute to calcification of the media, and can accelerate atherosclerosis in the presence of oxidized blood lipids.
We do not know for sure whether this man's heart attack was due to atherosclerosis, but if it was, there is another key finding to take into account. His Lp(a) level was incredibly high, in the 95th percentile for his race and sex. As described in my article on the cause of heart disease and my crash course on lipoproteins, Lp(a) appears to be a very strong marker for the presence of oxidized blood lipids, especially oxidized phospholipids from the membrane of LDL.
Thus, this case of heart disease seems to suggest that it is not the level of LDL that is important, but the rate of LDL oxidation. In this man, so many factors may have contributed to the oxidation of his LDL that the fact that this level of LDL was extremely low made little if any difference.
One critical finding of this study, however, is that clearance of the LDL from the bloodstream is one of the most critical factors affecting the risk of heart disease. If LDL is rapidly cleared from the bloodstream, the rate of heart disease is nearly, but not entirely, abolished! Therefore, our focus should be understanding the nutritional and lifestyle factors that affect the rate of LDL utilization.
Curcumin Increases LDL Receptor and Suppresses Atherosclerosis
Chinese researchers recently published a paper showing how curcumin, a compound in tumeric, increases the expression of the LDL receptor. They had previously shown that curcumin has anti-atherosclerotic effects in humans and animals and in cell studies showed it upregulates the LDL receptor, which clears LDL from the blood, brings it into cells, and thereby prevents its oxidation. This study showed that curcumin increased expression of the LDL receptor and LDL uptake by isolated liver cells, and showed that it acted at the level of the gene-regulating factors that control the expression the LDL receptor.
The study leaves us with more questions than answers. The concentrations the researchers used were much higher than reached in human plasma during supplementation, and they did not show exactly how — whether directly or indirectly — it interacted with the regulatory molecules.
The basic finding that it has a primary effect on LDL receptor expression, increases clearance of LDL from plasma, and counters atherosclerosis, however, seems to lend further support to the basic concept that rapid clearance of LDL from plasma and into cells is desirable. Moreover, this study and others like it may stimulate research into the nutritional control of the LDL receptor.
We must also remember that thyroid hormone is a critical booster of LDL receptor function. Many dietary compounds interfere with thyroid function, called goitrogens. These are covered in my Special Report, Thyroid Toxins: Double-Edged Swords of the Kingdom Plantae.
Benefits of EPA/DHA End at 250 mg/Day
A recent review published in the American Journal of Clinical Nutrition by Dariush Mozaffarian of Brigham and Women's Hospital and Harvard Medical School concluded that omega-3 fish oil fatty acids EPA and DHA help prevent heart disease, but that the benefits only extent to taking 250 mg/day. This conclusion was based on the convergence of data from prospective cohort studies and randomized clinical trials.
This is just under 0.1 percent of calories for someone consuming 2500 calories per day. In my Special Report, How Essential Are the Essential Fatty Acids? I have emphasized the fact that the need for these fatty acids is incredibly low. If one were eating grass-fed butter, egg yolks, and meat and occasional fatty fish, one could easily obtain 250 mg/day of these fatty acids. Moreover, these studies are conducted in people consuming a massive excess of omega-6 fatty acids, which raises the requirement for omega-3 fatty acids.
There is one more interesting finding in the report. Mozaffarian writes, "Many, although not all, expreimentally characterized effects of EPA and DHA are similar (references), but some experiments suggest that DHA may be more preferentially antiarrhythmic (reference), and DHA tissue levels may more strongly predict lower CHD risk (reference)." As I wrote in my PUFA Report, I believe the evidence suggests that EPA is not natural to the mammalian body and does not belong there. It can, however, be converted to DHA, and this conversion is most robust when the total intake of PUFA is low, the intake of omega-6 linoleic acid from vegetable oil in particular is low, and the intake of vitamin B6 is high. The finding that EPA should have some benefits but DHA should be superior lends further support to this belief.
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Please take notice that the contents of this newsletter and Cholesterol-And-Health.com are copyright of Chris Masterjohn, 2007, and that this information is not to be construed or understood as any form of advice. Please visit my disclaimer page here.