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Bill Sardi
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Posted August 5, 2013: by Bill Sardi
Something huge is going on in the cholesterol world. Those lipoproteins we have been taught to be phobic over – LDL (low density “bad” cholesterol), total cholesterol and triglycerides, as well as HDL cholesterol (high density “good” lipoproteins), believed to clog arteries and induce heart attacks, are losing scientific ground as true measures of your risk for a mortal heart attack. Another lipoprotein that was cast aside decades ago is gaining attention.
That lipoprotein is called lipoprotein(a). Readers may recall it is the cholesterol particle that was temporarily made famous by vitamin C researchers Drs. Linus Pauling and Matthias. Since their research in the 1990s lipoprotein(a) has been largely shunned and ignored.
Before I go on to write about lipoprotein(a), I am forced to address the shortcomings of the cholesterol theory of heart disease. It takes a strong amount of evidence to convince anyone, especially gullible statin drug users, that cholesterol is a mistaken direction in modern medicine.
Despite the fact 25 million Americans take statin drugs to lower circulating levels of cholesterol, when Dr. John Abramson, author of Overdosed America, analyzed the top ten statin drug studies he couldn’t find any evidence their use prevents mortality from coronary artery disease among healthy adults.
The real risk of heart attack is much lower than the hype would suggest. Because heart attacks only occur in about 8-12 adults in 1000 over a 5-year period, it takes a lot of people taking statin drugs to derive a measurable benefit. Only about 1 in 200 healthy adults and 1 in 70 at-risk patients avert a non-mortal heart attack by taking statin drugs.
Statin cholesterol-lowering drugs are said to reduce the risk of a non-mortal heart attack by a third, but that is a relative number, not a hard number. The misleading impression is that statin drugs prevent heart attacks in 33 of 100 users. However, reduction of LDL cholesterol from 190 to 90 reduces the risk for a heart attack from 12 in 1000 to 8 in 1000, about a third. In hard numbers however that is only 4 in 1000 (4/10ths of one percent).
Meanwhile, the rate of side effects produced by statin drugs (muscle aches, diabetes, loss of memory, mental depression, liver toxicity), said to be ~3% is more like 10-15%. One recent study says the side effect rate for statin drugs is 17%. So the risk of serious side effects far outnumbers any alleged health benefits. So much for modern medicine’s dictum “first do no harm.”
The FDA gets itself off the hook because it issues warnings of side effects. But these warnings haven’t dented the number taking these drugs. So the unstated policy in practice at the FDA appears to be “if the patients are dumb enough to take these drugs there is nothing we are going to do to stop them.”
The most feared heart problem, sudden-death heart attack, is not prevented by cholesterol reduction. That is primarily because circulating cholesterol is not a measure of the static plaque that builds up inside arteries which is a result of inflammation.
A landmark study published in the New England Journal of Medicine in the year 2000 showed that unstable arterial plaque is responsible for most sudden mortal heart attacks. More disconcerting is the fact vitamin C has been clearly identified as a natural agent that prevents unstable plaque, but it has been ignored.
About half of the people who experience heart attack have low to normal total circulating cholesterol, lowering cholesterol in adults with normal-range cholesterol is of no benefit, even elevated levels of the so-called “bad” LDL cholesterol do not increase heart attack risk, and HDL “good” cholesterol doesn’t make any difference for heart disease risk either.
Facts like these are not likely to alter what is prescribed. Statin drugs bring patients to doctors’ offices and cholesterol phobia is now so ingrained it is unlikely the cholesterol train will ever be derailed. Statin drugs are a big cash cow for pharmaceutical companies. However, the Food & Drug Administration has given license to sell statin drugs on what appear to be false advertising claims.
Dr. Arthur Agatston, a leading Miami cardiologist, says “the cholesterol number is essentially worthless.”
In fact, a 30-year follow-up study reported that for each 1% milligram/ deciliter drop in cholesterol there was an 11 percent increase in all-cause mortality! The implication here is that cholesterol reduction with statins may kill rather than save lives.
Sadly, even when confronted with data like this, patients still want numbers to give them (false) assurance their heart is healthy.
I’ve taken nearly 700 words to rattle the nerves of statin drug users before I identify the long ignored lipoprotein that DOES have cardiologists concerned. But many others have written about the drawbacks of statin drugs and haven’t put a dent in their sales. I don’t live under the illusion my words will dissuade the average cholesterol-phobe either.
The long-ignored lipoprotein that is the subject of this report is lipoprotein(a), often called “lipoprotein little a.” Discovered 50 years ago, it is only now being reconsidered after a flurry of research beginning in the 1970s.
Published reports about lipoprotein(a) are noted by these recent titles:
“Fifty years of lipoprotein(a) – the magical mystery continues.” – Journal of Internal Medicine, January 2013
“Lipoprotein(a): more interesting than ever after 50 years.” -Current Opinion in Lipidology, April 2012
“Lipoprotein(a): resurrected by genetics.” – Journal Internal Medicine, January 2013
What is known about lipoprotein(a) is that it is an LDL-like particle. It is produced in the liver and some people produce gobs of it because of a genetic predisposition. Lipoprotein(a) is transported on LDL-cholesterol particles.
In the 1970s lipoprotein(a) was largely dismissed as a fatty particle that induces heart and blood vessel disease. Then modern medicine followed by introducing a number of statin drugs that interfered with the natural production of cholesterol particles in the liver. But in a full-turn circle, modern genetic studies have truly resurrected lipoprotein(a). It is now considered the “strongest genetic risk factor for coronary heart disease.”
Unexpectedly, there is no correlation between lipoprotein(a) and other known risk factors for heart disease such as age, sex, blood pressure, body mass index, inflammation (C-reactive protein) and albumin. Lipoprotein(a) (or Lp(a) for short) stands alone as a risk factor and there is reason why.
A report published in 2008 in the Archives of Internal Medicine said: “Contrary to previous reports that there was no association between lipoprotein(a) with coronary heart disease”… lipoprotein(a) represents a risk factor in adults that is “very high, considerably higher than blood pressure, blood serum cholesterol and C-reactive protein.” Elevated levels of Lp(a) can cause atherosclerosis without elevated cholesterol. But, uh, how did they miss it for all these years?
More striking is the fact lipoprotein(a) is a particle that is particularly pathogenic to humans. Lp(a) is only found in humans, old world monkeys, guinea pigs and hedgehogs, not in other animals. All are animals that do not produce vitamin C naturally due to a genetic mutation.
How did modern medicine get side tracked about the importance of lipoprotein(a) when Drs. Linus Pauling and Matthias Rath conducted ground-breaking experiments in the 1990s that clearly showed Lp(a) replaces ascorbate (vitamin C) in artery walls when vitamin C levels are low, resulting in a weakened arterial wall? It has been known for some time that injury to the internal walls of arteries are milder in areas that have higher levels of ascorbate.
A report published in 1957 in the Canadian Medical Association Journal, thirty-three years prior to the animal study conducted by Linus Pauling and Matthias Rath, clearly demonstrated that arterial plaque can rapidly form in animals without intentionally over-feeding them cholesterol but by depriving them of vitamin C. Early plaque formation could actually be reversed with provision of vitamin C!
Experiments conducted at the Cleveland Clinic, published in 1988, demonstrated that as Lp(a) levels increase, arterial narrowing worsens. At a blood serum level of 31.6 milligrams/deciliter or higher 92% of postoperative coronary artery bypass surgery patients exhibited arterial narrowing (stenosis).
This oversight is beginning to look more like dereliction of duty rather than inattentiveness. The anti-vitamin biases of cardiology were manifest even decades ago, before the era of statin drugs. Inexplicably modern medicine still declares Lp(a) to be a mystery today as it did nearly 25 years ago! There is no mystery surrounding Lp(a). There is a just a covert effort to distract and cover up what Drs. Pauling and Rath discovered over two decades ago.
Let us not overlook the fact that Dr. Linus Pauling published a book in 1970 entitled Vitamin C And The Common Cold and the intake of vitamin C (largely from dietary supplements) rose 300% and a steep decline in mortality from coronary heart disease was clearly documented.
The latest “definitive” paper on the subject of Lp(a) makes no mention of the work of Matthias Rath or Linus Pauling. Neither do any of the other papers written on Lp(a) in the past few years. Science is being censored.
I’m sure readers are eager now to learn more about Lp(a) and vitamin C. At what precise point do Lp(a) numbers represent an elevated risk for coronary heart disease? What natural agents or drugs aside from vitamin C lower Lp(a)?
The reason why cardiologists are not treating patients with elevated Lp(a) levels with known agents that lower it is largely because there is no medication that lowers Lp(a) below known risk levels.
Furthermore, the range of Lp(a) in humans is quite variable, with some individuals exhibiting almost no Lp(a) in their blood (0.1 mg/deciliter), the vast majority of people having relatively low Lp(a) levels (under 200 mg/deciliter), and some people having Lp(a) blood levels greater than 1000 mg/deciliter, with African Americans exhibiting very high concentrations.
Elevated Lp(a) levels are present at birth, but obviously do not represent a risk till later in life, a fact that will be revisited later in this report.
Adding to the Lp(a) puzzle is that while it is assumed that elevated Lp(a) levels are not favorable for survival, studies reveal high Lp(a) levels are found more frequently among centenarians. This fact should not lead to the mistaken conclusion that elevated levels of Lp(a) are desirable, just that there may be compensating factors in the diet or environment that negate its effect. Elevated Lp(a) numbers in centenarians may reflect accumulation of iron in body tissues, another factoid that is discussed below.
Experts believe circulating blood levels of Lp(a) above 30 mg/deciliter represent elevated risk for coronary heart disease. Lp(a) levels above 25 mg/deciliter are present in ~30% of Caucasians and 60-70% of African Americans. However, none are being treated today.
Elevated Lp(a) has been called an “untreatable” condition for a variety of reasons.
First, elevated Lp(a) is genetically predetermined in many individuals.
Second, there is no conclusive study to show that any technology employed to lower circulating Lp(a) levels actually reduces mortality rates from heart disease. Shame on modern medicine for dragging its feet on this important issue. Isn’t this evidence that the National Institutes of Health is playing footsy with the statin drug makers so as not to reveal their drugs, which do not reduce Lp(a), are ineffective against a major cause of death?
In fact, a recent report urged the academic and scientific communities, via grant support from the National Institutes of Health and investment by the pharmaceutical industry, to develop specific novel and targeted therapies that lower Lp(a). But that might mean the $30 billion in annual sales of statin drugs would vanish. Statin drugs actually raise Lp(a) levels. Big Pharma may have a lot to hide here.
Third, while there are a number of natural and prescription agents that significantly lower Lp(a), they may not lower it enough.
The best known agents that lower Lp(a), aspirin, niacin, L-carnitine, apple pectin, vitamin D, lower Lp(a) by 20-35%. A person with an Lp(a) level of 200 mg/deciliter taking an anti-Lp(a) agent that reduces Lp(a) to 130 mg/deciliter (-35%) still leaves the patient in the high-risk range.
Fourth, the only certain way to reduce Lp(a) (up to -80%) is to remove Lp(a) outside of the body in a process called apheresis, which is quite expensive and impractical.
Fifth, the cut-off point where Lp(a)-lowering treatment should begin lies somewhere between 30-50 mg/deciliter of blood serum. But recall, now, African Americans would all require treatment using this measure. Also there are confounding reports that show (1) elevated Lp(a) does not predict cardiovascular disease among adult-onset (Type 2) diabetes and (2) there is a greater risk for cancer among individuals with Lp(a) below 80 mg/deciliter. So there is a tradeoff between lowering Lp(a) below 20-30 mg/deciliter to prevent heart disease and raising Lp(a) above 80 mg/deciliter to prevent cancer.
Fifth, two studies, one that employed 1000 mg per day and another 4500 mg per day, show that supplemental vitamin C does not lower circulating Lp(a) levels.
Does all this sound confusing? It is. There is no straight forward relationship between higher Lp(a) levels and heart disease for all adults. Exceptions abound.
Modern medicine is repeating the same mistake it made with cholesterol, which was to equate circulating blood levels of cholesterol with arterial plaque.
In this instance, it is the lack of vitamin C and permits incorporation of Lp(a) into the arterial wall, which results in a weakened arterial wall and collapse of arteries and veins.
I postulate that this is why elevated Lp(a) is associated with retinal vein occlusion and unusual cases of childhood ischemic stroke. This is a likely reason why elevated Lp(a) has been shown to increase narrowing (stenosis) of arteries but not plaque area. Lp(a)-laden arteries simply collapse.
Elevated circulating Lp(a) is not only associated with unstable arterial plaque but also with clotting (thrombosis) in the venous return circulation.
A definitive report has been published about the pro-thrombotic (blood clotting) properties in lower-pressure veins and pro-atherosclerotic properties (unstable plaque) in higher pressure arteries.
Modern medicine characterizes elevated Lp(a) as causal for stenosis (internal narrowing) of arteries with the false assumption that narrowing is solely due to plaque. It is during the diastole (resting state rather than the systolic pumping phase of the heart) that arteries and veins are more likely to collapse, prompting formation of a clot.
Think of an Lp(a)-weakened artery or vein as one of those flat thin-walled garden hoses that only inflate with water pressure compared to a round thick-walled garden hose.
A lack of vitamin C can result in greater deposition of Lp(a) within the walls of arteries and veins. Veins are more likely to collapse and produce blood clots (thrombosis). The blood pools and becomes stationary with the passive (lower pressure) return to the heart and lungs. As arterial walls weaken due to lack of collagenous support as a result of a shortage of vitamin C, thrombosis (local blood clots) then form, which is a characteristic of elevated Lp(a).
A unique case where a prematurely born neonate presented with a blood clot in the heart is also explained by elevated lipoprotein(a) in the arterial wall due to an assumed a lack of vitamin C.
Again, where modern medicine is making a big mistake is measuring circulating Lp(a) as it mistakenly did with cholesterol. Circulating cholesterol does not equate with cholesterol plaque, nor does elevated circulating Lp(a) equate with Lp(a) deposition within arterial and venous walls. (Note: Doppler ultrasound can be utilized to estimate arterial wall thickness, such as in the carotid (neck) arteries.)
That supplemental vitamin C doesn’t reduce circulating Lp(a) is irrelevant. Nor can any natural Lp(a)-lowering agent (niacin, L-carnitine, apple pectin, or vitamin D3) replace vitamin C. Only supplemental vitamin C interrupts Lp(a) deposition within the inner-artery wall. Virtually any amount of circulating Lp(a) can result in intra-arterial deposition, just higher Lp(a) levels would hasten the onset of an undesirable cardiovascular event (heart attack or stroke) at an earlier point in time.
Because supplemental vitamin C is rapidly excreted (within 30 minutes) in urinary flow, optimal vitamin C levels can only be maintained by repeat supplementation throughout the day (500 mg X5/day), or by slowing the absorption of supplemental vitamin C with accompanying bioflavonoids or utilizing slow-release vitamin C tablets.
Secondarily, because arterial and venous walls are weakened due to Lp(a) deposition resulting from a shortage of vitamin C, calcium deposits are also more likely to form. Lp(a) is strongly associated with calcification of coronary arteries that supply the heart with oxygenated blood.
There is also a strong association between circulating Lp(a) and autoimmune atherosclerosis. This makes sense as blood vessel walls weaken due to poor collagen formation from a lack of vitamin C, with internal lesions in arteries attracting white blood cells in a protective immune response to prevent infection.
Given that all humanity is afflicted with a genetic mutation that negates liver synthesis of vitamin C (ascorbate), one would think arterial disease would be universally endemic from an early age. In fact, investigators have called attention to the fact that a third of healthy young adults exhibit elevated levels of Lp(a) which would theoretically increase their risk for heart attacks and strokes. But this is not the typical case. Humans do not experience strokes and heart attacks typically till later in life. This may be explained by the fact iron accumulation doesn’t begin till later in life.
Iron may be the culprit in raising Lp(a) levels. Iron is in short supply during the growing years of life as it is needed to make new red blood cells. Only when childhood growth has ceased does iron begin to accumulate, first in males and later in females when their monthly menstrual flow ceases with the change of life.
Examine these facts. In iron deficiency anemia, Lp(a) levels decline. Phlebotomy (blood letting), which is employed to reduce stored iron (ferritin) levels, reduces Lp(a) levels. Iron overload significantly decreases circulating ascorbate (vitamin C) levels which could result in greater incorporation of Lp(a) into artery walls. Only recently have investigators shown high stored iron levels (ferritin) increase the risk for acute heart attacks by an astounding 572%!
It is also interesting to note that high blood serum levels of Lp(a) are accompanied by high iron storage (ferritin) levels and low albumin levels (albumin helps to control iron) in cases of severe stroke.
There is evidence that the reduction of Lp(a) by blood filtration (apheresis) also removes iron. It is the accumulation of iron, as measured by the iron storage protein ferritin, that appears to be involved in the reduction of Lp(a). Ferritin (iron storage) is also independently associated with arterial calcification.
Iron appears to be a major underlying factor in the reduction of circulating levels of ascorbate (vitamin C) and resultant incorporation of Lp(a) and calcium within artery walls.
Furthermore, modern dietary habits can also help explain, with all of the medical technology available today, why mortal heart attacks still occur. The consumption of refined sugars in sweetened beverages raises circulating levels of Lp(a). High-fructose corn syrup, now added to many foods and beverages, increases the risk for iron overload in the liver, where Lp(a) is synthesized.
Despite convincing information that links low circulating levels of vitamin C (which may be due to poor intake or iron overload) with incorporation of Lp(a) and calcium into artery walls, modern day researchers have the gall to say “the lack of a definitive functional mechanism involving an Lp(a)-dependent pathway in coronary heart disease pathogenesis has limited the potential clinical connotation of Lp(a).” None are so blind as those who will not see.
In closing, dietary supplements can be safely and economically utilized to both lower circulating Lp(a) levels and inhibit Lp(a) substitution into artery walls.
A recently published animal study showed that the consumption of crushed flaxseed (flaxseed meal) significantly reduces circulating Lp(a) levels (-67% in the aortic arch, the first blood vessel outside the heart), which is comparable with Lp(a) removal by apheresis. Again, this reduction in circulating Lp(a) may not equate with reduced incorporation of Lp(a) into blood vessel walls, but it may serve to slow the disease process.
Another encouraging study showed that an undesirable blood protein known as homocysteine as well as Lp(a) are significantly reduced among adults when given a regimen of B vitamins (25 milligrams of vitamin B6, 2000 micrograms of vitamin B12 and 2500 micrograms of folic acid) over a period of four months. This can be achieved with a well-designed multivitamin.
Drs. Pauling and Rath successfully utilized the human equivalent of 2800 milligrams/day of vitamin C to prevent arterial aging in laboratory animals (40 mg per kilogram/2.2-lbs body weight, 60-lb human). A daily regimen of supplemental oral vitamin C (500 mg 5X/day) taken every 4 hours, preferably with bioflavonoids to slow absorption and reduce rapid excretion, will produce optimal blood levels and will likely inhibit incorporation of Lp(a) into blood vessel walls.
A low-iron diet (small amounts of red meat) and avoidance of multivitamins with iron and copper as well as avoidance of refined sugars and intake of calcium from the diet rather than supplements are all advised.
If obtaining a ferritin iron storage blood test, the healthy range for ferritin is 20-50 nanograms/milliliter of blood.
Professional advice that such a dietary supplement regimen is unproven needs to be weighed against the fact statin cholesterol-lowering drugs have already been disproven. Any physician who advises that patients should wait for some currently unknown Lp(a) lowering drug to be introduced at some indefinite time in the future does not fully recognize mankind’s total vulnerability to heart disease following a universal genetic mutation that ceased natural liver synthesis of vitamin C compared to most other animals that internally produce vitamin C.
This paper represents a master explanation that incorporates cholesterol, calcification, iron, homocysteine, lipoprotein(a) and genetics as factors that explain the age-related onset of cardiovascular disease.
Modern medicine’s cupboard is bare when it comes to prevention of coronary artery disease-related death. What harm could come from adding a tablespoon of flaxseed meal, a few B vitamins and some vitamin C to the daily diet? ©2013 Bill Sardi, Knowledge of Health, Inc.
Dynamic Factors That Influence Lipoprotein(a) |
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Raises Lp(a) |
Lowers Lp(a) |
Prevents incorporation of Lp(a) into walls of blood vessels |
| Statin cholesterol-lowering drugs Iron (red meat, iron pills) |
L-carnitine (-10 to 20%) Apple pectin (-35%) Vitamin D (-25%) Niacin (-30 to 35%) IP6 rice bran (unknown) Alcohol (-20 to 57%) Estrogen (-37%) |
Vitamin C pills 40 mg per kilogram (2.2 lbs.) body weight or 2800 mg for a 160-lb adult 500 mg/5 times a day Ascorbic acid Mineral ascorbate Ascorbyl palmitate |
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