Statins implicated in multiple sclerosis

This post includes a synopsis of a study published in the Journal of Neuroscience Research 2010 Nov 15;88(15):3361-75.

Study title and authors:
Simvastatin interferes with process outgrowth and branching of oligodendrocytes.
Smolders I, Smets I, Maier O, vandeVen M, Steels P, Ameloot M.
Biomedical Research Institute, School of Life Sciences, Hasselt University and Transnational University Limburg, Diepenbeek, Belgium.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/20857509

Oligodendrocytes are a type of brain cell. They are the cell type that is predominantly affected in multiple sclerosis. Myelin is the protective sheath coating our nerve fibers.

Any adverse effects on oligodendrocytes and myelin are detrimental and are implicated in multiple sclerosis.

The study focused on the effects of stain drugs on oligodendrocytes and myelin.

The study found:
(a) Cholesterol is required for the growth of oligodendrocytes.
(b) Statins inhibited the growth of oligodendrocytes.
(c) Statins inhibited the growth of myelin.

To conclude: Statin treatment has detrimental effects on oligodendrocyte growth, which is the prior step in (re)myelination, and thereby inhibits the healing of multiple sclerosis lesions.

Tip the scales towards plaque reversal

Tip the scales towards plaque reversalThere’s no one easy formula to achieve coronary plaque reversal: no single pill, supplement, food that guarantees that you drop your heart scan score.

But there are indeed factors which can work in favor or against the likelihood that you
gain control over your coronary plaque
.

Does everyone who tries to reverse coronary heart disease and reduce their heart scan score succeed? No, not everyone. There are indeed people who fail and see their heart scan score increase. There are usually identifiable and correctable reasons for this to happen. Occasionally, even someone who does everything right still sees their score increase. Thankfully, this is unusual.

There are a number of basic requirements that everybody needs to follow if you hope to gain control over your coronary plaque. There are also less common factors that need to be corrected only by some people. There are also factors that make it more difficult to drop your score.

What makes plaque reversal more likely?

Among the most important facets of the Track Your Plaque program are the recommended targets for conventional lipids: LDL 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl: 60-60-60. We call this the Track Your Plaque “Rule of 60”. (Refer to the Special Reports on each of these factors to see how we accomplish this. There’s no quick and dirty pill or supplement that immediately achieves these numbers, but there are indeed effective ways.)

The metabolic syndrome must be eliminated. This usually means weight loss, exercise, and reduction of high-glycemic index foods sufficient to achieve normal blood pressure (preferably 130/80 or less), normal blood sugar (≤100 mg/dl), a C-reactive protein <1.0 g/l. This is also good for your long-term health. The metabolic syndrome is a pre-diabetic condition. You can’t remain pre-diabetic for a lifetime. Unless corrective action is taken, you will convert to a full diabetic. You need to put a stop to this for lots of reasons, including gaining control over coronary plaque .

Lower scores are easier to control than higher scores. A level of 200 or less seems to represent a fairly distinct cut-off between easier and tougher. Having a higher heart scan score of, say 500, doesn’t means it’s impossible, but it will be somewhat tougher and may require a longer period. We’ve seen really high scores in the thousands take 2 to 3 years, for instance.

Taking fish oil. It’s truly shocking how few people take fish oil, even when they’ve suffered a heart attack. It’s simple, virtually harmless, and inexpensive. Yet the benefits are enormous. Fish oil is a crucial requirement for controlling coronary plaque.

Reaching a blood 25-OH-vitamin D3 level of 50 ng/ml. Though our appreciation for this fact is recent, it’s among the most exciting developments in coronary plaque reversal. In fact, we would rank vitamin D as among the most important heart health discoveries of the last 40 years, along with CT heart scanning and fish oil.

Having an optimistic attitude that allows you to see the bright side of problems, overcome difficulties, and engage in healthy relationships with family and friends. Optimists have an easier time in life and they seem to reduce their heart scan scores much more readily.

What makes plaque reversal tougher?

There are some obvious factors that make it less likely that you will drop your heart scan score: cigarette smoking; an unrestricted diet rich in donuts, fried chicken, spare ribs, and cookies; diabetes; uncontrolled high blood pressure; kidney disease. Chances are that, if these factors are uncorrected, you will simply not drop your heart scan score. It is much more likely that your score will increase, sometimes substantially, year after year. Eventually, heart attack or a major heart procedure (actually a lifetime series of procedures) will catch up to you.

More recently, we have seen several well-established diabetics drop their score, sometimes as much as 30%. However, it still remains more difficult if diabetes is part of the picture, as compared to a non-diabetic.

Pre-diabetes represents an intermediate between full-blown diabetes and non-diabetes. However, from a plaque reversal viewpoint, it does make it substantially tougher to drop your score.

Having lipoprotein(a), or Lp(a), also makes it more difficult. We have had more success in halting the increase in heart scan scores (i.e., holding the score steady without increase or decrease) in people with Lp(a), less success in dropping scores. Though our track record with Lp(a) is getting better and better, it still remains a tough nut to crack. With Lp(a), it is clear that you’ve got to work harder to succeed.

Higher scores are tougher to drop than lower scores. Someone with a starting score of, say, 1800, will have to try harder and for a longer period than someone starting with a score of 70. This holds true even if they share the same set of lipoprotein causes. The person with the higher score may even require 2 or 3 years before they see the score stop increasing or decrease, while the person with the lower starting score may drop their score in the first year. People with scores of <100 can even occasionally see zero again. This is not possible (with present-day knowledge) with high scores.

We’ve recently begun to appreciate that a pessimistic attitude may play an important role in your program. People who are angry, critical, see the bad in everything, are isolated and lack social involvement, have a much more difficult time reducing their scores.

Coronary plaque in the balance

In the Track Your Plaque program, we try to help you achieve as many advantages as possible to gain control over coronary plaque. While not perfect, the Track Your Plaque approach is, without question, the most effective program available anywhere.

Obviously, we can do nothing about our genetics, but we can identify and correct as many factors as possible. In this way, we tilt the scales heavily in favor of dropping your heart scan score.

Copyright 2007, Track Your Plaque, LLC
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What if your heart scan score is ZERO?

What if your heart scan score is ZERO?

Tremendous confusion persists about the implications about a heart scan score of zero.

A zero score is great! In fact, it’s the best result obtainable. But does it allow you to do anything you want, free of danger for the rest of your life?

A zero score can mean many different things

A score of zero is not a rare thing: Approximately 50% of people who get a CT heart scan have a score of zero—no detectable calcified coronary plaque. It’s the best score you can get, since heart scan scores never go below zero. By age 65, only 25% of people will maintain a score of zero.

But what exactly does a zero score mean? How long does it remain at zero? What implications does a zero score carry for cholesterol and other sources of heart disease risk?

Here’s what we know. If you are without symptoms of heart disease and your CT heart scan score is zero:

• Your risk for heart attack is very low, though not zero. Across all studies, if your score is zero, the likelihood of heart attack (or other major “event”) is in the range of 2-3% over the next 5 years, as compared, for instance, with a score of 100 in a 52-year woman carrying a risk of 20% over the same time period. Why isn’t your risk zero with a zero score? Well, statistically, nobody’s score is zero. That includes strapping 25-year old athletes and children. The exceptions (people who have heart disease with a zero score) include people who use cocaine or amphetamines, people with exceptionally high LDL cholesterol (“heterozygous hypercholesterolemia” with LDL cholesterols >225 mg/dl), those with severe hypertension, and some other rare disorders. In other words, for the vast majority of people with a zero score, your risk is indeed very low.
• Starting with a score of zero, you are unlikely to convert to a significantly positive heart scan score within the next 3–5 years. Approximately 90% of people with a zero score will remain at zero over that time period. For example, say your score was zero in 2005. In 2008, it’s probably still zero. But if it has turned positive (>0), it will likely be a modest score of only 10, 20, or 30—not 300 or 400. Positive scores are, of course, important for your prevention program, but they are rarely dangerous at a level of 10,20, or 30. This is the rationale behind recommending a heart scan score in 3–5 years if you have a zero starting score.

What a zero score does not mean

While a zero heart scan score is great short-term news, it does not mean that you are free of risk for a lifetime.

A heart scan score of zero does not mean that:

• You can ignore lipids and lipoproteins—These issues do, indeed, assume less urgency. Rather than weeks or months to correct your abnormalities, you may have years to do it. Since you are in far less imminent danger than, say, someone with a score of 700, you will likely not be treated with the same intensity. Your LDL target, for instance, might be 100 mg/dl, rather than <70 mg/dl. Perhaps you don’t need to reach an HDL of 60 mg/dl, and 50 mg/dl may be acceptable. (Your target values should be discussed with your doctor.) You may be less inclined to rely on prescription medication and can depend more on long-term lifestyle and nutritional approaches, as well as nutritional supplements. But a score of zero does not provide an open invitation to ignore lipids or lipoproteins.
• You can ignore other health issues—We’ve seen this happen: Someone has a heart scan score of zero, then completely neglects health, or becomes very lax. They skip exercise, eat unhealthy foods, over-snack, etc. Next thing you know, they’ve got high blood pressure, diabetes, bowel cancer, or any number of other diseases of lifestyle. Though our focus is heart disease risk, having no measurable coronary plaque does not provide license for health abuses.
• You are free of carotid or other atherosclerotic processes—With a heart scan score of zero, you’re far less likely to have carotid atherosclerotic plaque or plaque in any other artery, such as the aorta (causing stroke) and leg arteries. But you are not immune. Occasionally, someone with a substantial risk profile (e.g., smoker, diabetic, small LDL, low HDL, hypertension, etc.) will have no detectable coronary plaque but have a moderate quantity of carotid plaque. Should everyone, including people with zero scores, have carotid ultrasound to settle this question? Given the ease and safety of this test, we feel that this is actually a reasonable thing to do, though it is not yet conventional practice to screen people without symptoms for carotid disease. Should you prove to have carotid plaque of some degree but with a heart scan score of zero, then we feel that your prevention program should assume the same intensity as someone with a high heart scan score.
• .
• .
• .
• Do you know what’s even better than a heart scan score of zero? A second score of zero several years later. This means that, given your level of preventive efforts, no detectable plaque has developed. Two successive scores of places you into a very low-risk group. It means you have succeeded!

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Read the full article here. May require registration.

Statin Associated Myopathy and Exercise

Statin Associated Myopathy and Exercise

By Dr. Duane Graveline, M.D., M.P.H.
Not only can statin drugs cause myopathy ( muscle disease ) of varying degrees but this myopathy is greatly exacerbated by exercise. ( Ref 1 ). The effect of exercise is such that most experienced athletes will not use statins for fear of predisposition to muscle side effects of all kinds.

The severity of the muscle side effects from statins vary widely from relatively benign CPK elevation without symptoms, to muscle tenderness, aching, soreness and pain, and rarely, even to death from rhabdomyolysis.
The existing literature is lacking as to definite identification of mechanisms but a number of potential mechanisms include:
1. Induction of skeletal muscle fiber apoptosis ( cellular death, the usual result of accumulation of sufficient mitochondrial DNA mutations so the cell is taken out of service, so to speak ).
2. Alterations in ubiquitin-proteasome pathway activity ( a cellular system that identifies and degrades proteins ) leading to mitochondrial dysfunction ( the ultimate effect of CoQ10 inhibition secondary to mevalonate blockade ).
3. Terpenoid depletion ( consequence of dolichol inhibition and aberration in glycoprotein synthesis ).

These three pathways are also considered to be the primary channels by which we age - mitochondrial damage, CoQ10 depletion and dolichol inhibition. Additionally, I suspect that these three pathways that explain statin drug effects on muscle cells are the same for damage to other cell types as well.

Ten years ago an internet search would have come up with little to nothing on the subject of statin associated myopathy pathways but now the general pathophysiology has been defined by the many studies now in progress.

A major problem at present is that although these pathways are now well known to the research community, the clinical community of doctors is mostly lacking in the knowledge of even the basics of this statin effect and the very idea that statin damage uses the same pathways as aging is particularly difficult for clinicians to conceive.

The very idea that deficiency of this quaint supplement, CoQ10, is now considered by researchers to be a major foundation of statin damage and that many alternative medicine physicians are now far ahead of "regular doctors" in both their understanding and treatment of statin damage is particularly galling.

Dysfunction of the so called ubiquitin-proteasome pathway is a fancy way of saying CoQ10 inhibition, clearly defined in my first book, Lipitor®, Thief of Memory, years ago. What this refers to is the two-pronged statin attack on our mitochondria: first blocking the vital anti-oxidant role of CoQ10 and next blocking uptake of CoQ10 into the structure of complexes 1 and 2, major elements of electron transfer and ATP production. This occurs in every cell of our bodies.
It is difficult to understand how the developers of statins failed to recognize this potential, inevitable effect of compactin ( Mevastatin ) and lovastatin ( Mevacor ) the first statin drugs. The effect is there for all to see. What researchers are saying today had to have been clear to the original makers of statins. 

Next on this list of statin damage mechanisms currently reported by the research community is the consequence of terpenoid depletion. This is a fancy way of saying dolichol inhibition, additional collateral damage from mevalonate blockade. Remember, statin drugs are reductase inhibitors. To achieve reduction of cholesterol synthesis they have blocked the mevalonate pathway, inevitably blocking CoQ10 and dolichols ( and many other vital biochemicals as well ).

If the full range of CoQ10 deficiency on cellular function is difficult to accept, that of dolichols is nearly impossible for most clinicians since they have barely been introduced. Dolichols orchestrate the entire process of glycoprotein synthesis, the linkage of peptide fragments and certain sugars so the resulting strand not only determines our very emotionality but also cellular identity, communication and immunodefense. Without at least some basic understanding of dolichol biochemistry the possible effects of statins become unimaginable.

Not only do these processes of apoptosis, CoQ10 mediated mitochondrial damage and dolichol mediated glycoprotein dysfunction help to explain the full range of effects seen with statin myopathy but this same group of factors is involved in all other types of statin damage.

What we have found to be true as the underlying mechanism of statin injury to muscle cells is true for every other cell in our bodies as well. As to the aggravation of statin muscle damage from exercise, the ubiquitin-proteasome pathway in particular addresses this CoQ10 mandated process. When one's CoQ10 is at a minimal level, the slightest exercise is bound to aggravate.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

April 2011
1. http://www.ncbi.nlm.nih.gov/pubmed/20878737

Statin drugs do indeed provide real advantage...

According to cardiologist William R. Davis of Track Your Plaque...

 "...there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception."

Niacin and adrenochrome

 

We know that torectrapib was excellent at raising "good" HDL cholesterol, while simultaneously increasing the human death rate from heart attack to the point where it couldn't be ignored. We know that the Kitavans have low "good" HDL cholesterol and no heart disease. So we should forget good and bad cholesterol and concentrate on the things that really matter, which are probably
hyperglycaemia, hyperinsulinaemia and wheat. Plus a few other things like trans fats. But the HDL as "good" cholesterol hypothesis will not lie down, although it seems to have been dead for some time. The statins raise HDL, but can be ignored due to their host of confounding pleiotropic effects, inseparable from their cholesterol effects. The current flavour of the month for raising HDL,
since the demise of torcetrpib, appears to be niacin, vitamin B3, in multigram doses.

There is no doubt that niacin elevates HDL cholesterol levels and, according to those who follow these things, decreases overall mortality. Now niacin is a very interesting drug. Oh, at 2.0g a day niacin is a drug, not a vitamin. Its career began with Abraham Hoffer, who is still going strong, back in the 1950s. On the basis that "vitamin" doses of niacin had half emptied the psychiatric wards when the problem of pellagra was solved by Goldberger, Hoffer tried massive doses of B3 on schizophrenic patients. The idea was to see if they had a poor response to "normal" doses of B3 which could be overcome by high doses. It worked.

Hoffer's publication in 1954 was last-authored by Smythies, so I assume he was Hoffer's supervisor.

Smythies is also still going strong and has recently summarised the adrenochrome theory of schizophrenia in one of his many publications.

My guess is that niacin may be working by reducing adrenochrome in the brains of schizophrenics. I've no idea of how this works, but it is interesting to note that adrenochrome is an oxidation product and niacin is an effective antioxidant.

That dynamo of genuine cardiovascular research, Kummerow, has looked at adrenochrome in the blood of hypertensive patients. It's there and it mangles the vascular epithelium. Now, does niacin reduce adrenochrome in the blood stream as well as in the brain? It is, after all, a significant antioxidant and anti inflammatory agent. No one has looked at this as far as I know. I certainly don't know if this is the case, but I'm suspicious.

If it does, who cares about the HDL cholesterol effect? Like the statins, niacin appears to be a useful drug, possibly a very useful drug, chosen for the wrong reason. Unlike the statins, niacin has
relatively little "badness" attached to it. The problem with torcetrapib was that it ONLY adjusted cholesterol levels. Whatever its associated "badness" or "goodness" might have turned out to be.

That's what happens when you spend millions or maybe billions of dollars developing a drug based on a wrong hypothesis.

Peter

Krauss is in the HOUSE: 'Low-fat Message Was a MISTAKE'

"Everybody I know in the field -- e v e r y b o d y -- recognized that a simple low-fat message was a mistake," says Dr. Krauss, as interviewed in the latest Men's Health magazine, see below. Why is Men's Health interviewing Krauss?! What is this revolutionary MH reporter saying? Don't. S-W-A-L-L-O-W . . . ! ? ? *haa!!* Men's Health, Your Unstoppable Heart: Before you swallow what your doctor prescribes, we suggest you read this article By: Paul Scott CHOLESTEROL IS A NATURAL SUBSTANCE your body produces for a variety of uses. It is carried through the body in three containers -- LDL, HDL, and VLDL -- that deliver it to cells along with triglycerides. The average man reasons that the cholesterol in his scrambled eggs must surely end up in his arteries somehow, and this makes him do things like order egg-white omelets for breakfast. There is indeed a link between the cholesterol you eat and the cholesterol in your arteries. It's just not the "eat more, have more" worry that's been drummed into you for years. In fact, your body's production and uptake of cholesterol is highly regulated; eat a six-egg omelet and your body simply produces less cholesterol because of the dietary onslaught. "There is a very weak connection between the LDL cholesterol we measure and dietary cholesterol," Dr. Krauss says. "I spend a lot of time talking to reporters and trying to explain that dietary cholesterol is not the same as blood cholesterol." He adds that the 200 milligrams of cholesterol most people eat every day is NOTHING compared with the 800 milligrams their bodies produce [my EMPHASIS]. But you don't have to take his word for it. "It is now acknowledged that the original studies purporting to show a linear relation between cholesterol intake and coronary heart disease may have contained fundamental study design flaws," wrote the author of a recent review in the International Journal of Clinical Practice. [ HERE . Jones PJ citing Hu et al] The author suggests to lower small dense LDL, the actual heart disease culprit Targeting the Killer LDL Small changes, fewer small particles "Small, dense particles of LDL are much more inflammatory than larger particles," says Paul Ziajka, M.D., Ph.D., a clinical lipidologist with the Southeast Lipid Association. Here's how to snuff the little devils. Crack an egg Down an omelet every morning and you may lower your small-particle count, University of Connecticut researchers recently found. People who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent. Choose your meds wisely A class of drugs known as fibrates, which includes Tricor, specifically targets small, dense LDL, says Dr. Ziajka. The effect is significant only when your triglycerides are also elevated, he says. [Note: no statin mentioned...*haa*; actually low carb, sat fats and fish oil omega-3 work far FAR better than fibrates, PPAR drugs] Pop some niacin "Most drugs shift particle size after the cholesterol is made," Dr. Ziajka says. "Niacin causes the liver to produce larger particles." Try a no-flush variety (Dr. Ziajka recommends Slo-Niacin) starting with 500 milligrams a day and building to 2,000. There are side effects, so talk to your doctor first. [Note: no-flush doesn't work; slo-niacin is a lower-flush type of niacin] Lighten your load Deflating your spare tire may reduce your small, dense LDL cholesterol, say scientists at Children's Hospital Oakland Research Institute. The majority of overweight men who were pattern B (mostly small LDL) switched to pattern A (mostly large LDL) after they lost an average of 19 pounds. Have a glass That nightly beer does more than relax you -- it may also lower your small, dense LDL, a recent Journal of Clinical Endocrinology Metabolism study found. Men who drank 7 to 13 alcoholic drinks a week had 20 percent fewer small-LDL particles than men who didn't drink at all. [Note: beer aint paleo] Previous animal pharm: Men's Health interview with Mozzafarian MD on benefits of dietary saturated fats Read more about Krauss et al's newest research that redeems the role of saturated fats at my fave peeps and playgrounds: Tourgeman, holymoly ur so funny Nephropal Seth Roberts my Berkeley bud... Animal Fat Peter Hyperlipid Stephan WholeHealthSource Don Primal Wisdom Chris Masterjohn Daily Lipid Dr. Mike Eades THANKGODFORYOURSANENESS

BMJ Admits Competing Commercial Interests in Wakefield Attacks Warranted Disclosure

This post is not about the primary focus normally evident here but rather the related mis-steps of  scientific journals in their presentation of believable science. Tainted is the word that comes to mind. Thank you Health Impact News Daily (http://healthimpactnews.com) for this news item.
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BMJ Admits Competing Commercial Interests in Wakefield Attacks Warranted Disclosure

BMJ editor admits that they should have disclosed competing commercial interests in Wakefield attack

By John Stone Age of Autism

British Medical Journal’s editor has been forced into an embarrassing admission that the journal should have disclosed connections with MMR manufacturers Merck and GSK when publishing attacks on the integrity of Andrew Wakefield in January  (HERE). Godlee’s admission came eight days after my letter to the journal was submitted, and three days after the publication of my article on Age of Autism (HERE). My letter was occasioned by an article in Age of Autism by Martin J Walker (HERE ) subsequently also published in  Vera Sharav’s AHRP newsletter (HERE).  I had been responding to an article highlighting the issue of free access journals and advertising: BMJ apparently did not think this applied to them.

Godlee’s admission, “We did not declare these competing interests because it did not occur to us to do so”, underlines the complacence, and even arrogance, of large journals that think they are above having interests. Nor will her defence carry much water amid the hotly disputed claims of Brian Deer’s articles that the issue was fraud so who manufactured the products did not matter. BMJ in a breach of the basic traditions of peer review journals have been unwilling to allow their and  Deer’s  allegations to be discussed directly in its columns, many letters to the journal have been blocked, Deer has never been required to respond to criticisms, and the defence of their position has been crudely legalistic (HERE ).

Godlee was also reduced to make a technical defence of the journal decision to publish the Deer articles in Age of Autism (HERE) and BMJ Rapid Responses (HERE).

However, Godlee’s admission represents a major blow against scientific journals, however large, not declaring their commercial interests: the excuse “it did not occur to us” will scarcely wash again.

This is the latest episode in a long running series of battles between Age of Autism and the journal. In February 2010 BMJ were forced to admit that Prof Trisha Greenhalgh had not only contributed to Brian Deer’s website, but had also received £1.4m in Department of Health research grants since 2003 (HERE, HERE ). In March 2010 Age of Autism highlighted the removal by BMJ of a series of letters questioning how Brian Deer obtained confidential material about Royal Free patients and MMR litigants, while in May 2010 the journal refused to acknowledge that Brian Deer was the undisclosed complainant to the GMC against Wakefield and colleagues (HERE), which has been covered by tortuous language in the latest publications, though never acknowledged in the Sunday Times. Age of Autism has also focussed on the role of Harvey Marcovitch who doubles as a BMJ associate editor, co-authoring editorials against Wakefield, and chairman of panels at the GMC (HERE ).

Read the Full Article Here: http://www.ageofautism.com/2011/03/bmj-admits-competing-commercial-interests-in-wakefield-attacks-warranted-disclosure.html

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http://healthimpactnews.com

Is Your Bottled Water Killing You? By William Davis, MD

Health Benefits of Magnesium Replacement What can you expect from supplementing magnesium to optimal levels? Research over the past 20 years suggests that magnesium supplementation will accomplish several critically important goals: Magnesium improves insulin sensitivity. Magnesium helps correct impaired insulin sensitivity, the fundamental defect that characterizes pre-diabetes and metabolic syndrome. An intracellular enzyme called tyrosine kinase requires magnesium to allow insulin to exert its blood-sugar-lowering effects. In several studies, daily oral magnesium supplementation substantially improved insulin sensitivity by 10% and reduced blood sugar by 37%.21-23 Magnesium helps correct abnormal lipoprotein patterns. Improved insulin sensitivity from magnesium replacement can markedly reduce triglyceride levels.23 Reduced triglyceride availability, in turn, reduces triglyceride-rich particles, such as very low-density lipoprotein (VLDL) and small low-density lipoprotein (small LDL), both of which are powerful contributors to heart disease.24 Magnesium supplementation can also raise levels of beneficial high-density lipoprotein (HDL).24 Magnesium suppresses abnormal heart rhythms. Magnesium has gained a foothold in hospital care following coronary bypass surgery, when the abnormal heart rhythm known as atrial fibrillation commonly occurs. Magnesium may help suppress this rhythm outside of the hospital as well,25 suggesting a preventive role in averting abnormal heart rhythms. Magnesium reduces blood pressure. Magnesium regulates blood pressure by modulating vascular tone. Magnesium works in ways similar to the prescription hypertension drugs known as calcium-channel antagonists (such as diltiazem and nifedipine), which block calcium channels that trigger constriction of the arteries. Magnesium stimulates the production of prostacyclins and nitric oxide, which are potent artery-relaxing agents.26 Magnesium exerts a modest effect of reducing blood pressure, reflecting its whole-body artery-relaxing properties.27 Magnesium can block migraine headaches. Magnesium has been explored as a means to prevent or relieve migraine headaches. People suffering migraine headaches tend to have lower magnesium levels.28 A study from the State University of New York showed that intravenous magnesium relieved headache symptoms in 15 minutes in 80% of recipients.29 Other studies have since corroborated magnesium’s beneficial effect on migraine headaches, including a trial in children, in which oral supplementation with magnesium oxide reduced the frequency and severity of migraine.30 Magnesium may improve exercise performance. Extensive research in athletes has found that intensive exercise triggers magnesium loss through urinary excretion and perspiration. When magnesium is low, supplementation enhances exercise performance by reducing lactate blood levels (indicating brief, strength-based anaerobic muscle activity), decreasing oxygen requirements, and increasing muscle strength.31,32 Magnesium may benefit many other conditions. Other conditions in which magnesium is believed to exert positive effects include fibromyalgia,33 asthma (acute episodes have been treated successfully with both intravenous and aerosolized magnesium),34 prevention of osteoporosis,35 and premenstrual syndrome.36 Can you correct metabolic syndrome and its complications—such as insulin resistance and high blood pressure—without replacing magnesium? Of course you can, just as you can operate your car without changing the oil. However, magnesium deficiency will catch up with you, and consuming this basic supplement will help you to more easily achieve your health goals. Strategies for Optimizing Your Magnesium Intake According to the US Department of Health and Human Services, nearly all of us fail to achieve even the modest magnesium RDAs of 420 mg for adult males and 320 mg for adult females. Most American adults ingest about 270 mg of magnesium a day, well below the RDA and enough to generate a substantial cumulative deficiency over months and years.37 The magnesium RDA refers to elemental magnesium, defined as the amount of magnesium regardless of its source or form. Magnesium is generally available as various “salts” (not to be confused with table salt), and the amount of elemental magnesium contained in each varies depending on the salt. For example, the amount of magnesium in magnesium oxide is 60%; in magnesium carbonate, 45%; in magnesium citrate, 16%; and in magnesium chloride, 12%.38 Thus, magnesium oxide supplements tend to contain more elemental magnesium per pill than do magnesium citrate supplements. Magnesium salts differ in absorption. Magnesium oxide, though inexpensive and widely available, is thought to be relatively less absorbed than the citrate and chloride forms.39-41 You can also increase your magnesium intake by choosing foods rich in magnesium, which are listed in the table below.42 Foods rich in magnesium (magnesium content in mg) Almonds (1 oz; 24 nuts) 78 Oatmeal (1 cup, cooked) 56 Artichokes (1 cup) 101 Pumpkin seeds (1 oz; 142 seeds) 151 Barley (1 cup, raw) 158 Rice, brown (1 cup, cooked) 84 Beans, black (1 cup, cooked) 120 Soybeans (1 cup, cooked) 148 Beans, lima (1 cup, cooked) 101 Spinach (1 cup, cooked) 163 Brazil nuts (1 oz; 6-8 nuts) 107 Trail mix (1 cup) 235 Halibut (1/2 filet) 170 Walnuts (1 oz; 14 halves) 45 Filberts, hazelnuts (1 oz) 46 Wheat flour, whole grain (1 cup) 166 Oat bran (1 cup, raw) 221 Source: USDA National Nutrient database for Standard Reference, Release17 Dietary Sources of Magnesium Nuts, pumpkin seeds, spinach, and oat bran are particularly rich and healthy sources of magnesium. Another strategy for boosting magnesium intake is to supplement your diet with the soluble fiber known as inulin. Like other soluble fibers, inulin may exert modest cholesterol- and triglyceride-reducing effects. However, it also enhances magnesium absorption in the intestine.43 Inulin can be taken as a supplement, and is contained in some foods (for example, the Stonyfield Farms brand of yogurt). Inulin can help increase satiety (the sense of fullness you get with eating), resulting in decreased calorie intake throughout the day.44 Inulin thus holds promise in supporting efforts to lose weight.45 One more important way to optimize your magnesium intake is to choose water that is rich in magnesium. Unfortunately, in the US, this is easier said than done. The FDA regulates bottled water and mandates that the only additives permitted are fluoride and antimicrobials to deter bacterial growth. Magnesium cannot therefore be added to water labeled spring water or mineral water. Magnesium Content of Mineral Waters The following waters contain far more than the usual amounts of magnesium. Some, like Apollinaris and Pellegrino, are widely available in American grocery stores, while others are found only in upscale groceries or through websites of the water producers. Mineral Water Magnesium Content Original Fountain of Youth Mineral Water (Florida) 609 mg/L Apollinaris (Germany) (410 mg/L of sodium) 130 mg/L Adobe Springs (California and other western states) 110 mg/L Badoit (France) 85 mg/L Colfax (Iowa) 91 mg/L Deep Rock (Colorado) 60 mg/L Evian 24 mg/L Gerolsteiner (Germany) 108 mg/L Noah’s California Spring Water 110 mg/L Pellegrino Sparkling Mineral Water (Italy) (43.6 mg/L of sodium) 55.9 mg/L Manitou Mineral Water (Colorado) 43 mg/L Rosbacher 93 mg/L St. Gero 109.4 mg/L Both Apollinaris and Pellegrino contain more sodium than most other waters, and therefore should be avoided by those who are limiting their sodium intake due to existing hypertension, fluid retention, or kidney disease. Magnesium-rich mineral waters are not easy to find, but they are out there. By FDA definition, mineral waters must contain at least 250 parts per million (ppm) of total dissolved solids. Not all mineral water contains significant quantities of magnesium. For example, Napa Valley’s Calistoga Springs, labeled as “mineral water,” contains 0.61–0.96 mg/L of magnesium, or virtually none. Magnesium Dosage Guidelines The recommended dietary allowance (RDA) for magnesium is 420 mg a day for adult men and 320 mg a day for adult women.46 Most people fail to achieve the RDA, which may lead to magnesium deficiency.37 The most common adverse reaction from the use of magnesium supplements is diarrhea. Other gastrointestinal symptoms include nausea and abdominal cramping. Diarrhea and other gastrointestinal symptoms are less likely to occur if magnesium supplements are taken with food.46 Magnesium supplements are contraindicated in those with kidney failure. Those with myasthenia gravis (an autoimmune disorder that results in progressive skeletal muscle weakness) should avoid magnesium supplements.46 To determine the amount of magnesium contained in bottled water labeled “mineral water” but not listed above, go to the bottler’s website to determine the water’s composition. With the exception of Florida’s Original Fountain of Youth Mineral Water, drinking an entire liter of many so-called mineral waters provides only a modest amount of magnesium. Thus, for instance, if you are currently ingesting around 250 mg a day of magnesium from your diet, drinking a liter of Gerolsteiner a day (supplying 108 mg/L of magnesium) will increase your magnesium consumption only to about 350 mg per day. However, by adding a magnesium supplement that provides as little as 100 mg of elemental magnesium, you will have more than achieved the RDA for an adult male. Since many mineral waters are expensive (around $2-3 per liter), magnesium supplements are a far less costly way to optimize your magnesium intake. Conclusion The intensification of municipal water treatment has resulted in a growing epidemic of magnesium deficiency, with most Americans failing even to achieve the modest levels set by the government-recommended RDA. Most of us have daily deficiencies in magnesium intake of only 70-200 mg a day. The consequences of magnesium deficiency can be dramatic, including poor insulin response, migraine headaches, high blood pressure, and abnormal and even dangerous heart rhythms. Fortunately, there are plenty of healthy choices—foods rich in magnesium, low-cost magnesium supplements, and waters rich in magnesium—that can you help reach or exceed the magnesium RDA and attain the numerous health benefits conferred by optimal magnesium intake. Dr. William Davis is an author and cardiologist practicing in Milwaukee, WI. He is founder of the Track Your Plaque program, a heart disease prevention and reversal program that shows how CT heart scans can be used to track and control coronary plaque. He can be reached at www.TrackYourPlaque.com. The Basics of Water and Water Purification While the Environmental Protection Agency regulates the quality of tap water, the Food and Drug Administration (FDA) is responsible for regulating bottled water. In 1995, the FDA issued its most recent regulations classifying various waters: Artesian well water is water that naturally flows upward from an underground aquifer to a well, without the need for pumping. Mineral water is water from an underground source that contains at least 250 parts per million (ppm) of dissolved solids consisting of minerals and trace elements. Mineral content of 250-500 ppm is often called “low mineral content” or “light mineral water,” while content of 1500 ppm or greater is “high mineral content.” (In Europe, spring waters with dissolved solids equal to or less than 500 mg/L are considered “mineral with low mineral content” or simply “mineral water.”) Minerals and trace elements cannot be added artificially to water labeled as mineral. Spring water, like artesian well water, comes from an underground source but flows naturally to the earth’s surface. It cannot come from a public or municipal source. Spring water must be collected directly at the spring or through a borehole tapping the underground source. Mineral content is less than 250 ppm and cannot be added after collection. Well water is water from a hole bored or drilled into the ground, which taps into an aquifer and is drawn to the surface using a pump. Many homes in the US that do not have access to municipal water use well water. To make matters even more complicated, any water—regardless of the source—can be treated or filtered. This is usually done to modify its taste or to remove undesirable ingredients. Methods of treatment are defined as: Distillation. Water is vaporized and collected, leaving behind any solid residues, including minerals. Distilled water contains no minerals whatsoever. Reverse osmosis. In this common water-purifying process, water is forced through membranes to remove minerals in the water. Deionization. Also called demineralization or ion exchange, this process uses synthetic resins to remove ions and minerals from water. This is very effective at removing ionized impurities, but does not remove organic, bacterial, pathogenic, or particulate matter efficiently. Deionized water contains no magnesium. Absolute 1 micron filtration. Water is passed through filters that remove particles larger than 1 micron in size, including Cryptosporidium, a parasite that causes intestinal infestation. This process does not affect the water’s mineral content. Ozonation. Many bottled water companies use this process instead of chlorine to rid water of bacteria. Ozonation does not affect the mineral content of water. Many bottled waters are simply tap water processed using one or more of the above processes of distillation, reverse osmosis, deionization, or filtration. This leaves the water virtually devoid of both nutrients and contaminants. Of the 700 or so brands of bottled water available in the US, 80% are processed water. Many experts say that treated water like this is virtually identical to that produced by home water purifiers. The appeal of these waters is therefore a reduction in impurities like lead and pesticide residues, or better taste—but not enhanced mineral content. Bottled processed waters contain little or no magnesium. It should also be noted that unlike tap water, purified waters and water purifiers reduce or eliminate the fluoride that is added by many municipal treatment facilities to promote dental health. Although the FDA permits producers to add it back to purified water, few actually do. Waters derived from natural sources like artesian well water, well water, mineral water, and spring water are generally slightly richer in mineral content than are processed and tap waters. However, the difference is small. Nearly all American bottled waters obtained from natural sources—whether artesian, well, spring, or mineral waters—contain less than 6 ppm of magnesium, a trivial amount.

References

1. Available at: http://www.historyofwaterfilters.com/. Accessed November 14, 2006. 2. Azoulay A, Garzon P, Eisenberg MJ. Comparison of the mineral content of tap water and bottled waters. J Gen Intern Med. 2001 Mar;16(3):168-75. 3. Available at: http://lpi.oregonstate.edu/infocenter/minerals/magnesium/index.html. Accessed November 14, 2006. 4. Touyz RM. Magnesium in clinical medicine. Front Biosci. 2004 May 1;9:1278-93. 5. Liebscher DH, Liebscher DE. About the misdiagnosis of magnesium deficiency. J Am Coll Nutr. 2004 Dec;23(6):730S-1S. 6. Durlach J, Bac P, Durlach V, et al. Magnesium status and ageing: an update. Magnes Res. 1998 Mar;11(1):25-42. 7. Eisenberg MJ. Magnesium deficiency and sudden death. Am Heart J. 1992 Aug;124(2):544-9. 8. Dacey MJ. Hypomagnesemic disorders. Crit Care Clin. 2001 Jan;17(1):155-73, viii. 9. Eisenberg MJ. Magnesium deficiency and cardiac arrhythmias. NY State J Med. 1986 Mar;86(3):133-6. 10. Purvis JR, Movahed A. Magnesium disorders and cardiovascular diseases. Clin Cardiol. 1992 Aug;15(8):556-68. 11. Smetana R, Stuhlinger HG, Kiss K, Glogar DH. Intravenous magnesium sulphate in acute myocardial infarction—is the answer “MAGIC”? Magnes Res. 2003 Mar;16(1):65-9. 12. Kousa A, Havulinna AS, Moltchanova E, et al. Calcium:magnesium ratio in local groundwater and incidence of acute myocardial infarction among males in rural Finland. Environ Health Perspect. 2006 May;114(5):730-4. 13. Anderson TW, Le Riche WH, MacKay JS. Sudden death and ischemic heart disease. Correlation with hardness of local water supply. N Engl J Med. 1969 Apr 10;280(15):805-7. 14. Available at:http://www.nsf.org/international/press_release.asp?p_id=12041. Accessed November 14, 2006. 15. Laires MJ, Monteiro CP, Bicho M. Role of cellular magnesium in health and human disease. Front Biosci. 2004 Jan 1;9:262-76. 16. Berkelhammer C, Bear RA. A clinical approach to common electrolyte problems: 4. Hypomagnesemia. Can Med Assoc J. 1985 Feb 15;132(4):360-8. 17. Roffe C, Sills S, Crome P, Jones P. Randomised, cross-over, placebo controlled trial of magnesium citrate in the treatment of chronic persistent leg cramps. Med Sci Monit. 2002 May;8(5):CR326-30. 18. Bilbey DL, Prabhakaran VM. Muscle cramps and magnesium deficiency: case reports. Can Fam Physician. 1996 Jul;42:1348-51. 19. Bussone G. Pathophysiology of migraine. Neurol Sci. 2004 Oct;25 Suppl 3S239-41. 20. He K, Liu K, Daviglus ML, et al. Magnesium intake and incidence of metabolic syndrome among young adults. Circulation. 2006 Apr 4;113(13):1675-82. 21. Guerrero-Romero F, Tamez-Perez HE, Gonzalez-Gonzalez G et al. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes Metab. 2004 Jun;30(3):253-8. 22. Rodriguez-Moran M and Guerrero-Romero F. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care. 2003 Apr;26(4):1147-52. 23. Yokota K, Kato M, Lister F, et al. Clinical efficacy of magnesium supplementation in patients with type 2 diabetes. J Am Coll Nutr. 2004 Oct;23(5):506S-9S. 24. Rasmussen HS, Aurup P, Goldstein K, et al. Influence of magnesium substitution therapy on blood lipid composition in patients with ischemic heart disease. A double-blind, placebo controlled study. Arch Intern Med. 1989 May;149(5):1050-3. 25. Piotrowski AA, Kalus JS. Magnesium for the treatment and prevention of atrial tachyarrhythmias. Pharmacotherapy. 2004 Jul;24(7):879-95. 26. Sontia B, Touyz RM. Role of magnesium in hypertension. Arch Biochem Biophys. 2006 May 24. 27. Jee SH, Miller ER, III, Guallar E, et al. The effect of magnesium supplementation on blood pressure: a meta-analysis of randomized clinical trials. Am J Hypertens. 2002 Aug;15(8):691-6. 28. Gallai V, Sarchielli P, Morucci P, Abbritti G. Magnesium content of mononuclear blood cells in migraine patients. Headache. 1994 Mar;34(3):160-5. 29. Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulfate rapidly alleviates headaches of various types. Headache. 1996 Mar;36(3):154-60. 30. Wang F, Van Den Eeden SK, Ackerson LM, et al. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Headache. 2003 Jun;43(6):601-10. 31. Lukaski HC. Magnesium, zinc, and chromium nutrition and athletic performance. Can J Appl Physiol. 2001;26 SupplS13-S22. 32. Cinar V, Nizamlioglu M, Mogulkoc R. The effect of magnesium supplementation on lactate levels of sportsmen and sedanter. Acta Physiol Hung. 2006 Jun;93(2-3):137-44. 33. Sarac AJ, Gur A. Complementary and alternative medical therapies in fibromyalgia. Curr Pharm Des. 2006;12(1):47-57. 34. Blitz M, Blitz S, Hughes R, et al. Aerosolized magnesium sulfate for acute asthma: a systematic review. Chest. 2005 Jul;128(1):337-44. 35. Rude RK, Gruber HE. Magnesium deficiency and osteoporosis: animal and human observations. J Nutr Biochem. 2004 Dec;15(12):710-6. 36. Rapkin A. A review of treatment of premenstrual syndrome and premenstrual dysphoric disorder. Psychoneuroendocrinology. 2003 Aug;28 Suppl 3:39-53. 37. Ervin RB, Wang CY, Wright JD, Kennedy-Stephenson J. Dietary intake of selected minerals for the United States population: 1999-2000. Adv Data. 2004 Apr 27;(341):1-5. 38. Available at: http://ods.od.nih.gov/factsheets/magnesium.asp#h6. Accessed November 15, 2006. 39. Firoz M, Graber M. Bioavailability of US commercial magnesium preparations. Magnes Res. 2001 Dec;14(4):257-62. 40. Coudray C, Rambeau M, Feillet-Coudray C, et al. Study of magnesium bioavailability from ten organic and inorganic Mg salts in Mg-depleted rats using a stable isotope approach. Magnes Res. 2005 Dec;18(4):215-23. 41. Walker AF, Marakis G, Christie S, Byng M. Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study. Magnes Res. 2003 Sep;16(3):183-91. 42. Available at: http://www.nal.usda.gov/fnic/foodcomp/Data/SR14/wtrank/sr14w304.pdf. Accessed November 15, 2006. 43. Roberfroid MB. Introducing inulin-type fructans. Br J Nutr. 2005 Apr; 93 Suppl 1S13-S25. 44. Archer BJ, Johnson SK, Devereux HM, Baxter AL. Effect of fat replacement by inulin or lupin-kernel fibre on sausage patty acceptability, post-meal perceptions of satiety and food intake in men. Br J Nutr. 2004 Apr;91(4):591-9. 45. Hoeger WW, Harris C, Long EM, Hopkins DR. Four-week supplementation with a natural dietary compound produces favorable changes in body composition. Adv Ther. 1998 Sep-Oct;15(5):305-14. 46. Available at: http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/mag_0167.shtml. Accessed November 16, 2006.

Magnesium

Reduce High Cholesterol with Nutritional Magnesium   

Written By:  William Davis, MD       

February is Heart Health Month and heart health expert and cardiologist Dr. William Davis, M.D., talks about the importance of lowering high cholesterol naturally and reducing your chances of coronary heart disease with the use of magnesium and other nutritional strategies.

Tired of the media onslaught promoting statin drugs? What happened to the conversation about nutritional strategies that reduce cholesterol? Since February is Heart Health Month, now is a great time to highlight the importance of magnesium for the reduction of high cholesterol.

There are a number of ways to significantly reduce cholesterol using diet and nutritional supplements. Reductions in bad cholesterol, or LDL cholesterol, of 25, 30, 50, even 100 mg/dl are possible—if you have the right information.

At the top of the list of natural strategies to reduce LDL and supplement and/or sometimes replace your need for prescription medication (in consultation with your doctor) is magnesium.
Magnesium can act like a natural statin drug and lower bad cholesterol (LDL), reduce triglycerides and increase good cholesterol (HDL) (1).

In order for the body to make cholesterol, it requires a specific enzyme called HMG-CoA reductase. Magnesium regulates this enzyme so as to maintain only a proper amount of cholesterol in the body. When the body is magnesium deficient, cholesterol continues to be produced in excess, which can cause a cholesterol buildup and may lead to coronary heart disease.

The HMG-CoA reductase enzyme is the exact same enzyme that is targeted and inhibited by statin drugs. The inhibiting process is similar to magnesium's function, except that magnesium is the natural way that the body has evolved to use to control and limit cholesterol when it reaches a certain level; statin drugs are used to destroy the entire mechanism.

The term metabolic syndrome describes a set of conditions that many believe may be another name for the consequences of long-term magnesium deficiency. The list includes high cholesterol, hypertension and elevated triglycerides that lead to and promote coronary heart disease, stroke and type-2 diabetes. In a 2006 study (2) published in the American Heart Association's journal Circulation, entitled: Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults researchers concluded: “Our findings suggest that young adults with higher magnesium intake have lower risk of development of metabolic syndrome.”

In an age when statins dominate conventional heart disease prevention, an important role remains for nutritional approaches. Because statin drugs are principally LDL-reducing agents and do not address other causes of heart disease, nutritional strategies add a real advantage. Nutritional approaches can be used to minimize and sometimes eliminate the use of statin drugs altogether. Perhaps it would be better to regard statin therapy as a solution only when natural, nutritional means have been exhausted.

The adherence to a healthy diet is not enough in the majority of cases. The American Heart Association’s diet, for instance, yields a 7% drop in cholesterol. That’s too small to make any real difference (3) and, by itself, virtually guarantees a future of heart disease. The formerly popular ultra low-fat diets (≤10% of calories from fat) yield variable drops in cholesterol, but HDL or the good cholesterol is also substantially reduced and harmful triglycerides increased (4). The net effect can be increased risk of heart disease and diabetes.

The restriction of processed carbohydrates is an effective way to lose weight and thereby reduce cholesterol, particularly for people starting with lower HDL and higher triglycerides. Reducing intake of flour products (pasta, breads, bagels, pastries, cookies, cakes, pretzels, and other processed foods) may, in fact, yield larger drops in cholesterol than now outdated low-fat diets (5).
While dietary restriction of total fat intake has only limited power to reduce cholesterol, avoidance of saturated fat (e.g., in butter, greasy meats, cured meats, fried foods) and hydrogenated fat (“trans fats” in margarine, shortening, and many processed foods) remains a well-proven means of reducing LDL cholesterol modestly. Replacing saturated fat sources with healthy monounsaturated oils (olive, canola, flaxseed) provides even greater benefits for cholesterol reduction, as well as reduced triglycerides and VLDL (6, CM Williams, et al., 1999).

Weight loss (if you’re overweight) has broad effects on risk reduction: reduction of cholesterol levels (total and LDL), increased HDL, reduced triglycerides, and correction of small LDL, VLDL, and abnormal postprandial (after-eating) fat clearance (7).

Magnesium can help. Magnesium helps the body digest, absorb, and utilize proteins, fats, and carbohydrates and helps prevent obesity genes from expressing themselves.

As a practical solution, supplementation at a level of 2.3 milligrams of magnesium per pound of body weight per day (this comes to about 345 milligrams per day for a 150 lb individual) can really help. When supplementing with magnesium, start on a gradient of a low dose and gradually build up. If you get diarrhea you can lower the dose back down until you are at a comfortable level. While magnesium supplementation is generally quite safe, people on certain antibiotics should not take magnesium. If you have kidney disease (renal failure) or any kidney disorders, you should not take any magnesium supplements without consulting a physician.

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water and foods, supplemental magnesium is necessary for nearly everyone to ensure healthy levels. Not all forms of magnesium are equally absorbed by the body. One of the most absorbable forms of nutritional magnesium is magnesium citrate in powder form. Start out slow and build up to and find your body's tolerance level.

For most people, no single supplement or diet change will reduce LDL to your target. A combination of several strategies usually yields the large drops that we need to achieve dramatic LDL reduction, but nutritional magnesium and the above diet adjustments will help.

Heart health expert and cardiologist, William Davis, M.D., is the author  of "Track Your Plaque: The only heart disease prevention program that  shows how the new CT heart scans can be used to detect, track, and  control coronary plaque" (www.trackyourplaque.com). Dr. Davis is a  member of the Nutritional Magnesium Association and invites you to get  more information that will help you avoid the magnesium deficiency. Go  to www.nutritionalmagnesium.org.

The ideas, procedures and suggestions contained in this article are not intended as a substitute for consulting with your physician. All matters regarding your physical health require medical supervision. Neither the author nor the publisher shall be liable or responsible for any loss, injury or damage allegedly arising from any information or suggestion in this article. The opinions expressed in this article represent the personal views of the author and not the publisher.
References

1. Rosanoff A, Seelig MS, “Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals.” J Am Coll Nutr 2004;23(5):501S-505S.
2. Ka He, MD, ScD; Kiang Liu, PhD; Martha L. Daviglus, MD, PhD et al. Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults. Circulation 2006;113:1675-1682.
3. Pearson TA, Blair SN, Daniels SR, Eckel RH, Fair JM, Fortmann SP, et al. AHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 update. Consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases. Circulation 2002;106:388–91.
4. Krauss RM, Dreon DM. Low-density lipoprotein subclasses and response to a low-fat diet in healthy men. Am J. Clin Nutr 1995: 62:478S–87S.
5. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006 May;83(5):1025–31.
6. Gulesserian T, Widhalm K. Effect of a rapeseed oil substituting diet on serum lipids and lipoproteins in children and adolescents with familial hypercholesterolemia. J Am Coll Nutr 2002 Apr;21(2):103–8.
7. Miller WM, Nori-Janosz KE, Lillystone M, Yanez J, McCullough PA. Obesity and Lipids. Curr Cardiol Rep 2005 Nov;7(6):465–70.

Published online, Feb. 2010, WholeFoods Magazine
http://www.wholefoodsmagazineonline.com/