Monday, April 25, 2011

Statins implicated in multiple sclerosis


Study title and authors:
Simvastatin interferes with process outgrowth and branching of oligodendrocytes.



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.


Saturday, April 23, 2011

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

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.
  • .
  • .
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  • 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!
Read the full article here. May require registration.

Statin Associated Myopathy and Exercise

Statin Associated Myopathy and Exercise

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

Thursday, April 7, 2011

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."

Sunday, April 3, 2011

Niacin and adrenochrome













Why is Men's Health interviewing Krauss?! What is this revolutionary MH reporter saying?





Clinical Practice. [ HERE . Jones PJ citing Hu et al]

Targeting the Killer LDL Small changes, fewer small particles

"Small, dense particles of LDL are much more inflammatory

Crack an egg
small-LDL levels by an average of 18 percent.

Choose your meds wisely

Pop some niacin

Lighten your load
after they lost an average of 19 pounds.

Have a glass


Tourgeman, holymoly ur so funny Nephropal
Seth Roberts my Berkeley bud... Animal Fat
Peter Hyperlipid
Chris Masterjohn Daily Lipid

Friday, April 1, 2011

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.

BMJ Admits Competing Commercial Interests in Wakefield Attacks Warranted Disclosure







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


Is Your Bottled Water Killing You

Is Your Bottled Water Killing You?

By William Davis, MD

Health Benefits of Magnesium Replacement


Strategies for Optimizing Your Magnesium Intake

Foods rich in magnesium (magnesium content in mg)
Almonds (1 oz; 24 nuts) 78Oatmeal (1 cup, cooked) 56
Artichokes (1 cup) 101Pumpkin seeds (1 oz; 142 seeds) 151
Barley (1 cup, raw) 158Rice, brown (1 cup, cooked) 84
Beans, black (1 cup, cooked) 120Soybeans (1 cup, cooked)148
Beans, lima (1 cup, cooked) 101Spinach (1 cup, cooked) 163
Brazil nuts (1 oz; 6-8 nuts)107Trail mix (1 cup) 235
Halibut (1/2 filet) 170Walnuts (1 oz; 14 halves) 45
Filberts, hazelnuts (1 oz) 46Wheat flour, whole grain (1 cup) 166
Oat bran (1 cup, raw) 221Source: USDA National Nutrient database for Standard Reference, Release17

Dietary Sources of Magnesium

Magnesium Content of Mineral Waters
Mineral WaterMagnesium Content
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
Manitou Mineral Water (Colorado) 43 mg/L
Rosbacher 93 mg/L
St. Gero109.4 mg/L
Magnesium Dosage Guidelines


The Basics of Water and Water Purification


Written By:  William Davis, MD       


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).


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.

  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.
  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