Thumb your nose at swine flu

Judging from what we know about vitamin D, it is highly probable that it confers substantial protection from viral infections, including swine flu.

Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) first connected the dots, identifying the possibility of an influence of vitamin D on incidence of flu.

In 2006, Dr. Cannell reports noticing that the patients in his psychiatric ward in northern California were completely spared from the influenza epidemic of that year, while plenty of patients in adjacent wards were coming down with flu. Dr. Cannell proposed that the apparent immunity to flu in his patients may have been due to the modest dose of 2000 units vitamin D per day he had prescribed that the patients in other wards had not been given. (Since the hospital was run by the state of California, Dr. Cannell apparently had only so much leeway with vitamin D dosing.) While it’s not proof, it’s nonetheless a fascinating and compelling observation.

A similar conclusion was reached in a recent analysis of the National Health and Nutrition Examination Survey demonstrating that the higher the vitamin D blood level, the less likely respiratory infections were.

Personally, I used to suffer through 2 or 3 episodes of a runny nose, sore throat, hacking cough, fevers and feeling crumby every winter. Over the last 3 years since I’ve supplemented vitamin D, I haven’t been sick even once. The past two years I didn’t bother with the flu vaccine, since I suspected that my immunity had been heightened: no flu either winter.

And so it has been with the majority of my patients. Since I began having patients supplement vitamin D to achieve normal blood levels (we aim for 60-70 ng/ml), viral and bacterial infections have become rare.

New research is uncovering myriad new ways that vitamin D enhances natural immune responses to numerous infections, including tuberculosis, bacteria such as those causing periodontal disease and lung infections, and viruses like the influenza virus. Enhanced immunity against cancer is also an intensive area of research on vitamin D.

Will vitamin D supplementation sufficient to achieve desirable blood levels confer sufficient immunity to swine flu should it come to your door? From what we know and what we’ve seen in the few years of vitamin D experience, I think it will in the majority. But I do believe that we should still heed public health warnings to avoid contact with others, minimize exposure to crowds, avoid travel to affected areas, etc.

Will the real LDL please stand up?

The results of the latest Heart Scan Blog poll are in.

The question: How has your LDL been measured? The 187 responses broke down as:


I have only had a conventional calculated value
108 (57%)

NMR LDL particle number
35 (18%)

Apoprotein B
21 (11%)

Direct LDL cholesterol
21 (11%)

Non-HDL cholesterol
8 (4%)

I don't know what you're talking about
23 (12%)


Remember the TV game show, To Tell the Truth? Celebrities would have to guess which of three guests represented the real person, such as the notorious con man, Frank Abagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")

The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!"

If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:

--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation.

--Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL.

--Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.

--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.

--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL.


While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.

Vitamin D and inflammation

We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack.

A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.

In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.


Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.

Zitterman A, Frisch S et al.

BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis.
OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects.
DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program.
RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group.


(Calcitriol = 1,25-dihydroxy vitamin D.)


Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.

Even monkeys do it


It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound.

A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku:

Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.”

Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."
In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning.

Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves.

Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication.

If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?



Image courtesy Wikipedia

Cath lab energy costs

In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory.

A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).

All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging.

Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath.

Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing.

At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs.

If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold.

By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluids.

That's just one procedure. The amount of trash generated by these procedures is staggering, much of it plastic. I don't know how much of the U.S.'s annual plastic trash burden of 62 billion pounds (source: EPA) originates from the the cath lab, but I suspect it is a big number in total.

So if you are truly interested in reducing your carbon footprint and doing your part to be "green," avoid a trip (or many) to the cath lab.

Wag the Dog

What if the system to provide heart care has already gotten as big as it should be?

Worse (for hospitals), what if it’s already far larger than it needs to be? Can the system continue to increase revenues if they’ve already attained titanic proportions and outgrown demand? After all, darn it, there are only so many sick people around.

Hospital administrators might have to face an unpleasant choice: downsize to strip excess capacity and suffer the consequences in a competitive market, or . . . fabricate demand for their services.

Like the Dustin Hoffman and Robert DeNiro characters in the movie, Wag the Dog, about how two media-manipulators divert public attention away from a Presidential sex scandal by fabricating a war, spin is everything. It’s enough to sidetrack public attention from a scandal, obscure a truth, send us on a useless detour.

If healthcare for the heart isn’t driven by need, but many still desire to reap the benefits of the procedure-focused system, why not increase the perceived need?

That’s precisely the course that many hospital systems have chosen to follow. If the market you serve has been tapped to its full potential, then grow the market.

Imagine if a company like General Motors were to operate this way. In 2006, for instance, GM sold 9.1 million automobiles. If GM executives were to decide that they’d like to outstrip Toyota by boosting sales by 10% to 10 million, how would they do it? They would first have to determine whether it was feasible to grow demand for their product. If deemed possible, the company would need to ramp up manufacturing capacity to anticipate increased demand. If they miscalculate, GM could be stuck with a costly surplus and have to swallow the costs, maybe selling leftovers at a loss. (We don’t mean to pick specifically on GM; they’re a fine company as far as we’re concerned. This is just a hypothetical illustration.)

But what if a company could concoct some sort of scheme to persuade the car-buying public that they just had to have their cars or trucks? In other words, they could, in effect, create demand for their products.

As perverse as it sounds, that is exactly what occurs in healthcare for heart disease. The system long ago exceeded the necessary level of infrastructure to maintain a high-quality level of care accessible to most Americans. Instead, it continues to grow through a distortion of perception, delivering more services of increasing complexity to larger and larger numbers of people.

The size of the market is therefore a manipulable thing, something that can be massaged and cultivated. There are a variety of clever ways to exaggerate the need for heart procedures.

Why not raise the alarm for heart disease every chance you get? When a local sports figure survived a heart attack here in Milwaukee, St. _____ marketing department was right there, broadcasting the process in TV ads after his recovery. What could be more American than baseball, apple pie . . . and St. _____ Hospital? After his hospital discharge, the 57-year old local icon was shown on the sidelines with his team, back on the job, and at home with family, all beaming, just three months after a bypass operation. “I received only the very best care at St. _____ Hospital. They treated me like family. St. _____ doctors and nurses are the best!” Predictably, a two-month long spike in hospital testing followed filled with people worried whether they, too, might be in imminent danger. Several local cardiologists boasted of the many sports figures who came through the stress testing and heart catheterization labs, though virtually all checked out to be fine.

Though it can serve a legitimate purpose in some situations, stress tests are the ultimate example of a heart scam built on the perception of danger. Pull people in with promises of reassuring them whether or not they have heart disease, only to provide murky results that usually do no such thing. The pitfalls of the test are turned to advantage. The all too common equivocal or mildly abnormal result can be converted into a hospital procedure. (Imagine you could perform such alchemy on the uncertain calculations on your income taxes.)

With millions of stress tests performed every year and the push to perform more and more screening tests, the market has, in effect, been expanded—even though no increase in the disease itself has actually occurred.

Beware: As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine.

Heart scan book



There are only two books on heart scans available.

One, of course, is Track Your Plaque.

The other is the basic book on heart scans, What Does My Heart Scan Show?

Lost in the navigation column to the left on this blog is the link to get the electronic version of the book. In case you didn't know, we make this available for free.

If you're interested, just go here. This book can provide many basic answers to the questions that often arise regarding heart scans, such as the expected rate of increase in score, how your score compares to other people, when should a stress test be considered. Many heart scan centers use this book for educational purposes to help patients understand the importance of their heart scan scores.

(The sign-up for the book requires that an e-mail address be entered.)

The hard copy of What Does My Heart Scan Show? is available from Amazon, also, for $12.99.

Lies, damned lies, and statistics

In the last Heart Scan Blog post, I discussed the question of whether statin drugs provide incremental benefit when excellent lipid values are already achieved without drugs.

But I admit that I was guilty of oversimplification.

One peculiar phenomenon is that, when plaque-causing small LDL particles are reduced or eliminated and leave relatively benign large LDL particles in their place, conventional calculated LDL overestimates true LDL.

In other words, eliminate wheat from your diet, lose 25 lbs. Small LDL is reduced as a result, leaving large LDL. Now the LDL cholesterol from your doctor's office overestimates the true value.

Anne raised this issue in her comment on the discussion:

I eliminated wheat - and all grains - from my diet nearly three years ago (I eat low carb Paleo). My fish oils give me a total of 1680 mg EPA and DHA per day, and my vitamin D levels since last year have varied between 50 ng/ml and 80 ng/ml. However, my lipid profile is not like either John's or Sam's:

LDL cholesterol 154 mg/dl
HDL cholesterol 93 mg/dl
Triglycerides 36 mg/dl
Total cholesterol 255 mg/dl

My cardiologist and endocrinologist are happy with my profile because they say the ratios are good, no one is asking me to take a statin. My calcium score is 0.



However, if we were to measure LDL, not just calculate it from the miserably inaccurate Friedewald equation, we would likely discover that her true LDL is far lower, certainly <100 mg/dl. (My preferred method is the bull's eye accurate NMR LDL particle number; alternatives include apoprotein B, the main apoprotein on LDL.)

So Anne, don't despair. You are yet another victim of the misleading inaccuracy of standard LDL cholesterol determination, a number that I believe should no longer be used at all, but eliminated. Unfortunately, it would further confuse your poor primary care doctor or cardiologist, who--still believe in the sanctity of LDL cholesterol.

By the way, the so-called "ratios" (i.e., total cholesterol to HDL and the like) are absurd notions of risk. Take weak statistical predictors, manipulate them, and try to squeeze better predictive value out of them. This is no better than suggesting that, since you've installed new brakes on your car, you no longer are at risk for a car accident. It may reduce risk, but there are too many other variables that have nothing to do with your new brakes. Likewise cholesterol ratios.

Aspirin, Lipitor, and a low-fat diet

Despite all the hoopla heart disease receives in the media, I continue to marvel at how many people I meet who still think that aspirin, Lipitor, and a low-fat diet constitute an effective heart attack prevention program.

It doesn't. No more than washing your hands prevents all human infections. It helps, but it is a sad substitute for a real prevention program.

Of course, aspirin, Lipitor, and a low-fat diet is the same recipe followed by the unfortunate Tim Russert and his doctors. You know how that turned out. Mr. Russert's experience is far from unique.

What is so magical about aspirin, Lipitor and a low-fat diet?

There is a simple rationale behind this approach. Aspirin doesn't reduce atherosclerotic plaque growth, but it inhibits the propagation of a blood clot on top of a coronary plaque that has "ruptured," thereby reducing likelihood of heart attack (which occurs when the clot fills the artery). So aspirin only provides benefit if and when a plaque ruptures.

Lipitor and other statin drugs reduce LDL cholesterol, promote a modest relaxation of constricted plaque-filled arteries (normalization of endothelial dysfunction), and exerts other effects, such as inflammation suppression.

A low-fat diet is intended to reduce saturated fat that triggers LDL cholesterol formation and to encourage intake of whole grains that reduce cardiovascular events and LDL cholesterol.

If that is the extent of your heart disease prevention program, you will have a heart attack, bypass surgery, or stent--period. It may not be tomorrow or next Friday, or even next month. Aspirin, Lipitor, and a low-fat diet may delay your heart attack or procedure for a few years, but it will not stop it.

Some flaws in the aspirin, Lipitor, low-fat program:

--Aspirin can only exert so much blood clot-blocking effect. It can be overwhelmed by many other factors, such as increased blood viscosity, increased fibrinogen (a blood clotting protein that also triggers plaque), and plaque inflammation.
--Lipitor reduces LDL, but does not discriminate between the relatively harmless large LDL and the truly plaque-triggering small LDL--it reduces all LDL, but small LDL can still persist, even at extravagant levels since neither aspirin nor Lipitor specifically reduces small LDL, while a low-fat diet increases small LDL.
--Low-fat diet--A diet reduced in fat and loaded with plenty of "healthy whole grains" will trigger increased small LDL (an enormous effect), c-reactive protein, high blood sugar, resistance to insulin, high blood pressure, and an expanding abdomen ("wheat belly").


Aspirin, Lipitor and a low-fat diet do not address:

--Vitamin D deficiency
--Omega-3 fatty acid deficiency and the eicosanoid path to inflammation
--High triglycerides
--Small LDL particles
--Distortions of HDL "architecture"
--Lipoprotein(a)--the worst coronary risk factor nobody's heard of
--Thyroid status

In other words, the simple-minded, though hugely financially successful, conventional model of heart disease prevention is woefully inadequate.

Don't fall for it.

Statin drugs for everybody?

Who is better off?

John takes Crestor, 40 mg per day:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl




Or Sam:

LDL cholesterol 60 mg/dl
HDL cholesterol 60 mg/dl
Triglycerides 60 mg/dl
Total cholesterol 132 mg/dl


who obtained these values through vitamin D normalization (to increase HDL); wheat elimination (to reduce triglycerides and LDL); and omega-3 fatty acids (to reduce triglycerides).


Believe the drug industry (motto: If some statin is good, more statin is better!), then John is clearly better off: He has obtained all the "benefits" of statin drugs. They refer to the "pleiotropic" effects of statin drugs, the presumed benefits that extend outside of cholesterol reduction. The most recent example are the JUPITER data that demonstrated 55% reduction in cardiovascular events in people with increased c-reactive protein (CRP). Media reports now unashamedly gush at the benefits of Crestor to reduce inflammation.

However, on Sam's program, elimination of wheat and vitamin D both exert anti-inflammatory effects on CRP, typically yielding drops of 70-90%--consistently, rapidly, and durably.

So which approach is really better?

In my experience, there is no comparison: Sam is far better off. While John will reduce his cardiovascular risk with a statin drug, he fails to obtain all the other benefits of Sam's broader, more natural program. John will not enjoy the same cancer protection, osteoporosis and arthritis protection, relief from depression and winter "blues," and increased mental and physical performance that Sam will.

If our goal is dramatic correction of cholesterol patterns and reduction of cardiovascular risk, for many, many people statin drugs are simply not necessary.
When MIGHT statins be helpful?

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are 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.

Comments (17) -

  • Might-o'chondri-AL

    4/8/2011 12:21:11 AM |

    I don't know how individuals with mis-sense SNP for gluco-kinase regulatory protein (ex: GCKR rs780094) fit into the pattern. They get more liver steatosis (fat build up) with attendant elevated LDL and triglycerides, despite less fasting glucose and less fasting insulin numbers; while their 2 hour blood glucose runs high (GCK gene is very determinate of 2 hour glucose levels), showing down-regulation of the homeostatic model for Beta cell function (HOMA-B).

    Normally GCKR regulates triglycerides and determines persons glycemic traits by governing how glucose is stored and how it is dispersed. GCKR also geneticly regulates the availablility of substrate used for de-novo lipo-genesis.

    Gene SNP of protein phosphatase 1regulatory (inhibitor) subunit 3 B (PP1R3B rs4240624) manifests increased liver steatosis  and both elevated LDL and elevated HDL; with low fasting glucose. PPP1R3B codes for controling protein and modulates the break down of glycogen (storage glucose moleccule).

    Together PPP1R3B and GCKR are integral to blood sugar dynamics and the levels of lipids in circulation.

    If Doc's regimen counter-balances individual missense genetic workings, like those above, then that is impressive corrrection achieved through intervention . I presume for people with liver steatosis missense mutations (ie:  SNPs like above) elevated LDL treatment using statins would be bad for their liver.

  • Dr. John

    4/8/2011 1:10:14 AM |

    Statins might be helpful if you have bacterial pneumonia:
    http://www.bmj.com/content/342/bmj.d1907.extract?sid=f762e55c-1a0b-4ef3-81c4-f31cc472a372

    That's because the rapidly growing pneumococcal bacteria are very susceptible to HMG-CoA reductase inhibitors (statins). The bacteria have similar cholesterol compounds (hopanoids) in their membranes, essential for their membrane function. With the statins blocking the hopanoids, they die....very quickly.

    All bacteria have a mevalonate pathway.  The HMG-CoA reductase enzyme is inhibited in bacteria and are VERY toxic to bacteria. So thus, you have a "statin-benefit" because it kills the bacteria, before it kills or injures the patient.

    Statins can essentially inhibit biological life forms.
    Dr. John

  • Dr. William Davis

    4/8/2011 1:11:01 AM |

    HI, Might--

    As usual, you've come out of left field with a totally unexpected issue!

    I'm not sure how this genetic variant fits into this argument. It is, to my knowledge, a very rare diagnosis.

  • Might-o'chondri-AL

    4/8/2011 6:40:15 PM |

    I don't envy Doc trying to sort out who needs what treatment. Genetic high cholesterol entails over 50 amino acid variations out the jumble of 692 amino acids assembled into relevant complexes.

    Pro-protein convertase subtilisin/kexin-9 (PCSK9)is involved in familiar hyper-cholestemia. Those who make too much PCSK9 (in the liver and small intestine) rapidly degrade their cholesterol receptors and can't pluck much LDL out of circulation; plasma cholesterol rises.

    Should one's genetics foster making too little PCSK9, then cholesterol receptors don't degrade. This promptly shunts cholesterol into the liver lysosome (an organelle inside a cell)for break down; thus they  measure low cholesterol in the blood.

    I speculate Doc's diet, in "normal" genetic people up-regulates cholesterol reception. Which means his program has the epigenetic effect (from diet dynamics) on "normal" liver/small intestine genes in a way that less PCSK9 is expressed

    The caucasian anglo-saxon PCSK9 D374Y mutation causes 4 times the normal cholesterol in patients. Their risk factor for pre-mature death is 10 years earlier than even more benign PCSK9 mutations; so Detective Doc Davis is willing to prescribe statins for people like them.

  • Anonymous

    4/9/2011 2:59:55 AM |

    I might be one of these poor souls.

    Eating a strict diet, one Dr Davis would be very proud of... I'm lean as can be, feel great, but my cholesterol shot through roof (while HDL dropped).    

    Frown

  • Might-o'chondri-AL

    4/9/2011 4:53:48 AM |

    Hi Annon.,
    Internet self-diagnosing shouldn't replace a good medical consultant. My comments are not qualified medical assesments; am a layman.  

    My favorite cousin has had her cholesterol testing well over 300for several decades, and is now in her late 70s. Like Doc chided me earlier, there are "genetic variant" being "very rare diagnosis."

  • Lucy

    4/9/2011 11:47:29 AM |

    What do you think about KIF6?   I was tested and found to be a non-carrier, and I was subsequently told that statins would likely not benefit me as much as diet/lifestyle changes (I'm ApoE 3/4 as well).  Does that also mean that niacin would not help?

  • Anonymous

    4/9/2011 12:52:56 PM |

    To say the least, I am very disappointed in Dr. Davis' stance regarding ApoE 4 & statins. There is abundant evidence suggesting statins are counterproductive to brain health, which is much more pronounced in Apo E4's who are already at high risk for alzheimers disease. It isn't only about lipids, there is a larger picture to consider. The brain requires cholesterol.  Also, high cholesterol levels are associated with longevity in the elderly.

  • Might-o'chondri-AL

    4/9/2011 7:44:42 PM |

    Alzheimers and the relationship of ApoE4 is different than other ApoE isoforms (like ApoE 2 & 3). In normal people ApoE is integral to clearing amyloid Beta from the brain; it forms a conjugate (ApoE/AmyloidB)that is moved out across the brain blood barrier by LRP-1 (lipo-protein related protein 1).

    ApoE4 is acted upon (cleaved) in brain neurons, yielding rump fragments with unique Carbon- terminals; and,  ApoE4 degrades easier than ApoE 2 &/or 3. These ApoE4 fragments, when in a brain cell's cytosol, influence that cell's mitochondria hydro-phobic pattern of lipid binding.

    The ApoE4 fragment properties  do 2 unwanted things to the brain cell mitochondria. It decreases the mitochondria ability to perform tasks involved in glycolysis (glucose energy). And is antagonistic to PPAR gamma; PPAR gamma is what would otherwise promote adequate mitochondria bio-genesis.

    ALzheimer lesions show higher amounts when measured in individuals with concurrent Type II diabetes and the ApoE4 isoform. The ratio of insulin in the cerebro-spinal fluid to the amount of insulin in the blood also shows a difference depending on the specific ApoE geno-type.

    Alzheimer brains are using less glucose; patients show less receptors for insulin-like growth factor and insulin, as well as less insulin degrading enzymes. It is postulated that depending on the individual's ApoE variation there is a different amyloid Beta response to brain insulin.

    Normally one goes from glucose intolerance to hyperglycemia and then elevated insulin circulating as become diabetic. Yet experiments show that giving insulin improves diabetic neuro-pathy in the brain; it seems to be a way peripheral insulin resistance causes different tissues to respond.

    In Alzheimer experiments with supplemental insulin (nasal, etc.)administration cognitive function improved. This response was more significant in those with the ApoE4 allele (compared to other ApoE types with Alzheimers, who also improved cognition ).

    So, the Alzheimer enigma seems to involve energy format dynamics for ApoE isoforms more than specific levels of cholesterol. This is not a comment on ApoE homo-zygote genes relationship to cardio-vascular risk factors, or brain lipid metabolism.

  • homertobias

    4/11/2011 3:36:34 PM |

    Mito
    You sound like Suzanne Craft.  I like her work.

  • Medicomp INC.

    4/12/2011 4:06:52 PM |

    You make an excellent point here:

    ...eat more healthy whole grains" diet that introduces grotesque distortions into metabolism

    We are encouraged by transient sources that this is almost always the best alternative for other fattening foods, yet people never really delve deep into the cons of this transition either.  It truly does take dedication to be well-informed about the dietary changes you make in your lifestyle.

  • Anne

    9/18/2011 5:58:38 PM |

    I had a body scan a few years ago, and my plaque count was 1050, when they told me that 150 was considered high, I thought  I would implode at any moment, I went to a lot of different cardiologists and had all kinds of tests and they said to exercise and not  worry about the plaque. One Dr. put me on lipitor and 3 days later I could hardly walk from the muscle pain, he told me to stop taking it and I tried niacin and red rice with the same results. I don't know how to reduce the plaque, the Dr's all said it was hereditary . I am open to any advice.

  • Dr. William Davis

    9/20/2011 12:43:37 PM |

    Hi, Anne--

    Note that this is the blog that accompanies the Track Your Plaque program that focuses on just this issue. It means 1) identify all causes of plaque, then 2) correct them, preferably using natural means.

  • JK

    10/30/2011 4:52:34 PM |

    Dr. Davis,
    I don't know if you have already addressed this topic in prior posts but allow me to suggest that in lieu of consuming statin drugs, even for the aforementioned outliers, it is possible to achieve reduced LDL cholesterol and increased HDL cholesterol by supplementing with magnesium.
    (All the ensuing statements below I humbly attribute to Mildred S. Seelig and Andrea Rosanoff, "The Magnesium Factor," pages 139-147.)
    1. Statins (Lipitor, Zocor, Baycol, Mevacor, etc.) are designed to lower cholesterol by inhibiting HMG-CoA reductase, which is the enzyme responsible for the synthesis of cholesterol.
    2. These drugs when studied, not only lower cholesterol, but also reduce total mortality, cardiac mortality, the total incidence of heart attacks, angina, and other non-fatal cardiac events. (p.140.)
    3. They also made the blood platelets less sticky, they slowed the progression of plaques and stabilized them, and they reduced inflammation in the blood vessel tissue. (ibid.)
    All these results, and more, Seelig further informs the reader, are a result of reduced mevalonate in the cells, which is the direct result of an inhibited HMG-CoA reductase, which is the enzyme that statins are designed to inhibit.
    Now stay with me for a second because here is where it gets interesting.
    4. Magnesium is a natural inhibitor of HMG-CoA reductase. Here magnesium and statins are comparable (p. 141.)
    5. Magnesium also acts on two enzymes, phosphatase reductase and phosphohydrolase which reactivate HMG-CoA reductase. By its effects on these enzymes, which contrast one another, magnesium can either stop cholesterol formation or allow it to continue depending on the body's needs.
    6. Magnesium also activates another enzyme, lecithin cholesterol acyltransferase (LCAT) which, through this action, converts LDL cholesterol to HDL cholesterol -- increasing HDL and reducing LDL.  (Statins cannot do this.)
    In the interest of brevity, I'll conclude by saying that whereas statins are known to reduce cholesterol and perhaps achieve other cardiovascular benefits, this is due in large part to their suppression of mevalonate, brought about by their inhibition of HMG-CoA reductase.
    In contrast, magnesium not only inhibits HMG-CoA reductase, meaning that it would achieve the same results as statins in "1, 2, and 3 above," but it also converts LDL cholesterol to HDL cholesterol, achieved by its activation of LCAT, which is something that statins do less consistently.
    Further, instead of poisoning HMG-CoA reductase as statins do, magnesium inhibits it in ways that can be reactivated by other (magnesium dependent) enzymes so that the body can naturally make the mevalonate and cholesterol it needs.
    This is important because vitamin D is synthesized from cholesterol (when using the sun's rays), and cholesterol is also the precursor to testosterone, estrogen, and other steroids.
    So I encourage you to consider using Magnesium for those Apo-B cases that cannot be addressed by carbohydrate restricted diets.

  • JK

    10/30/2011 4:58:10 PM |

    Sorry, meant to say Apo-E cases.

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