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From the Townsend Letter
May 2016

Head-On Collision Kills Millions Yearly
by John Parks Trowbridge, MD
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For the fearless driver, here's an interesting detour: infarctions can occur without any clot being found in the artery; a clot can form in a coronary artery days or even weeks before a myocardial infarction; a clot can fully obstruct a coronary artery without causing an infarction.24 And why does plaque not form in your veins or your pulmonary artery, exposed to almost all of the same "risk factors" as coronary arteries? The story is gigantically complex, not merely as simple as, "Start here, turn there, and X marks your destination." Quite possibly it is an infarction that first occurs and then the clot forms. With all the emphasis on the cholesterol hypothesis, kick these tires: systemic lupus erythematosus (SLE) increases the risk for cardiovascular disease 83 times (8300%!) more than having an elevated level of LDL cholesterol.25 Answering these challenging issues will provide future treatment strategies.

Conventional physicians have long relied on Coumadin to impair clotting tendency of the blood. The annual market for anticoagulant drugs is estimated to be over $10 billion in the US. Side effects of Coumadin are not trivial: brain hemorrhages and other forms of internal bleeding, making it one of the leading causes of emergency room fatalities. More recently, Eliquis, Pradaxa, and Xarelto have emerged as drug "favorites," claiming that frequent blood testing (PT, protime assessment of the in vitro time to reduce fibrinogen to an intact fibrin clot or the derived INR [international normalized ratio]) is not needed nor are dietary limitations (such as salads, green leafy vegetables containing forms of vitamin K that competitively interfere with the blocking of liver production of fibrinogen by Coumadin). I have long advocated dosage levels that achieve 18 to 20 seconds (PT) or about 1.8 to 2.2 (INR) for many patients, to reduce bruising/bleeding risks while providing a desirable anticoagulant effect.26 Comfort and convenience certainly are promoted for the newer drugs, so long as the side effects can be ignored: unexpected or uncontrolled bleeding leading to injury or death. The list of common drugs that interact with these recent medications is long indeed. Taking aspirin or other over-the-counter or prescription NSAIDs while on any anticoagulant prescriptions can dramatically raise the risk of deadly bleeding. (Remember 1-800-BAD-DRUG? In May 2014, a short 3½ years after Pradaxa was introduced, the manufacturer reportedly settled more than 4000 lawsuits for $650,000,000.)

Alternative physicians need not rely solely on conventional prescription drugs to create desired effects. We often look to nutritional supplements that improve blood rheology (viscosity relating to ease of flow, such as ketchup versus syrup) and reduce inflammatory (oxidant) reactivity of the blood compartment (whether circulating constituents or endothelial lining). Sadly, some conventional doctors strongly protest or discourage their patients from taking "any vitamins or such" that they unknowingly surmise would "cause problems." Critical examples of useful natural substances are fibrinolytic enzymes – classically nattokinase (subtilisin, produced by bacteria from boiled/fermented soybeans), serrapeptase (from bacteria found in the silkworm intestine), and lumbrokinase (enzymes from earthworms) – along with nonesterified tocopherols/tocotrienols (vitamin E), carotenoids and beta-carotene with vitamin A activity, ascorbic acid (vitamin C), omega-3 fatty acids (EPA and DHA) from marine sources, even ubiquinone, liposomal glutathione (GSH), L-carnitine, alpha-lipoic acid, curcumin, Pycnogenol from grapeseeds or tree bark, and several bioflavonoids.

How many conventional physicians strongly discourage pro-inflammatory foods – not just sugars and starches but also those processed, preserved, stabilized, enhanced, and other "foods of commerce"? The standard American diet ("SAD") is a simmering cauldron, ready at any moment to slide you off the road to healthy as easily as a wet oil slick kills your traction on pavement.

Where appropriate, physicians skilled in the management of Coumadin readily rely on that valuable prescription (see sidebar). In my almost 40 years of clinical care, I never have needed to severely reduce vegetable intake; all I do is have the patients stay on a reasonable fresh food diet (always limiting sugars and starches!) and then adjust Coumadin dosage around their personal food choices. After optimizing antioxidant status, erythrocyte deformability, platelet reactivity, endothelial function, and blood viscosity, some patients can be reduced in prescriptive dosages or even removed from such support.

Screeching Halt
Talk about a deadly accident! Deep vein thrombosis (DVT) and thrombophlebitis have grabbed the attention of the public more recently due to the television ads for the recent (expensive) anticoagulants noted above. Lest we forget that some emergencies really are life-threatening and might require urgent surgery, a high index of suspicion must be maintained by all physicians so that dire consequences can be avoided. When ultrasound or other modalities confirm the presence of an obstructive pattern, hospital care is often most advisable. At discharge, however, the routes take different directions: conventional cardiologists and cardiovascular surgeons often pursue a treatment plan similar to that outlined above for disturbing arrhythmias.

Successful treatment merely begins when your patient is stabilized and recovering for discharge. Alternative physicians follow the same map outlined above for arrhythmias, but they emphasize a plan to reduce inflammation and improve rheology (flow characteristics). More importantly, they devise a program of inquisitive investigations trying to explain how this "accident" developed in this individual at this time. The answers could suggest the direction to be pursued as foundational treatment, aimed at reducing the chances of recurrence in coming months or years. Surprisingly, each search might turn up a different "answer," since we're sleuthing for the specific pathways by which this particular patient finally hit the wall and suffered such a potentially catastrophic event. Not just the high road, not just the low road, many "roads lead to Rome"!

Perhaps it goes without saying … diagnostic and treatment programs for cerebrovascular accidents (strokes) and TIAs (transient ischemic attacks), gangrene, and retinal or optic nerve occlusions are pursued by alternative physicians in very much the same way as for DVTs. Although the "theme" is the same, a personalized program will be designed for each suffering patient.

Where the Rubber Meets the Road
Cholesterol is not the culprit! Stealing the title from research scientist Fred Kummerow's book was surprisingly easy, just cut-and-paste from Amazon.com.27 Hey, if that's not the culprit, then what is? And why is cholesterol "so high"? And what should we be doing about it? Sadly, I find few heart specialists of any ilk who pause to ask these questions in a genuine search for "the" answers. Lipitor has $14 billion in sales each year. "You're down with Crestor" has a snazzy ring to it. Clearly the "statin drugs" are favorites for cardiovascular surgeons, cardiologists, internists, and family/general practitioners, even physician assistants, independent nurse practitioners … and pharmacists!(Seems that everyone is a professional backseat driver, even your family and neighbors.)

What isn't so clear is whether … those devotees are simply not aware of the real basic science or clinical literature, or haven't read the relevant literature, haven't read the product warning information, or really couldn't care less because "they heard at a meeting or exhibit hall booth all they need to know." Lowering blood cholesterol levels by drugs is not the answer to saving lives, to reducing heart attacks, strokes, or blocking of other blood vessels … because cholesterol is not the cause of these potholes on the road through life.

Popular books are sharing the facts on serious adverse results, but apparently doctors haven't read these materials or simply didn't understand or believe them.42-44 After all, if the prime dictum in medicine is "First, do no harm," then how could they prescribe these toxic drugs so casually? Maybe the problem is that they're so busy "taking care of patients" that they simply don't have time to evaluate the issues carefully to avoid predictable problems while they are "busy taking care of patients."

Reluctant to conclude that statin drugs are worthwhile? You too can share the tunnel vision of cardiologists, who don't accept that patients can ease on over into the fast lane and find their bodies trashed, crashed, and "totaled" even more with two upcoming injectable "PCSK9 inhibitor" drugs on the approval/marketing track. While statins can lower cholesterol by 30 to 40%, the PCSK9 protein-blockers confront your physiology head-on, plummeting levels by 60 to 70%, for a trivial reduction in heart attacks.28 The cost for charging full speed into the body shop is only $500 to $1,000, for an injection every 2 to 4 weeks. Rest assured, both the manufacturers and the FDA consider potential side effects to be minimal.

But wait – there's more! Does this mean that alternative physicians are (or should be) ignoring a "high" cholesterol problem? I certainly hope so! Sadly, some of them have drunk the Kool-Aid and can be charged with DUI. From the view out my windshield, you should have a cholesterol check only three times in your life: first, as a growing child if you have slowed development or odd recovery from usual illnesses or injuries – or even more severe or puzzling ones; then, when you're about 20, to confirm that your metabolic systems have developed well, perhaps to alert you to a "fix" that needs to be put "in" to help avoid preventable complications; and finally, when you're 45, to confirm the results of any "bad" eating habits: sugars and starches. This article is far too short for me to share my distress at family doctors and specialists who are scaring patients into taking prescriptions for total cholesterol levels "above 200." [Caveat: Rarely folks have genetic settings that produce seriously high blood cholesterol levels, especially oxidant-promoting VLDL, LDL, or other lipoprotein subtypes; these need specific treatment.]

Many conventional doctors appear to have misplaced their commonsense when looking at the "issue" of cholesterol and its "control." Some frighten or bully their patients into avoiding such wholesome foods such as eggs, butter, cream, marbled red meats, and so on. Few physicians expect that statin use can result in increased coronary artery plaque calcifications.29 Cholesterol can be elevated in people with inadequate antioxidant protection, such as vitamins C and E, because your body has it ease on over to quench free radical injuries of the vessel endothelium.30 Unfortunately, oxidized cholesterol is not reduced and recycled by glutathione as are those vitamins; indeed, it is a much better predictor of heart disease than either HDL or LDL, with 82% accuracy.31 This fatally altered molecule stimulates an immune response and collects in your LDL particles and at the injured site, where it can form a gummy, gunky plaque, even promoting coronary artery disease.32 Wait – we haven't even addressed how oxidized lipid products can induce or aggravate platelet reactivity, leading more easily to thrombotic occlusions.33 Do you notice the red-flag waving? This patient showing elevated cholesterol might be compromised with regard to his ability to control inflammation (the root of all degenerative diseases) and not actually "statin deficient" – because inflammation is the culprit.34

The astute physician – conventional or alternative – will pay attention to underlying causes of deviations from optimal for a variety of inflammatory markers, including Lp(a), homocysteine, uric acid, fibrinogen, C-reactive protein, LDL particle number (measured as apolipoprotein B), small LDL particles, HDL, IDL (intermediate-density lipoproteins, especially persisting longer than postprandial), sedimentation rate (ESR), platelet aggregability, and blood viscosity to name a few. Other contributory diseases need to be identified as well, such as glucose intolerance/diabetes mellitus, autoimmune illnesses, hormonal imbalances, even unsuspected infections. The only answers are the right answers for each particular patient.

Road Signs That Doctors Ignore
From a physiological perspective, cholesterol plays a pivotal role in your bodily structures and operations.35 Every cell is wrapped by a bilayer phospholipid membrane containing cholesterol, keeping "out things out" and "in things in," moving specific things in or out, and providing membrane fluidity. Each of the organelles inside cells is involved with cholesterol. Major lipids and cholesterol are made continuously by the smooth endoplasmic reticulum inside cells, as are steroid hormones. Your brain contains about 20% of your body's total cholesterol. Nerve conduction is possible because of multiple wrapping layers of myelin/cholesterol as a protective insulator, just like on electric wires. Many of our hormones are made starting with cholesterol – as is cholecalciferol (vitamin D3 – it's really a hormone) and most importantly, ubiquinone (coenzyme Q10), the queen molecule in the electron transport energy production pathway inside the mitochondria, and also bile acids, so that you can digest fatty foods, oils, and fat-soluble vitamins (A, D, E, and K).36 The list goes on and on, because bodies are very expert at adapting basic molecules to serve essential needs.

In a novel twist, MIT senior scientist Dr. Stephanie Seneff presents a tight biophysical schema wherein high LDL cholesterol levels resulting in heart disease actually signal a deficiency of cholesterol itself and crucial biosulfates in the cardiovascular system, especially cholesterol sulfate: your body is crying out for sulfur and possibly vitamin D.37 Literature reviews suggest that atheromatous plaque uses local superoxide to liberate sulfate from homocysteine and glycosaminoglycans of the protective endothelial glycocalyx (glycoprotein-polysaccharide), leading to induction of nitric oxide release and subsequent microvascular relaxation with increased perfusion.38 Just imagine for a moment: what "accidents" could be caused by impairing cholesterol synthesis with the favorite drugs promoted by conventional doctors?39,40

Interestingly, any effect that statin drugs have in lowering heart attack risk might have little or nothing to do with their depression of circulating cholesterol. A 2014 report sums it up easily: "Recent studies have shown that statins reduce thrombosis via multiple pathways, including inhibiting platelet activation and reducing the pathologic expression of the procoagulant protein tissue factor."41 Could it be that statins act pretty much the same as aspirin does … but with a nasty and unfortunate side effect of lowering cholesterol?

What should you do right now about cholesterol-lowering statin drugs (HMG-CoA reductase inhibitors)? From either conventional or alternative perspective, start by reading the side effects that are more than just possible. Check the Internet for articles and books documenting serious adverse effects that arise that physicians poorly identify,17,18 including memory loss, muscle and liver damage, fatigue, and the list goes on and on, because cholesterol is not just floating in the blood but is essential in so many normal processes.42-44 Then you can make unbiased, informed decisions about whether your prescribing is doing more harm than good. Disappointingly, few of your patients will believe that their doctors have "steered them wrong" – until they, too, become aware of the documented risks they are taking … hopefully not by suffering adverse reactions!

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