I’ve Been Invited to Join the Board of Directors of The FH Foundation

“The mission of the FH Foundation is to raise awareness of FH (familial hypercholesterolemia) through education, advocacy, and research. Our goal is to save lives through increasing the rate of early diagnosis and encouraging proactive treatment. If left untreated this life-threatening genetic disorder leads to aggressive cardiovascular disease in men, women, and children.”

I am proud to have been invited to serve on the Board of Directors for this very impactful organization. It is a wonderful opportunity to help make a difference.

For the full press release announcing Seth’s appointment click here.

Please learn more about preventive cardiology at www.preventivecardiologyinc.com.

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Learn to Read the Label: What to Look for When Choosing an Omega-3 Fish Oil Supplement

Omega-3 fish oil supplement labels can be very deceiving. This video explains how to choose the appropriate fish oil supplement.

Get more info on the world’s most potent omega-3 fish oil supplement at vitalremedymd.com

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Cholesterol and Vascular Disease Part 4: The Great Statin Debate

September is National Cholesterol Education Month. In support of this important educational initiative we are republishing our six part series on cholesterol and the role it plays in cardiovascular disease.

Note: Seventy-one million American adults have high cholesterol, but it is estimated that only one-third of them have the condition under control.

It has been unequivocally established that high levels of LDL can lead to heart attacks and strokes. Parts 1- 3 of this blog described the history of cholesterol, the superiority of LDL particles over LDL cholesterol, and the pathophysiology associated with an overabundance of LDL particles. In addition to our understanding of the biological process whereby LDL particles cause vascular disease, we also have a plethora of clinical trials demonstrating the efficacy of lowering LDL.

Everyone–lay people, physicians, and scientists–is plagued by the overabundance of clinical trials involving all aspects of health and medicine, many of which clearly contradict one another. In order to practice medicine in a fashion that appropriately considers the outcomes of these clinical trials, one must find a way to make sense of them. My approach has been to evaluate the clinical trials not just individually, but as a whole. I look for trends. When studies repeatedly reach the same conclusions (especially when they pathophysiologically “make sense”) I feel much more comfortable concluding that they are correct. In the case of LDL we find a commonality that is indisputable. The studies repeatedly demonstrate that statins–a class of cholesterol lowering medications I will momentarily describe–uniformly decrease the risk of cardiovascular events by about 30%. This event reduction is consistent among patients in the setting of both primary and secondary prevention. And so we must listen to the studies and lower our patients’ LDLs accordingly.

Statins are the class of medication for cholesterol management that unequivocally possess the greatest amount of science supporting their use. These medications work by blocking a critical enzyme in our body’s production of cholesterol. In response to lower levels of cholesterol within our cells, the cells increase surface receptors to bring in more LDL particles. The result is a diminution in the number of LDL particles – as well as the LDL cholesterol – in our bloodstream. Read More…

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Our Bodies are Truly Temples

woman doing yoga outdoors
Last week my son started Veterinary Medicine School. As with Medical School, the quintessential class for indoctrination in the Medical Arts is Gross Anatomy. He is dissecting a dog; I dissected a human being. Remarkably, they are quite similar. In order to help him and contemporaneously restore my own misplaced memories I took the opportunity to dust off my thirty-year-old Clemente Atlas of the human body. What I discovered was both astonishing and unanticipated. First the bad news – I had forgotten much more than I had remembered. Second and far more interesting and uplifting was my reinforcement that countless marvels abide within us all. Each of us is a universe of infinite possibilities. To say we are complex, intricate, amazing, unparalleled falls so short of the mark that it is nearly not worth saying. Our complexity is ineffable. Over the past decade my focus in cardiovascular prevention has been on our bodies’ microscopic goings-on; biochemistry, cell biology, molecular biology, and organic chemistry have been my playgrounds. Each time I’ve learned something new I’ve recognized how little I (we) know. With all we appreciate, we have merely scratched the surface of the elaborate, multifarious activities engaging each of our trillions of cells at every moment of life. And that’s the microscopic. I had neglected the macroscopic: our bones, muscles, nerves, organs, and network of vascular tributaries. Looking at the visible is no less remarkable than the invisible. Do this now. Lift your arm to scratch your head. In performing this singular simple act you have activated countless neural, muscular, vascular, and skeletal systems. And that doesn’t include all the cell-cell communications requiring the activation of genes and creation of proteins as well as the intentional movement of made-to-order bio-chemicals as well as armies of cells. All this just to scratch your head! Try to imagine how spectacularly intricate are our bodies’ activities when there’s a crisis, say a pneumonia or deep wound to your leg. The coordinated responses of layers of participants in maintaining our health and physical prosperity become fully activated. These reactions are so far beyond our wildest imagination that I predict no supercomputer will ever crack the code.

Yes we can pound our chests and pretend we are gods when we clone sheep. The truth is, to god, we are no god.

Visit vitalremedymd.com for more preventive healthcare solutions.

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Prostate Cancer and Omega-3 Fish Oils: Beware Conclusions Born of Misinformation

The recent conclusions of Brasky et al must be examined closely as they are not only misleading but potentially dangerous. This statement may appear extreme, but omega-3 fatty acids have been repeatedly shown to protect us against cardiovascular disease (CVD), the leading cause of death in the Western World. Therefore, if men stop eating fish and taking fish oil pills for fear of prostate cancer, they may be putting themselves at risk for CVD, a disorder that kills seven times as many men as does prostate cancer. Such a decision would be not only unwise, but potentially damaging. To better understand this, let’s examine Brasky’s findings in the context of prior data as well as our understanding of the biology of DHA and EPA.

First, many earlier trials have demonstrated a correlation between high fish consumption and low rates of prostate cancer. Some examples are: Lancet, 2001 Terry et al showed a significant correlation between high fish consumption and a low incidence of prostate cancer. The Physician’s Health Study in 2008 revealed a correlation between high fish consumption and improved survival in men with prostate cancer. A 2003 Harvard study of 48,000 men showed a higher intake of fish to be associated with a lower risk of prostate cancer. There are many other examples, but this should suffice.

Second, let’s look at plasma levels of EPA and DHA in Brasky’s trial. The reported EPA+DHA level in the plasma phospholipids was 3.62% in the non-cancer control group and 3.74% in the high-grade cancer group. This difference between controls and the worst cases is extremely small, frankly with no clinical significance.  It is simply within the normal laboratory variation.

Third, is association tantamount to cause? No. Even if there were a clear association between prostate cancer and high EPA and DHA levels, that would not prove causality. Other plausible explanations exist. In fact, this would more likely be a case of reverse causation. We know that two cancer-related phenomena will increase DHA and EPA levels. First, cancerous tissues can upregulate the genes for enzymes that cause long chain fatty acids to “grow” into EPA and DHA – the desaturases and elongases. Second, we know that genetic polymorphisms in the fatty acid desaturases are associated with an increased risk of cancer. So what may be occurring here (if anything is occurring at all) is that cancer-induced changes in desaturases, or cancer-producing genetic polymorphisms in these same enzymes are causing an increase in EPA and DHA. DHA and EPA are not causing the cancers.

Fourth, we are not told the source of omega-3s in this study group. Is it mostly from fish? Some fish have very high levels of PCBs, substances known to be carcinogenic. To conclude that people should stop their fish oil supplements when some supplements are actually far “cleaner” than fish, might therefore be very misguided.

Fifth, let’s examine another population with vastly different omega-3 levels to see whether Brasky’s assertions are relatable to real life. The Japanese consume eight times as much EPA and DHA as do Americans, yet their risk of prostate cancer is about one eighth of ours. If anything, one should conclude that omega-3s are protective here.

Sixth, we can’t ignore the biology of the fatty acids. A plethora of data has demonstrated the anti-inflammatory impact of the omega-3 fatty acids EPA and DHA. Data have also uniformly shown the pro-inflammatory effects of trans-fatty acids. When trial conclusions fly in the face of our understanding of human biology (in this case, trans fats not being harmful while omega-3s causing harm) we must consider them to be highly suspect.

Finally, let’s not forget that EPA and DHA are considered by experts to be “essential” fats. In other words, we must consume them in order to live. Before we discard these indispensable fatty acids, let’s await better clinical trials, and ones that are plausible in the context of prior literature and well-documented pathophysiology.

Additional resource : Dr. Gerald Chodak’s article entitled “Fish Oil’s Link to Prostate Cancer Unproven”  featured on Medscape.

Learn more about the world’s most potent omega-3 fish oil supplement at vitalremedymd.com

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The Inclusiveness of Modern Medicine

Western Medicine has been branded non-inclusive, even close-minded. In many respects it deserves this designation. After all, medical guidelines have been constructed on dogma derived almost solely from “outcome trials”. Such trials are uniformly difficult to perform and have inherent constraints such as limited applicability to the specific patients we all see every day in practice. At times doctors do rely too heavily on guidelines and by so doing limit their own ability to think outside the box. Interestingly, doctors often utilize techniques and procedures in an “off label” fashion, meaning they are being used in ways for which they have not been approved, but they do so to benefit their patients. Still, most doctors fail to acknowledge the pervasiveness of “off label” practices and this self-blinding permits frequent condemnation of alternative or complementary strategies. For example, for years doctors have condemned chelation as pure quackery. Recently (TACT), a large clinical trial presented at both the American Heart Association (AHA) and American College of Cardiology (ACC) meetings, showed clinical benefit of this purportedly charlatan-based procedure. Another recent study noted that osteopathic maneuvers (also deemed useless by many western-minded physicians) appear to have real value. The long-awaited revised cholesterol guidelines are still in the process of being approved (this has been going on for many years). The hold-up – difficulty in creating guidelines based solely on high-level evidence. Translation; we recognize that we simply don’t know as much as we think, and sometimes pretend, to know.

So why, you may ask, is my title so optimistic? It’s because the winds of change are upon us. The subtle acceptance of methods such as chelation and osteopathy along with our guideline-related struggle to come to terms with our lack of knowledge speak volumes. We are coming to the point I believe, when we will be able to accept our imperfection. We will acknowledge the unique and permanent blend of art and science that is medicine. We will embrace our science-based creativity. By doing all this, we will enter a new, better, and more inclusive stage in the evolution of modern medicine.

Visit vitalremedymd.com for more preventive healthcare solutions.

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Cholesterol and Vascular Disease Part 3: How Tiny LDL Particles Can Cause Such Harm

Last week we discussed the relevance of LDL particles, emphasizing their role as the main drivers of vascular disease. We did not, however, discuss how they wreak such havoc upon our blood vessels. Today we will do so.

LDL particles do wonderful things. They transport cholesterol and triglycerides to various parts of our body for fuel, storage, or even to serve as building blocks for other important molecules. They even transport vitamin E to our brains in order to enhance growth and development in infants, and proper brain function in adults. So how can something so good, be so bad? The answer lies in numbers. The aphorism “too much of a good thing can be bad” applies perfectly to LDL particles; they are necessary for a healthy body, but only in small quantities. The numbers most of us possess are so far out of range, they are literally killing us. But how? What happens when these tiny particles make their way beneath the delicate yet vital single cell layer (called the endothelium) that lines our blood vessels?

When LDL particles penetrate the boundary that separates blood from the blood vessel wall, they often cause a chain reaction that leads to plaque accumulation.

First they become oxidized. Oxidation leads to activation of an enzyme called LpPLA2 (lipoprotein associated phospholipase A2). Enzymes are biological molecules that initiate chemical reactions. In this case, LpPLA2 destroys a type of fat (a phospholipid) that sits within the surface membrane of LDL particles. The fat is broken in two, creating two independent but highly inflammatory elements – an oxidized fatty acid and Lyso-phosphatidylcholine (Lyso-PC). These “freed” fats summon other agents of atherogenesis (plaque formation) – adhesion molecules and cytokines are released bringing in specialized white blood cells called macrophages which then consume the oxidized LDL particles. As more oxidized particles are consumed, the macrophage weakens and ultimately dies, releasing its atherogenic contents and essentially pouring fuel on the fire beneath the endothelium. Other “bad” substances are also produced – MMPs (matrix metalloproteinases) for example chew away at the cap that has formed over the budding plaque in an attempt to contain the fire below. As MMPs thin the cap it becomes more likely to tear. (Dr. Abela, Professor and Chief of Cardiology at MSU produced spectacular images of cholesterol crystals helping MMPs tear through the thinning cap. Remember, cholesterol that floats freely will crystallize. Once the cap tears, the fire rages into the vessel lumen (where our blood is freely flowing in order to bring nourishment to the tissues it feeds – in this case the heart muscle). The blood in turn attempts to quench the fire, but by doing so produces a blood clot, which in turn can entirely block the bloods passage. The end result – a heart attack and death of heart muscle. And it all started with the excessive LDL particles! Next week we will discuss methods to lower LDL particles to diminish our risk of heart attacks.

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Cholesterol and Vascular Disease: Part 2: LDL-Cholesterol is Important, but LDL-Particle Number is Far More Revealing

We left off with part 1 of the Cholesterol and Vascular Disease blog concluding that the two key assumptions made by cholesterol scientists in the 1940s and ‘50s were wrong. These assumptions were: 1. All LDL particles are the same size and 2.  All similarly-sized LDL particles have the same cholesterol content. Had these assumptions been correct there would have been no need to evaluate any other LDL parameter beyond LDL cholesterol. Given the fact that they are wrong however, means that looking simply at LDL cholesterol allows for the persistence of significant and dangerous “hidden risk”.  And risk that is hidden is risk that will not be corrected. Therefore we must dig deeper into this issue and how it can translate into a higher risk for developing arterial plaque.

First, let’s deal with the size issue. We now know that many individuals have very small LDL particles, while others have large, normally-sized particles. The larger the LDL particles, the more cholesterol they can fit within them. Smaller particles on the other hand cannot carry nearly as much cholesterol as their larger brethren. (That is simple enough. A large bucket holds far more water than a tiny cup.) Therefore, if you have very tiny LDL particles, you need many more of them to generate an LDL cholesterol content (LDL-C) than someone with very large particles. (Back to the water analogy –  If you need to carry a quart of water and you have one quart-sized bottle, you can carry all the water in one bottle. If you have only cups available, you will need four of them to carry the same amount of water.) The result of this disparity in LDL size is that two people with the same LDL-C (130 mg/dL for example) will have very different LDL particle numbers when their LDL particles are very different sizes.

The second erroneous assumption was that similarly-sized LDL particles always carry the same amount of cholesterol within them.  This too has turned out to be false.  Under certain metabolic conditions – diabetes, obesity, overweight, high triglycerides, low HDL– LDL particles tend to be under-filled. Once again in these patients in order to generate a particular LDL-C level, more particles are required.  (Back to the water analogy – if you have only cups available to fill, but are permitted to fill them only half way, it will take twice as many cups to carry the same amount of water as your friend who is allowed to fill the cups to the very brim.) Therefore, two individuals with precisely the same LDL-C can have vastly different LDL-Ps. So the bottom line is that LDL-C is NOT a good surrogate for LDL-P after all. OK, you buy that, but you might now be asking yourself,” Does it really matter if I have a lot of LDL particles?” A common and excellent question with a simple answer – YES! This is because more particles translate into a higher risk for developing plaque.  And the reason this is so, is actually quite intuitive. The more LDL particles a person has bouncing around in the blood stream, the more likely the particles are to encounter and penetrate the walls of his/her arteries. (The shotgun vs. the pistol is another helpful analogy. Even if you are an expert marksman, you are much more likely to hit your target with a shotgun than a single-shot pistol.) This is important because the penetration of our arteries by LDL particles initiates the process of atherosclerotic plaque formation. Yes, it all begins with a single particle. Next week we will discuss how such simple LDL particles can initiate a process that still kills more Americans than any other disease.

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Dr. Seth Baum Interview: Non-Invasive Heart Testing

In my interview (below) on WPTV’s “Ask the Doctor” segment I discuss non-invasive heart testing, women’s preventive cardiology, as well as the positive impact proper diet and moderate exercise can have on heart health.

Learn more about preventive cardiology at www.preventivecardiologyinc.com.

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