Friday, April 27, 2007

Will Someone Please STOP the Insanity

I recently completed another one of those online "Heart Disease Risk Analyses" that are becoming more and more frequent on hospital websites (You can find this particular one at They all involve filling out an online questionnaire asking questions about height, weight, blood pressure, cholesterol, etc. They then electronically compare your answers with the motherload of all heart health studies, the Framingham Heart Study experience.

Now, don't get me wrong, the Framingham Study is the "motherload" of all heart disease risk analyses. It has an unbelievable amount of data catalogued over decades of experience. It's problem, like most risk analysis of this ilk, is that all it tells you is your risk. It does not tell you whether you actually have heart disease. BUT A HEART SCAN WILL!!!

For example, my risk for developing heart disease, based on all the data I supplied, was a mere 9%! Nine percent?!!! My actual risk for heart disease is 100%! I have it and it has been confirmed by a half dozen heart scans over the last six years! If all I did was take this online test I might still be eating McDonald's hamburgers and fries for lunch everyday.

This type of health care practice is INSANE! Look, all the "risk factors" tell you is whether you might have heart disease. Regardless of risk factors and "probabilities" the answer is maybe "yes" and maybe "no." There are plenty of people like me with low "risk factors" that still have heart disease and others whose risks are high yet never develop heart disease. A heart scan will tell you with damn near 100% certainty whether you do or do not.

It amazes me that so-called health care professionals still engage in such "hocus pocus" (perhaps for profit, maybe). Remember, I am still a numbers guy. Risk factors are a wonderful tool when you do not have the means to determine an outcome with any certainty. BUT, THIS IS NO LONGER THE CASE WHEN IT COMES TO HEART DISEASE. Stop the insanity. Get a heart scan and learn the truth. Gee whiz! This ain't rocket science!



Wednesday, April 18, 2007

Fish Oil + Low-Dose Statins = 19% Heart Attack Reduction!

I once asked Dr. William Davis of Track Your Plaque fame if he could use only one supplement what it would be. He quickly answered, "Fish Oil!"

Many have touted the heart health benefits of the Mediterranean Diet (high in fish products) or simply taking fish oil as a supplement. Now, the new JELIS study (PubMed Abstract, HeartWire Article), an 18,645 participant study over 5 years shows that major cardiac events are reduced 19% when fish oil is used to supplement a low-dose statin regimen.

This finding could be a real boon to many heart disease sufferers who cannot tolerate high-dose statin therapy!



Sunday, April 15, 2007

Round 2: Cocoa Kicks Tea's Butt

Yes, another study is out and cocoa is the clear winner over tea as far as lowering blood pressure is concerned. In a study recently released in the Archives of Internal Medicine (see the free PubMed Abstract), the polyphenols (the group composed of phenols and the more abundant and popularly known flavonoids) in cocoa products (such as dark chocolate) produced significant reductions in both diastolic blood pressure (-4.7 mmHg) and systolic blood pressure (-2.8 mmHg) as compared to tea (both black and green).

The study made some rather dubious claims that the drop in blood pressure was comparable to monotherapy with either beta-blockers or ACE inhibitors but my limited experience (I don't have high blood pressure) suggests that is a bit of a stretch (i.e. most people I know have significantly greater drops on prescription drugs). But, hey, it's nice to know a little cocoa goes a long way. The authors were also quick to point out that this only works if the cocoa calories ingested did not exceed a healthy total caloric intake. Sorry, you cannot pig out and then eat chocolate to get healthy. If you take a cocoa supplement you must cut back an equal number of calories elsewhere!

Bon Appetit!


Saturday, April 14, 2007

Eagle Eye: New Gene Research Target

The 'Eagle Eye' is a new recurring blog item that will look at cutting edge research into the root causes and potential 'cures' for heart disease. The latest item is the research into the 'kalirin' (KALRN) gene and the 'Rh0-GTPase' signaling pathway. The abstract can be found at Let's break it down in layman's terms for all those who slept through Bio-Chem lecture with special thanks to University of Wisconsin Honors Bio-Chem major - and my daughter - Caitlin (you didn't really think I was that smart did you?).

Researchers looked at chromosome 3q13-21 (a specific section of a human DNA strand), a site already established as playing a role in early onset atherosclerosis. We remember (yeah, sure) that DNA is simply a 'biological program' for creating the basic proteins that make up living organisms. It is composed of a long sequence of nucleotides (a fancy word for a group of four chemical compounds adenine, cytosine, guanine, thymine abbreviated A, C, G, and T respectively) that are organized into what we know as 'genes'. These sequences of A, T, C, and G, our genes, determine what proteins are made (thousands of them) and ultimately determine what the end result of the process is (an artery for example).

The researchers also considered little glitches in our genes called 'Single Nucleotide Polymorphisms' (SNP). SNPs are simply gene sequences where a single nucleotide (remember A, G, C, T) is replaced with another, incorrect, nucleotide. SNPs in genes sometimes code to produce the same protein, but they can also create subtle differences that are beyond the space in this blog to describe.

Finally, researchers used the '1-LOD-unit-down' method which is a statistical method of determining whether a gene is likely to be linked or associated with another gene in a given chromosome (wonks can review Genetic Linkage for a complete description and the math).

Now to the good stuff. Here is what they found.

A strong association between SNPs and heart disease was found in the KALRN (kalirin) gene. Three SNPs in the kalirin gene in particular were found in patients with early-onset heart disease. The kalirin gene is also responsible for the inhibition of 'inducible' (i.e. endothelial) nitric oxide synthase (iNOS/eNOS) which we all know regulates artery dilation (the body synthesizes endothelial nitric oxide from l-arginine which is why this is such a popular supplement). Finally, researchers discovered the kalirin gene is part of the Rho-GTPase signaling pathway that regulates behaviors such as clotting (see, reverse cholesterol transport (see, and arterial stenosis (see

What does this all mean?

The bottom line is that if you find ways to manipulate the kalirin gene or its manufactured proteins you may be able to do things like increase eNOS (like we do with l-arginine), improve the reverse-cholesterol transport efficiency of HDL, inhibit the formation of the clots associated with heart attack, and affect the process by which arteries accumulate plaques. One study (see found that statins actually inhibit Rho-GTPases which might account for the additional or pleiotropic effects they have beyond LDL cholesterol reduction. Realistically, commercial applications of these findings are at least 5-10 years away. So work extra hard with what you've already got and buy that extra decade! There is more than this exciting research already in the pipeline. LET'S BEAT HEART DISEASE TO A PULP! The way to do it is one day at a time.



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