As most of us know, heart disease is the leading cause of death for men and women and most ethnicities in the United States. However, the majority of physicians in this country are still ignorantly diagnosing and malignantly prescribing medications to those affected by the disease.
Health care is on the rise, billions of dollars are made from cholesterol-lowering medications, and millions of Americans continue to take these drugs each year. These numbers continue to steadily rise, along with obesity and diabetes. However, the gap between money being spent on creating new cholesterol-lowering drugs and the number of deaths each year from heart disease is widening.
It is a sad truth that there are millions of misinformed Americans when it comes to their health. Dr. William B. Kennel, who is considered the pioneer of cardiovascular epidemiology, coined the term “risk factor” in 1961, and the “Framingham risk score” was born. Dr. Kennel’s study has been acknowledged as one of the top ten medical advances of the last century, and we have been predisposing people for heart disease ever since. These risk factors are based on age, sex, total cholesterol, blood pressure, and family history. Five decades later, the mortality numbers from cardiovascular disease (CVD) is still on a steady incline. Granted, our growing obesity epidemic and sedentary lifestyle aren't doing these “risk factors” any favor in helping them live up to their higher standard for predicting heart disease. However, even for the rest of the “healthy” adult population, the traditional risk factors and the majority of blood work are still simply not enough of a prediction and are even becoming irrelevant when it comes to diagnosing America’s number one killer.
A national study in 2009 showed that 75 percent of patients hospitalized for a heart attack had cholesterol levels that would indicate they weren’t at high risk for a cardiovascular event based on current national cholesterol guidelines. Fortunately, a few institutes and physicians are implementing their first attempt at improving the prevention of the major source of death in the United States. This attempt begins with a set of blood work. A much more thorough or complete lab panel than just your ordinary cholesterol levels, this blood work is becoming the hallmark to telling us what our risk factors are for CVD. But before we start bashing the cholesterol industry, let’s take a look at some of the markers that we should be aware of in order to be preventative with our health.
The uniqueness of these tests is that the genetic markers, inflammatory markers, and lipid profiles give us a more direct approach to identifying those individuals who may be at an increased risk for developing heart disease. It is also important to be aware that experts are still beginning to understand how these markers play a role in disease and that this research is still very new. However, as I have mentioned before, many physicians are still quick on the trigger when prescribing powerful drugs such as statins when their diagnosis isn't that clear cut. “Low risk and high risk” aren't as black and white as we once thought.
Approximately 2,200 Americans die of CVD daily. Even though we're still looking for more evidence on how these markers affect our health, I think we can all agree that we need to look further than just age, race, total cholesterol, family history, and blood pressure. It is negligent to believe that just because we don't have any family history of heart disease and have normal cholesterol numbers that we aren't at risk for pathology.
The interesting thing to note is that not all of these markers are treated equally. Some of these risk factors can be treated with nothing more than a lifestyle change. Statins will not make up for a crappy diet and lack of exercise. However, we still need to forge a paradigm shift in medicine, creating a more proactive approach that is critical to our future health.
Genetic markers
The first segment of blood work is what we called genetic markers or markers found on our DNA that will make us prone to CVD. These markers may explain why some people can live a perfectly healthy lifestyle according to our standards and still develop heart disease. Even individuals without any family history of heart disease can still have these genes present. The understanding of why these genetic markers contribute to CVD is still relatively new, and scientists are still developing research in the pursuit of these genetic variants. Nevertheless, the genetic markers I will be alluding to are the KIF 6 genotype, apolipoprotein E (Apo E), and chromosome 9p21.
- KIF 6: KIF 6 is a genotype that is comprised of tiny proteins called kinesins. These proteins play a role in the intracellular transport of organelles, protein complexes, and mRNAs. According to the Berkley Heart Lab, a polymorphism (rare variant) in KIF 6 can result in an amino acid change within the gene that can affect the development and acclimation of the kinesin protein. Individuals who are carriers of this variant have a 55 percent greater chance of developing CVD than non-carriers.
- Apo E: Apo E is associated with lipoprotein metabolism (packaging cholesterol and other fats and carrying them throughout the bloodstream) and has three major isoforms—ApoE2, ApoE3, and ApoE4. All three play a role in influencing the risk of CVD. However, only ApoE4 plays a significant role in developing atherosclerosis, Alzheimer’s disease, and impaired cognitive function. It is still unclear how the ApoE4 allele is related to the risk of disease, and not all people who carry the ApoE4 allele will develop the disease and vice versa. However, scientists have found that the ApoE4 allele is associated with sticky build ups of protein or plaque that accumulate in the nerve cells of brain tissue in affected people.
- 9p21: The 9p21 chromosome is another rare variant (polymorphism) that can cause early onset myocardial infarction or abdominal aortic aneurysm. According to the Scripps Translational Science Institute, the 9p21 genotype is the strongest genetic marker for CVD that has thus far been identified. Scientists have discovered that these polymorphisms can trigger an outpouring of molecular actions that contribute to inflammatory signaling in endothelial cells.
Inflammatory markers
The second set of blood work is what I believe to be the precursor for heart disease and really most other diseases as well. For decades, we've been told that cholesterol is the culprit when it comes to these diseases. Dr. Stephen Sinatra, the author of The Great Cholesterol Myth says, “You know cholesterol is found at the scene of the crime for heart disease, but it is not the perpetrator.” Far too many Americans are being told that statins and other cholesterol-lowering medications will save their life when, in reality, altering cholesterol levels is much more dangerous. Elevated cholesterol levels might just be a natural response to dealing with high inflammation. We need cholesterol to repair the body.- Myeloperoxidase (MPO): MPO is a protein-based enzyme that can easily be oxidized. It contributes to tissue damage during inflammation. It is associated with atherosclerosis and instability of plaque.
- F2 isoprostanes/creatine ratio: F2-IsoPs are inflammatory markers produced by free radical oxidation. They promote platelet activation resulting in thrombosis or blood clots.
- Microalbumin/creatine ratio: Microalbumin appearing in the urine is a marker for loss in vascular integrity and endothelial dysfunction. People who have high urinary microalbumin levels are three times more likely to develop CVD and are also at increased risk for diabetes.
- PLAC test (PLA 2): This test measures Lp-PA 2, which is an enzyme that promotes inflammation inside the arteries and can lead to the acclimation of unstable, rupture prone plaques. This test is unique from a standard cholesterol test because it can provide information on the stability of these rupture-prone plaques that standard tests can't.
- C-reactive protein (CRP): A CRP test is the most widely available out of all the inflammatory marker tests and should be less than 1.0 mg/L in most individuals. It is a protein produced by the liver and levels can rise due to inflammation.
Lipid profiles
Hopefully, by this point, we have learned that being aware of our cholesterol is helpful, but cholesterol alone isn’t as important as we once thought. Instead of just looking at thetotal number of HDL and LDL in our blood, we need to take a look at the cholesterol particle size. The real question our doctors should be asking is, “What makes up your cholesterol particles?” Small, dense particles are more atherogenic (more likely to cause the plaque in the arteries that leads to heart attacks) than large, buoyant, fluffy cholesterol particles. These smaller particles can sneak through the tiny holes in the walls of our arteries, causing an atherogenic response. Our health risk has less to do with our cholesterol numbers than it does with the quantity and size of the cholesterol particles. We should now be aware of these lipid profiles as a better index for measuring our risk of CVD.- Apolipoprotein B (ApoB): ApoB is the predominant apolipoprotein attached to the LDL and is the “scientifically accepted gold standard measurement for LDL particle number.” Elevated ApoB levels (>120 mg/dl) may triple the risk of CVD even when the total LDL cholesterol number is within normal range. Again, individuals with seemingly normal LDL levels may in fact have high ApoB values, identifying the presence of small, dense particles.
- Lipoprotein (a) (Lp(a)): Lp(a) is an LDL particle with an inherited apoprotein attached. High levels of Lp(a) (>=30 mg/dl) are associated with atherosclerosis and puts an individual at three to five times the risk for a heart attack. This risk increases even further when Lp(a) is in combination with other abnormal markers.
Miscellaneous laboratory markers
- Fibrinogen: Fibrinogen is another protein produced by the liver that assists with the formation of blood clots inside a blood vessel. Just like C-reactive protein, fibrinogen rises when there is damage or inflammation. Most heart attacks are known to be due to acute thrombosis. It makes sense then that elevated fibrinogen levels would be associated with an increased risk of heart attack.
- Homocysteine: Homocysteine is an amino acid found in the blood. Although research showing that high homocysteine levels increase the risk of CVD is lacking, evidence has made one believe that it may cause narrowing of arteries as well as blood clots.
The uniqueness of these tests is that the genetic markers, inflammatory markers, and lipid profiles give us a more direct approach to identifying those individuals who may be at an increased risk for developing heart disease. It is also important to be aware that experts are still beginning to understand how these markers play a role in disease and that this research is still very new. However, as I have mentioned before, many physicians are still quick on the trigger when prescribing powerful drugs such as statins when their diagnosis isn't that clear cut. “Low risk and high risk” aren't as black and white as we once thought.
Approximately 2,200 Americans die of CVD daily. Even though we're still looking for more evidence on how these markers affect our health, I think we can all agree that we need to look further than just age, race, total cholesterol, family history, and blood pressure. It is negligent to believe that just because we don't have any family history of heart disease and have normal cholesterol numbers that we aren't at risk for pathology.
The interesting thing to note is that not all of these markers are treated equally. Some of these risk factors can be treated with nothing more than a lifestyle change. Statins will not make up for a crappy diet and lack of exercise. However, we still need to forge a paradigm shift in medicine, creating a more proactive approach that is critical to our future health.