Part of the problem is that there are many stratifications that must be considered in order for a doctor to make a sound recommendation to his or her patient in respect to cholesterol, and the simple reflex of “your LDL is over 200” hardly makes the grade. Is the patient older or younger; male or female? Does he or she have diabetes, or perhaps a strong family history (genetic) risk for cardiovascular disease? Has the individual had a previous event, such as a heart attack, stroke or chest pain? Is she African American, Caucasian, or Asian? What does the patient weigh? Clearly there are many considerations that should be taken into effect before a lifelong drug is chosen. I am not fully convinced that in the majority of cases a drug is required at all.
I like to refer to a 2005 study, while admittedly small in number, pointed to the potential for diets and foods in the control of elevated cholesterol levels. The title of the study was “Diet compared to Statin for Cholesterol Reduction”, and was published in the prestigious American Journal of Clinical Nutrition. The link to the study is below.
The research compared the use of a “portfolio” diet consisting of almonds, soy products, plant sterols (a type of plant-based cholesterol), and fiber in a head-to-head trial against one of the first generation statin drugs. The study showed that both groups, dietary and pharmacologic, showed a 30% reduction of LDL cholesterol relative to a control diet, with no difference between the two intervention groups. This dietary reduction of cholesterol occurred without significant interventions in exercise, or other dietary changes.
There are basically two conversations going on in the discussion of cholesterol and prevention of heart disease. The first conversation, addressing the measurement of cholesterol, divided simply into "good" cholesterol (HDL) and "bad", (LDL, which is typically not measured but calculated) only partially explains what is going on in the cardiovascular system. The truth is that sub-intimal (behind the lining of the blood vessel) atherosclerosis is a factor of cholesterol, but also of inflammation. A cholesterol molecule, while not totally without blame, is often found at the proverbial “scene of the crime”, and implicated in all the wrongdoing, when the picture in its entirety is much more complex.
The immune system, in making an atherosclerotic plaque, or hardened artery, is responding to oxidized LDL. This is cholesterol that has been exposed to unregulated inflammatory processes. The problem that I find with these "official" assessments is that there is little consideration of the fact that a basic cholesterol study: calculated (not measured) LDL, HDL, Triglycerides, and Total Cholesterol is not addressing the correct questions of what truly influences cardiovascular health. We need to be looking at things like LDL particle number and particle subtyping such as 'small dense particles'. We need to be measuring markers of inflammation, and of oxidative stress and damage. The American Heart Association doesn't seem to acknowledge, or take these things into consideration. A full review of their most recent manuscript and recommendations, the “2013 Guidelines on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults”, doesn’t even mention that there are well studied, FDA approved, testing alternatives that could be used to make a more thorough investigation of an individual’s cardiovascular risk.
The second discussion has to do with what testing is most informative, appropriate and cost effective, and how this testing could be generalized to the population as a whole. There is ample data that an individual exposed to many small, dense LDL (Low Density Lipoprotein) particles, in a background of increased inflammation, is at higher risk for cardiovascular disease. But the "experts" are still using the old studies to judge an individual's risk. A more thorough assessment, I believe, includes measurement of lipoprotein A2 , homocysteine, fibrinogen and HS-C reactive protein to measure for clot-promoting states and inflammation. The newer tests also qualify the types of lipoproteins into small-dense, intermediate or large-sized particles. Fibrinogen is another important marker for cardiovascular risk, as is the PLAC test- a test that measures the activity of an enzyme associated with oxidized LDL- and quantifies an individual’s progressive risk of plaque rupture with subsequent heart attack or stroke. You should know that 50% of heart attacks occur in people with normal LDL- so obviously this in and of itself does not fully reflect true CV risk. But it still seems to be the primary "signpost" for the AHA experts when making assessments for risk reduction (read: statin use).
In conclusion, I feel that the American public should demand a more comprehensive understanding, laboratory evaluation, and treatment approach to the cholesterol question. It is clear that simply assessing a value for Low Density Lipoprotein (LDL), and basing a lifetime therapy with a drug such as a statin drug, is grossly underestimating the complexity of the factors that contribute to cardiovascular disease. There is ample data to stress the importance of dietary changes and modifications to reduce the load of cholesterol in the body. We have to remember that cholesterol is an essential part of our cellular membranes, and the absolute starting point for all of our hormone synthesis in the body. I believe that the real culprit is the presence of LDL cholesterol that has been oxidized- tagged with an inflammation inducing electron- that sets up the process for damage to the vascular walls and subsequent atherosclerosis. So to initiate a therapy that solely decreases the production of cholesterol in the body, without taking a good, long look at the factors that promote the inflammatory part of the equation, is only giving short-shrift to what we understand as the etiology of cardiovascular disease.
Are heart attacks and strokes fully preventable? I doubt it, but I do feel that with a functional approach that incorporates a more comprehensive look at the factors contributing to inflammation and oxidative stress, we can begin to decrease the scourge of the number one killer of both male and female Americans.
What different steps will your functional medicine physician undertake to optimize your personal risks of Cardiovascular Disease?
I recommend that all patients with even limited cardiovascular risk take advantage of what current science and nature have to offer in the evaluation and management of heart disease. The majority of “Western” medical providers are ignorant (in the literal sense: “not knowing”) towards the potential that is available to our patients other than the rote prescription of a cholesterol lowering drug such as Lovistatin or Crestor. This is an excellent opportunity to take your health care into your own hands; to find a provider who understands the complexities of the biological systems, and who knows the opportunities that exist in testing and treatment that can make a lasting difference in your health, wellness and longevity.
Dr. Scott Resnick