C-Reactive Protein:
The Track Your Plaque Perspective
We met Phyllis because her husband, Dick, had undergone
two prior bypass operations and was seeking an opinion regarding why his
disease kept progressing. Although Dick was too far along to engage in
the usual Track Your Plaque approach (since his disease was no longer
“scorable” due to bypass operations), we believed that he could still
benefit from our preventive approach. We proceeded to uncover small LDL
particles, low HDL, and lipoprotein(a), among a few other lesser
patterns. As Dick became angina-free (chest pain-free) for the first
time in years and the causes behind his heart disease came under control
for the first time in his life, Phyllis decided it was time for her to
explore her own heart health with a CT heart scan.
Phyllis’ CT heart scan score: 598. At age 63, this put her well into the
99th percentile (a score in the worst 1% of women in her age group).
Phyllis was shocked: her standard cholesterol panel had been
near-perfect for years, including HDL cholesterol of 80 mg/dl. We dug
deeper. Phyllis proved to have:
- Moderate excess small LDL particles (45% of total LDL)
- Moderate intermediate-density lipoprotein (IDL)
- Severe vitamin D3 deficiency with 25-OH-vitamin D3 of 14 ng/ml (in September)
- C-reactive protein (CRP) elevated at 8.9 mg/l
We surmised that inflammation, as evidenced by the dramatically elevated
CRP, was a major factor behind Phyllis’ substantial degree of coronary
plaque, along with the modest lipoprotein abnormalities and severe
vitamin D3 deficiency. We decided that reduction of CRP would be a
priority for Phyllis.
C-reactive protein (CRP) is another blood test that many hope will
improve the power to predict whether heart attack is in your future.
“We have to think of heart disease as an inflammatory disease, just as we think of rheumatoid arthritis as an inflammatory disease.”
Paul Ridker, MD
Harvard University
Why another blood test?
Keep in mind that the majority of physicians and the
public have not yet gained an understanding of CT heart scans and the
superior information they provide. Instead, many cling to the notion
that “risk factors” like cholesterol can be used to predict future heart
disease.
Cholesterol is an obvious failure to reliably predict future heart
attack. While in large groups (thousands of people), cholesterol values
(LDL cholesterol, HDL cholesterol, triglycerides, and the least helpful
of all, total cholesterol) do indeed predict a spectrum of risk, when
applied to a specific individual, it falls apart utterly. Only at
extremes do cholesterol values predict the future with any sort of
reliability. Very high LDL cholesterol, for instance, of 225 mg/dl, does
predict increased risk. So does a very low HDL of, say, 26 mg/dl.
But let’s say a person has the sort of average values shared by most of
us: LDL 140 mg/dl, HDL 44 mg/dl, triglycerides 150 mg/dl, total
cholesterol 214 mg/dl. Does this person have heart disease? Will they
have a heart attack in the next year, 2 years, 5 years, 10 years?
The answer is that you cannot reliably predict the future with
cholesterol values. So, CRP has emerged as another test, another “risk
factor,” that some advocate adding to conventional cholesterol values to
yield a clearer glimpse into the future.
But those of us following the Track Your Plaque program already know
that it’s not risk factors we’re looking for. We already know what heart
attack risk is based on our CT heart scan scores, a reliable measure of
the disease itself, coronary atherosclerosis. Why add another risk
measure?
First of all, what is CRP?
CRP is nothing more than a blood protein
expressed by the liver whenever any inflammatory process is active in
the body, whether or not you’re aware of it. Obvious sources of
inflammation, like pneumonia and knee arthritis, will raise CRP, usually
to high levels. Inflammatory responses increase blood levels of the
signaling molecule, interleukin–6 (IL–6) which, in turn, triggers the
liver to increase CRP production for release into the blood. Although
its exact function in the body is unknown, the blood concentration of
CRP does seem to parallel the degree of inflammation.
Over the past decade it has been recognized that people who feel well
and lack any obvious or perceptible source of inflammation may have
modest elevations of CRP, so low it was previously felt to fall within
the normal range. CRP at these low levels appears to add to the power of
cholesterol values to predict whether or not you’re at increased risk
for heart attack (Everett BM et al 2006; Tsimikas S et al 2006).
A high C-reactive protein (>0.5 mg/l) suggests that inflammation may be
a contributor to growth of coronary atherosclerotic plaque. It can also
act as a trigger for heart attack. Inflammation is the fuel for the fire
that leads to coronary plaque rupture, the event that results in heart
attack. Inflammation also drives other conditions like diabetes, cancer,
and arthritis. While very high C-reactive protein levels >10 mg/l nearly
always represent inflammation outside of the heart (e.g., arthritis) and
do not necessarily indicate increased coronary risk, lower levels (<10
mg/l) can be used to gauge low-grade inflammation that stimulates
coronary plaque activity.
Dr. Paul Ridker of Harvard University, the nation’s authority on CRP,
has shown that high CRP levels (of 3 mg/l) increase heart attack risk
3-fold, even when LDL cholesterol is low (Everett BM et al 2006;
Tsimikas S et al 2006). When elevated CRP occurs in the company of small
LDL particles, heart attack risk is 7-fold greater (St-Pierre AC et al
2003).
Studies are also now beginning to emerge suggesting that reducing CRP
also yields a reduction in likelihood of heart attack, though the great
bulk of this treatment experience is focused on the application of
statin drugs (Willerson JT et al 2004).
Predictably, drug manufacturers have tried to persuade us that the only
effective way to reduce CRP is with statin drugs, which reduce CRP from
20–50% (Deveraj S et al 2007). This is simply not true: there are many
ways to reduce CRP as well as, or even more effectively, than the statin
drugs. In the Track Your Plaque experience, we commonly see CRP drop
dramatically, usually back to the perfectly normal range of ≤0.5 mg/l,
with strategies listed below—whether or not a statin drug was part of
the treatment picture.
How to Reduce CRP
Here are approaches to consider that reduce CRP and thereby help remove inflammation as a contributor to your risk for heart disease:
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Copyright 2007, Track Your Plaque.