First off, here is another study (actually a meta-analysis of other studies) showing that increased bilirubin is related to decreased risk of atherosclerosis.
http://www.ebmonline...tract/228/5/568...
Inverse Relationship Between Serum Bilirubin and Atherosclerosis in Men: A Meta-Analysis of Published Studies Ladislav Novotn* and Libor Vítek,1 * EuroMISE Center-Cardio and Institute of Hygienic Medicine and Epidemiology, and
4th Department of Internal Medicine and Institute of Clinical Biochemistry and Laboratory Diagnostics, 1st Medical Faculty, Charles University, Prague, Czech Republic Abstract Bilirubin, a major intravascular product of heme catabolism,
is a potent antioxidant compound. Numerous studies have been
published showing the relationship between serum bilirubin levels
and atherosclerosis. In the present investigation all the epidemiological
studies available on the effect of serum bilirubin levels and
atherosclerotic disease were analyzed. Studies on the epidemiology
of atherosclerotic diseases in relation to serum bilirubin levels
were searched in the MEDLINE database. Selected studies were
subdivided according to serum bilirubin levels and severity
of atherosclerotic disease. Because of the limited number of
females involved in the studies, only males were included into
meta-analysis. Associations for ordered categorical variables
(bilirubin and natural history of graded atherosclerosis) were
assessed to find correlation and linear trend between analyzed
variables. A stratified analysis was conducted to compare risks
of clinical outcomes. Eleven relevant studies were used for
analysis. A close negative relationship was found between serum
bilirubin levels and severity of atherosclerosis (Spearman rank
coefficient
r = -0.31,
P < 0.0001). The linear trend was confirmed
in analysis of proportions with x
2 values for both disease conditions
to be very significant (
P < 0.0001). Unambiguous inverse
relationship between serum bilirubin levels and atherosclerosis
was demonstrated in this preliminary meta-analytic study. These
results indicate the importance of hem oxygenase-related products
in the prevention of oxidative stress-mediated diseases.
Key Words: atherosclerosis • oxidative stress • ischemia • artery disease
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To be fair, there are still questions about whether it is the increased bilirubin or the increased heme oxygenase (the enzyme that breaks down the red blood cells to start the process that produces bilirubin eventually) that is responsible for reduced atherosclerosis. Now those with Gilbert's Syndrome, depending on their specific mutation, may have both a decrease in bilirubin conjugation as well as an increase in bilirubin production (through extra heme oxygenase activity). This is documented in the following study.
<A href="
http://www.ncbi.nlm....pubmed/11915038...
Hemolysis and bilirubin conjugation in association with UDP-glucuronosyltransferase 1A1 promoter polymorphism.Kaplan M,
Hammerman C,
Rubaltelli FF,
Vilei MT,
Levy-Lahad E,
Renbaum P,
Vreman HJ,
Stevenson DK,
Muraca M.Department of Neonatology, Clinical Genetics Service, Shaare Zedek Medical Center, Faculty of Medicine of the Hebrew University, Jerusalem, Israel. kaplan@cc.huji.ac.il
Hemolysis may contribute to hyperbilirubinemia in Gilbert's syndrome. The authors examined blood carboxyhemoglobin corrected for inspired CO (COHbc) to index heme catabolism and serum conjugated bilirubin fractions to reflect bilirubin conjugation. Both parameters were related to UDP-glucuronosyltransferase 1A1 (UGT) promoter polymorphism, associated with Gilbert's syndrome, in term male newborns. COHbc was expressed as percentage of total hemoglobin, and total conjugated bilirubin (TCB) value as a percentage of serum total bilirubin (STB), (TCB/STB[%]). A production/conjugation index, COHbc/(TCB/STB[%]), represented bilirubin production divided by conjugation. UGT promoter genotype was designated according to the number of promoter TA insertions in each allele: 6/6, homozygous normal; 6/7, heterozygous; 7/7, homozygous variant. STB and COHbc values were higher in the 7/7 subgroup than the other counterparts (P <.01). The COHbc/(TCB/STB[%]) was higher in the 7/7 than either the 6/6 or 6/7 subsets (1.93 [1.31-2.88] vs. 0.85 [0.51-1.72] and 0.84 [0.53-1.87], respectively; P <.01). In conclusion, 7/7 UGT promoter polymorphism was associated with increased blood COHbc values (unexpected finding) as well as diminished serum total conjugated bilirubin ratios (expected finding). The increased hemolysis may contribute to the pathogenesis of increased STB values seen in Gilbert's syndrome, and exacerbate neonatal hyperbilirubinemia associated with the promoter polymorphism.
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I recently had an EBCT (electron beam computed tomography) scan done to assess my atherosclerosis level. I just got the results and they rate me with a score of zero. From this page on
identifying asymptomatic coronary artery disease, we get the following information on what the scores mean.
...
<H3 class=dynamic>How Do I Interpret My Coronary Calcium Score?</H3>
- 0 - No plaque is present. There is less than a 5% chance of having heart disease. Risk of a heart attack is very low.
- 1 – 10 - A small amount of plaque is present. There is less than a 10% chance of having heart disease. Risk of a heart attack is low.
- 11 – 100 - Plaque is present. There is mild heart disease. The chance of a heart attack is moderate.
- 101 – 400 - A moderate amount of plaque is present. There is heart disease; plaque may be blocking an artery. The chance of a heart attack is moderate to high. Your health professional may want to do more tests and may start treatment for heart disease. Aggressive treatment may be started for risk factors such as high blood pressure and high cholesterol.
- Over 400 - A large amount of plaque is present. There is more than a 90% chance that plaque is blocking one of the arteries. The chance of a heart attack is high. Your health professional will want to do more tests and will start treatment.
<H3 class=dynamic>What Are The Risks Of Having A Heart Scan?</H3>
- Critics raise the issue of false negative results in heart scanning especially in younger populations. A negative result may not detect soft plaques.
- Although calculated risk is present, actual risk (of course) cannot and is not and must be assumed as such. Critics note that further invasive tests may be performed (cardiac catherization and/or angioplasty).
- CT scanning increases radiation exposure comparable to multiple chest x-rays.
<H3 class=dynamic>What Are The Benefits?</H3>
- Knowing your risk.
- Dependent on the results, identifying the risk of cardiac event in the immediate future spurs lifestyle changes and fosters a proactive approach by both the patient and the physician towards targeted medical prevention and/or timely intervention.
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Now, one of the reasons I had the test done (probably the main reason) is that my father has been told that he has higher than expected atherosclerosis, given his level of cholesterol (which isn't low, but isn't extremely high either). I wanted to see if I was genetically predisposed to atherosclerosis. I theorized that if I was, I might show some level of build-up, even though I'm only 37 years old.
As the test shows, I have no plaque present (that can be detected with this test -- might still have non-calcium plaques). However, according to the information I was given with the results, it has statistics showing that 80% of people my age have a score of zero.
Personal analsysis:
1) I could have the same issue that my father has, but my Gilbert's Syndrome is countering it, thus I have no atherosclerosis.
2) I could have the same issue that my father has, but the issue may not show build up at my age, even if I didn't have Gilbert's Syndrome.
3) I could not have the same issue that my father has and even without Gilbert's Syndrome, I'd have an 80% chance of having a score of zero.
4) I could not have the same issue that my father has, and the Gilbert's Syndrome is helping me stay within the 80% percentile.
In other words, this test really says nothing conclusively about my personal relationship between Gilbert's Syndrome and atherosclerosis. It does provide peace of mind that I don't show calcification of my arteries at this point in my life. The other reason I may have had some concerns is that my HDL cholesterol levels are lower than I'd like (35 and 32 mg/dL in my last two tests in the last 4 months, which is lower than the bottom end of "normal", with normal being 40-50 mg/dL).
I should also add that my self assessment that I gave to the technicians was a rating of 2/10 on how much I exercise and 5/10 on how low fat my diet is. In other words, very little exercise and middle of the road fat content. I do plan on increasing my exercise when I'm done with some other personal tests regarding resveratrol mitochondrial biogenesis potential that exercise may confound.
My current plan is to have this test done once every 5 years. By keeping an eye on this, I hope to get an early handle on atherosclerosis if it does begin to rise. It is normal for it to rise as you age, but I'd much rather be abnormal in this regard, to increase my chances of longevity.
If anyone reading this who has Gilbert's Syndrome and who is older has this test done, I'd be very interested in the results.
David