Lipoprotein A and B, how to reduce levels by Ray Sahelian, M.D.
A lipoprotein is a molecule that contains both proteins and lipids. Many enzymes, transporters, structural proteins, antigens, and toxins are lipoproteins. Examples include the high density and low density lipoproteins of the blood. Dietary and lifestyle factors that lower cholesterol and triglyceride levels will also lower lipoprotein a levels.
Lp(a) lipoprotein A
When LDL cholesterol combines with Apoliprotein (a), the result is a compound known as Lp(a). High levels of Lp(a) can increase a person's risk of heart attack. Lp(a) is measured through a blood sample and can be tested as part of a lipoprotein panel. Lp(a) levels are influenced by genetics. Any dietary steps or nutritional supplements that reduces inflammation and cholesterol levels could be helpful to reduce the risk for heart attack.
High Lp(a) and heart disease
As with elevated high-sensitivity C-reactive protein, an elevated Lp-PLA(2) level approximately doubles the risk for primary and secondary cardiovascular events. Interestingly, when both inflammatory markers are increased together, they provide an even greater predictive capability to help identify very-high-risk individuals who would benefit most from aggressive lipid-lowering therapy, hopefully by natural means.
Danish researchers report people with higher levels of lipoprotein (a), which varies up to a thousand fold from one person to another, also more likely to have heart attacks. Statin drugs -- taken by millions to cut heart attack and stroke risk -- do not affect lipoprotein (a) levels. People with the highest lipoprotein (a) levels are two to three times more likely to have a heart attack than those with the lowest levels. Niacin, a vitamin often prescribed generically to lower cholesterol, also lowers lipoprotein (a) levels.
Lipoprotein (a) and stroke.
Minerva Med. 2008.
The Lp(a) is a low density lipoprotein produced by the liver and it seems to be related to vascular diseases. There is a large individual variability of Lp(a) in the blood levels in the different subjects. The mechanism of the Lp(a) in the pathogenesis of atherosclerosis is not completely clear. There are a lot of different hypotheses and, one of these, is based on the structural analogy of apo(a) with plasminogen. According to current knowledge, it seems that there is a strong relationship between Lp(a) levels and coronary artery disease. Instead, there are still doubts about the real relationship between Lp(a) and stroke. Furthermore, Lp(a) levels seems to be influenced by some other cardiovascular risk factors: fibrinogen, cigarette smoke, and other. Actually, the dosage of the protein is not very useful in clinical practice.
Consensus panel recommendation for incorporating
lipoprotein-associated phospholipase A2 testing into cardiovascular disease risk
Am J Cardiol. 2008.
A consensus panel was formed to review the rapidly emerging literature on the vascular-specific inflammatory marker lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) and to update recommendations for the appropriate use of this novel biomarker in clinical practice. The recommendations of the panel build on guidelines of the Adult Treatment Panel III (ATP III) and the American Heart Association/Centers for Disease Control for cardiovascular risk assessment. Consistent with the ATP III guideline recommendations for the use of inflammatory markers, Lp-PLA(2) is recommended as an adjunct to traditional risk assessment in patients at moderate and high 10-year risk. As a highly specific biomarker for vascular inflammation, elevated Lp-PLA(2) levels should prompt consideration of increasing the cardiovascular risk category from moderate to high or high to very high risk, respectively. Because intensification of lifestyle changes and low-density lipoprotein (LDL) cholesterol lowering is beneficial in high-risk patients, regardless of baseline LDL cholesterol levels, consideration should be given to lowering the LDL cholesterol target by 30 mg/dL in patients with high levels of Lp-PLA(2). Lp-PLA(2) is recommended as a diagnostic test for vascular inflammation to better identify patients at high or very high risk who will benefit from intensification of lipid-modifying therapies. However, at this time Lp-PLA(2) cannot be recommended as a target of therapy.
Q. it seems u have discussed almost everything in your site but little about Lipoprotein (a), the lipid which they say maybe related to heart attacks.
A. Sometimes those who are not familiar with the complexity of the body or the varied influences of heart attack occurrence focus on one blood study and think that is the most important factor in causing a heart attack. There are many factors that influence hardening of the arteries, arterial spasm, and blood clot formation. Dietary and lifestyle factors that lower cholesterol and triglyceride levels will also lower lipoprotein a levels.
Q. Do you have any thoughts or advice where I might
look to discover more about controlling the lipoprotein a factor that I have?
A. See the cholesterol link above.
Q. I have a 120 LPa. My Dr. is a wonderful integrative
GP who took the time to address possible inflammation, which he says otherwise
is not seen on other markers. I am 35 with chronic hypothyrodism, history of
endometriosis, current dermoid cyst, (although not a painful chronic issue
currently - I am taking Neprinol for possible fibringen issues, I tested
negative for Hashimoto's several times-once positive-but yrs now later always
negative). CRP is I have had possibly all tests done related to inflammation,
always low or negative. What on earth could be causing supposed
inflammation-high LPa at 120? Without other markers that would suggest
rheumatism or other inflammation? I don't get it. Is it genetics? It's the only
marker that's off, my cholesterol is normal, and my BP normal. My weight is an
issue, I have a BMI of 29 which is borderline...I am taking supplements for
neurotransmitters and all my vitamin levels are in range. Is it all because of
extra weight? Is it because of chronic stress? I was put on Pauling therapy to
lower it, and was also told that Inositol / Proline / Lycine / Niacin lower LP(a).
Should I be concerned about dropping dead of a heart attack any minute with a
high LPa with no other indicators (other than chronic high stress)? My leptin
levels are consistently right over the normal range at 27-is that it? Isn't that
a bit odd its - LPa the only thing 2x normal and out of range? What causes that?
Is it genetic? I know you can't respond directly to my health, but what is the
deal with LPa? What does it mean? What would make it be off? We can't figure it
A. When LDL cholesterol combines with Apoliprotein (a), the result is a compound known as Lp(a). High levels of Lp(a) may increase a person's risk of heart attack. Lp(a) is measured through a blood sample and can be tested as part of a lipoprotein panel. Lp(a) levels are influenced by genetics. Any measure that reduces inflammation and cholesterol levels could be helpful to reduce the risk for heart attack. To evaluate overall health, one should review and take into account the results a complete medical history, physical exam and laboratory studies rather relying too much on the results of one test alone.
I saw where Linus Pauling talked about lysine as a way
to prevent arteriosclerosis. Linus Pauling and Matthias Rath discovered that
substances that inhibit the binding of lipoprotein-(a) also cause
lipoprotein-(a) to be released from the arterial wall. According to the patent,
a binding inhibitor (e.g., lysine or lysine analog) used alone or in conjunction
with ascorbate, finds Lp(a) in the blood and binds with it before the molecule
can reach the walls of arteries. At high enough concentrations, the lysine in
the blood attracts Lp(a) in the existing plaques and will dissolve the plaque.
AM Scanu of the University of Chicago published an article that suggested
apolipoprotein(a), a component of Lp(a) rather than only Lp(a) should be
emphasized along with the apolipoprotein B100, which is found mainly in
low-density lipoprotein (LDL). The latter is often called the “bad” form of
cholesterol to which apolipoprotein(a) and Lp(a) are linked. According to recent
studies, small-size apolipoprotein(a) isoforms may represent a cardiovascular
risk factor either by themselves or synergistically with plasma Lp(a)
concentration. Moreover, the density properties of the LDL moiety may have an
impact on Lp(a) pathogenicity. It has also become apparent that Lp(a) can be
modified by oxidative events and by the action of lipolytic and proteolytic
enzymes with the generation of products that promote atherosclerosis and
thrombus formation. For this reason more sophisticated tests may be used to
better classify risks. Wondered if this theory was ever tested?
I prefer not to get too technical about these matters or to order to many blood tests, but rather focus on the overall picture of reduction in cardiovascular risk factors through various lifestyle habits. I am a clinician rather that a laboratory scientist. One can get quite lost in focusing too much on these fine lipoprotein distinctions and biochemical interactions. Rather it is best to focus on consuming as healthy a diet as possible that reduces overall inflammation in the body and provides a wealth of antioxidants, exercising more, sleeping deeper, reducing stress, reducing intake of alcohol and avoiding smoking. Certain supplements could be helpful for reducing levels of high triglycerides, cholesterol, lipoproteins, and these are discussed on my cholesterol page.