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  • Lipoprotein(a) - Friend or Foe?

    If you know that you have elevated Lp(a), you know it is associated with cardiovascular disease. But, there is debate over if Lp(a) is the cause of CVD itself or if is it an indicator of something else gone wrong. Maybe Lp(a) is part of a process that is intended to heal our arteries when they become damaged from inflammation. Few doctors actually check Lp(a) levels.

    There is a longstanding and still somewhat unproven theory that increases of plasma Lp(a) levels act as an acute-phase reactant. In other words, a person’s average Lp(a) level will rise, and sometimes sharply, in response to an acute injury to the endothelium of the artery wall. That response has been very well documented in people who have normal baseline Lp(a) levels and have had myocardial infarctions and cardiovascular surgeries and shortly after their Lp(a) levels will spike.

    That theory also proposes that the Lp(a) particles act as an healing agent to help repair the surgical site by sticking to the damaged arterial wall and patching the damage, if you will. So is Lp(a) our friend? And what about the millions of people who have high Lp(a) levels and have not had myocardial infarctions or cardiovascular surgery?

    Perhaps arterial injury may mean arterial damage from diabetes, insulin resistance, sub-clinical chronic infection, oxidative damage, heavy metals, toxins, high blood pressure, homocysteine, just to name a few. Sustained elevated Lp(a) levels may indicate the underlying cause of the arterial damage has not been properly diagnosed and therefore remains inadequately treated.

    Back in the ’80’s, Linus Pauling proposed that oxidative damage to the endothelium was a result of human’s lost ability to produce their own vitamin C, and that in turn initiated the atherosclerotic process. Hence, he proposed that high dose vitamin C, along with the amino acids lysine and proline, could protect the endothelium from oxidative damage which would in-turn result in a drop in Lp(a) levels. I tried that approach for 18 months and my Lp(a) levels never budged.

    I’ve tracked my Lp(a) levels on an average of 3 times per year since 2009. I live a pretty clean life in terms of diet, exercise, BMI, blood pressure, fasting blood sugar, HbA1c, low stress and adequate sleep. I have seen my Lp(a) rise unexpectedly on three occasions to a maximum of 217 nmol/L and drop on two occasions to a low of 8.0 nmol/L. That’s a whopping 27-fold variation. My 9-year average Lp(a) level is 124 nmol/L. I’ve never been able to determine the cause for my variations. Maybe I am the cause of my Lp(a) and not my genetics. I have to wonder.

    Getting a onetime Lp(a) level snapshot in a doctors office may tell us nothing. Doctors often say Lp(a) levels don’t change. I say nay! I will be curious to see when, and if, my elevated MACR (microalbumin creatine ratio) level drops from following a low carb diet and taking Metformin. An elevated MACR is a marker of damage (cracks) to the arterial wall.

    If I see improvement in the "cracks in my tennis court" perhaps it may also have a beneficial effect on lower my Lp(a). Time will tell.


    References:

    Lp(a): an acute-phase reactant? https://www.ncbi.nlm.nih.gov/pubmed/7514505

    Relation between lipoprotein(a) concentrations in patients with acute-phase response and risk analysis for coronary heart disease http://clinchem.aaccjnls.org/content/43/10/1891

    Lipoprotein (a) as an acute phase reactant in patients with chronic hemodialysis http://www.old.bjbms.org/archives/2010-1/Shufta.pdf

    Transient changes of serum lipoprotein(a) as an acute phase protein http://www.atherosclerosis-journal.com/article/0021-9150(89)90218-9/abstract

  • #2
    This is a great introduction to the topic. My guess is that it’s both...friend AND foe. Pardon me if this seems a digression, but I think it is similar to the issue with Apo(e)4; the acute phase reactant function is a healer and protector short term. But in a workd where we’ve made to late middle age and beyond - it tends to create more chronic inflammation.

    Comment


    • #3
      Thanks John, you're really on the ball, I'm considering getting a series of blood tests done and was wondering of you've tried the PULS test yet? or what your thoughts are on it? Ideally I'd like to get quite a few tests but they are expensive in the UK and our Dr's- consultants are still working with LDL. Thanks

      Comment


      • #4
        No, I haven't had the PULS test done. I think it's a bit overrated (at least in my case) for the reasons Dr. Brewer mentions in his video. https://www.youtube.com/watch?v=0nCofPbwa8A . My CIMT done in Dr. Brewer's office showed no soft plaque which is the inflamed and unstable plaque, so adding a PULS test would not likely show inflamed and unstable plaque either. My MPO was low and my Lp-PLA2 dropped significantly into the normal range after switching from atorvastatin to rosuvastatin. I do think the PULS test is valid but may not give anymore information than the MPO, Lp-PLA2, MACR tests, and a well done CIMT, all which I previously had performed.

        Comment


        • #5
          Thanks John, I think I'll wait and see what the consultant has to say regarding getting a CIMT before rushing into more blood tests just yet.

          Comment


          • #6
            That sounds like a good plan. Proceed with caution as many medical providers who perform CIMT's are also interventional cardiologists who make their money by performing carotid endarterectomies (surgery) or carotid artery stenting. Some use the CIMT to promote those procedures which may not always be necessary. You want an objective diagnoses, but not be rushed into having a procedure performed.

            Comment


            • #7
              Thanks for the warning

              Comment


              • #8
                According to Dr. Rath LPa was and a life saving mechanism to prevent fatal blood loss though the arteria wall. Of course with vitamin deficiency over decades it over shoots and causes the dangerous coronary plaques.

                Comment


                • #9
                  Everyone on this forum who has coronary artery disease should watch this video, then ask yourself these questions. Why infarction mainly happen in a few centemeters of the heart while the miles of blood vessel's remain largely unaffected.

                  https://youtu.be/O0lEmXJD7p4

                  Comment


                  • #10
                    Welcome, Guitarplayer007:

                    Yes, I think Pauling was correct on elevated Lp(a) being a surrogate for Vitamin C deficiency. Unfortunately, there hasn't been much research on that since his day. With that said, following the Pauling Protocol for 18-months did not lower my Lp(a).

                    There are other likely offenders that attack our endothelium besides Vitamin C deficiency. Inflammation from insulin resistance, toxins such as heavy metals, infections, oxidative stress, poor diet, just to name a few.

                    Comment


                    • #11
                      Yes. Paulinn and Rath. I agree there is something there. But John’s right. There is more to it.

                      Comment


                      • #12
                        Originally posted by dobe762 View Post
                        Thanks John, I think I'll wait and see what the consultant has to say regarding getting a CIMT before rushing into more blood tests just yet.
                        Consultant recently got back to me and told me that CIMT is not offered in the UK, not even privately, but that might change over the next few years!

                        I also contacted another private clinic regarding getting specific tests done, namely those in your most recent video, they never even replied! It appears many of these clinics don't like the clients being so well informed!

                        Comment


                        • #13
                          That is a shame. It’s a simple, non-invasive and inexpensive test. Did you talk to these people in London? They claim they offer it. You may have to pay out-of-pocket.

                          http://www.drholdright.co.uk/dynamic...ns&pageid=NTg=

                          Comment


                          • dobe762
                            dobe762 commented
                            Editing a comment
                            Thanks John I hadn't found that site, I have droppedt hem an email for further info and to see if they run the necessary blood tests.

                        • #14
                          Originally posted by John Lorscheider View Post
                          If you know that you have elevated Lp(a), you know it is associated with cardiovascular disease. But, there is debate over if Lp(a) is the cause of CVD itself or if is it an indicator of something else gone wrong. Maybe Lp(a) is part of a process that is intended to heal our arteries when they become damaged from inflammation. Few doctors actually check Lp(a) levels.

                          There is a longstanding and still somewhat unproven theory that increases of plasma Lp(a) levels act as an acute-phase reactant. In other words, a person’s average Lp(a) level will rise, and sometimes sharply, in response to an acute injury to the endothelium of the artery wall. That response has been very well documented in people who have normal baseline Lp(a) levels and have had myocardial infarctions and cardiovascular surgeries and shortly after their Lp(a) levels will spike.

                          That theory also proposes that the Lp(a) particles act as an healing agent to help repair the surgical site by sticking to the damaged arterial wall and patching the damage, if you will. So is Lp(a) our friend? And what about the millions of people who have high Lp(a) levels and have not had myocardial infarctions or cardiovascular surgery?

                          Perhaps arterial injury may mean arterial damage from diabetes, insulin resistance, sub-clinical chronic infection, oxidative damage, heavy metals, toxins, high blood pressure, homocysteine, just to name a few. Sustained elevated Lp(a) levels may indicate the underlying cause of the arterial damage has not been properly diagnosed and therefore remains inadequately treated.

                          Back in the ’80’s, Linus Pauling proposed that oxidative damage to the endothelium was a result of human’s lost ability to produce their own vitamin C, and that in turn initiated the atherosclerotic process. Hence, he proposed that high dose vitamin C, along with the amino acids lysine and proline, could protect the endothelium from oxidative damage which would in-turn result in a drop in Lp(a) levels. I tried that approach for 18 months and my Lp(a) levels never budged.

                          I’ve tracked my Lp(a) levels on an average of 3 times per year since 2009. I live a pretty clean life in terms of diet, exercise, BMI, blood pressure, fasting blood sugar, HbA1c, low stress and adequate sleep. I have seen my Lp(a) rise unexpectedly on three occasions to a maximum of 217 nmol/L and drop on two occasions to a low of 8.0 nmol/L. That’s a whopping 27-fold variation. My 9-year average Lp(a) level is 124 nmol/L. I’ve never been able to determine the cause for my variations. Maybe I am the cause of my Lp(a) and not my genetics. I have to wonder.

                          Getting a onetime Lp(a) level snapshot in a doctors office may tell us nothing. Doctors often say Lp(a) levels don’t change. I say nay! I will be curious to see when, and if, my elevated MACR (microalbumin creatine ratio) level drops from following a low carb diet and taking Metformin. An elevated MACR is a marker of damage (cracks) to the arterial wall.

                          If I see improvement in the "cracks in my tennis court" perhaps it may also have a beneficial effect on lower my Lp(a). Time will tell.


                          References:

                          Lp(a): an acute-phase reactant? https://www.ncbi.nlm.nih.gov/pubmed/7514505

                          Relation between lipoprotein(a) concentrations in patients with acute-phase response and risk analysis for coronary heart disease http://clinchem.aaccjnls.org/content/43/10/1891

                          Lipoprotein (a) as an acute phase reactant in patients with chronic hemodialysis http://www.old.bjbms.org/archives/2010-1/Shufta.pdf

                          Transient changes of serum lipoprotein(a) as an acute phase protein http://www.atherosclerosis-journal.com/article/0021-9150(89)90218-9/abstract
                          Hi John, I like what you summarized. I've checked twice in 6 months and mine has dropped by half....so is it the niacin and Vit. C? How will I ever know?

                          Comment


                          • #15
                            I would wage a strong bet it's the niacin. C might be of some help, who knows. I did the Pauling protocol years ago with no measurable effect whatsoever. That's the problem using more than 1 strategy as you never know what was responsible for the improvement.

                            Comment

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