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Lipoprotein A Variance...

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  • Lipoprotein A Variance...

    Hi All and hope all are well.
    Got a quick question for the forum.
    I have the Lovely LPa which was identified 6 months ago
    at 97. Had done early this month and went to 166 :-(
    Needless to say I am going to try Niacin, enduracin this time as per my Bale Donneen Doc.
    I held off on Nicain initially as I had AFib and AFlutter where I had a successful Catheter Ablation 2 months ago.

    Could the meds for AFib (which I'm off now less the Eliquis) or something around that condition have affected this?
    Is it normal to get variances on LPa levels as such in short amount of time?
    Eat real healthy (heavy veg, low simple carbs, lots of healthy fat), daily meds are Fish oil, Ubiquinol, Pepcid, Vitamin D3, Cinammon, Chromium, B12,
    Magnesium, and Crestor 5g (Every other day).

    Thanks To All in Advance!

  • #2
    To my limited understanding on this topic, people seem to have a genetically set amount of Lp(a) and more can be expressed due to health issues. Two or three grams of niacin daily seems to result in a 25-30% reduction in genetically set levels for most people who have an elevated Lp(a) level, and John Lorscheider mentioned in the past that his Lp(a) level went down something like 70% or more over time. He was taking niacin and improving his health.
    Some people have liver issues with the larger doses of niacin, and Chris Masterjohn speculated that it is caused by depletion of methyl group donors as those are necessary as part of the liver processing niacin with some relatively small amount going to a nicotinamide pool for the whole body and the rest peed out after a methyl group is added. He recommends taking some TMG to offset those methyl groups lost to niacin. Search for Chris Masterjohn and niacin videos if you want to know more.

    Comment


    • #3
      Thank you Tom, I really appreciate your feedback here.
      There is a lot of inconsistent info about LPa and what
      may Increase or decrease. I did find in one journal article
      “Lp(a) do fluctuate with stress, infections and injury.”
      interesting that I had a catheter ablation 6 weeks before that
      bloodwork and the LPa went up 69 points from 6 months before.
      trying niacin and I’ll see how that will help it!
      thanks again! :-)

      Comment


      • Joe Reilly
        Joe Reilly commented
        Editing a comment
        I'm taking niacin Enduracin 2.5 grams a day. This reduced my Lp (a) from 450 to 373. I'm keen to hear how it works for you.

    • #4
      I copied below a posting by John Lorscheider a while back on niacin which I thought you might find useful.


      The benefits of niacin in the form of nicotinic acid are many:

      1. Raises HDL cholesterol

      2. Lower LDL cholesterol

      3. Lowers Lp(a)

      4. Reduces total cholesterol

      5. Reduces triglycerides

      6. Reduces VLDL cholesterol

      7. Reduces arterial inflammation


      Many doctors don't believe in the value of niacin. The science is there but they don't choose to believe it.


      Yes, Niacin can be very effective. It can be purchased without a prescription. I've been taking it for 10 years. Dosages of 1,000 to 2,000 MG, once per day, of extended release formulas like Endur-Acin, Rugby, Slo-Niacin can work well.


      As far as niacin goes, be sure the base ingredient is nicotinic acid which is the only form of niacin that has a beneficial effect on lipids and Lp(a). Niacinamide and Inositol Hexanicotinate don't work for lipids. Start niacin at low doses and work up as it takes time to get used to it.


      There are three types:


      Instant-Release - Lowest possible concern for elevated liver enzymes. Highest level of flushing. Usually taken 2-3 times daily.


      Extended-Release (releases over 8-12 hours) - Low to moderate concern for elevated liver enzymes. Less flushing. Doses of 2,000 MG or less, once daily, are usually not a problem. Endur-Acin, Slo-Niacin, Niaspan are typical examples of ER Niacin.


      Sustained-Release (releases over 12+ hours) - Highest level of concern for elevated liver enzymes. Least flushing.


      That is a lot of bang for $8 to $16 per month.


      https://www.amazon.com/ENDUR-ACIN-Ni...pSrc=srch&th=1


      Start with 500 MG with dinner once per day. Add 500 MG more in 4 weeks until you get to 1,000 MG. Then after 4 weeks at 1,000 MG get your labs. The flush is mild and diminishes the longer you use it. Some people report drinking a large glass of ice water or taking an aspirin 1-hour before taking niacin helps to reduce the flush.


      You can add more from that point as dictated by your labs.

      Comment


      • sthubbar
        sthubbar commented
        Editing a comment
        Tom, this is a great summary for Niacin. Thank you.

    • #5
      Thank you again To,m. My new and now Bale Doneen dr wants me to start at 250 mg for 3 weeks and increase to 500 mg . Take baby asa 1/2 hour before as well as tbs. of fiber he says.
      I guess he's playing safe for now. Maybe he wants to run liver enzymes and since I'm on Crestor 5 mg, albeit QOD (every other day) dosing. Prior cardiologist said crestor has half life of 19 hrs. and
      recommended.
      My lipid panel by the way on Crestor 5 QOD (eating very healthy) is as follows:
      Total: 120, HDL: 41, Trigs: 70, LDL: 64.
      Have fair amount of plaque. New Bale Doneen Dr. Sneered at QOD dosing but has not yet talked to me about these results, that's my next appt with him. CRP = .3 All else good except LPa :-(........................
      What you think? Should I keep QOD and with Niacin see what does?

      Thank You a million again.
      You are truly awesome :-)
      Roland

      Comment


      • #6
        To be honest I don't remember the particulars for your health status other than there was an obvious issue. I know that Dr. Brewer generally recommends a low dose of statins for patients at moderate/high risk. To my thinking the higher the risk that you have going forward, the higher the dose of statin because you might not have enough time to gradually lower cardiovascular inflammation with a lower dose statin along with diet/lifestyle changes.

        A lot of doctors would prescribe 40 mg/daily of rosuvastatin to a patient after a major cardiovascular health event (or test showing that the patient is at high risk) in order to knock down their LDL-C levels. I transitioned from 10mg/daily simvastatin to 20 mg/daily rosuvastatin after my CAC score indicated that I had some heart disease. After a couple of years I reduced that to 10 mg/daily rosuvastatin once my lipid tests were improved. In retrospect I think that my heart disease (cardiovascular disease) pre-dated my starting the simvastatin which likely did improve my overall cardiovascular plaque burden (CIMT test showed my plaque burden as ten years lower than usual for a male my age).

        I am not a doctor, and so I can only say have an informed conversation with your cardiologist. My liver enzyme AST did elevate after starting a statin along with some supplements, but it is still ok from what Dr. Brewer has said in multiple videos. Your doctor will obviously watch your liver enzymes for indications of issues.

        Comment


        • #7
          Roland, your lipid panel looks great. HDL might be a little low, but hopefully the niacin will raise it. And it should lower your LDL some as well. Watch LDL because too low may be a problem.

          Any idea what your ldl particle number is?

          Are you doing plant based or keto or something else?

          Comment


          • #8
            Ty again Tom and will have a serious talk with new bale
            doneen talk. After all that’s what I’m paying for.

            Hi Rich, LDL-P is 1088, not bad but not great is my understanding?
            I am going to try to post my complete labs in here and after discussion with new bale Dinesen doc and have forum weigh in.
            All of you and Fatmax as well are the best! From helping
            others you are getting great Kharma!
            Anyway, I was Esselstyn plant based for a bit but it was
            not sustainable for me. I am now more along the ways
            of Dr. Fuhrman with nearly vegan, that is I’ll have fatty fish about
            once a week but consume a good bit of healthy fats like
            avocado, walnut, almond milk. I am looking heavily at diet though and will make a post here shortly. I have read Esselstyn, fuhrman,
            bernard, Kahn, but also Ozner, Davis, Sinatra, Berry, and Fung. I think there are valid points to be taken from each BUT WE MUST KEEP FOCUSED ON NOT BEING INSULIN RESISTANT so
            simple carbs and most sugars are VERY bad, as has been shown
            high insulin is 5 TIMES WORSE FOR HEART DISEASE
            than CHOLESTEROL.

            Comment


            • rich
              rich commented
              Editing a comment
              Out of all your numbers, particle number is probably the most important. What you want to ask the doc is with your LDL so low, why is particle number so high? Why isn't LDL being cleared? That's the same thing I'm trying to figure out.

              If you have them, could you post some of your older lipid labs along with what kind of diet you were on at the time? I'd like to check them against mine to see if they follow the same pattern. I've got some going back 9 years, but my primary doctor of most of the last 10 years closed her office, and I just found out the patient portal no longer gives access to old labs so I'm missing a bunch of labs. I have a few I ordered myself, so I think I can make a graph of the last 8 or 9 years.

          • #9
            Hi Rich,
            I had bloodwork done in January as per my prior cardiologist ,
            god forgive me I’m changing cardiologists quicker than shoes
            - SERIOUSLY! Anyway, it was baseline bloodwork where I was not on a statin for 3 months prior and it was: Total: 138, LDL: 97,
            HDL: 33 (Was not on fish oil here), Trig: 103, LDL-P: 1448.
            So to answer your question Rich, for me LDL-P did come down 360
            points since January of this year.
            You bring up an excellent point here Rich and now have me thinking
            , if I were to switch to Crestor QD from QOD, can this go down further?? I welcome all commentary here and thanks and god bless you all!

            Comment


            • rich
              rich commented
              Editing a comment
              I'm on my 6th cardiologist, so I'm guessing you've got a ways to go to catch up. Not one seems to have a clue as to what causes arterial plaque.
              Last edited by rich; 07-31-2019, 06:44 AM.

          • #10
            Rich, It's really sad as these guys all seem sharp like spoons when it comes to causation and prevention of heart disease!
            I mentioned something about inflammation to one doc a little while ago and he looked at me like I had 3 eyes, :-(...
            We'll see how my new Bale Doneen guy is here where I live. Seeing his nurse this week and him within a few weeks.

            Comment


            • David
              David commented
              Editing a comment
              It's quite disturbing that nobody seems to agree on what causes plaque build up. Sure, all things equal, we want our blood sugars low, insulin low, inflammation low, blood pressure low, etc etc. But nobody seems to know what really causes the build up. Lots of theories. No agreement.

            • fatmax
              fatmax commented
              Editing a comment
              Plaque build up, also called atherosclerosis, is caused by insulin resistance.

            • rich
              rich commented
              Editing a comment
              My guess is that it is a lot like Bredesen's approach to Alzheimer's. It is a cascade of a whole bunch of things. There are certainly multiple things that can cause damage to blood vessels. I think when looking at the cholesterol side, we need to be looking at everything that keeps particles from being cleared resulting in high number of remnants, high LDL particle number, sdLDL, and oxidized LDL.

          • #11
            Been looking at ALOT of data just recently and while I agree it’s a culmination of events that cause plaque to include LDL-P, in the lead is in fact sugars coupled with insulin resistance. As we all say
            it would be nice to have a time machine here! Lol

            Comment


            • rich
              rich commented
              Editing a comment
              But that doesn't really tell us much. It is associative at best. What is it that sugar does that causes heart disease?

              It appears sugar increases the level of triglycerides and cholesterol. So just maybe we are back to remnants and LDL particle number again.

          • #12
            Hi Rich,
            more than anything it is acknowledged high sugar
            and insulin resistance correlate with metabolic syndrome
            and inflammation. Inflammatory = disease.
            i don’t have equation for chemical pathways here.
            a bit of a crude but accurate explanation that I’ve heard various times stated differently:

            Dr. Razani explains the link between macrophages and atherosclerosis, as well as the motivation behind the research:
            "In atherosclerosis, macrophages try to fix damage to the artery by cleaning up the area, but they get overwhelmed by the inflammatory nature of the plaques. Their housekeeping process gets gummed up. So their friends rush in to try to clean up the bigger mess and also become part of the problem. A soup starts building up - dying cells, more lipids. The plaque grows and grows," he says.

            "We are interested in enhancing the ability of these immune cells, called macrophages, to degrade cellular garbage - making them super-macrophages."

            Comment


            • #13
              I think these may explain what Dr Razani is referring to. The 1st link is an easy to understand article and the 2nd is the study that the 1st link references,

              Glucose-guzzling immune cells may cook up coronary artery disease, Stanford study finds

              The glycolytic enzyme PKM2 bridges metabolic and inflammatory dysfunction in coronary artery disease

              Comment


              • #14
                2nd article is very interesting. Thank You Rich!
                Would love to get Dr. Brewers input here as well.

                Comment

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