You wrote: “I take 2.125g of immediate release metformin”

You take two, 125 grams immediate release metformin–that’s a mighty big tablet, I would think since each would contain 125,000mgs Metformin… ??

Pioglitazone seems scary… But then diabetes is scary too…

No, I don’t take it all in one go, and I have cut back on the total dose of metformin I now take. As it’s immediate release, I take it (1/2 of 750mg tablet) an hour before meals, and just before bedtime.

I’m going to order some extended release metformin and do a head-to-head study whilst wearing a CGM.

Yes, Pioglitazone is a bit ‘scary’, with its risk of bone fractures etc, I used to work (in drugs research) with its cousin Rosiglitazone. I take a micro dose 1/4 of a 30mg tablet, so 7.5mg dose, which has been shown to be efficacious

I take the pioglitazone along side a 1g omega 3 soft gel to boost the efficacy

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30237-0

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Interesting info! How long have you taken the pioglitazone and did you notice any changes in blood parameters?

I’ve taking it for about a year now, I’ve only started taking measurements recents HbA1c etc so can really say.

Now I’ve got my blood pressure meds sorted, I’m planning on stopping my glucose meds (to get a baseline) and re introducing them slowly to see what works for me and what doesn’t.

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Thanks for the feedback, keep us updated!

This is a link to register for clinical trial for Lp(a) - lowering med (I’m not sure which one)

I registered and got a text saying they’ll let me know if/when a trial is taking place in my area :unamused:

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A post was merged into an existing topic: The Carnivore Diet and Rapamycin

In fact, not in any way related to the topic of new Lp(a) lowering drugs or Lp(a). Why post it here? You could create a new thread instead of derailing the subject of this one.

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Not quite true what you are saying. I thought level of Lp(a) is in fact somehow related to what people eat, no? I guess you could swipe left if you don’t like something you read! Plus, sharing what works and what doesn’t for certain health condition should be considered kosher for these boards, no?

No. Diet has minimal impact on Lp(a), unlike LDL/ApoB.

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One of / the top Lp(a) doc in the world is answering questions via twitter tomorrow

https://twitter.com/lpa_doc/status/1781362823689535524?s=46&t=zJMJ1xVdRJYEDYz-DHipTw

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https://x.com/Lpa_Doc/status/1781723202785583371

Edit: here’s the link to the actual paper from the photo in the tweet. I think the “may even increase Lp(a)” comment is specific for statins, not “any 3rd med”.

So my interpretation is that if you’re just looking at LDL-C, it can be confusing in those with high Lp(a) because some of that cholesterol is actually carried on Lp(a) not LDL. Which is all the more reason for looking at the actual particle numbers of LDL and Lp(a) instead of a secondary surrogate like cholesterol, or at the very least ApoB instead of LDL-C, since it’s a better surrogate for atherogenic particle number.

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Published: 08 May 2024

Discovery of potent small-molecule inhibitors of lipoprotein(a) formation

Pelacarsen, an antisense oligonucleotide that targets LPA , and olpasiran, an LPA small interfering RNA, are both injectable therapeutics that are currently in phase 3 clinical studies. These interventions have shown a robust Lp(a)-lowering effect, with good tolerability16,17. Results from ongoing phase 3 cardiovascular outcome trials, such as HORIZON and OCEAN(a), will provide much-needed evidence about the therapeutic utility of Lp(a)-lowering treatments18,19.

So far, no small molecule that specifically targets apo(a) has been studied in humans; however, the plasminogen inhibitor tranexamic acid was found to reduce the levels of Lp(a) in a small clinical study20. The goal of our research was to develop a potent and selective orally delivered small-molecule therapeutic to inhibit the formation of Lp(a) by blocking the first interaction between apo(a) and apoB to reduce the circulating levels of Lp(a). A potent and selective small-molecule Lp(a)-reducing therapeutic could provide a way to decrease the number of primary and/or secondary major adverse cardiovascular events in patients who are at risk of cardiovascular disease because of their high levels of Lp(a).

Open access:
https://www.nature.com/articles/s41586-024-07387-z

Published: 09 May 2024

Development and multinational validation of an algorithmic strategy for high Lp(a) screening

https://www.nature.com/articles/s44161-024-00469-1

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This is what I already did to lower my Lp(a);

  • daily 400mg bezafibrate from 16 november to 16 februari; Lp(a) dropped from 96 mg/dL to 54 mg/dL, so a 43% reduction.

  • daily fenofibrate nanoparticle 145mg from 17 februari to 6 june; Lp(a) dropped from 54 mg/dL to 39 mg/dL, so an additional 28% reduction

The only downside: homocysteine has increased from 8,6 to 12,2 mcmol/L, although I take a lot of supplements to lower it (5g creatine, 3g glycine, 0,5g TMG, methylated B vitamins). I have a MTHFR mutation and since I found this out, I try to eat at least 4 biological eggs a day, for cholesterol I take 5mg ezetimibe and 5mg rosuvastatin every other day.

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would be interesting to know what exactly “biological eggs” are?

Probably “organic” (“biologique” in French, a false friend).

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You’re right, I am Dutch speaking, so I made a wrong translation :blush:

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Congratulations Ludovic, that’s a great result.

I was just wondering did you change medication in February for a specific reason? Also, are you now going to continue with either fibrate or are you going to stop and retest to see whether your Lp(a) has permanently stabilised or will go back up without the fibrates?

I changed the medication to see what kind of a result I would get with the fenofibrate nanoparticle which is cheaper and easier to get here in Belgium. I actually expected worse results with the bezafibrate.
I now plan to keep taking the fenofibrate, since I think lowering Lp(a) is more important then a little higher homocysteine. Is there evidence that Lp(a) could stabilise permanently?

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I don’t know why, but mine came down quite a bit and then has hovered around 5.7 nmol/l. It went up as high as 13 in February and then was below 5.2 a couple of times recently.