Because of my low Lp(a), should I be concerned about Repatha?
Low Lp(a)? Consider yourself lucky!
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From Gemini Pro:
Clinically low levels of Lipoprotein(a) [Lp(a)]âtypically defined as <10 mg/dL or <25 nmol/Lâare overwhelmingly established as cardioprotective and beneficial for human longevity due to a drastically reduced risk of atherosclerotic cardiovascular disease (ASCVD) and aortic stenosis,
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That statement from Gemini Pro is kind of confusing â makes it sound like having some (very low level) is cardioprotective when I think it means to say that the absence of Lp(a) is what is beneficial.
Actually I think there is some small protective benefit of Lp(a) as a protection against infection but over around 30mg/dl it is bad --causes inflammation in the blood vessels.
My Lp(a) was 40 mg/dl before I started Repatha. It went down to 27.
My Lp (a) is 9. Will Repatha make it even lower? And if itâs that low why it didnât protect me from having a high calcium score? I suspect that either my Lp (a) or CAS were calculated incorrectly.
Having a low Lp(a) doesnât guarantee a low calcium score if your LDL particles have been elevated much or most of your life and/or if youâve had some chronic low grade inflammation. Things would likely be considerably worse if you also had high Lp(a).
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You have side effects from those 3 different classes of medication? I donât know how to explain that. Are you being prescribed these by a doctor?
LDL 5.5 = ~200mg/dl, which is very high. And you have a positive calcium score. That means you already have established cardiovascular disease. Youâve built plaque, and itâs been going for long enough to go through cycles of repair and calcification. And with LDL of 5.5 mmol/L, you will be building more plaque as time goes on.
How old are you?
Tadalafil may be cardioprotective by lowering cardiac stress, but it doesnât affect lipids. Rapamycin may be protective by lowering inflammation, but it generally makes lipids worse.
Mine wasnât affected at all by Repatha. I think itâs quite unreliable as an Lp(a)-lowering agent.
The CAC might have been worse if your Lp(a) was higher. And of course there are contributions from ApoB (LDL-C etc), and others. Atherosclerosis is generally âarea under the curveâ thing, where the longer you went with higher lipids and other risk factors, the higher the CAC will go, with some lag time. You can roughly imagine that 10 years at 200mg/dl is equivalent to 20 years at 100mg/dl in terms of total accumulation.
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Exgenous androgens lower Lp(a) 25 to 75%, but then you have to contend with low hdl, lĂber strain, and elevated ldl. No free lunch!
Iâm currently experimenting with oral enobosarm (ostarine) 6mg daily, which has completely normalized my Lp(a). LDL and ApoB are extremely low thanks to modern pharma and liver enzymes are normal, courtesy of TUDCA. Iâm going with the theory that any risk from low HDL is more than offset by the 75% drop in Lp(a) and my very low LDL/ApoB. Next Iâll lower the enobosarm dose to 3mg and retest Lp(a) to see what the lowest effective dose is.
To be clear, enobosarm is still experimental (in stage 3 clinical trials) and is not approved for any use at this point and comes with risks of serious side effects such as (but not limited to) suppression of endogenous testosterone/estrogen synthesis. Its effect on Lp(a) has never been tested in clinical trials.
Note: I posted a few months back that it was IGF1-LR3 that was responsible for my decreased Lp(a), but I had no idea at the time that the enobosarm I was also taking off/on could have such a dramatic effect on Lp(a). Stopping enobosarm while continuing LR3 caused my Lp(a) to climb back to 175. Stopping LR3 and restarting enobosarm quickly dropped Lp(a) back to 50.
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I donât think Lp(a) could ever be too low. I am pretty sure lower is better with no floor.