Agian
Well-known member
390 divided by 2.5 = 156
Doesn't sound right
Chemistry wasn't my forte.
Anyone?
Doesn't sound right
Chemistry wasn't my forte.
Anyone?
Lp(a) of 390 nmol/L!
- Thread starter Nocturne
- Start date
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The conversion is for Lp(a) yes. The quote from Wikipedia you'll see also uses that conversion for the reference ranges they list.
https://en.wikipedia.org/wiki/Lipopr...nostic_testing
390 divided by 2.5 is 156, yes.
PS In that Wiki article you'll note it says: Approximate levels of risk are indicated by the results below, although at present there are a variety of different methods by which to measure Lp(a). A standardized international reference material has been developed and is accepted by the WHO Expert Committee on Biological Standardization and the International Federation of Clinical Chemistry and Laboratory Medicine. Although further standardization is still needed, development of a reference material is an importance step towards standardizing results.
Perhaps that's part of the problem, different measuring methods ?
https://en.wikipedia.org/wiki/Lipopr...nostic_testing
390 divided by 2.5 is 156, yes.
PS In that Wiki article you'll note it says: Approximate levels of risk are indicated by the results below, although at present there are a variety of different methods by which to measure Lp(a). A standardized international reference material has been developed and is accepted by the WHO Expert Committee on Biological Standardization and the International Federation of Clinical Chemistry and Laboratory Medicine. Although further standardization is still needed, development of a reference material is an importance step towards standardizing results.
Perhaps that's part of the problem, different measuring methods ?
Nocturne
Well-known member
156 mg/dL is a bit more than triple the "very high risk" cutoff, which is what 390 nmol/L is. So Paleowoman's conversion makes sense.
So if I cut it by 66% it is still "extremely high".
From what I have read, my Lp(a) level combined with extant AS and CAD would qualify me for apheresis treatments in Germany and maybe some other European countries.
My Lp(a) is freakshow high. There is a reason there aren't any other people on this forum who have degenerative calcific AS in their early 40s.
But there are drugs just on the horizon that can lower Lp(a) by 90% or more! So there is hope, especially for my kids.
So if I cut it by 66% it is still "extremely high".
From what I have read, my Lp(a) level combined with extant AS and CAD would qualify me for apheresis treatments in Germany and maybe some other European countries.
My Lp(a) is freakshow high. There is a reason there aren't any other people on this forum who have degenerative calcific AS in their early 40s.
But there are drugs just on the horizon that can lower Lp(a) by 90% or more! So there is hope, especially for my kids.
Agian
Well-known member
Even a weekly dose of Evolocumab.
Anyway, here's the blurb on Fenofibrate:
https://www.ebs.tga.gov.au/ebs/picm...t&id=CP-2010-PI-07176-3&d=2017042416114622483
Educate your cardiologist
Anyway, here's the blurb on Fenofibrate:
https://www.ebs.tga.gov.au/ebs/picm...t&id=CP-2010-PI-07176-3&d=2017042416114622483
Educate your cardiologist
Nocturne
Well-known member
Agian;n875695 said:
Looks like you did not finish your first sentence there.
I read the whole blurb on Fenofibrate but I must have missed the part where it mentioned how it can bring down Lp(a).
It is evident to me that my heart issues were caused primarily by FH and extremely extremely high Lp(a).
I just found out an old schoolmate of mine also has Lp(a) in the 300s (nmol/L) and she just had a heart attack this past January. She is 43. I asked her what her doc put her on to lower her Lp(a). No response yet.
Agian
Well-known member
I meant weekly Evolocumab. It's usually prescribed fortnightly, but it can be given weekly if the response is 'inadequate'. Good luck convincing your cardiologist after she sees what the fortnightly dose does to your ldl. That would get it down to the 50s. You could essentially normalise it after that with some of the other crap. Apheresis is like dialysis. They essentially filter your blood and pump it back into your body. It's quite a big deal.
Good point: it mentions lp(a) in passing, but it doesn't specifically say Fenofibrate reduces it. Otherwise it would be in their data.
i used an online converter specifically for lp(a) but it uses micromoles instead on nmol/L. Just moved the decimal point to convert and got 109, which sounds right. I'd upload the link but I don't know how to on my iPad and don't have access to my PC tonight.
Lercanidipine (for bp which went up post-op) may have helped reduce mine as well, but it's hard to tell, because I started that and dhea around the same time.
Good point: it mentions lp(a) in passing, but it doesn't specifically say Fenofibrate reduces it. Otherwise it would be in their data.
i used an online converter specifically for lp(a) but it uses micromoles instead on nmol/L. Just moved the decimal point to convert and got 109, which sounds right. I'd upload the link but I don't know how to on my iPad and don't have access to my PC tonight.
Lercanidipine (for bp which went up post-op) may have helped reduce mine as well, but it's hard to tell, because I started that and dhea around the same time.
Agian
Well-known member
Probably nothing; a lot of these guys are muppets. You're in America, right?Nocturne;n875696 said:
Why don't you get in touch with William Davis? He's vocal about this stuff. You could even get an appointment. He wrote the 'Track your Plaque' book and is all over this CAC thing. Milwaukee.
Nocturne
Well-known member
Agian;n875708 said:
Agian, I found the same converter and it seems wonky. I'm not sure how 109 makes any sense when it is double the "extreme risk" cutoff in mg/dl and 390 nmol/L is more than triple the same cutoff of 125 nmol/L. Paleowoman's calculation of 150-something really does make more sense. In any event I'll trust my cardiologist when she tells me, as she has been pretty impressive so far.
If you can find any literature, other than your own conjecture, revealing high doses of Evolocumab being used to cut Lp(a) levels in half, I'd love to read it so I can bring it to my cardiologist. So far I have found only evidence that it is NOT indicated for such use. Yes, it lowers Lp(a) by up to 30% in most people, but that benefit appears to vanish at high ends of the scale.
In the end, I'll trust a preventative cardiologist over a well-meaning fellow on the internet who says he knows a guy...
Let me just clarify -- did YOU actually lower YOUR Lp(a) by a significant amount somehow? Where you had it tested before and after and it went down significantly?
Because if it really that easy, there is an entire foundation out there that I have linked to that would like to know about it.
I'll let you know what my cardio doc says when I talk to her about it.
Nocturne
Well-known member
So this is interesting... Checked the forums on the Lp(a) foundation website and learned that you can find the SNPs associated with high Lp(a) in the raw data from 23andme (which I have already gotten).
Checked my data and found that I am homozygous for one of the alleles associated with high Lp(a). That means I inherited the defective allele from BOTH of my parents. It also means that ALL of my kids inherited it from me (because it's the only one I can give).
Checked my data and found that I am homozygous for one of the alleles associated with high Lp(a). That means I inherited the defective allele from BOTH of my parents. It also means that ALL of my kids inherited it from me (because it's the only one I can give).
Agian
Well-known member
It's not 'indicated' because lp(a) is not a widely accepted risk factor. Evolocumab was marketed for FH patients, not lp(a).
So you are unlikely to find any literature on it's use for this. It only came out last year.
Yes, my lp(a) has normalised on evolocumab, Niacin, dhea, lercanidipine, almonds, flaxseed.
All the best.
So you are unlikely to find any literature on it's use for this. It only came out last year.
Yes, my lp(a) has normalised on evolocumab, Niacin, dhea, lercanidipine, almonds, flaxseed.
All the best.
Nocturne
Well-known member
Agian, what level was your Lp(a) prior to treatment? How far down did it go?
I have looked around on the Lp(a) Foundation forum and seen a few people claiming to have Lp(a) levels in excess of 150 mg/Dl. There really are some people with crazy high Lp(a) levels out there. It is unfortunate but not unbelievable. I myself am triple the level that would qualify me for apheresis (blood cycling) treatments in the UK or Germany.
I did a bit more reading and learned that the particular bad Lp(a) allele I am homozygous for is the one most associated with calcific aortic stenosis.
It is good to know WHY. I don't have to wonder about whether it was the air quality of the room where I work, or the stress level from dealing with the students, or my testosterone, mouthwash, or something else that caused me to have calcific AS at such a young age -- I know what the cause was, and what it is I need to learn about and fight as I can.
Also learned that the new drug is being trialed (it is really a newish form of gene therapy called antisense(?)) in Massachusetts, which is the state next to my home state -- probably about an hour drive from home. I am going to try to get onto the phase 3 drug trial -- with my particular situation, I am exactly the sort of person they are trying to market the treatment to (extremely high Lp(a) and extant heart disease).
Lowering my Lp(a) level by over 90% with a pill? Yes, please.
Amusingly, the name of the company developing this treatment used to be ISIS, but they changed it for some reason (what could it have been?) to Ionis.
I have looked around on the Lp(a) Foundation forum and seen a few people claiming to have Lp(a) levels in excess of 150 mg/Dl. There really are some people with crazy high Lp(a) levels out there. It is unfortunate but not unbelievable. I myself am triple the level that would qualify me for apheresis (blood cycling) treatments in the UK or Germany.
I did a bit more reading and learned that the particular bad Lp(a) allele I am homozygous for is the one most associated with calcific aortic stenosis.
It is good to know WHY. I don't have to wonder about whether it was the air quality of the room where I work, or the stress level from dealing with the students, or my testosterone, mouthwash, or something else that caused me to have calcific AS at such a young age -- I know what the cause was, and what it is I need to learn about and fight as I can.
Also learned that the new drug is being trialed (it is really a newish form of gene therapy called antisense(?)) in Massachusetts, which is the state next to my home state -- probably about an hour drive from home. I am going to try to get onto the phase 3 drug trial -- with my particular situation, I am exactly the sort of person they are trying to market the treatment to (extremely high Lp(a) and extant heart disease).
Lowering my Lp(a) level by over 90% with a pill? Yes, please.
Amusingly, the name of the company developing this treatment used to be ISIS, but they changed it for some reason (what could it have been?) to Ionis.
Agian
Well-known member
From 60ish to mid 20s.
Nocturne
Well-known member
OK, so not from 150 to mid 20s. But yes, very impressive for a factor that is supposedly intractable.
And yes, I am in the States where apparently we have decided to pretend that Lp(a) is not a thing.
A word about conversions from the Lp(a) Foundation forum:
* * * * *
Converting Lp(a) from mg/dL to nmol/L
In years past, LP(a) was typically measured in mg/dL units by Labcorp, Quest and other labs. mg/dL is a weight based measurement that is biased toward the less atherogenic larger and less atherogenic form of apoA. The experts said at the time just take your mg/dL result x 2.5 to convert to nmol/L. nmol/L is a volume based measurement that is said to be more reflective of atherogenicity.
Multiplying mg/dL x 2.5 didn't turn out to be so accurate and can be anywhere from 2.85 for small, dense and more atherogenic molecules to as low as 1.85 for the large Lp(a) molecules.
As Dr. Thomas Dayspring put it:
"The conversion factor from mg/dL to nmol/L varies from 2.85 for a small Lp(a) size to 1.85 for a large one. Therefore, a factor of 3.5 is too high, and we suggest a mean conversion factor of 2.4, even though the conversion can be more or less imprecise depending on the apo(a) size. However, the major problem of Lp(a) values is not the units used to report the results but is related to the inaccuracy of the methods that are affected by apo(a) size heterogeneity. These methods overestimate the levels of Lp(a) in individuals with large Lp(a) molecules and consequently underestimate the levels in individuals with small Lp(a) molecules."
In other word, don't rely on old mg/dL Lp(a) values and get retested by a lab using nmol/L values. Hopefully there will be particle size testing for Lp(a) someday just as there now is for LDL.
http://www.lipidcenter.com/pdf/Entire_Lpa_Complexities.pdf
And yes, I am in the States where apparently we have decided to pretend that Lp(a) is not a thing.
A word about conversions from the Lp(a) Foundation forum:
* * * * *
Converting Lp(a) from mg/dL to nmol/L
In years past, LP(a) was typically measured in mg/dL units by Labcorp, Quest and other labs. mg/dL is a weight based measurement that is biased toward the less atherogenic larger and less atherogenic form of apoA. The experts said at the time just take your mg/dL result x 2.5 to convert to nmol/L. nmol/L is a volume based measurement that is said to be more reflective of atherogenicity.
Multiplying mg/dL x 2.5 didn't turn out to be so accurate and can be anywhere from 2.85 for small, dense and more atherogenic molecules to as low as 1.85 for the large Lp(a) molecules.
As Dr. Thomas Dayspring put it:
"The conversion factor from mg/dL to nmol/L varies from 2.85 for a small Lp(a) size to 1.85 for a large one. Therefore, a factor of 3.5 is too high, and we suggest a mean conversion factor of 2.4, even though the conversion can be more or less imprecise depending on the apo(a) size. However, the major problem of Lp(a) values is not the units used to report the results but is related to the inaccuracy of the methods that are affected by apo(a) size heterogeneity. These methods overestimate the levels of Lp(a) in individuals with large Lp(a) molecules and consequently underestimate the levels in individuals with small Lp(a) molecules."
In other word, don't rely on old mg/dL Lp(a) values and get retested by a lab using nmol/L values. Hopefully there will be particle size testing for Lp(a) someday just as there now is for LDL.
http://www.lipidcenter.com/pdf/Entire_Lpa_Complexities.pdf
Nocturne
Well-known member
From the above, it would seem that my Lp(a) of 390 nmol/L could be converted as something between 137 and 211, depending on particle size(s). The recommended conversion would be 162 mg/Dl.
That's the sort of high you get from having homozygous alleles for bad Lp(a).
That's the sort of high you get from having homozygous alleles for bad Lp(a).
Nocturne
Well-known member
Interesting JACC article about Lp(a) that mentions its role in AVS:
http://www.sciencedirect.com/science...35109716372540
* * * * *
What is the clinical evidence that Lp(a) mediates CAVS?
Although it has long been suspected that Lp(a) is a risk factor for CAVS; only recently has Lp(a) become appreciated as a potent risk factor (33). Recent studies have shown that of >2.5 million single-nucleotide polymorphisms (SNPs) analyzed, the LPA SNP rs10455872, which is associated with markedly elevated Lp(a) levels, was the only monogenetic risk factor for aortic valve calcification and CAVS in multiple racial groups 34; 35; 36 ; 37. Similar to the studies with myocardial infarction, a strong case for causality can be made because these studies linked a genetic trait (LPA SNPs) that could not be altered by environment or diet to a quantitative and substantial (5- to 20-fold) increase in plasma Lp(a) levels, and to a clinical phenotype of aortic valve calcification and CAVS.
* * * * *
LPA SNP rs10455872 is the one I am homozygous for the bad allele of, and the paper goes on to explain how it speeds up the progression of AVS. So -- fun, fun.
http://www.sciencedirect.com/science...35109716372540
* * * * *
What is the clinical evidence that Lp(a) mediates CAVS?
Although it has long been suspected that Lp(a) is a risk factor for CAVS; only recently has Lp(a) become appreciated as a potent risk factor (33). Recent studies have shown that of >2.5 million single-nucleotide polymorphisms (SNPs) analyzed, the LPA SNP rs10455872, which is associated with markedly elevated Lp(a) levels, was the only monogenetic risk factor for aortic valve calcification and CAVS in multiple racial groups 34; 35; 36 ; 37. Similar to the studies with myocardial infarction, a strong case for causality can be made because these studies linked a genetic trait (LPA SNPs) that could not be altered by environment or diet to a quantitative and substantial (5- to 20-fold) increase in plasma Lp(a) levels, and to a clinical phenotype of aortic valve calcification and CAVS.
* * * * *
LPA SNP rs10455872 is the one I am homozygous for the bad allele of, and the paper goes on to explain how it speeds up the progression of AVS. So -- fun, fun.
Nocturne
Well-known member
So, finally met with my lipid doc again. I was a bit disappointed that she clearly had not read any of the emails I had sent her as it was clearly news to her that high Lp(a) is associated with calcific aortic valve stenosis and appears to accelerate progression. And she was not even aware that my Lp(a) test results had come in. And she did not recommend any treatments to lower it (she actually made that suck-air-through-teeth noise when she saw my score, but then said, "Well, this won't actually change your treatment, but we should definitely get your kids tested.")
BUT! Her group will be starting a trial of Ionis' new antisense drug and she said my Lp(a) was so high (5th highest on the list of people they are compiling for the study) that, combined with my high CAC score, I should qualify for the study. She suggested this before I had mentioned the drug and was surprised that I already knew what it was and what company was developing it.
Her concern was that I had not actually had a heart attack yet -- this may disqualify me from the study as they are not looking at CAVS progression (she did not even know the association), but rather "heart events".
When I pushed, she said she would help me with niacin treatments if I could not get in the study, but shook her head at everything else mentioned in this thread.
The USA, it seems, it just putting all of its hope on this new drug, when it even thinks about high Lp(a) at all.
And it is very unnerving to me that I seem to know more about what is going on with me than my doc does.
But I'm calling this one a win, at least for now, if I can get in on that study.
Still convinced that it will become policy to give this drug to CAVS patients to greatly slow down progression immediately AFTER I have my AVR surgery. Because that would be funny, at least to the sort of sick ******* of a universe that would give someone heart trouble in the first place. Ha ha! Get the joke?
BUT! Her group will be starting a trial of Ionis' new antisense drug and she said my Lp(a) was so high (5th highest on the list of people they are compiling for the study) that, combined with my high CAC score, I should qualify for the study. She suggested this before I had mentioned the drug and was surprised that I already knew what it was and what company was developing it.
Her concern was that I had not actually had a heart attack yet -- this may disqualify me from the study as they are not looking at CAVS progression (she did not even know the association), but rather "heart events".
When I pushed, she said she would help me with niacin treatments if I could not get in the study, but shook her head at everything else mentioned in this thread.
The USA, it seems, it just putting all of its hope on this new drug, when it even thinks about high Lp(a) at all.
And it is very unnerving to me that I seem to know more about what is going on with me than my doc does.
But I'm calling this one a win, at least for now, if I can get in on that study.
Still convinced that it will become policy to give this drug to CAVS patients to greatly slow down progression immediately AFTER I have my AVR surgery. Because that would be funny, at least to the sort of sick ******* of a universe that would give someone heart trouble in the first place. Ha ha! Get the joke?
Agian
Well-known member
Share THIS with your cardiologist
Nocturne
Well-known member
The term "muppets" you are using is not in popular usage here in the USA, at least not outside of banking circles. I'm not entirely sure of the meaning you are trying to convey myself, although I get the gist of it.
Nocturne
Well-known member
What the godless people in your country do not understand, Agian, and what Americans understand COMPLETELY, is the Power of Prayer. Treatments are, in fact, a swat to the face of the LORD. God is Great, God is Good, and God is what makes 'Murrica STRONG! You can KEEP your fancy egghead godless SCIENCE "treatments" (AKA sinful perversions that waste the hard-earned money of the insurance companies) -- *I* will have all the protection of PRAYER! And THAT is REAL prevention -- just wait and see!
Nocturne
Well-known member
Remember -- here in the USA, spending the $150 required to identify someone with high Lp(a) is NOT WORTH IT. "Those people" and their long-term health just aren't worth $150. Besides, if enough of them realized they had a problem, they'd start demanding treatment -- and we can't have THAT, now, can we? It'd meddle with insurance company profits! Just tell 'em all that keeping their LDL low with statins'll solve everything. Statins for everyone!
