Lp(a) [Lipoprotein(a)] - the hidden killer lipid marker

[Marco N Cognito]

1) I had on my last blood test a line on the lipid panel of Lp-PLa2. My level was 271(<325 in range) Is the Lp level you reference?

2) I had a talk with my wife tonight about the 23 and me. She and her sisters are against this because it leaves your biological info available to insurance companies for denial of claims at a later date if something should develop. Is there any validity in this?
I know that for a fact the juvenile profiles done at a youth court, if you take them up on the free offer of a pysch exam, can haunt you in your future. I have a niece who is still fighting this. It is still being dug up.

Lp-PLa2 is a different marker than Lp(a). When elevated, they are both atherogenic. In response to your second question, I would say that sounds like a conspiracy theory. I had my 23andMe.com test done 6 years ago and have filed probably hundreds of claims since with no issues.

 

[Gianluca]

these oil are dangerous for sure, I do remember a well known Doctor from Italy mentioning PUFAs being more prone to oxidation, althoguh I don't think intake from Walnuts, for example, being as dangerous, here the study suggested on my nutrition text book showing better benefit of CVD replacing SFA's with PUPAs, https://www.ncbi.nlm.nih.gov/pubmed/19211817

Omega 6 PUFAs (corn, safflower, canola, soy oil) are all highly oxidative and inflammatory oils. Omega 3s are also PUFAs, but are supposedly less prone to oxidation/rancidity. SFAs are not prone to any oxidation, second to that are MUFAs. For heart health, I therefore would keep PUFAs (other than Omega 3s) to an absolute minimum.

Here's a simple view:
https://blog.bulletproof.com/omega-3-vs-omega-6-fat-supplements/

 

[Gianluca]

At the end the most important thing is to probably avoid those Omega 6 that are converted more to Arachidonic Acid, that may seems contradictory http://blog.lifeextension.com/2011/09/how-to-manage-inflammation-by-eating.html

these oil are dangerous for sure, I do remember a well known Doctor from Italy mentioning PUFAs being more prone to oxidation, althoguh I don't think intake from Walnuts, for example, being as dangerous, here the study suggested on my nutrition text book showing better benefit of CVD replacing SFA's with PUPAs, https://www.ncbi.nlm.nih.gov/pubmed/19211817

 

[Gianluca]

Thank you Marco

Congrats on a zero score! If you want to proceed with advanced lipid testing I would recommend either the NMR LipoProfile or Quest's Cardio IQ® Advanced Lipid Panel and Inflammation Panel.

 

[Gianluca]

Marco, we discussed about this last month, well I got my Lp(a) checked and it turns out elevated 136 nm0l/L on a scale of less than 75, LabCorp not quiet optimal I believe, along with my HDL of 34

Did you measure your Lp(a)?

 

[Marco N Cognito]

Marco, we discussed about this last month, well I got my Lp(a) checked and it turns out elevated 136 nm0l/L on a scale of less than 75, LabCorp not quiet optimal I believe, along with my HDL of 34

Welcome to the high Lp(a) club, lol! Well, at least you know to take some proactive steps to keep it in check for now until the new drug, AKCEA-APO(a)-LRx, gets final FDA approval (http://www.lipoproteinafoundation.org/)

Until then, high-dose niacin and/or tocopherol nicotinate, lysine, vitamin C, TRT, DHEA, l-carnitine, saturated fat (yes, SFAs lower Lp(a)) is pretty much all we have to at least keep it in check for the time being. Neither dietary intervention nor exercise has any effect on reducing level, as Lp(a) is genetically-determined. I do notice mine increases with weight gain and coincides with elevation in other deleterious markers as well, so keeping your BMI/bodyfat levels healthy, along with common sense health habits should always be a mainstay in reducing risk. Your HDL is suppressed, and I would guess that your other lipid biomarkers may be off as well; the only way to confirm this is to have an advanced lipid panel like the one I posted on upthread.

I just happened on this article today. Apheresis is not something I would do, but it is at least an option:
http://www.dailymail.co.uk/health/a...BLOOD-machine-help-prevent-heart-attacks.html

 

[Davet]

Here in the Uk you can run the labs...called fractions where they drill down into whats going on with your ldl looking for the bad guys.
As my LDL is raised and tends to stay there I thought I better have a closer look at where i was so I had the fraction labs run in Jan...all was good but its definitely one to keep an close eye on. So i will be running these labs once yearly.

 

[Gianluca]

My HDL is suppressed due to high Free T, I'm lowering the dose to aim for a healthy 25 FT level or so, I have been at 30/35 most of my TRT due to low SHBG, I remember you mentioning about SFA's lowering Lp(a) and saw the evidences, although you told me that with ApoE people actually the opposite occur, so I did a little research and find out ApoE 4 people do get elevated LDL and guessing Lp(a) also with Saturated Fat, so being proactive LifeExtention has a sale going on for lab test, they sell the ApoE gene test for about $100! so I think that it will tell me about my diet, but I have a feeling Carbohydrates rich/Mediterrenen Diet is what best may work for me

I had an discussion with one of the Senior Wellness Specialist at LE, so I was trying to make a point, as we know the Cholesterol myth where the actual Oxidized LDL is the dangerous one and that Inflammation plays a huge role in determining if that cholesterol will stick in the arteries or not, I was tying to get to the same point with Lp(a), although we came to a conclusion that there are not studies yet out there proving the same, that an elevated Lp(a) with low inflammation markers such as CRP or AA/EPA becomes innocuous. I really hope is the case, what are your thoughts about that?

Welcome to the high Lp(a) club, lol! Well, at least you know to take some proactive steps to keep it in check for now until the new drug, AKCEA-APO(a)-LRx, gets final FDA approval (http://www.lipoproteinafoundation.org/)

Until then, high-dose niacin and/or tocopherol nicotinate, lysine, vitamin C, TRT, DHEA, l-carnitine, saturated fat (yes, SFAs lower Lp(a)) is pretty much all we have to at least keep it in check for the time being. Neither dietary intervention nor exercise has any effect on reducing level, as Lp(a) is genetically-determined. I do notice mine increases with weight gain and coincides with elevation in other deleterious markers as well, so keeping your BMI/bodyfat levels healthy, along with common sense health habits should always be a mainstay in reducing risk. Your HDL is suppressed, and I would guess that your other lipid biomarkers may be off as well; the only way to confirm this is to have an advanced lipid panel like the one I posted on upthread.

I just happened on this article today. Apheresis is not something I would do, but it is at least an option:
http://www.dailymail.co.uk/health/a...BLOOD-machine-help-prevent-heart-attacks.html

 

[Nelson Vergel]

I added this test on DiscountedLabs.com

https://www.discountedlabs.com/lipoprotein-a

 

[Vince]

Case # 277 Niacin, statin or both or neitherin a high risk woman?
THE CASE: The case is a 49 year old woman who has a family history of early CAD in her father. She does not have hypertension or diabetes nor does she smoke. Her BMI is 31, but otherwise her vitals are normal. A recent CIMT revealed increased risk of CAD. Her labs done at Health Diagnostic Labs in Richmond VA are as follows:

TC = 116, LDL-C = 56, HDL-C = 40, TG = 58, Non-HDL-C = 55 (all in mg/dL) TC/HDL-C = 2.9 TG/HDL-C = 1.45 ApoB = 44 mg/dL, ApoA-I = 124 mg/dL Total LDL-P = 707 nmol/L Total HDL-P = 25.1 umol/L HDL2 = 11 mg/dL

http://www.lipidcenter.com/pdf/lipidaholics/Case277.pdf

 

[Marco N Cognito]

I had my OxLDL level measured and it is elevated! So was hsCRP. So, despite my "perfect" modified keto diet free of any processed sugars or anything processed and tons of anti-inflammatory supplements, I am a victim of inflammation. I also have a long history of Pattern B particles, elevated TMAO, sdLDL-C, LDL-P, APOB, and Lp-PLA2 - all the bad biomarkers which contribute to that inflammation and atherogenesis. These are in addition to elevated Lp(a). I am lucky that my CAC score is as low as it is, and my CIMT was normal, probably due to my diet and exercise regimens.

It is important to test APOE to determine what genetic variant you are. I am 3/3 which is neutral as is 85% of the population, so at least I don't need to worry about SFAs https://www.ncbi.nlm.nih.gov/pubmed/26574962

If I had to guess the reason for my dyslipidemia, other than as-yet unknown genetic predispositions, I'd blame it on chronic long-term suboptimized thyroid function (subclinical hypothyroidism). Thyroid optimization is key for lipid metabolism and affects ALL of the above, including Lp(a) https://www.ncbi.nlm.nih.gov/pubmed/10601541. The two other major influences: your microbiome (gut) and insulin signaling. The jury is still out as whether elevated TMAO is harmful and directly impacts plaque risk. Nonetheless, it's an indication of an imbalance in the gut microbiome (too much Firmicutes bacteria which are the species mainly responsible for converting choline to TMA<TMAO which, in studies, has shown increased risk for CVD).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5127123/

Despite that there aren't any studies showing increased risk of atherogenesis when Lp(a) is combined with all the baddy biomarkers I mentioned, I still think it best to err on the side of caution and fix what I can to minimize overall morbidity.

And to make things even more confusing, here's some evidence that refutes oxLDL as being the bad guy: https://www.sciencedaily.com/releases/2014/09/140904121247.htm

I have just recently resumed using hi-dose extended-release niacin, starting @ 1g/day; will increase to 2g/day. Also, will be starting a new RYR supplement from a well-respected co. which is devoid of monocolin-K (statin) but has been shown in studies to be as effective (we'll see): https://aorhealth.com/products/red-yeast-rice-with-ankascin-568-r/
I also recently started citrus Bergamot, plants sterols, Sytrinol, L-lysine and food-based vitamin C (3g/day) to help manage lipids.

Am going to add tocopherol nicotinate to the mix as it has been shown to reduce Lp(a) independent of niacin alone. Unfortunately, it is not available stateside, but from Italy, Germany, and Japan:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384183/
https://www.ncbi.nlm.nih.gov/pubmed/2149270

We are all experimental works in progress!

 

[Marco N Cognito]

TC/LDL-C that low is just as bad, if not worse, than elevated TC. The pt's CIMT results proves that. Throwing statins in the mix will just make things worse and does NOTHING to directly reduce Lp(a) and, in fact, could increase it. https://www.ncbi.nlm.nih.gov/pubmed/28183512

Better to evaluate inflammation, diet, thyroid and other hormones, blood sugar/insulin first!

 

[Gianluca]

Jesus! my head is spinning right now, I'm definitely going to test this week for AepoE gene, at least is good to know what macro best suits my body, probably later on will do the NMR as well,

the use of anticoagulant/platelets for high Lp(a) people may be a good idea? cialis as well,

what is your take on controlling AA (arachidonic acid)? as we know AA is thrombogenic and inflammatory, egg yolks for example is a good source, I had an AA/EPA test done by ZoneLabs the company where I usually get my fish oil from, I take 3gr of EPA+DHA and my blood result was 10% of AA and 5.4%EPA a sort of 2:1 ratio AA/EPA, considered as low inflammation level, according to Berry Sears Optimal AA is btw 7/9% and EPA is 4/6%,

good thing for us would be to keep AA low side

I had my OxLDL level measured and it is elevated! So was hsCRP. So, despite my "perfect" modified keto diet free of any processed sugars or anything processed and tons of anti-inflammatory supplements, I am a victim of inflammation. I also have a long history of Pattern B particles, elevated TMAO, sdLDL-C, LDL-P, APOB, and Lp-PLA2 - all the bad biomarkers which contribute to that inflammation and atherogenesis. These are in addition to elevated Lp(a). I am lucky that my CAC score is as low as it is, and my CIMT was normal, probably due to my diet and exercise regimens.

It is important to test APOE to determine what genetic variant you are. I am 3/3 which is neutral as is 85% of the population, so at least I don't need to worry about SFAs https://www.ncbi.nlm.nih.gov/pubmed/26574962

If I had to guess the reason for my dyslipidemia, other than as-yet unknown genetic predispositions, I'd blame it on chronic long-term suboptimized thyroid function (subclinical hypothyroidism). Thyroid optimization is key for lipid metabolism and affects ALL of the above, including Lp(a) https://www.ncbi.nlm.nih.gov/pubmed/10601541. The two other major influences: your microbiome (gut) and insulin signaling. The jury is still out as whether elevated TMAO is harmful and directly impacts plaque risk. Nonetheless, it's an indication of an imbalance in the gut microbiome (too much Firmicutes bacteria which are the species mainly responsible for converting choline to TMA<TMAO which, in studies, has shown increased risk for CVD).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5127123/

Despite that there aren't any studies showing increased risk of atherogenesis when Lp(a) is combined with all the baddy biomarkers I mentioned, I still think it best to err on the side of caution and fix what I can to minimize overall morbidity.

And to make things even more confusing, here's some evidence that refutes oxLDL as being the bad guy: https://www.sciencedaily.com/releases/2014/09/140904121247.htm

I have just recently resumed using hi-dose extended-release niacin, starting @ 1g/day; will increase to 2g/day. Also, will be starting a new RYR supplement from a well-respected co. which is devoid of monocolin-K (statin) but has been shown in studies to be as effective (we'll see): https://aorhealth.com/products/red-yeast-rice-with-ankascin-568-r/
I also recently started citrus Bergamot, plants sterols, Sytrinol, L-lysine and food-based vitamin C (3g/day) to help manage lipids.

Am going to add tocopherol nicotinate to the mix as it has been shown to reduce Lp(a) independent of niacin alone. Unfortunately, it is not available stateside, but from Italy, Germany, and Japan:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384183/
https://www.ncbi.nlm.nih.gov/pubmed/2149270

We are all experimental works in progress!

 

[Gianluca]

Something that I don't understand, so my CAC score was 0, but that doesn't mean that I don't have plaques in my CA, correct? is there an actual test to check how many plaques and calcification there are on major arteries?

till now I have done: EKG, ECG, stress test, CAC score, all good, but this elevated Lp(a) makes me think I have collected many plaques already at 32yo, I also smoked for 12 years,

Marco what is your take on K2? good or not so good, some would argue that remove calcium from plaque is not so smart

 

[Marco N Cognito]

Jesus! my head is spinning right now, I'm definitely going to test this week for AepoE gene, at least is good to know what macro best suits my body, probably later on will do the NMR as well,

the use of anticoagulant/platelets for high Lp(a) people may be a good idea? cialis as well,

what is your take on controlling AA (arachidonic acid)? as we know AA is thrombogenic and inflammatory, egg yolks for example is a good source, I had an AA/EPA test done by ZoneLabs the company where I usually get my fish oil from, I take 3gr of EPA+DHA and my blood result was 10% of AA and 5.4%EPA a sort of 2:1 ratio AA/EPA, considered as low inflammation level, according to Berry Sears Optimal AA is btw 7/9% and EPA is 4/6%,

good thing for us would be to keep AA low side

My AA is actually low, probably because I consume a ton of n-3s to reduce it, so I don't worry about it. Got bigger fish to fry!

 

[Marco N Cognito]

Something that I don't understand, so my CAC score was 0, but that doesn't mean that I don't have plaques in my CA, correct? is there an actual test to check how many plaques and calcification there are on major arteries?

till now I have done: EKG, ECG, stress test, CAC score, all good, but this elevated Lp(a) makes me think I have collected many plaques already at 32yo, I also smoked for 12 years,

Marco what is your take on K2? good or not so good, some would argue that remove calcium from plaque is not so smart

AFAIK, the CAC is a specific CT scan that directly measures any detectable calcium in your coronary arteries. Other than that - CCTA, MRI, PET, angiogram will show visible plaque.

Yes, you're right, there are some that feel that removing hardened plaque can be dangerous as it can dislodge and TRAVEL. I'm taking K2 anyway for now until I can research more. There's a thread I started about CAC scores on the forum in which member Michael Gaiso made some interesting points. I see that you were in that thread as well. We need to do more research! Unfortunately, time is limited.

If you want to take a step further in CV preventive diagnostics, I would suggest doing the panel at CHL: http://www.clevelandheartlab.com/

They have labs that are available nowhere else. They are now owned by Quest.

 

[Gianluca]

good would be to know if there is a K2 dose that will just move enough calcium from food to the bones and not removing it from deposit in the arteries, for now I'm taking 45mcg of MK7

AFAIK, the CAC is a specific CT scan that directly measures any detectable calcium in your coronary arteries. Other than that - CCTA, MRI, PET, angiogram will show visible plaque.

Yes, you're right, there are some that feel that removing hardened plaque can be dangerous as it can dislodge and TRAVEL. I'm taking K2 anyway for now until I can research more. There's a thread I started about CAC scores on the forum in which member Michael Gaiso made some interesting points. I see that you were in that thread as well. We need to do more research! Unfortunately, time is limited.

If you want to take a step further in CV preventive diagnostics, I would suggest doing the panel at CHL: http://www.clevelandheartlab.com/

They have labs that are available nowhere else. They are now owned by Quest.

 

[bp]

As we learn more about how elevated levels of Lp(a) can potentially kill us before anyone can determine the cause, it is imperative that everyone get this lipid marker tested frequently, especially those on any type of HRT regimen. It is entirely possible that one of the leading culprits behind the upsurge of recent untimely deaths we've been seeing pop up left and right in the sports and bodybuilding community, in which "enhanced" athletes are pushing beyond human limits, could very well be unchecked elevated Lp(a) levels.

Standard lipid panels are pretty much worthless for many reasons, one being that Lp(a) levels are never included. Thus, millions go unchecked that potentially could have avoided that MI (heart attack) or TIA (stroke), etc. had they known they were at risk. Only advanced lipid panels (i.e. Quest's Cardio IQ® Advanced Lipid Panel and Inflammation Panel) include Lp(a). Alternatively, you can test for it individually. I would also urge everyone 35+ to have a calcium score test done (EBCT or CCTA) to determine the levels of arterial plaque, as elevated Lp(a) can promote calcification.

I have been tracking my Lp(a) for the last several years. My last level was 118 which is considered moderate risk. However, back in 2012, I suffered from two episodes of idiopathic thrombophilia (blood clots of unknown origin) in both legs. I have been on a low-dose anticoagulant (blood thinner) prophylaxis since. As Lp(a) is thrombogenic (clot-producing) in nature, I was already at risk without knowing I had slightly elevated Lp(a), as all genetic thrombosis and other routine (i.e. RBC, HGB, HCT, E2) blood markers were normal. Neither exercise, diet or supplements have any impact, as one's Lp(a) are genetically-determined from birth.

For those who've had the 23andMe.com test done early on, you have access to your raw data which includes the genetic markers that can help determine your predisposition for elevated levels of this marker. If interested, PM me, as I have done some research and have the actual genetic data (SNPs) that can help you see if you're at risk in addition to blood work.

There is now an excellent Lp(a) foundation that is in place to help answer questions and educate those that are unfamiliar. It is also important to have all family members tested if your levels are elevated.
Click here: Lipoprotein(a) Foundation

2020
My issue was always massively raised Lp(a) in the LDL-c partition.
(Heterozygous Fh)

before Nandrolone decanoate added to trt protocol
2.64 micromol/l

after 8weeks ND + test cyp (30mg/60mg) qwk outlier.

1.435 micromol/l

almost in range for first time in my life. (Interestingly, atorvastatin therpy had it over 3.0 !)

I’m considering adding oxandrolone in microdose, in addition to the microdose of ND in attempt to attenuate Lp(a) further.

 

[bp]

Am familiar with this combo and the research. AOR has a specific powdered formula for this: http://www.aor.ca/en/product/tlc-3.0

I have tried pretty much everything in the past and continue to try OTC natural remedies that have shown limited success in some, and perhaps it's what is keeping my levels from increasing, but nothing thus far has pushed my levels down far enough to get completely out of the risk zone. A drug trial is underway that looks promising, but it's indeterminate how long it will take for FDA approval + there are always side effects: http://www.lipoproteinafoundation.org/page/AkceaPhaseII

Nandrolone and oxandrolone attenuate Lp(a)

I’ve pm’d you Marco.

 

[Marco N Cognito]

Nandrolone and oxandrolone attenuate Lp(a)

I’ve pm’d you Marco.

Interesting. Thanks. Keep us posted on more results from this protocol.

Testosterone-induced suppression of lipoprotein(a) in normal men; relation to basal lipoprotein(a) level - PubMed

The concentration of lipoprotein(a) [Lp(a)] in human plasma is largely genetically determined and is inversely correlated to the size of apolipoprotein(a) [apo(a)]. Additionally, Lp(a) values are relatively stable within individuals and are only marginally susceptible to therapeutic treatment...

www.ncbi.nlm.nih.gov

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