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

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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
 
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Vince

Super Moderator
Some people I know believe that vitamin c along with lysine will lower Lp(a).
The issue with the Pauling/Rath "stuff" is the amount you have to take. It requires powders and a good powder delivery system.

Biochemical fact is that if the body does not have enough Vit C then it is replaced with Lp(a)


http://raysahelian.com/lipoprotein.html
 
Some people I know believe that vitamin c along with lysine will lower Lp(a).
The issue with the Pauling/Rath "stuff" is the amount you have to take. It requires powders and a good powder delivery system.

Biochemical fact is that if the body does not have enough Vit C then it is replaced with Lp(a)


http://raysahelian.com/lipoprotein.html

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
 

Jinzang

Member
Lipoprotein(a) as a cardiovascular risk factor: current status

The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. ... Treatment should primarily be niacin 1–3 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment.
 

Vince

Super Moderator

Decreases lipoprotein(a)—Among the most serious of heart disease risk factors, no other treatment approaches the power of niacin to reduce this genetically-determined pattern.

Extended- or intermediate-release niacin are time-release preparations, but not as slow as slow-release. This has made them safer than the slow-release preparations that can cause liver side-effects. It also provokes less hot flush than immediate-release. Over-the-counter Slo-Niacin®, is one such preparation and has been proven to be safe (Brown 2001). Niaspan® (Kos Pharmaceuticals) is a prescription extended-release preparation.
 

Gianluca

Well-Known Member
i Have just got to know about Lp(a) from the book I'm studying Nutrition from, in the book elevation of Lp(a) is linked with increase intake of dietary Fat, especially Saturated and Trans

Now, some studies has shown there is not correlation between Saturated Fat intake and increase in LDL therefore eliminating all the guessing on it, but Lp(a) seems to be far more dangerous to me, do you guys have more "out of the box" info about the correlation between Saturated Fat and Lp(a)?
 
i Have just got to know about Lp(a) from the book I'm studying Nutrition from, in the book elevation of Lp(a) is linked with increase intake of dietary Fat, especially Saturated and Trans

Now, some studies has shown there is not correlation between Saturated Fat intake and increase in LDL therefore eliminating all the guessing on it, but Lp(a) seems to be far more dangerous to me, do you guys have more "out of the box" info about the correlation between Saturated Fat and Lp(a)?

First off, Lp(a) levels are entirely genetically-determined. Secondly, SFAs have been shown to reduce Lp(a) levels, not increase them:
http://atvb.ahajournals.org/content/17/9/1657
https://www.healthcentral.com/article/what-your-doctor-didnt-tell-you-about-lipoproteina
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0114859
https://wellnessmama.com/1265/saturated-fat/

The only risk of SFA intake is to those with the APOE polymorphism and familial hypercholesterolemia. SFAs WILL increase LDL and thus TC (which means nothing), yes, however, they raise the more beneficial Pattern A particle (large, fluffy particles), not the more harmful Pattern B particle (small, dense particles). Not all subfractions of LDL are bad and not all subfractions of HDL are good. Lipidology is complex science. I suggest researching more cutting edge and current science, i.e.:

Dr. Peter Attia, MD: https://peterattiamd.com/the-straight-dope-on-cholesterol-part-viii/
Chris Masterjohn, PhD: https://chrismasterjohnphd.com/2017/03/19/what-to-do-about-high-cholesterol/

And insightful blogs from Animal Farm: https://drbganimalpharm.blogspot.com/2009/10/cardio-controversies-lpa-dangerous-at.html

Interesting perspectives on Lp(a) from Dr. William Davis, MD:
http://www.cureality.com/blog/post/2012/08/08/i-wish-i-had-lipoproteina.html
https://www.healthcentral.com/article/what-your-doctor-didnt-tell-you-about-lipoproteina

No one knows lipid disorders and cardiovascular health better than the folks at Cureality/Track Your Plaque: https://www.cureality.com/forum/

Carbs are the killer, not fat!

My favorite snack - which happens to be a great Lp(a) killer: raw goat milk cheese eaten with my own home-made mayo (extra virgin olive oil, mac nut oil, avocado oil, algae oil, organic eggs, extra virgin coconut oil, apple cider vinegar, fresh-squeezed lemon juice, sea salt) and 5-10 cloves of raw garlic! I eat at least 100g of healthy fats daily, zero trans fats (except the incidental ones in whole foods), <75g carbs, 150-180g protein.

Going to be trialing TOCOPHEROL NICOTINATE which is basically niacin with an ester of vitamin E attached that has been show to reduce Lp(a), perhaps more effectively than niacin alone:
https://www.ncbi.nlm.nih.gov/pubmed/2149270
http://www.atherosclerosis-journal.com/article/0021-9150(90)90093-X/abstract
https://spacedoc.com/board/viewtopic.php?t=699


 
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Gianluca

Well-Known Member
First off, Lp(a) levels are entirely genetically-determined. Secondly, SFAs have been shown to reduce Lp(a) levels, not increase them:
http://atvb.ahajournals.org/content/17/9/1657
https://www.healthcentral.com/article/what-your-doctor-didnt-tell-you-about-lipoproteina
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0114859
https://wellnessmama.com/1265/saturated-fat/

The only risk of SFA intake is to those with the APOE polymorphism and familial hypercholesterolemia. SFAs WILL increase LDL and thus TC (which means nothing), yes, however, they raise the more beneficial Pattern A particle (large, fluffy particles), not the more harmful Pattern B particle (small, dense particles). Not all subfractions of LDL are bad and not all subfractions of HDL are good. Lipidology is complex science. I suggest researching more cutting edge and current science, i.e.:

Dr. Peter Attia, MD: https://peterattiamd.com/the-straight-dope-on-cholesterol-part-viii/
Chris Masterjohn, PhD: https://chrismasterjohnphd.com/2017/03/19/what-to-do-about-high-cholesterol/

And insightful blogs from Animal Farm: https://drbganimalpharm.blogspot.com/2009/10/cardio-controversies-lpa-dangerous-at.html

Interesting perspectives on Lp(a) from Dr. William Davis, MD:
http://www.cureality.com/blog/post/2012/08/08/i-wish-i-had-lipoproteina.html
https://www.healthcentral.com/article/what-your-doctor-didnt-tell-you-about-lipoproteina

No one knows lipid disorders and cardiovascular health better than the folks at Cureality/Track Your Plaque: https://www.cureality.com/forum/

Carbs are the killer, not fat!

My favorite snack - which happens to be a great Lp(a) killer: raw goat milk cheese eaten with my own home-made mayo (extra virgin olive oil, mac nut oil, avocado oil, algae oil, organic eggs, extra virgin coconut oil, apple cider vinegar, fresh-squeezed lemon juice, sea salt) and 5-10 cloves of raw garlic! I eat at least 100g of healthy fats daily, zero trans fats (except the incidental ones in whole foods), <75g carbs, 150-180g protein.

Going to be trialing TOCOPHEROL NICOTINATE which is basically niacin with an ester of vitamin E attached that has been show to reduce Lp(a), perhaps more effectively than niacin alone:
https://www.ncbi.nlm.nih.gov/pubmed/2149270
http://www.atherosclerosis-journal.com/article/0021-9150(90)90093-X/abstract
https://spacedoc.com/board/viewtopic.php?t=699



Marco wow mind blowing, I appreciate you sharing this, at least the course I took taught me the existence of Lp(a), I could try to link the studies that were showing increase in Lp(a) with SFA but I assume already is "main stream" data


Doc Chris Masterjohn at mn 49.25 of the Podcast says he would replace Fat with Carbohydrates for CV health, I'm sure he means whole grain and of course in a balanced fashion till at some extend, I do think refined sugar and carbohydrates are the killer but not the whole grain, we should make a distinction of the two, there is a good place for whole grain, and gauging them based on physical activity is the key
 
Marco wow mind blowing, I appreciate you sharing this, at least the course I took taught me the existence of Lp(a), I could try to link the studies that were showing increase in Lp(a) with SFA but I assume already is "main stream" data


Doc Chris Masterjohn at mn 49.25 of the Podcast says he would replace Fat with Carbohydrates for CV health, I'm sure he means whole grain and of course in a balanced fashion till at some extreme, I do think refined sugar and carbohydrates are the killer but not the whole grain, we should make a distinction of the two, there is a good place for whole grain, and gauging them based on physical activity is the key

From everything I've researched, insulin resistance (IR) is the main driver for CVD in general (elevated Lp(a) included) so, unless one has the APOE4 variant, whole food fats (MUFAs and SFAs, and NOT PUFAs) are not the enemy and are beneficial to lipid profiles. According to Dr. William Davis, carbs and especially grains, as is standard fare for the SAD (wheat being the most deleterious) is to blame for the inflammation and IR that stems from a diet high in carbs. Also, modern wheat is garbage, GMO'd "Frankenwheat", nothing like the ancient wheat eaten for thousands of years in ancestral diets. I think a modified keto diet (55% fat, 30% protein, 15% carbs) is the safest way to go for most with periodic refeeds of healthly, non-grain carbs from starchy root vegetables and resistant starch (non-glycemic/prebiotic) carbs. It's complex science, and one needs to do a lot of self-experimentation with before and after bloodwork using advanced lipid panels (not the useless standard lipid panels) and see what works best for them. I'm in that spot now, trying to tweak and figure out what I've done right and what I'm doing wrong with respect to my lipid profile including factoring in genetic tendencies toward IR/T2D, thyroid function, and gut microbiome (gut health, BTW, is huuuge).
 
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it's down for my next month blood draw for sure, I'm always fine on EKG ECG stress test, done CRP and Homocysteine but I do have a grandfather who died at 40 of Heart attack so better looking forwarder

IMO, do the CAC score test for sure to determine if you have any arterial plaque. Costs $100 out of pocket, worth every penny to find out where you stand. If zero, you needn't worry much about your other markers as much.
 

Gianluca

Well-Known Member
Marco I have done it a year an half ago, my score was "0", I have been using 3gr of EPA+DHA for about 5 years, I think that helped, I introduced K2(mk7) just lately, although, I believe, it doesn't necessarily means I'm fine, still want to do some advance Lipid testing, one thing, starting TRT had my HDL down to 32/34, trying to increase my aerobic and see where I can get at, in case I may consider Niacin

btw I appreciate your taking the time to respond

IMO, do the CAC score test for sure to determine if you have any arterial plaque. Costs $100 out of pocket, worth every penny to find out where you stand. If zero, you needn't worry much about your other markers as much.
 

Gianluca

Well-Known Member
I agree, I always say to anyone even though not gluten sensitive to avoid wheat, so actually you say Polyunsaturated fat could be an enemy?

From everything I've researched, insulin resistance (IR) is the main driver for CVD in general (elevated Lp(a) included) so, unless one has the APOE4 variant, whole food fats (MUFAs and SFAs, and NOT PUFAs) are not the enemy and are beneficial to lipid profiles. According to Dr. William Davis, carbs and especially grains, as is standard fare for the SAD (wheat being the most deleterious) is to blame for the inflammation and IR that stems from a diet high in carbs. Also, modern wheat is garbage, GMO'd "Frankenwheat", nothing like the ancient wheat eaten for thousands of years in ancestral diets. I think a modified keto diet (55% fat, 30% protein, 15% carbs) is the safest way to go for most with periodic refeeds of healthly, non-grain carbs from starchy root vegetables and resistant starch (non-glycemic/prebiotic) carbs. It's complex science, and one needs to do a lot of self-experimentation with before and after bloodwork using advanced lipid panels (not the useless standard lipid panels) and see what works best for them. I'm in that spot now, trying to tweak and figure out what I've done right and what I'm doing wrong with respect to my lipid profile including factoring in genetic tendencies toward IR/T2D, thyroid function, and gut microbiome (gut health, BTW, is huuuge).
 

Gianluca

Well-Known Member
I just opened my text book again, there they would actually link Saturated Fatty Acids from Meat to CVD when SFA from Dairy actually have a benefits on CVD, agree?
 

blackebob

Member
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.
 
I agree, I always say to anyone even though not gluten sensitive to avoid wheat, so actually you say Polyunsaturated fat could be an enemy?

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/
 
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Marco I have done it a year an half ago, my score was "0", I have been using 3gr of EPA+DHA for about 5 years, I think that helped, I introduced K2(mk7) just lately, although, I believe, it doesn't necessarily means I'm fine, still want to do some advance Lipid testing, one thing, starting TRT had my HDL down to 32/34, trying to increase my aerobic and see where I can get at, in case I may consider Niacin

btw I appreciate your taking the time to respond

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.
 
I just opened my text book again, there they would actually link Saturated Fatty Acids from Meat to CVD when SFA from Dairy actually have a benefits on CVD, agree?

SFAs from CAFO-raised meats and pastured, organic, grassfed meats are like comparing apples to oranges. I've never seen CV studies using the latter, and until I do, I would not take them to heart (no pun intended). I've read both pro and con of dairy fats effect on CVD. Again, never seen a study in which they use raw, whole fat dairy that some of the longest-lived humans have been consuming for thousands of years vs the pasteurized, homogenized, low-fat (Elmer's glue) garbage. I feel there's a huge difference in terms of how the body, and in particular, our CV system, handles fats from whole, unprocessed, non-commercial foods vs. fats from the SAD. Check out the Weston Price site for more info: https://www.westonaprice.org/
 
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