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Unusually High Lipoprotein A / Lipo(a) - Niacinamide Effective?

Antarehs

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Joined
Oct 1, 2015
Messages
16
My most recent labs came back with an off-the-charts high lipoprotein(a) level of 519 nmol/L, which combined with the high number of small and medium LDL particles, TC 277, LDL 180, HDL 78, LP PLA2 Activity 111 and mild hypertension it's very scary indeed.

Considering that lipo(a) levels over 75 nmol/L are considered an extremely high risk for all types of CVD, a 519 nmol/L is more than horrifying. My mother died of a heart attack at 48, her brother at 50, grandfather at 60 of his third heart attack, other grandfather likewise, a cousin had an angioplasty at 46, and the list goes on... I clearly didn't win the genetic lottery and I fully expressed the high lipo(a) genes. The question is what to do.

Has anyone had success with niacinamide combined with CoQ10 and vit C? If so, at what dose? I was reading that niacinamide is not effective at lowering lipo(a), but 1000-3000 mg of regular niacin (the amount apparently needed to lower it) are likely to damage the liver, so niacinamide would be preferable.

Thank you!
 

CLASH

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Sep 15, 2017
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1,163
Hey Antarehs,
Before I begin, I'd like to stipulate that I have not experienced elevated lipoprotein a, so the information I am going to provide you with is solely based on my research into the area, not my personal experience. Also, I am not a doctor, so anything I offer is simply opinion and not medical advice. I'd encourage you to corroborate anything I say (I'll provide some links) and also to do your own research.

From what I've read elevated lipoprotein is hypothesized to be a function of damage to the arterial wall in the absence of adequate vitamin C to repair the tissue. Vit C functions as a cofactor for a specific enzyme in cross linking the collagen fibers of the endothelium within the vasculature, it also has anti-oxidant function. When there is an inflammatory stimulus over time in conjunction with mechanical tension, the walls of the arterial bed, much like a corroded pipe, are slowly damaged. Being that we are living organisms, unlike the pipe, we have the ability to address this damage and continually repair the "pipes" as long as we have the correct structural materials available

Humans, among guinea pigs, a bat species, a few other primates and a few other obscure animals are the only animals that do not produce their own Vit C, for whatever reason. In the absence of endogenous Vit C production, if we do not eat adequate vit C we develop heart disease. Tests done on guinea pigs in the absence of vit C have corroborated these findings, such that if guinea pigs are provided vit C they do not develop heart disease whereas if vit C is withheld they do develop heart disease. These findings where essential in the work of Dr. Linus Pauling and his partner Dr. Matthias Rath. You can find numerous studies discussing this hypothesis here: http://www4.dr-rath-foundation.org/NHC/researcharchive.html

Furthermore, these cross linked collagen fibers that vitamin C is a co-factor in creating, seem to provide structure for a glycolax with which sulphur molecules are attached in order to provide propulsion for the red blood cells. These sulphur groups attached to the collagen structure provide a particular charge that is the same as the RBC's (the RBC's also have sulphur molecules on their surface) thus leading to repulsion such as seen with magnets (similar charges repel). The easiest way I can describe this visually is to think of the RBC's as the ships utilized in the movie The Matrix that move via magnetic propulsion and the vasculature as the tunnels with which they navigate. In the absence of this structure, blood pressure is elevated as a means of avoiding the RBC's from adhering to the wall of vasculature, at least this is what I gleaned from reading this article: A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome | Theoretical Biology and Medical Modelling | Full Text

Furthermore, the elevation of cholesterol, is a means to provide sulfate molecules to the damaged areas in attempt to possibly rebuild structure. Thus the high blood pressure and the elevated cholesterol are protective in this instance. The plaque that forms in the vessels is the accumulation of this cholesterol, platelets and other components that are attempting to heal the site, however without adequate structure i.e. scaffolding provided by the collagen structure created by the Vit C dependent enzyme, the tissue cannot properly heal.

Thus in order to possibly treat the situation, based on what I read, If I were in this situation, I'd look into Vit C (ascorbic acid) in high doses, and possibly some sulphur containing compounds such as MSM. I have not supplemented MSM, so I can't provide much info on my own experience. I have researched MSM and it seems safe from what I've read but again I would do your own research. I am not sure what the consensus is on the forum of MSM as people here seem to dislike DSMO and they are related compounds. If you'd prefer to avoid sulphur supplements perhaps some raw milk, some shellfish, or some red meat would provide you with sulphur. Raw milk is actually one of the highest sources of MSM, interestingly.
In conjunction with the above, I'd try to eliminate the inflammatory stimulus. From what I seen from my own research it seems that enhanced inflammatory states can lead to increased damage to the vascular system. Such inflammatory stimuli seem to be PUFA, endotoxin, possibly plant toxins and inadequate nutrition. To help with these things:

-some aspirin may help, I'd take it with glycine to avoid stomach issues

-avoidance of PUFA

-supplementing the fat solubles (specifically vit k2, as if your arteries have plaques they may begin to fibrose and calcify as the inflammatory histological changes generally follow that progression and K2 is great for decalcification of soft tissue)

-some of the B's as seen in Haiduts energin perhaps (niacin is actually directly mentioned in this article by Dr. Rath: http://www4.dr-rath-foundation.org/THE_FOUNDATION/About_Dr_Matthias_Rath/publications/pub13.htm, as a means in lowering lipoprotein a. I think the mechanism is by providing precursor to NAD thus providing substrate for mitochondrial function and thus increasing utilization of LDL which is the precursor for steroids and the precursor for lipoprotein a. So yes, niacinamide may help (obviously niacin isn't ideal, at least from a Peat perspective)

-The last aspect I'd address would be endotoxin. Everyone here seems to recommend the carrot salad, I haven't found much benefit from it. Nor have I found benefit from antibiotics. What I have found benefit from was a no fiber diet (Milk, kefir, butter, shellfish, beef meat and organs, tallow, raw honey, invert syrup, fresh fruit juice) and using raw fermented goat milk kefir (made from kefir grains not industrial starter) to provide the necessary flora to digest milk and displace the negative bacteria that I had in my gut. This obviously is not directly in line with Peat, I recognize that, but this is the only thing that has really exacted a change on my gut. Also, avoidance of all vegetables has been key.

Good luck to you Antarehs, hope this helps,
CLASH
 

Antarehs

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Thank you very much for all this information! Much appreciated.
 

Diokine

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Mar 2, 2016
Messages
552
I share your concern, that's got to be a scary revelation. I agree with the importance of vitamin C, @Travis has shared some great information with me that has thoroughly convinced me of it's fundamental role in atherosclerosis. I would also examine the role of tryptophan, derangement of it's metabolism is also fundamental in this case. Substitutions of arginine for tryptophan in genes encoding the Apolipoprotein B complex are probably at the heart of many cases of familial hypercholesterolemia.

Inflammation in the gut can cause improper absorption of tryptophan, and over time can accumulate into a chronic deficiency of its vital roles and an exaggeration of its disease causing ones. An improper NAD/NAD+ ratio is one manifestation of it's derangement, which niacinamide and nicotinic acid can address. Nicotinic acid increases thromboxane and prostacyclins, which are toxic when not managed properly but are important for some aspects of tissue repair. Pyridoxine has similar effects but is less toxic.

Improper protein assimilation can cause issues with estrogen detoxification, which can increase free copper and ceruloplasmin, leading to greatly increased lipid peroxidation.

ceruloplasmin and atherosclerosis

Excessive dietary tryptophan enhances plasma lipid peroxidation in rats.
(lol soybean oil controls)
Low density lipoprotein (LDL) was peroxidized by incubation with copper ions in the presence of tryptophan or serotonin. Serotonin was shown to enhance LDL peroxidation whereas tryptophan had no effect on LDL peroxidation. We conclude that excessive dietary tryptophan may be atherogenic since it enhanced plasma lipid peroxidation in hypercholesterolemic rats and increased macrophage uptake of plasma cholesterol. These effects are probably associated with increased plasma concentration of serotonin following the consumption of a tryptophan supplemented diet.

Disturbed Tryptophan Metabolism in Cardiovascular Disease
The review leads to a novel framework for successful therapeutic modification of several cardinal pathophysiological processes leading to adverse cardiovascular outcome.

 

Antarehs

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Oct 1, 2015
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Thank you. Food for thought... My diet is probably too rich in tryptophan and I suppose I should eliminate it. Pyridoxine is not something I can make use of, as I suspect an impaired ability to absorb it. Even supplementing at 20 mg daily resulted in very high plasma B6, too high of a level for just 20 mg a day. I have now increased the niacinamide to 1500 mg and will have to increase Vitamin C as well.

I share your concern, that's got to be a scary revelation. I agree with the importance of vitamin C, @Travis has shared some great information with me that has thoroughly convinced me of it's fundamental role in atherosclerosis. I would also examine the role of tryptophan, derangement of it's metabolism is also fundamental in this case. Substitutions of arginine for tryptophan in genes encoding the Apolipoprotein B complex are probably at the heart of many cases of familial hypercholesterolemia.

Inflammation in the gut can cause improper absorption of tryptophan, and over time can accumulate into a chronic deficiency of its vital roles and an exaggeration of its disease causing ones. An improper NAD/NAD+ ratio is one manifestation of it's derangement, which niacinamide and nicotinic acid can address. Nicotinic acid increases thromboxane and prostacyclins, which are toxic when not managed properly but are important for some aspects of tissue repair. Pyridoxine has similar effects but is less toxic.

Improper protein assimilation can cause issues with estrogen detoxification, which can increase free copper and ceruloplasmin, leading to greatly increased lipid peroxidation.

ceruloplasmin and atherosclerosis

Excessive dietary tryptophan enhances plasma lipid peroxidation in rats.
(lol soybean oil controls)
Low density lipoprotein (LDL) was peroxidized by incubation with copper ions in the presence of tryptophan or serotonin. Serotonin was shown to enhance LDL peroxidation whereas tryptophan had no effect on LDL peroxidation. We conclude that excessive dietary tryptophan may be atherogenic since it enhanced plasma lipid peroxidation in hypercholesterolemic rats and increased macrophage uptake of plasma cholesterol. These effects are probably associated with increased plasma concentration of serotonin following the consumption of a tryptophan supplemented diet.

Disturbed Tryptophan Metabolism in Cardiovascular Disease
The review leads to a novel framework for successful therapeutic modification of several cardinal pathophysiological processes leading to adverse cardiovascular outcome.
 

Travis

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Linus Pauling recommended lysine to keep Lp(a) from sticking to the arterial wall. Lipoprotein(a), like plasminogen, has a very specific lysine-binding domain. It has such a high affinity for lysine that lysine-sepharose chromatography is the standard technique used to separate it.
 

Antarehs

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Do you know how much lysine and if there are any side effects or counter-indications to its use? Thank you.

Linus Pauling recommended lysine to keep Lp(a) from sticking to the arterial wall. Lipoprotein(a), like plasminogen, has a very specific lysine-binding domain. It has such a high affinity for lysine that lysine-sepharose chromatography is the standard technique used to separate it.
 

Diokine

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The high plasma B6 makes me think excess estrogen-copper also, as it disrupts zinc metabolism and zinc is a required cofactor for pyridoxal kinase. Do you have high homocystine as well? I would look at possible methylation issues and cobalamin disruption.

In my opinion therapy should focus on restoring proper digestion, reducing tryptophan, and elimination of excess copper through appropriate zinc intake. Also 1500mg niacinamide in my opinion is too much. 50mg every 2 hours should be plenty.
 

Antarehs

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Yes, I have high homocysteine, which is why I was supplementing with B6 and methylfolate. And yes, I have two copies of an MTHFR gene mutation. I used to also have extremely low B12, but after supplementing with methylcobalamin my plasma B12 went over 1000. Now it's over 1400 without supplementation.

I also have very, very severe GERD, for which I'm stuck on dangerous omeprazole to avoid bleeding in the esophagus, I haven't had a gallbladder for more than 20 years, and I've been under a lot of stress for a very long time, so my digestion is impaired at best.

The high plasma B6 makes me think excess estrogen-copper also, as it disrupts zinc metabolism and zinc is a required cofactor for pyridoxal kinase. Do you have high homocystine as well? I would look at possible methylation issues and cobalamin disruption.

In my opinion therapy should focus on restoring proper digestion, reducing tryptophan, and elimination of excess copper through appropriate zinc intake. Also 1500mg niacinamide in my opinion is too much. 50mg every 2 hours should be plenty.
 

Diokine

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How long have you been on omeprazole? It has destroyed your ability to effectively absorb minerals. I would suspect some kind of persistent allergy in your case, probably gluten. This leads to hypothyroidism, swelling of nerves, vagal nerve irritation and low stomach acid output with esophogeal sphincter dysfunction. Gallbladder irritation is usually from hypometabolism and viral intereference.

You need to stop the omeprazole to allow true recovery, and this may indicate serious food restrictions for some time. I usually recommend a period of steeped broth made from greens, parsley, cilantro, etc.,. Mushroom broth is delicious and nutritious as well. Apply salt to taste. It might also be a benefit to find a competent chiropractor who can address any anatomical issues with the cervical-thoracic atlas and vagus nerve.
 
Last edited:

Mito

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Yes, I have high homocysteine, which is why I was supplementing with B6 and methylfolate. And yes, I have two copies of an MTHFR gene mutation.
You can't solve a MTHFR problem with methylfolate. You would need to supplement multiple grams of methylfolate to make up for MTHFR's reduced action. Especially of you are homozygous for C677T.

You might find this podcast interesting. Includes strategy to deal with MTHFR problems.
https://chrismasterjohnphd.com/2017/08/12/living-with-mthfr/

Here is a forum thread with some discussion on the topic.
Lack Of Methyl Donors, Demethylation, Folic Acid, B12
 

Travis

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Yes, I have high homocysteine, which is why I was supplementing with B6 and methylfolate.
This is yet another reason to limit methionine.
 

Lucenzo01

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May 17, 2016
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Linus Pauling recommended lysine to keep Lp(a) from sticking to the arterial wall. Lipoprotein(a), like plasminogen, has a very specific lysine-binding domain. It has such a high affinity for lysine that lysine-sepharose chromatography is the standard technique used to separate it.

This. And proline has even higher affinity.
 

Travis

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This. And proline has even higher affinity.
Wow. That certainly makes sense. Proline and hydroxyproline is a primary component of collagen, and could be exposed in frayed and damaged collagen leading to Lp(a) deposition: Lysine is a relatively minor component.

Looks like we're now in a race to first patent proline–sepharose chromatography beads to separate fibrinogen and Lp(a) from the blood. :penguin:
 

ddjd

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Jul 13, 2014
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My most recent labs came back with an off-the-charts high lipoprotein(a) level of 519 nmol/L, which combined with the high number of small and medium LDL particles, TC 277, LDL 180, HDL 78, LP PLA2 Activity 111 and mild hypertension it's very scary indeed.

Considering that lipo(a) levels over 75 nmol/L are considered an extremely high risk for all types of CVD, a 519 nmol/L is more than horrifying. My mother died of a heart attack at 48, her brother at 50, grandfather at 60 of his third heart attack, other grandfather likewise, a cousin had an angioplasty at 46, and the list goes on... I clearly didn't win the genetic lottery and I fully expressed the high lipo(a) genes. The question is what to do.

Has anyone had success with niacinamide combined with CoQ10 and vit C? If so, at what dose? I was reading that niacinamide is not effective at lowering lipo(a), but 1000-3000 mg of regular niacin (the amount apparently needed to lower it) are likely to damage the liver, so niacinamide would be preferable.

Thank you!
How are you getting on with the lysine?
 

TreasureVibe

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Joined
Jul 3, 2016
Messages
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High dose ascorbic acid powder (with no additives) atleast 6000 mg divided in 1000 mg per serving + L-Lysine 5000 mg + L-Proline 2000 mg. This is the only studied and proven natural way of treating CVD/CHD associated with lipoprotein (a). Linus Pauling protocol.

China free vitamin C is the best, like Quali-C from DSM. Multiple brands sell it.

You need this! The L-lysine will bind to the lipoprotein(a) in the blood, while vitamin C will repair lesions in the blood vessels whilst the body will then release the lipoprotein(a) from the lesions again, with once again Lysine binding to it.

L-lysine = lipoprotein(a) binder!!

L-proline will boost the effects of L-lysine and vitamin C.

At first in the Pauling therapy, your lipoprotein(a) will temporary increase in the blood. This is a good sign, indicating that the body is releasing lipoprotein(a) from the plaques, because the vitamin C is repairing the lesions. Don't let this scare you! Just make sure you get those doses named above everyday!

Google for the Pauling protocol! And see this: http://www.paulingtherapy.com/

Are you using fish oil? If so, stop them at once! And get your cysteine in check to prevent cardiovascular damage and disease! Don't listen to the fish oil recommendations by Pauling's work!

Okay, so, the point is, your lipoprotein(a) is raised for a reason. Probably if CVD/CHD runs in the family, it is typically because of vitamin C deficiency, with lesions forming in the blood vessel walls.

Get enough vitamin C daily, atleast 6000 mg! You have a vitamin C deficiency.

Minerals: What is your daily calcium, magnesium, potassium intake in miligrams?

Also: No gallbladder perhaps means worse absorption of fat soluble vitamins, vitamin A, D, E and K? Someone should elaborate on this. Perhaps oxbile salts should be indicated, or bile-boosting nutrients.

PPI drugs are dangerous, omeprazole should be stopped. GERD is probably because of low/no stomach acid and perhaps magnesium deficiency which causes the esophageal sphincter not too close, allowing acid to travel to the esophagus.

I really feel bad for her, as she hasn't logged back on ever since posting this topic, I hope she is still fine!
 
Last edited:
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