please advise.. 3 heart attacks & stenosis

[jimmylesante]

Also as Johnwen et al mention taking Vit C at the right times is very important and i'm sure overlooked, at least 1hr before meals and 2hrs after meals.

[jpoww]

Jimmy, my husband takes carnitine in 3 different forms along with all the minerals and vitamins that linus pauling recommends. My husand is gluten intolerant and we have been following a low carb and low yeast diet. We eliminated all processed sugars. The only thing, is that lately we have been eating a little more fruit than usual and we ususally dont eat much of that. we grow our own.
I just cant find out what could possible cause this, he has been excerising also.

[jimmylesante]

Would Vitamin B3 as Niacin clear out the blood levels of LP(a)??
I thought the pauling therapy prevented LP(a)from attaching to plaque as the amino acids had already done that, then the LP(a) was also lifted out of the plaque-thus there will be higher levels of LP(a) in the blood but no where for them to attach.
My simplistic view- and it is that,- simplistic. Is that 3 major things make up plaque, 1)fat 2)calcium 3)Cholesterol
Therefore if it was me i'd use the Pauling therapy, plus plenty of magnesium and vitamin K2 to redistribute calcium to where it should be and i would definitely nail a good Omega 3- 3times a day

[jpoww]

My husband use to take B3 Niacin and he stop taking it because he could not put up witht he flushing effect.
Yeah I thought the pauling therapy would lower LP(a) levels also..thats why i'm shocked by his recent blood work of LP(a) increase.
Pauling says any levels of LP(a) above 20 starts to deposit on arterial walls. so your statement of
"then the LP(a) was also lifted out of the plaque-thus there will be higher levels of LP(a) in the blood but no where for them to attach."
is confusing to me.
My husband takes 1800mg-2000mg of magnesium a day. he does take fish oil and hemp oil. He doesnt take vitamin k because he is on blood thinners

[Johnwen]

They found out that Prasugrel is not the one shoe fits all it suppose to be although the manufacture is standing fast on this, Doctor’s are finding that smaller frame people are having some serious reactions to it such as sporadic hematoma’s and vision problems and a lot of docs are putting their patients back on plavix or having their smaller patients to half their dose even though the pill isn’t scribed. At his weight he should be ok.
According to this report which I’ll try to find a free copy of and post it for you. Be warned it’s techy as all get out. The subscription version is 42 pages long so we’ll see what the free version looks like (if I can find one.) It has to do with the DNA and when genes start changing it just don’t happen over night unless it’s a poison then who knows what will happen, but takes time to institute it’s changes which will then have reactions else where. So there’s a good possibility his LP(a) may continue to rise if he remains on this drug. This report did state that 162mg. Of aspirin was the minimum to countered this effect. With that in mind maybe he should up his dose of aspirin to 2 times a day. If his doc ok’s it! Which I don’t see any problem with but he may have other ideas.
I could go into a lot of detail and confuse you, so I’ll be as simple as possible on the effect of Lysine on LP(a). LP(a) hunts through our bodies in search of dead tissue if the liver receives signals of dead tissue in the system it’ll increase the amount of LP(a) to go hunt for the source of the problem and start a cascade of events to correct it. Lysine when it’s metabolized into the system looks like dead tissue but doesn’t produce the signals to the liver to up production but when the LP(a) comes in contact with it, it attaches to it like a magnet to iron changing both to a useless particle that the liver then removes.
So as you can see it stops the action of the LP(a) it doesn’t stop the liver from producing it, only correcting the problem within the system will cease it’s production. The problem you maybe running into is maybe one of his readings is a calculated reading and one maybe actual readings or both could be calculated. The error probability in calculating is +or- 10% depending on the lab. If you want actual reading his doc must specify this is what he wants but like most docs they don’t think LP(a) is of any value but that’s up to him and how knowledgeable he is or if he’s just a robot.
Technically he’s not on blood thinners but Anti-Platelet medicine. Blood thinners increase the time it takes for blood to clot known as pro thrombin time. These are used when the circulation is slowed at some point in the body which would cause the blood to clot and allow the clot to block the pipes stopping blood flow. Basically this is like cutting yourself and timing how long it takes to stop bleeding.
Anti-platelets keeps platelets from sticking together. This happens in non penetrating injuries such as a bruise. The black and blue spot is a result of platelet’s sticking together to help in the healing of the injury. Anti-platelets change the release of the agent that causes them to attach to each other when there is a injury. The marks he gets on his body from this medicine when he taps a part or bangs it on something are what happens when platelets don’t stick together and leech out to uninjured tissue around the injured point. You probably noticed their color is more like the color of blood then the regular black and blue mark people get. That’s because what your seeing is circulating blood most of the time these marks disappear as fast as they came that’s the healing power of fresh blood. This doesn’t work so good if he scrapes a knee he’ll probably think he’s going to bleed to death. I see a lot of these people. They tend to get concerned when I just stand there looking at my watch and like a miracle it stops.
With your husbands case I think you’ll see that when they placed the stent they obviously did some injury within the artery. It’s probably a drug eluding stent which is stopping the formation of plaque over this injury. Which is natures band aide and patch for injury but it doesn’t stop the platelet formation. So he takes anti-platelet drugs to stop this. Now the problem DE Stents have a useful life span which means after a certain amount of time they lose their potency and nature will resume it’s effort to heal the damage done. This is where the power of Pauling’s therapy will come’s into play. Plaque will form over it but how much is the key, a light coat with a calcium cover is ideal but not a plug that keeps closing down. This is what it’s all about allow nature to do it’s job but not get carried away with it. There loading him down with statins thinking this will stop it but one problem the body needs cholesterol to survive so even if he’s in range there’s still enough to clog an artery that’s injured. Giving the body the tools to fix things Vitamin C, lysine and proline) will give better results then trying to remove tools (cholesterol) and see what happens.
Hope this clears some things up for you.

[jpoww]

This clears up some of my confusion. So you think at his weight he is ok on 10mg of effient?
If the effient is causing the lp(a) to increase then your saying he should up his asprin to twice a day to counteract this. Do you think 162mg of aspirin is ok in addition to the 10mg of effient?

Should I try to see if i can get his effient decrease to 5mg? or see if he should switch back to plavix? is plavix better with the lp(a)? or the same.

If the lp(a) is in fact going to continue to go up would that mean he will be at an increase risk of another heart attack? i'm assuming the more it goes up the more plaque build up will happen right?

Now to figure out if his lp(a) on his lab was a calculation or reading, how do I know which it one is it?
The lab was done at Berkley Labs.

[Johnwen]

As I said before check with his doctor to make sure he agrees with it before changing any thing.
He knows him better then anyone here does.

Don't change to many things at one time. I would say if his doc agrees on the other increase hold a steady course and see if there is a change. Flipping things around in bulk would just add to the confusion of what does what?

This is why he's on Pauling therapy to counter the effects of the LP(a) So if there is a increase make sure he's getting the proper dosage. I would like to say it will stop it but thats something no one here on earth could give you a deffinite answer on. All we can do is make sure were doing our part to try and prevent it.

If you have a copy of their report there should be a Reference number on it. Call them and ask they can use that number to give you details on the test. If not they can check by name but it will probably require more questions. So just call them and Ask!

[jpoww]

Johnwen,

I will call Berkley Lab and find out if those LP(a) were readings or caculations? and let you know.
I will talk to his doctor about the increase in asprin and see what he says.
He is currently taking that maximum lysine amount Linus Pauling recommended. I think he is taking the following dosage
26,000 mg of vitamin c
6,000 mg of lysine
2,000 mg of proline

if you think we need to change this dosage, let me know.
Thank you for all your advice.

[jpoww]

Johnwen,

I spoke to the lab and she said she is pretty sure both of those readyings for the lp(a) are calculated readings. so what does that mean to me?

the test he took in october was lp(a) of 14 and the one he took in may the lp(a) was 20

[Johnwen]

What it means is you should probably wait till he has a third test and then average them out and use this for a base number. You also have to realize that a direct reading test is a 15 step process which then evaluates the results with a standard chart which there is 330 different patterns for and the results have to match one which is then compared for results which then gives a figure that is reported. Margin of error is -2% to +8% so it’s really a figure that’s only as good as the people doing it. The test kit wholesales for about $175 plus the tech’s time and you can see why they would opt to calculate using figures that come available when the sample is machine processed. This is also why the ranges are so broad. Right now I wouldn’t be changing too much he’s on a good dose of Pauling. But I thought you might be interested in the fact that statins do increase APO-A1.

Apo A-I may increase with:
Drugs such as: carbamazepine, estrogens, ethanol, lovastatin, niacin, oral contraceptives, phenobarbital, pravastatin, and simvastatin
Physical exercise
Pregnancy
Weight reduction
Use of statins

http://labtestsonline.org/understanding ... a/tab/test

APO-A1 is one of the factors used in calculating LP(a) I see a connection! Do You??
Also if you wouldn’t mind Could you give us, his glucose readings from the same tests where the LP(a) was reported??

[jpoww]

So the "calculated readings" are not the best way to go. There could be some errors done there but a 7 point difference is kind of alot for the two test being six months apart. I see what your saying about the statins but the first test he did when the lp(a) was 14 he was on 80mg of lipator and the second test he did he was on 40mg of lipator with the lp(a) being 20 so if you the statin was an issue shouldnt the lp(a) reading done on 80mg be higher then the reading he had done on 40mg of lipator?
I just dont see how the decrease in lipator could cause an increase in LP(a)

The glucose reading on the first test in october was 84
The glucose reading on the second test in may was 94

I also wanted to tell you these readings just in case they mean anything:
APO B- Particle reading in october was 75
APO B- Particle reading in may was 67
Q-LDL IIIa+b in october was 12.4
Q-LDL IIIa+b in may was 12.3
Q-LDL IVb in october was 1.5
Q-LDL IVb in may was 1.4

On the october test he had more LDL-I size particles which are the large fluffy kind and on the may test he decreased in this size particle and started to increase in the medium to small sizes so that along with the increase in the LP(a) I started to freak out thinking he is heading to making more plaque .

[Johnwen]

This what I was talking about. You’ll notice his APO-B dropped substantially, Using stainolgy “It Dropped a by a Massive 11%!!”
APO-B is the latest Buzz as to the cause of CVD. Their saying it’s more of a predictive indicator then LDL. Unfortunately for the statinators this massive drop was caused by your husbands reduction of statins from 80mg. to 40Mg.HMMM!!!

first test he did when the lp(a) was 14 he was on 80mg of lipator and the second test he did he was on 40mg of lipator with the lp(a) being 20

The glucose reading on the first test in October was 84
The glucose reading on the second test in May was 94

I also wanted to tell you these readings just in case they mean anything:
APO B- Particle reading in October was 75
APO B- Particle reading in may was 67
Q-LDL IIIa+b in October was 12.4
Q-LDL IIIa+b in may was 12.3
Q-LDL IVb in October was 1.5
Q-LDL IVb in may was 1.4

This is another reason I don’t put too much credence in these figures each LP(a) has a APO-B particle in it’s make up. So a lower APO-B should result in lower LP(a) calculations since it’s also used in calculating the LP(a).
I’m going to check with our guru lab rat Monday and get the pro opinion, Their into this everyday and can give me the true answer. I just see their results and try to figure out what’s going on.
Normally I wouldn’t even consider this rise to be of any consequence because his levels are well within normal range however the reason behind it would be good to know for future reference. You need to settle down a little you can’t base everything on one number and panic because it changed. The other numbers you presented all show signs of improvement this is good and without a baseline figure it’s hard to say what a change would mean. If you had a LP(a) reading before his incident you could have a concern but for now till you establish a good baseline, it should be a observe for symptoms type situation.
I did some searches and came up with these, some get techy but you’ll see there’s many possibilities to explore.

In this one it looks at glucose changes across a varying of people, conditions and times for changes in LP(a).
http://atvb.ahajournals.org/content/18/8/1335.full

Here’s a simpler article about Lipids.

http://www.dearpharmacist.com/2013/01/1 ... erol-news/

This one talks about APO-B

http://www.clinchem.org/content/48/3/484.full

Hope this gives you some insight into this complex issue.

[jpoww]

The only reason I was freaking out was because of the increase in smaller LDL size which I know are more dangerous and the LP(a) because Linus Pauling said anything about 20 will start building plaque. I will chill out and wait til we get another Lab test done. How long do you think we should wait before getting another test done?

I wanted to ask you. My husband mixes is lysine and proline in his powdered vitamins with water and drinks it throughout the day. Do you think that will cause the lysine to breakdown and cause him not to be absorbing it much?

Please let me know what your lab guru person says about the inscrease in LP(a)

Thank You so much!

[Johnwen]

APO(a) Size Heterogeneity! Ever hear of it? Neither did I till today, anyway I talked to our Lab Guru today and my head is still buzzing. Well the results that they use, is the ELISA test which is the 15 step compare to chart type test I mentioned earlier. When they see a reading above 50 mg/dl they check the APO(a) size because it seems the size has a lot to do with the LP(a) levels.
The larger the APO(a) tends to lower the LP(a) but it also increase fibrin which is for clotting of the blood. The smaller the APO(a) size the higher the LP(a) will be and the smaller the fibrin.
Drugs that reduce fibrin size will see an increase in LP(a). He brought up effient and I just said, “YEP!” He said, “There you Go!” So I did “GO”
Anyway he also confirmed a 14 to 20 is Not a big deal if it continues, “you know what to do!”
So there you have it, my suspicions on effient were more or less confirmed.
Now I guess I’ll have to do a little more research to find the who, what and why in a free site???

[jpoww]

I dont have any readings of APO(a) on his blood works but only APO(b). All we know is that is APO(b) and fibrogen decreased and LP(a) increased. So it sounds like your saying this is a result of the effient he is taking.
It all sounds ligit but my confusion is if it is the effient doing this, then why was his lp(a) low on the october test when he was on the effient and had been on effient since nov. of 2010 and before that he was on plavix since 2005. its not like he wasnt on effient when he had a low lp(a) reading. you see what i'm trying to say?
you said if this increase in lp(a) continues "I know what to do". What is that? increase the current 81mg of ecotrin asprin to 2? or should I see if the doctor is willing to decrease the effient from 10mg to 5mg or should I see if the doctor should switch him back to plavix?
You know I thought looking at the lp(a) would be a good indicator to see if the lysine and vitamin c are working and I thought it would be a good gauge of his increase of a threat of another heart attack but that seems to be ruined now...what number do I look at in his lab work now to help me figure out if he is doing good?