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Re: Got new VAP labs back-not good
Posted: Sat Jun 25, 2011 5:32 am
by Cobraman
John, already take niacin 1000mg three times a day. Are you saying more than that? As I have already posted, I do not have a problem w/ the flush. It is possible that I may need more time. I don't think that I want to take warfarin, but just found some studies that aspirin also lowers Lp(a). I will add a low dose aspirin to my supplement regimen. Since Lp(a) is thought to be hereditary perhaps mine may be more difficult to bring down. I am confident that I will be able to do it. I will post next week on results of 28 iv edta chelations that I have done. They do an ankle/brachial pulse to see if circulation has increased. I realize that this isn't the best test, but may provide some interesting information.
Johnwen wrote:What Owen said and
Up your B3 Niacin. I'll repeat this! Take right B4 you jump in bed for the night you'll sleep thru the flush. I've been taking 1500 mg like this for 4 years don't have any Idea if I get a flush or not now. LP(a) = 0 zero zip nada!!! Always comes back NR (None recordable)
It takes time to get it down but 12 isn't that bad Pauling gave us 14 is when trouble starts.
Or you could take Warfarin (Rat poison) it knocks LP(a) right out along with a few other things you need to live.
Re: Got new VAP labs back-not good
Posted: Sat Jun 25, 2011 7:03 am
by jknosplr
Cobra your pretty close to your goals, are your engineering units mg/dl?
Lipoprotein(a) - Lp(a)[27]
Desirable: < 14 mg/dL (< 35 nmol/l)
Borderline risk: 14 - 30 mg/dL (35 - 75 nmol/l)
High risk: 31 - 50 mg/dL (75 - 125 nmol/l)
Very high risk: > 50 mg/dL (> 125 nmol/l)
http://en.wikipedia.org/wiki/Lipoprotein%28a%29
Re: Got new VAP labs back-not good
Posted: Sat Jun 25, 2011 7:39 am
by ofonorow
but just found some studies that aspirin also lowers Lp(a). I will add a low dose aspirin to my supplement regimen. Since Lp(a) is thought to be hereditary perhaps mine may be more difficult to bring down.
Under what theory? I would like to see the links to these studies (hoping they weren't funded by Bayer) and even if there is some effect here, taking vitamin C and lysine deal with heart disease, strengthen the blood vessels, etc. Lowering Lp(a) while doing this makes sense.
Trying to lower Lp(a) while taking aspirin does not compute. I think taking aspirin is generally a mistake, although you can get away with it if you are also taking high vitamin C (as far as aspirin has a known tendency to create lesions in the stomach).
A willingness to take even low dose aspirin is a clue that if you started reading HOW TO LIVE LONGER AND FEEL BETTER, you probably didn't finish it!
Re: Got new VAP labs back-not good
Posted: Sat Jun 25, 2011 5:06 pm
by jknosplr
An interesting bit of information on the subject.
http://www.drlam.com/opinion/Lp%28a%29.asp
Re: Got new VAP labs back-not good
Posted: Sat Jun 25, 2011 8:17 pm
by Johnwen
I think this link will give a better understanding. Dr lam is kind of out there in left field right behind Barrett (quack something) at short stop.
Asprin affects platelets were looking at the fibrin component
http://www.drkaslow.com/html/lipoprotein__a_.html
Re: Got new VAP labs back-not good
Posted: Wed Jun 29, 2011 7:05 pm
by Cobraman
My willingness to try something new is only a clue to the fact that I am doing all I can to defeat this problem and your snide comments are not helpful. Since you do this website you should know that one of the bad effects of Lp(a) is that it contributes to blood clots. Aspirin has long been established to affect platelet aggregation. Even Johnwen suggested taking warfarin to lower Lp(a),though perhaps tongue in cheek. The study I found is this J Stroke Cerebrovasc dis, 2007 Sep-Oct: 16(5) 220-4 Effect of Aspirin on Lipoprotein(a) in Patients with Ischemic Stroke. Also, studies have found that people w/ high lp(a) that take aspirin do not have higher bleeding times than a control group. .
ofonorow wrote:but just found some studies that aspirin also lowers Lp(a). I will add a low dose aspirin to my supplement regimen. Since Lp(a) is thought to be hereditary perhaps mine may be more difficult to bring down.
Under what theory? I would like to see the links to these studies (hoping they weren't funded by Bayer) and even if there is some effect here, taking vitamin C and lysine deal with heart disease, strengthen the blood vessels, etc. Lowering Lp(a) while doing this makes sense.
Trying to lower Lp(a) while taking aspirin does not compute. I think taking aspirin is generally a mistake, although you can get away with it if you are also taking high vitamin C (as far as aspirin has a known tendency to create lesions in the stomach).
A willingness to take even low dose aspirin is a clue that if you started reading HOW TO LIVE LONGER AND FEEL BETTER, you probably didn't finish it!
Re: Got new VAP labs back-not good
Posted: Wed Jun 29, 2011 7:21 pm
by Cobraman
Thanks for the support J. Yes the units are mg/dl. From Labcorp they state anything over 10 is high. I plan on working more on my diet and see what happens. One of the biggest positives of doing edta chelation is that it is supposed to effect endothelial function in a positive way. As I have already stated will be checking my circulation tomorrow. Will post results.
jknosplr wrote:Cobra your pretty close to your goals, are your engineering units mg/dl?
Lipoprotein(a) - Lp(a)[27]
Desirable: < 14 mg/dL (< 35 nmol/l)
Borderline risk: 14 - 30 mg/dL (35 - 75 nmol/l)
High risk: 31 - 50 mg/dL (75 - 125 nmol/l)
Very high risk: > 50 mg/dL (> 125 nmol/l)
http://en.wikipedia.org/wiki/Lipoprotein%28a%29
Re: Got new VAP labs back-not good
Posted: Thu Jun 30, 2011 8:14 am
by ofonorow
Since you do this website you should know that one of the bad effects of Lp(a) is that it contributes to blood clots. Aspirin has long been established to affect platelet aggregation. Even Johnwen suggested taking warfarin to lower Lp(a),though perhaps tongue in cheek.
No, I am not aware that Lp(a) contributes to blood clots.
I was reacting to your finding a study that "aspirin lowers Lp(a)." That is what does not compute under any theory I am aware of, but I am ready to be educated.
Re: Got new VAP labs back-not good
Posted: Thu Jun 30, 2011 9:25 am
by Johnwen
Re: Got new VAP labs back-not good
Posted: Thu Jun 30, 2011 8:22 pm
by Cobraman
Re: Got new VAP labs back-not good
Posted: Fri Jul 01, 2011 4:55 am
by jknosplr
Cobra
As I understand it the higher the Lp(a) value the more % of change you will see when treating it. Mine constantly ran between 6 mg/dl and 12 mg/dl for the past 3 1/2 years on the PT. I have no base line before the MI 2007 to reference to so who knows what it was, it may not of been high at ll, I don't know. The second MI fed 2011 it was 9mg/dl, in fact all the numbers were just where the experts said they should be.
My brother started taking a baby aspirin some 25 years ago, he does not have any CVD. We ate the same food all through our lives, I exercised more than he and was much more physical. We drank about the same amounts of alcohol, no smoking at all. He favors my mothers side and I my father side..............genetics! Only difference in our lives was stress load, he worked from home and I from an airport for 30 years.
J
Re: Got new VAP labs back-not good
Posted: Fri Jul 01, 2011 10:21 am
by ofonorow
if I have a genetic predisposion to high Lp(a)
We learn here from people's experiences. (But I don't remember your number being that high?) The case in the book showed the vitamin C/lysine by themselves, over a long period, did not lower elevated Lp(a). (And even the Pauling/Rath studies in guinea pigs only showed the low vitamin C leads to elevated Lp(a), not the reverse. There is little scientific evidence that the apo(a) switch can be turned off by taking more vitamin C/lysine, at least in the short term.)
That case was included because it showed that by changing only one factor, adding proline, Lp(a) could be lowered. In the case of the medical professor, some time after 6 months but before 14 months, his elevated Lp(a) dropped to zero.
There is no way to know if this is an isolated case. If and when you decide to experiment with proline, we will be interested.
But as Johnwen points out, the Pauling/Rath theory is Lp(a) has a purpose, it is compensating for low vitamin C leading to less collagen and weaker blood vessels. I would think that if you have genetically high Lp(a), trying to find tools to "inactivate" any excess Lp(a) makes sense. Wait a minute, vitamin C lysine and proline are Lp(a) binding inhibitors! (Thank you Linus Pauling and Matthias Rath) That means, lysine and proline in the blood fill receptors in the Lp(a) molecules making them "less sticky." So if you do have elevated Lp(a), the correct approach, in my opinion, is to take more vitamin C, lysine and proline (and vitamin B3 - also listed in the U.S. patents.) Miraculously, these substances are also the building blocks of collagen, so you are fixing the underlying problem at the same time. (Every time I go over this I appreciate Linus Pauling's genius.. But I digress.)
My problem, in theory, with aspirin is that it has an effect on vitamin C something like smoking. The body considers it a toxin. It is my understanding that when people take aspirin, it uses up some of the vitamin C in their system. So, in theory, aspirin would be more likely to raise Lp(a) from this C lowering effect. But other anti-platelet factors may override this concern.
Finally, I have wondered what signals the liver to stop making apo(a). (Lp(a) is and LDL particle that has a sticky apo(a) particle attached. The apo(a) part has the lysine binding sites.) I saw work from the University of Chicago which found the proline binding site on the Lp(a) molecule (analogous to the lysine binding sites). And it is my understanding that it is the proline binding site which is used to create Lp(a) molecules in the liver. Proline binding site attaches to something on the LDL. Proline is not essential, meaning the body has the means to produce its own and doesn't require it in the diet. I have speculated that the amount of proline entering the liver may be the "signal" that is used to turn off the production of Lp(a), perhaps by interfering with the attachment to the LDL.
Re: Got new VAP labs back-not good
Posted: Fri Jul 01, 2011 3:15 pm
by Cobraman
As I have stated previouly, I have been taking 10000mg vit c, 6000mg lysine, 2000mg proline, and 3000mg niacin daily since November. I will be continuing this forever because I feel it is helpful no matter what the values are. I am doing the aspirin as a test for only 4 weeks which is what was done in the studies. If it does not do anything significant I will discontinue its use and perhaps move in a slightly different direction. My liver enzymes were slightly elevated so I am dropping to 2000mg a day of niacin. According to William Parsons, MD it is only a concern if lab values are double the norm, but I would rather be safe. I will resume the higher level if chol. goes up again.
Since I have been taking the Proline all along I was hoping it would drop the Lp(a). I will find out in 4 weeks with the aspirin. I will post results then.
Re: Got new VAP labs back-not good
Posted: Sun Jul 03, 2011 6:16 am
by Cobraman
Owen, is it your contention that the Lp(a) level may be less important if doing Pauling Rath therapy since the binding sites would all be occupied? I believe this is what you are implying and I apreciate that. I will also be taking this into consideration as I figure this out.
Also, circulation has improved from doing the edta chelation as shown from a better arterial stiffness index though wasn't bad before.
Re: Got new VAP labs back-not good
Posted: Thu Jul 07, 2011 3:48 pm
by ofonorow
Yes - lp(a) binding inhibitors are said to turn sticky Lp(a) into teflon - as they fill the lysine and proline binding sites.
How often to you measure Lp(a)? We have a time frame of 6 to 14 months when at least one person's went to zero with that much proline.My liver enzymes were slightly elevated
Why not start liposomal GSH - in case low glutathione is the cause of the elevated enzymes?
Glutathione (GSH) is the major detoxification molecule in all cells, and the liver is the bodies major detoxification organ. While studying Life Extension's position on acetaminophen (Tylenol) which is the number one cause of acute liver failure in the USA, found that Life Extension scientists "thinking outside the box" are convinced that acetaminophen depletes GSH in liver cells, and that this is the reason liver cells die causing liver failure.
Other drugs may also be toxic to the liver for the same reason - depleting intracellular GSH,
And thanks to environmental and other science, we know that there are only two reliable ways to increase intra-cellular GSH via supplementation. 1) with vitamin C, and 2) with liposomal GSH. (Ordinary GSH, even IV, in the blood does not enter cells.)