trying to understand LPA, lil help?

The discussion of the Linus Pauling vitamin C/lysine invention for chronic scurvy

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Joanna45
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Re: trying to understand LPA, lil help?

Post Number:#1  Post by Joanna45 » Sat Apr 29, 2017 4:40 pm

Lpa goes down because the vitamin C and Lysine have repaired your arteries and no longer needs the sticky Lpa to come on board and fix them..

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Re: trying to understand LPA, lil help?

Post Number:#2  Post by Joanna45 » Sun Apr 30, 2017 11:12 am

To get Lpa down you have to stay on vitamin C and Lysine and proline forever not even missing one day..my Lpa was down to 12 after 10 months but may have been lower earlier but had to find a private lab to do it..as my doctor would not order it done again..also I am a very active person walk every day and in the winter ski every day I can..Skied forty five days this winter..and work out with weights also..

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Re: trying to understand LPA, lil help?

Post Number:#3  Post by Joanna45 » Sun Apr 30, 2017 2:53 pm

I think the body stops producing Lpa when the scurvy of the arteries is taken care of then Lpa is no longer needed..but you think excercise or any stress bring it back up ..well I have been excercising a lot laately so will have my blood test done again in a month and see if the Lpa is staying low.

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Re: trying to understand LPA, lil help?

Post Number:#4  Post by pamojja » Mon May 01, 2017 5:24 am

zarfas wrote:so why does a cac have a high score and a lpa is a bad score?


CAC score doesn't have to be high. If it is high it shows the actual amount of already present calcification of plaque, and therefore possible higher risk of rupture.

Lp(a) is considered a risk-factor, like homocystein, fibrinogen, hs-CRP, etc. If it is high you have a statistically 'calculated' risk of an adverse event. However, since it's only a statistical calculation that might still not portrait your real risks.

In presence of a zero cac score, all calculated risks mean nothing. With a higher cac score they meant the more, because you already do have proven plaques from arteriosclerosis, which could rapture.

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Re: trying to understand LPA, lil help?

Post Number:#5  Post by pamojja » Mon May 01, 2017 7:35 am

CAC score shows the extent of existing disease. Lp(a) only increased risk without asseing how far, if at all, it has progressed. Therefore high CAC is worse.
With high Lp(a) it is even more so.
While high Lp(a) with no CAC score doesn't have to mean anything.

Since we obviously disagree how to reduce CAC score - the only one which actually measures the disease (and not only speculates) - I'll others answer the second question.

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Re: trying to understand LPA, lil help?

Post Number:#6  Post by pamojja » Tue May 02, 2017 7:15 am

zarfas wrote:I appreciate the answer
so having a low LPA score doesnt mean much in relation to risk of CAD?
what is a good CAC score?

Im not understanding the difference of CAC and LPA? Lpa is increased risk? and CAC tells you how much heart disease has progressed?
what are your thoughts on how to lower
LPA
CAC?

thanks


Lp(a) is a protein measured in blood, which, when high enough, could indicate some damage to the arteries it is about to fix. It tells nothing how far the damage has progressed. You still could have totally unobstructed arteries.

CAC score measures the already deposited calcium in the coronary arteries. Since calcium is mainly found in plaque in a certain percentage, it measures the actual amount of calcified plaque and therefore the progression of the disease - of various degrees blocked arteries.

The best CAC score is zero. However, since calcification of arteries comes naturally with age there are 'normal' ranges for each age group. Personally would shoot rather for 'optimal' ranges. The problem with any positive CAC score is, that it usually increases at a 30% yearly rate. So if you're first CAC is, let say 300, it could be 400 the 2nd year, 520 the 3rd, 676 the 4th, 878 the 5th, and so on exponentially heading for disaster.

Like I wrote in the other thread, my own Lp(a) only decreased when hormone levels normalized. I nevertheless would try all other methods I listed there, including Pauling's therapy. Also take a look at the video I linked in a post there.

CAC can be driven by many things in combination. Mainly, markers of inflammation (CRP, ESR, homocysteine, fibrinogen, Lp(a), etc., even low testosterone or low fT3 could be markers for low-level inflammation). So anything that brings it down helps.

However, most of the time inflammation and an increase in CAC seem really driven by increasing insulin resistance. Which could be calculated here: http://www.dtu.ox.ac.uk/homacalculator/index.php

The method I've learned at TrackYourPlaque is simple as it is effective: First test a few times where your highest peak of blood-glucose is after a meal (1 hr after eating in my case). And then try to keep this as low as possible (ideally below 110, 140 is already in the danger zone) by singling out and eliminating those foods which caused such high blood-glucose spikes.

However, be aware that a 15% yearly CAC score increase is already a exceptional deceleration and the fruit of such efforts. Though there are a few who really could decrease their CAC score again, with the methods used a TrackYourPlaque (now it's called Cureality). Here for example a thread where some member there tried to summarize all lab markers they shoot for, for decreasing CAC score: https://www.cureality.com/forum/topics.aspx?id=18881

With a 80% blockage at my abdominal aorta I considered myself already in the highest risk group 8 years ago. Therefore didn't needed a CAC score to tell I'm about to die. That I meanwhile could reverse intermittent claudication (and with it a 60% disability) assures me what I've done was right, despite the blockage remaining unchanged.

With diet it's pretty simple. Test, don't guess. Rarely any of us reacts to a specific diet with the same response as the statistical mean. Already Pauling talked about bio-chemical individuality. By testing important lab markers one sees correlations which otherwise remain hidden. By testing you know first-hand what a change in diet will cause.

I got sick as a life-long vegan (since age 10) and avoiding fats like plaque. Adding in eggs, fish and loads of healthy fats turned my health around for me. While an other might find out by testing, that contrarily by cutting down on meats and certain fats would help.

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Re: trying to understand LPA, lil help?

Post Number:#7  Post by pamojja » Tue May 02, 2017 9:39 am

zarfas wrote:huh? how is that?


Sub-clinical scurvy due to loosing the endogenous ascorbate producing gene explains it sufficiently to me.

zarfas wrote:so eventually everyone will die from blocked arteries?


CVD is the no. one cause for premature death, cancer the second, injuries from medication or hospitalization 3rd. It's a bid of being between a rock and a hard place. Since what's promotes cancer (angiogenesis) is counter to CVD. And vice-versa. In the end we have to die from something..

zarfas wrote:how do you lower your CAC?


By applying known interventions (comprehensive supplementation like with Pauling therapy, diet and lifestyle interventions) and monitoring progress (or regress) with any interventions with laboratory testing - or something cheap as blood-glucose monitoring. And adapt interventions according to your results. As already written above:

CAC can be driven by many things in combination. Mainly, markers of inflammation (CRP, ESR, homocysteine, fibrinogen, Lp(a), etc., even low testosterone or low fT3 could be markers for low-level inflammation). So anything that brings it down helps.

However, most of the time inflammation and an increase in CAC seem really driven by increasing insulin resistance.

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Re: trying to understand LPA, lil help?

Post Number:#8  Post by pamojja » Tue May 02, 2017 2:57 pm

zarfas wrote:ok so let me run this by you


First, self-directed care can only be run by oneself. :wink:

For that I would test to get a baseline. Try to get as many lab-markers tested your physician is willing too. Then get the most important missing out of your own pocket (see the link of lab-markers at cureality posted above). Get a blood-glucose monitor and test post-prandial blood glucose. Try to get one with which the test-strips don't cost too much, since that can add substantial costs.

Only that way you know where you're at, and from there you will know where to make adjustments. Without testing it's just guessing. A fasting glucose means nothing, without repeated postprandial testing, HbA1c, fasting Insulin or C-peptide.

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Re: trying to understand LPA, lil help?

Post Number:#9  Post by pamojja » Wed May 03, 2017 1:45 am

You asked how to reduce CAC. In retrospect you changed your question to what is Pauling therapy for your usual ridicule. - You're just too afraid to know your real numbers.


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