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        <title>What makes an episode stop? cont&amp;#039;d,</title>
        <description> It will soon be one month since Hans posed 3 tough questions:
==========

Author: Hans Larsen 
Date:   07-24-10 10:45

Erling,

I have reread your &amp;quot;theory&amp;quot; as to why afib episodes eventually stops. It is clearly pretty well identical to the one advanced in my &amp;quot;play&amp;quot;. Great minds do indeed think alike :~)

The questions remaining to be answered are:

1. Why does not everybody convert spontaneously?

2. Why is potassium supplementation at the beginning of an episode not effective in stopping/shortening the episode for all afibbers?

3. Is, as Mike suggests, the important &amp;quot;terminating factor&amp;quot; different for vagal and adrenergic afibbers, ie. for vagal afibbers reestablishing the proper K/Na ration is key, while for adrenergic afibbers reducing aldosterone is key. And what about mixed afibbers who are neither consistently vagal nor consistently adrenergic?

Hans
==========

My answers:

1. Just because? 

2. See 1

3. See 1

it&amp;#039;s very late, so I&amp;#039;ll sleep on it and try to do better tomorrow. (Great mind indeed...)

Erling</description>
        <link>https://www.afibbers.org/forum/read.php?9,107994,107994#msg-107994</link>
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            <guid>https://www.afibbers.org/forum/read.php?9,107994,108902#msg-108902</guid>
            <title>Re: What makes an episode stop? cont&#039;d,</title>
            <link>https://www.afibbers.org/forum/read.php?9,107994,108902#msg-108902</link>
            <description><![CDATA[ Jackie, I know its pretty late to jump into this conversation but it could be what the body perceives as homeostasis also changes over time so that in the end there is very little correction of the imbalance hence persistent afib becomes the norm.<br />
<br />
Adrian.]]></description>
            <dc:creator>Adrian</dc:creator>
            <category>AFIBBERS FORUM</category>
            <pubDate>Sat, 04 Sep 2010 06:43:14 +0000</pubDate>
        </item>
        <item>
            <guid>https://www.afibbers.org/forum/read.php?9,107994,108031#msg-108031</guid>
            <title>Re: What makes an episode stop? cont&#039;d,</title>
            <link>https://www.afibbers.org/forum/read.php?9,107994,108031#msg-108031</link>
            <description><![CDATA[ First, this is to highlight our Fearless Leader's  enduring theory of why a paroxysmal afib episode eventually stops, and also to commemorate the very beginnings of the Conference Room:<br />
<br />
Cunference Room Session 2: LAF AND THE HORMONE CONNECTION<br />
Jan 15  Jan 31, 2003<br />
[<a href="http://www.afibbers.org/conference/session2.pdf"  rel="nofollow">www.afibbers.org</a>];<br />
<br />
You are all invited to attend 'A play in three acts: The LAF Cycle or The Theory of Everything' by Hans Larsen.<br />
===============================================================================================================<br />
<br />
<br />
Hi again, Jackie!<br />
<br />
Thanks for your reply and as-always keen understanding. I would like to go even deeper in an attempt to answer The Three Questions. In my view it will first be necessary to understand some ways in which the atrial muscle tissue - the substrate - might lose its 'compliance', its ability to comply only with signals from the sinus node. Being an engineer of the mechanical ilk I tend to think in terms of structure, in this case that of muscle, how it is structured in order to function properly, and what might damage it to defeat it's designed function. A few things that come to mind are fibrotic infiltration separating muscle elements (you covered that superbly well in CR session 24), calcific infiltration doing the same thing, and clogged arterial capillaries, where "the action" is, possibly causing muscle cell death. It seems to me that any of these, via interruption or rearrangement of electrically conductive pathways, would be able to account for the individual differences. <br />
<br />
I've been re-reading two important books, The Homocysteine Revolution by Kilmer McCulley, MD, 1999, and Methyl Magic by Craig Cooney, PhD, also '99. At the same time I've been going into the vast CR library looking to see if any of this had been covered, and found this gem by our dogged co-researcher Richard. He posted a dialogue between you and Lorraine and me in '03, which I wish I could pull up, but have not been able to - yet.  <br />
<br />
The session is very educational to read, and it was nice to hang out with old friends again, Richard, Fran, Angus, Adrian, you, with nice Xmas greetings from all... Wow, we sure were busy and productive in '03, '04! I'm kinda hesitant - I guess - because it has my name on it, but since Richard thought it was good, and he'd know, I'm using it again because it serves the purpose well. I haven't even read it, just pasted it in, trusting Richard. Do you remember Lorraine? Her last post via Search was on 10-01-04?   <br />
<br />
Conference Room Session 20: METHYLATION<br />
Dec 21 - Jan 8, 2004<br />
[<a href="http://www.afibbers.org/conference/session20.pdf"  rel="nofollow">www.afibbers.org</a>];<br />
<br />
Richard led the session and then wrote: "I pulled this from the archives, 2/11/03, that Erling wrote, using the word "methylation":<br />
<br />
"Hi Jackie, and Lorraine,<br />
<br />
Jackie, your comments are always to the fact-filled point, and they are very much appreciated. In an earlier post you<br />
said that "DNA irregularities definitely influence membrane ion channels and pumps," and that in Metagenics seminars<br />
"they emphasize the major influence that nutritional factors have on healthy gene expression, protein synthesis and<br />
metabolism with their goal being the achievement of optimal genetic expression."<br />
<br />
Your statements bring up the subject of adequate "methylation" to limit DNA mutations and enhance gene expression.<br />
This might be of great interest to you, Lorraine, since you had said "I would like to know what I can do to improve the<br />
functioning of my calcium ion pump which I'm assuming may be faulty because my intracellular calcium level is 5.5<br />
which is above the range upper limit of 5.0." Craig Cooney, PhD biochemistry, UC Davis, has become a leading<br />
researcher and writer on the subject of methyl metabolism. His book Methyl Magic (1999) is written in a laypersons<br />
style, very easy to read and understand. He writes,<br />
<br />
"Methylation... it starts at the moment of conception (even before,<br />
actually) and continues, billions of time every second, until the day we die... methylation is a vital key to how we feel -<br />
physically, mentally, and emotionally. Lets put it as simply as possible: Methylation helps give life, and it can take it<br />
away. In fact, without methylation there would be no life at all. So what is methylation? Technically it starts with the<br />
small parts of molecules called methyl groups. A methyl group is a carbon atom with three hydrogen atoms attached to<br />
it. Any other molecule that adds this methyl group, whether it be a molecule of DNA or a protein molecule - any of the<br />
body's enormous inventory of molecules - is considered methylated. Methylation is so crucial a part of our body's<br />
machinery that it has a name of its own: methyl metabolism. Methyl metabolism refers to the making of methyl groups<br />
and their passing from one molecule to another. Methylation happens in everything that's alive - sponges, birds, bees,<br />
chimps, mice, and humans. As we said, without methylation there is no life - period. Methylation helps regulate the<br />
switching on and off of genes (technically this is known as gene expression) - one of the most crucial regulators of<br />
health and life itself. When gene expression goes awry the results can be horrifying: birth defects, cancer, and maybe<br />
even autoimmune diseases such as lupus. When other aspects of methyl metabolism go awry the downside can be<br />
equally terrible: heart disease, mental retardation, and diseases of the nervous system, among others."<br />
(It will not surprise me at all to someday learn that derangements of the complex structures of ion pumps and channels<br />
(proteins) from lack of adequate methylation can bring about cardiac arrhythmias)<br />
<br />
"Among the most important of methylation's many functions is the maintenance and protection of DNA, the basic stuff<br />
of heredity and of life itself. Adding methyl groups to DNA is enormously important in maintaining healthy cells. Many<br />
other proteins need periodic repair, and methylation is essential for this crucial repair work. Methylation, to put it in a<br />
nutshell, is vital to the healthy functioning of all our body's calls. Why? Because it makes the membranes that surround<br />
each of our cells more fluid. This in turn allows better regulation of life sustaining minerals like sodium and potassium<br />
into and out of our cells, so that a healthy balance of these minerals is maintained. In most people the fluidity of cell<br />
membranes decreases with age, and this loss of fluidity may be one of the features that defines aging itself."<br />
"Obviously methylation is a key player in giving us life, keeping us healthy, and perhaps enabling us to live longer,<br />
more vital lives. Scientists have known this for quite some time, but I still find it amazing that there's been so little<br />
discussion of methylation in the popular press and in the media. It's a shame, and we scientists bear much of the<br />
responsibility for not making the public aware of what we know."<br />
<br />
So this subject is the closest thing that I've come across to a real way of protecting, perhaps rebuilding, faulty ion<br />
pumps and channels (proteins all), and membranes (the fluidity of which is also enhanced with good fats such as DHA<br />
and EPA fish oils, and the elimination of bad fats such as hydrogenated oils and many plant oils). The book goes on to<br />
explain that the way to determine if ones methyl metabolism is adequate for repair and maintenance is with a<br />
determination of homocysteine (HCY) levels in the blood, a routine and quite inexpensive test (the recommended<br />
upper limit is 7 micromoles per liter of blood -- above that lie all sorts of health problems). And if ones HCY level is too<br />
high, the book lays out the methyl metabolism enhancing supplements that are needed and the recommended doses:<br />
trimethylglycine (TMG), choline, inositol, folic acid, vitamins B6, B12, and E, zinc, selenium, fish oils."<br />
<br />
The following are highly recommended reading:<br />
<br />
Book: Methyl Magic by Craig Cooney, PhD. ISBN 0-8362-3585-1<br />
Article: [<a href="http://www.lef.org/magazine/mag98/dec98_meth.html"  rel="nofollow">www.lef.org</a>];<br />
Article: [<a href="http://www.lef.org/magazine/mag2001/apr2001_briefs.html"  rel="nofollow">www.lef.org</a>];<br />
Article: [<a href="http://www.lef.org/magazine/mag99/mar99-report2.html"  rel="nofollow">www.lef.org</a>]; (this article shows the desirable HCY level)<br />
<br />
]]></description>
            <dc:creator>Erling</dc:creator>
            <category>AFIBBERS FORUM</category>
            <pubDate>Mon, 16 Aug 2010 14:02:43 +0000</pubDate>
        </item>
        <item>
            <guid>https://www.afibbers.org/forum/read.php?9,107994,108004#msg-108004</guid>
            <title>Re: What makes an episode stop? cont&#039;d,</title>
            <link>https://www.afibbers.org/forum/read.php?9,107994,108004#msg-108004</link>
            <description><![CDATA[ Erling -   Homeostasis.  The body&#039;s innate wisdom always tries to restore homeostasis or the correct balance in every cells and organ system to as close to ideal as possible with the nutrients available.   Without the basic nutrients to do that, that&#039;s often not possible, but when compensatory measures can be taken, the body will manage that automatically.   <br />
<br />
In the case of the AF self conversion, I can only speculate that if the deficiencies are not too great, eventually, the Na/K balance or that issue of Tissue Compliance  becomes adequate or close to it.  Adding critical nutrients at the onset of AF  probably helps as well. <br />
<br />
Obviously, it&#039;s much more complicated than that simplistic observation. <br />
<br />
Most likely, in most of our cases, we knew nothing about adding additional electrolytes at the onset... and yet, we converted in the early years rather quickly so the innate ability for homeostasis was working well.  Perhaps we wear it out, in time, as our AF journey progresses and without supplementation and adjustments to whole foods etc, self-conversion is less efficient and eventually, not at all.  The homeostasis mechanism may become exhausted.<br />
<br />
Jackie]]></description>
            <dc:creator>Jackie</dc:creator>
            <category>AFIBBERS FORUM</category>
            <pubDate>Mon, 16 Aug 2010 04:42:43 +0000</pubDate>
        </item>
        <item>
            <guid>https://www.afibbers.org/forum/read.php?9,107994,107994#msg-107994</guid>
            <title>What makes an episode stop? cont&#039;d,</title>
            <link>https://www.afibbers.org/forum/read.php?9,107994,107994#msg-107994</link>
            <description><![CDATA[ It will soon be one month since Hans posed 3 tough questions:<br />
==========<br />
<br />
Author: Hans Larsen <br />
Date:   07-24-10 10:45<br />
<br />
Erling,<br />
<br />
I have reread your &quot;theory&quot; as to why afib episodes eventually stops. It is clearly pretty well identical to the one advanced in my &quot;play&quot;. Great minds do indeed think alike :~)<br />
<br />
The questions remaining to be answered are:<br />
<br />
1. Why does not everybody convert spontaneously?<br />
<br />
2. Why is potassium supplementation at the beginning of an episode not effective in stopping/shortening the episode for all afibbers?<br />
<br />
3. Is, as Mike suggests, the important &quot;terminating factor&quot; different for vagal and adrenergic afibbers, ie. for vagal afibbers reestablishing the proper K/Na ration is key, while for adrenergic afibbers reducing aldosterone is key. And what about mixed afibbers who are neither consistently vagal nor consistently adrenergic?<br />
<br />
Hans<br />
==========<br />
<br />
My answers:<br />
<br />
1. Just because? <br />
<br />
2. See 1<br />
<br />
3. See 1<br />
<br />
it&#039;s very late, so I&#039;ll sleep on it and try to do better tomorrow. (Great mind indeed...)<br />
<br />
Erling]]></description>
            <dc:creator>Erling</dc:creator>
            <category>AFIBBERS FORUM</category>
            <pubDate>Sun, 15 Aug 2010 21:04:31 +0000</pubDate>
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