I came across this while doing some "AFIB Research" and thought it would be interesting. I searched to make sure this hadnt been posted before and I couldnt find any evidence that it had. There has been "some" discussion of the impacts of oxidative stress on AF but not much that I could find. Full report can be read here....(http://www.e-emm.org/article/article_files/EMM035-05-02.pdf).....below is a copy of the Abstract.

******************************************
Atrial Fibrillation (AF) is thought be caused by
oxidative stress. Oxidative stress at the cellular
level results from many factors, including exposure
to alcohol, medications, cold, toxins or radiation.
In this study we investigated gene transcriptional
profiles on the human myocardial tissues
from AF and oxidative stress conditions.
Right atrial appendages were obtained from AF
patients (n = 26) undergoing the Maze procedure,
and from control patients (n = 26) who were in
normal sinus rhythm and undergoing coronary artery
bypass graft operation. To examine the effects
of oxidative stress on AF, we used radioactive
complementary DNA (cDNA) microarrays to evaluate
changes in the expression of 1,152 known
genes. This technology, which monitors thousands
of genes simultaneously, gives us a better
picture of the interactions between AF and oxidative
stress. Total RNAs prepared from the retrieved
tissues were used to synthesize 33P-labeled
cDNAs by reverse transcription and hybridized
to cDNA microarrays. Gene expression profiles
showed that 30 genes were upregulated and
25 were downregulated in AF patients compared
with control patients. Moreover, comparison rank
analysis revealed that the expression of five genes
related to reactive oxygen species (ROS)-including
flavin containing monooxygenase 1, monoamine
oxidase B, ubiquitin specific protease 8, tyrosinase-
related protein 1, and tyrosine 3-monooxygenase-
increased by more than 2.0 of the Z-ratio,
and two genes related to antioxidantsincluding
glutathione peroxidase 1, and heme oxygenase
2-decreased to the Z-ratio levels of ≤ -2.0. Apparently,
a balanced regulation of pro- and anti-oxidation
can be shifted toward pro-oxidation and
can result in serious damage similar to that of
human AF. Western blotting analysis confirmed
the upregulation of tyrosinase-related protein 1
and tyrosine 3-monooxygenase and the downregulation
of heme oxygenase 2. These results suggested
that the gene expression pattern of myocardial
tissues in AF patients can be associated
with oxidative stress, resulting in a significant
increase in ROS. Thus, the cDNA microarray
technique was useful for investigating transcription
profiles in AF. It showed that the intracellular
mechanism of oxidative stress plays a pivotal role
in the pathologic progression of AF and offers
novel insight into potential treatment with antioxidants.

**************************************************


I think diet plays a large role for many VAFers and more to the point the consumption of Monosodium Glutamate. As Dr. Russell Blaylock states, "Again, it should be realized that excessive glutamate stimulation triggers a chain of events that in turn sparks the generation of large numbers of free radical species, both as nitrogen and oxygen species".

The same can be said for those who get AF through years of strenous exercise which also greatly enhances oxidative stress.

But why do some people get AF and not others? Is it the genes? If so, what can be done? I also read that Taurine is an anti-oxidant which could be another reason why it is so helpful.

Has anyone else read studies or had success by taking a lot of anti-oxidant supplements?

Hi Ben,

Atrial Fibrillation Increases Production Of Superoxide By The Left Atrium And Left Atrial Appendage: Role Of The NADPH And Xanthine Oxidases.
[www.ncbi.nlm.nih.gov]

So, it's basically a "which comes first - the chicken or the egg". I opt for the AF coming first, at least in LAF, because my inflammatory markers dropped precipitously after a successful ablation.

But I certainly think ROS play a critical role in "AF begets AF," whether lone or pathologic.

PC,

Thanks for the response. Out of curiousity, what was the % decrease in your inflammatory markers after the ablation? And how soon before the ablation and after were you tested? Do you continue to test and have you had any post ablation afib? Thanks.

Ben,

My first ablation by Prof Haissaguerre was on 7/12/05. AF recurred five days later (12 hours) and the touch-up took place on 7/19/05. Prof H was delighted to note a five second episode of AF at 6PM on the telemetry recording on the evening of that second ablation. After that second ablation my substrate obviously no longer supports AF (and I no longer support its unwelcome visits).

Date hs-CRP (mg/dL)

1/24/2003 0.083
1/27/2005 0.11
6/22/2005 0.12
8/18/2005 0.26
9/20/2005 0.07
10/3/2005 0.17 shortly after a 5 mile run
11/7/2005 0.03
3/1/2006 0.02
7/31/2006 0.16 1 hour after a run
10/25/2006 0.17 3rd day of a URI
12/5/2006 0.06
1/16/2007 0.03

I have a Holter monitor and have numerous 24 hour recordings that demonstrate no AF. Although silent episodes of short duration could occasionally occur during sleep, no episode of any duration has ever been detected by Holter or by my personal observation. However, I have noted occasional bursts of tachycardia (< 5 sec) and rare bigeminy (completely prevented by potassium supplementation), while refereeing soccer games.

I've stopped testing hs-CRP for now, but will no doubt repeat down the road.

Ben,

I take a lot of vitamin C as well as the usual Magnesium (600 mg daily), and Taurine (3 grams daily). I am happy to say that is has been almost a year and I have had no a-fib, I still get pacs on occasion but thats it. Before the diet and supplement use I was getting afib 3-4 times weekly for a couple of hours each. I still pretty much stick with a paleo diet, though I do have a cookie and a taste of bread every once in a while .

Also I should mention I still take 25 mg of atenalol daily and that was the dose I was on from the beginning.

Ken

PC,


Just to give you some background and why I think my diet along with, stress and a genetic disposition for AF is what originally set me off.

I am only 29 (had my first episode about a year ago and 2 others since then) but my dad and his mother both have AF episodes. My grandmother getting it late in life and my dad getting it around 50. So genetics does play a role.

I have eaten the Standard American Diet all of my life which of course is proccessed everything. I also stayed very active as a teenager including competitive basketball. In my 20's I stopped a lot of the activity and gained about 80lbs (of which I have now lost about 50lbs).

My first afib episdoe started about about a year after I began to consume diet coke. Months before the afib though I started to show signs of IBS. The IBS showed up very quickly after I began the diet coke. I should have taken the hint then. Anyway, the first epsisode occured in the middle of the night, after a late night of pizza, diet coke and sweets.

The second episode occured 6 months later after a late night Chinese Food meal. Exact same as my first occured in the middle of the night, very high heart rate and 24 hours to convert on my own.

After this episode I went Paleo diet (eat very little processed food and try and stay away from MSG as best as possible but that is a tricky proposition) and started Mg, Potassium and Omega 3 Fish Oil.

The 3rd episode occured again the middle of the night after a late night 2 scoop chocolate and peanut butter ice cream. I thought I would tempt the AFIB deamon, stupid choice. This time however I didnt have the really high heart rate and I converted in about 4 hours. So maybe the diet and supplements are having some sort of an effect.

Anyway, long story short, this is why I think in my case it is diet (mostly MSG) and genetics. Although the MSG doesnt trip AFIB everytime, everytime I have had AFIB it was after a meal high in MSG.

This my be a stupid question but can oxidative stress be independant of inflammation? In other words can oxidative stress elude the CRP test? Also have you changed your diet due to AFIB?

Thanks again for all the information.

Ben,

Good questions.

As far as your oxidative stress and hs-CRP question, I'd say that it is a matter of sensitivity of the test. ROS damages the cells and certain proteins are released that can be measured in the blood. Certainly the damage can be such that the amount released is below threshhold for the test. But there are many mechanisms by which cellular damage can be occur.

This problem comes up a lot wrt heart attack and the enzymes heart cells release when damaged. Damage is going on constantly even in "normals."

Although I've changed my diet a bit, I haven't gone paleo. Just more fruits and vegetables and more attention to fluid intake.

Genetics is definitely operative in LAF/AF. I'm working on a new view of LAF that might interest you. Perhaps we can get a discussion going in the CR.

Might I ask your birth weight?

Thanks much

With respect to antioxidants and a-fib, I have had success increasing antioxidants. I take as much vitamin C as I can tolerate and about 1200 mg of full spectrum E. Whenever I have a-fib, I will take another 500-1000mg of vitamin C and another 1200mg of E. It seems to have caused my a-fib events to become very much shorter, rarely lasting over 2 hours now and the number of events has declined.

Tish

PC,

My birth weight was around 7.5 lbs. I was a week or two premature though.

I read some very interesting CR topics from a few years ago (CR 4,5) in which you and Fran mostly discussed GABA and Glutamate.

As for Genetics and Glutamate. Dr. Blaylock said something to the effect of, exictotoxins arent an allergy. It isnt as if some people are allergic and some people arent. It acts on everyone but it may not rear its head till later in life after the damage is done, say Alzheimers. I guess it finds the chink in the genetic armour and possibly that chink happens to be heart rhythm for most LAFers. Also one of the main areas Glutamate attacks due to its lack of blood brain barrier is the hypothalamus, which controls the ANS.

It is such a complex topic it is hard for me to wrap my head around. Especially considering I am a civil engineer by trade and have little understanding of anatomy.

Tish,

I'm try and get most of my Vit. C from natural sources (OJ, fruits, veggies). But I think I will take a little extra next time AFIB comes to visit. I'm guessing it can't do anything but help, especially to keep the oxidative stress at a minimum during an attack.

Toni,

I believe glucose is the energy substrate of choice for the heart.

Ben,

If you're worried about oxidative stress, make sure you supplement with Vit C, A, and E, Mg and glutathione (or better yet NAC = N-acetyl cysteine).

My personal viewpoint on glutamate and LAF is that it works its effect through its neurotransmitter substance properties either directly or via cross stimulation of adjacent nerve fibers. This is not to say that it is not damaging as an excitotoxin. The latter has been definitively proven. Incidentally Mg++ is an MNMDA receptor antagonist. NMDA receptors are the site of action of excitotoxins.

As stated, the hypothalamus does not have a blood brain barrier (BB, but glutamate can cross the BBB during certain conditions, e.g., hypoglycemia.

PC:

Here is my problem: I can't take regularly: vitamin C, A or E due to hemochromatosis, osteopenia and due to taking blood thinners respectively.

What does someone like me do? I try to get my anti-oxidents from fruit and veggies. I am allowed up to 500mg of vitamin C from whole foods.

Isabelle

Hi Isabelle,

About all I know wrt supplements and hemochromatosis is that Vit C can exacerbate the problem.

Sorry I can't be of more assistance.

PC